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Volume 2 EIA: JACOS Hangingstone Expansion Project Appendix 19A: Human Health and Ecological Risk Assessment – Technical Report April 2010

APPENDIX 19A Human Health and Ecological Risk

Assessment – Technical Report


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Executive Summary

JACOS currently operates a Steam Assisted Gravity Drainage (SAGD) demonstration project in the Hangingstone area approximately 50 kilometres southwest of Fort McMurray, Alberta in Township 84, Range 11 W4M. The demonstration project is in its tenth year of operation of a project 20 – 25 year lifespan. The facility started producing bitumen in July 1999 and production has increased to its current level of 8000 barrels per day. The licensed maximum capacity is 11 000 barrels per day.

An Environmental Impact Assessment (EIA) has been prepared for the Expansion Project under the Alberta Environmental Protection and Enhancement Act (EPEA) and in accordance with the JACOS SAGD Project Public Disclosure Document and Final Terms of Reference. A requirement of the EPEA is that environmental effects that Expansion Project-related changes in the environment may have on human and ecological health be considered in the EIA. Through many years of study and research, government agencies and scientists around the world have developed a process to understand the movement of chemicals in the environment and to assess whether or not exposure to these chemicals by people and wildlife may be linked with potential environmental effects on health. This process is called human health and ecological risk assessment (HHERA). To address the requirements of the EPEA, as well as concerns of stakeholders and the general public regarding the environmental effects of Expansion Project-related chemical emissions, an HHERA was conducted for the Expansion Project.

RISK ASSESSMENT FRAMEWORK

The purpose of the HHERA technical study was to evaluate the potential for adverse health outcomes from both short-term (acute) exposures and long-term (chronic) exposures resulting from Expansion Project-related activities, because even with the use of pollution control technologies and best management practices, Expansion Project-related activities will result in the release of chemicals into the environment. The HHERA consists of two main components: the HHRA is an assessment of the potential toxicological risks of the Expansion Project on human receptors and the ERA is an assessment of the potential ecotoxicological risks of the Expansion Project on ecological receptors.

All chemicals (from anthropogenic and natural sources) have the potential to cause environmental effects. However, the level of environmental effect (i.e., risk) depends on the receptor (i.e., person or wildlife) being exposed, the route of exposure (e.g., soil ingestion), and the hazard (i.e., inherent toxicity) of the chemical. As illustrated in the diagram to the right, if all three components are present (i.e., where the three circles intersect), the possibility of a risk exists. If one or more of these three components is missing, then there would be no potential for risk. For example, a receptor could be exposed to a chemical, but if that chemical is essentially hazardless (low toxicity) and present at only very low levels, then no unacceptable risk would be expected. Alternatively, an extremely hazardous chemical may be present, but if there is no route of exposure, then that receptor is not at risk for contact with the chemical.

Receptor

Exposure HazardRisk

Volume 2 EIA: JACOS Hangingstone Expansion Project

Appendix 19A: Human Health and Ecological Risk Assessment – Technical Report April 2010

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The current HHERA was conducted according to widely accepted risk assessment methodologies and guidance published and endorsed by regulatory agencies, including Alberta Environment, Canadian Council of Ministers of the Environment, Environment Canada, Health Canada, and the United States Environmental Protection Agency. The risk assessment framework used in the HHERA technical study followed the standard paradigm that progressed from a qualitative initial Problem Formulation step, through Exposure and Toxicity Assessment, and concluded with a quantitative Risk Characterization. Following this, a discussion of the uncertainties inherent to ERA, and conclusions and recommendations stemming from the assessment are discussed.

ASSESSMENT CASES, SPATIAL BOUNDARIES AND RECEPTOR LOCATIONS

Air dispersion modelling was used to estimate Expansion Project-related emissions to the atmosphere for three distinct assessment cases. Each assessment case is intended to represent the contribution of chemicals of potential concerns (divided into two categories; criteria air contaminants (CAC) and non-criteria air contaminants (non-CAC)) to ambient air from operational conditions or ones that may be reasonably expected in the future. The three cases used in this HHERA are

• Baseline Case - Includes industrial facilities that are currently operating and those that have regulatory approval and not yet operating, as well as non industry sources such as communities and traffic

• Application Case - Includes emissions from existing and approved regional sources (i.e. Baseline Case) in combination with Expansion Project emissions

• Planned Development Case - Includes emissions from the Application Case in combination with emissions from publicly disclosed future planned facilities. For the purpose of this assessment, the publically disclosed facilities only include those facilities for which a regulatory application has been submitted.

An additional scenario was considered as part of the assessment. A “Project” scenario was included to allow identification of potential project effects for the Expansion Project only.

The study area for the HHERA was established to evaluate the potential for emissions to result in changes to the quality of the environmental media. The HHERA was conducted at specific locations within the Local and Regional Study Areas for specific human and ecological receptors. The Expansion Project area falls within the central mixedwood sub region of the boreal forest natural region, and is characterized by low, rolling lands with a wide diversity of soils, deciduous and coniferous forests, and small lakes and wetlands. Receptor locations were selected based on incorporated land use, preliminary air modelling results, and input from consultation and included:

• The City of Fort McMurray - The City of Fort McMurray (pop. 100 000) is located approximately 50 km to the north of the Expansion Project

• The community of Anzac - The community of Anzac (pop. 550) is located approximately 40 km to the east of the Expansion Project, along the eastern shore of Gregoire Lake

• Clearwater Indian Reserve - The Clearwater Indian Reserve 175 is located approximately 25 km to the east of Fort McMurray and 50 km to the northeast of the Expansion Project


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• Gregoire Lake Indian Reserve - The Gregoire Lake Indian Reserve is located on the southern shore of Gregoire Lake (also known as Willow Lake), immediately to the west of Anzac and approximately 40 km to the east of the Expansion Project

• Janvier Indian Reserve - Located 75 km southeast of the Expansion Project, along a roadway

• Gregoire Lake Provincial Park Campground - Located in Gregoire Lake Provincial Park, along the western shore of Gregoire Lake, immediately to the north of the Gregoire Lake Indian Reserve

• Trapper Cabins – Five trapper cabins are located within 3 km of the Expansion Project, one of which is located within the lease area

• Stony Mountain Wildland Provincial Park - This park is located approximately 25 km to the east of the Expansion Project

• Grand Rapids Wildland Park - This park is located 35 km northwest of the Expansion Project, along the Athabasca River

• The central processing facility of the Expansion Project (i.e., where the maximum predicted air concentrations at the fenceline of the Expansion Project is expected)

RECEPTORS EVALUATED IN THE HHERA

Five distinct groups of people were assessed in the HHRA, including:

• Resident: local residents and recreational users who live in the LSA, and enjoy recreational activities within the LSA

• Hunter: local residents who are hunt and eat local wild game, all from within the LSA

• Camper: visitors who camp at the local campgrounds

• Aboriginal Resident: First Nations or Aboriginal resident in the LSA who rely exclusively on local wild game for their meat/poultry from the LSA and obtain traditional foods from the LSA

• AENV/AHW AR: although the Aboriginal receptor represents the best available, current research regarding the current practices of First Nations and Aboriginal groups within Alberta, at the request of AENV, consideration was given for a potential, future scenario in which Aboriginal residents would also rely exclusively on fruit and produce from the LSA for their fruit and vegetable consumption needs. In the text of this Appendix the Aboriginal resident refers to Aboriginal, Métis and First Nations people who live in the study area and who use the area for hunting, fishing, harvesting, trapping and gathering.

In the technical appendices which detail the results of the model the Aboriginal receptor is referred to the First Nations receptor.



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With the large number of wildlife species present in and around the LSA, it is neither practical nor necessary to conduct an assessment for each individual species. Rather, after reviewing the known species inventories of the LSA a carefully selected, representative subset of receptors was selected as the basis for the ERA:

• Canada lynx (Lynx canadensis)

• masked shrew (Sorex cinereus)

• meadow vole (Microtus pennsylvanicus)

• snowshoe hare (Lepus americanus)

• woodland caribou (Rangifer tarandus) (Species at Risk in Alberta)

• American robin (Turdus migratorius)

• red-tailed hawk (Buteo jamaicensis)

• short-eared owl (Asio flammeus) (Species at Risk in Alberta)

• spruce grouse (Falcipennis canadensis)

• terrestrial plants and invertebrates

CHEMICALS OF POTENTIAL CONCERN

Identification of chemicals of potential concern (COPC) for a project that has yet to be constructed involves the review of several sources of information to develop an expected atmospheric emissions inventory for the Expansion Project. Human and ecological receptors will not only be exposed to COPC in air, but also to those COPC that deposit on to the ground. As such, this initial chemical inventory underwent subsequent screening following nationally and internationally accepted criteria for the categorization of persistent and bio-accumulative chemicals. Briefly, chemicals having a soil half-life greater than or equal to 182 days (6 months) and/or a log octanol-water partition coefficient (log Kow) greater than or equal to five were considered persistent, and carried forward as COPC for evaluation in the HHERA. Those COPC expected to persist and bioaccumulate were evaluated in the HHERA through a multi-media risk assessment (i.e., exposure to COPC is from oral/dermal routes). COPC assessed in the HHERA, along with the pathways evaluated are listed in Table 1.


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Table 1 Chemicals of Potential Concern Evaluated in the Human and Ecological Health Assessment

COPC Pathways Evaluated

Inhalation (Air) Oral/Dermal (Multi-media) Criteria Air Contaminants (CAC) Sulphur Dioxide (SO2)

Nitrogen Dioxide (NO2)

PM2.5

Carbon Monoxide (CO) Petroleum Hydrocarbons Benzene

Toluene

Ethylbenzene

Xylenes

Aliphatic C5-C8

Aliphatic C9-C16

Aromatic C9-C16

Aromatic C17-C34

PAHs Anthracene

Benz(a)anthracene

Benzo(a)pyrene (BaP)

Benzo(e)pyrene

Benzo(b)fluoranthene

Benzo(g,h,i)perylene

Benzo(k)fluoranthene

Chrysene

Dibenzo(a,h)anthracene

Fluorene

Fluoranthene

Indeno(1,2,3-cd)pyrene

Naphthalene

Phenanthrene

Pyrene

Perylene

VOCs Acetaldehyde

Acrolein

Benzaldehyde

Carbon disulfide



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Table 1 Chemicals of Potential Concern Evaluated in the Human and Ecological Health Assessment (cont’d)

COPC Pathways Evaluated

Inhalation (Air) Oral/Dermal (Multi-media) VOCs (cont’d) Dichlorobenzene

Formaldehyde

Hexane

Hydrogen sulfide

Thiophene Metals Aluminum (Al)

Chromium (Total)

Cobalt (Co)

Copper (Cu)

Lead (Pb)

Manganese (Mn)

Molybdenum (Mo)

Nickel (Ni)

Strontium (Sr)

Vanadium (V)

Zinc (Zn)

METHODS OF RISK EVALUATION

Two chemical hazard categories are commonly recognized by regulatory agencies depending on the COPC’s mode of toxic action: the threshold approach typically used to evaluate non-carcinogens, and the non-threshold approach typically used for carcinogenic compounds. These toxicity estimates are generally referred to as toxicity reference values (TRVs) for both human and ecological receptors and must be exceeded for toxicity to occur.

The assessment of health risks from non-carcinogenic COPC was expressed as a Concentration Ratio (CR) or as a Hazard Quotient (HQ). The incremental lifetime cancer risk (ILCR) was used to evaluate the probability or likelihood of a population, exposed over a lifetime to carcinogenic emissions from the Expansion Project itself, to develop cancer. ILCR values are calculated by multiplying the predicted exposure concentration (via inhalation) or dose (via multiple pathways) by the unit risk factor or cancer slope factor, respectively. The unit risk factors and the cancer slope factors are provided by regulatory agencies and reflect the potential of a given chemical to cause cancer.

Concentration ratios were used to evaluate the health risks from short-term and long-term exposure to chemicals in air. Concentration ratios were calculated by dividing the predicted ground-level air concentration (1-hour, 24-hour, or annual average) by the appropriate TRV. For assessment of non-carcinogenic health risks due to short- and long-term direct inhalation of COPC by people, a benchmark


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of 1.0 was used for comparison of calculated CR. In general, the risks associated with direct inhalation are distinct from those associated with oral and dermal exposures and are therefore assessed separately.

For chemicals that persist in the environment, multi-media HQ were calculated. This approach is used where the exposure to the chemicals occurs through multiple pathways, and shows the additional risks related to the oral and dermal exposure pathways. HQ values for multi-media are calculated by dividing the predicted exposure dose (via multiple pathways) by the appropriate toxicity reference value (i.e., TRV: reference dose, as provided by regulatory agencies).

The incremental lifetime cancer risk (ILCR) was used to evaluate the probability or likelihood of a population, exposed over a lifetime to carcinogenic emissions from the Expansion Project itself, to develop cancer. ILCR values are calculated by multiplying the predicted exposure concentration (via inhalation) or dose (via multiple pathways) by the unit risk factor or cancer slope factor, respectively. The unit risk factors and the cancer slope factors are provided by regulatory agencies and reflect the potential of a given chemical to cause cancer.

HQ values were also used to evaluate health risks to ecological receptors. However, for the assessment of potential risk to community-based receptors (e.g., soil invertebrates, terrestrial plants), the HQ was calculated by dividing the toxicological benchmark by the chemical concentration in an associated environmental, rather than by a daily dose.

CR and HQ less than or equal to 1.0 indicates that the exposure concentration is less than or meets the threshold of toxicity for the COPC being evaluated (but does not exceed it), and given the conservative approach to the estimation of exposure and selection of TRVs, adverse environmental effects are not expected. On the other hand, an HQ of greater than 1.0 does not necessarily indicate an unacceptable level of risk. Health Canada and Alberta Environment consider an ILCR of less than or equal to 1-in-100 000 as the de minimus (essentially negligible) risk level that is protective of public health.

RESULTS OF THE HHRA

Project Alone Scenario: The health risks estimates associated with acute and chronic exposures to Expansion Project-related emissions via inhalation and oral and dermal contact were less than the applicable benchmark for each of the COPC, with the exception of the 1-hour maximum concentration of SO2 and the maximum 24-hour concentration of hydrogen sulphide at the fenceline of the Central Processing Facility. Even then, 99.9% of the time the concentrations of SO2 and hydrogen sulphide in air near the fenceline meet the benchmarks, and the nature of the health effects (respiratory and nasal irritation) are reversible. As noted previously, the Expansion Project is located in a relatively remote area; human receptors would not likely be found at this location of any appreciable length of time. Based on these results, the likelihood that a person would be exposed to Expansion Project-related concentrations that are greater than the benchmarks is very low.

Baseline Case, Application Case, Planned Development Case: The cumulative health risks estimates associated with acute and chronic exposures to emissions of COPC via inhalation and oral and dermal contact were less than the applicable benchmark for each of the COPC, with a few exceptions. Elevated 24-hour exposures to PM2.5 and hydrogen sulphide, and annual average exposures to acrolein are



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generally limited to the cities of Fort McMurray and Fort McKay, each of which are located at least 50 km from the Expansion Project. The assessment demonstrated that the contribution of the Expansion Project to these elevated concentrations was negligible.

The CR values based on the maximum 24-hour concentrations of acrolein are higher than 1.0 throughout much of the LSA; however, the assessment indicates that the contributions of the Expansion Project to acrolein concentrations are negligible. The lowest concentration at which mild eye irritation has been observed in humans (i.e., 140 µg/m3) is more than 100-times higher than the maximum modelled 24-hour air concentration of acrolein at the receptor locations and as such, it is unlikely that the concentrations of acrolein would result in a substantive health risk.

The health risks associated with each of the metals (chromium, cobalt, lead, manganese, and zinc) did not change from the Baseline Case to Application Case to Planned Development Case, indicating that contributions from the Expansion Project and other planned projects are negligible. As indicated previously, given the conservatism in the exposure assessment associated with food concentrations, ingestion rates, and bioavailability, and that the HQ values are generally low, it is unlikely that multi-media exposures to these metals would result unacceptable levels of human risk.

RESULTS OF THE ERA

Project Alone Scenario: The HQ estimates associated with exposures of receptors to Expansion Project-related emissions via were less than the applicable benchmark of 1.0 for each of the COPC. Therefore, with the proposed mitigation, the Expansion Project-related environmental effects for a Change in Ecological Health are predicted to be not significant.

Baseline Case, Application Case, Planned Development Case:

Hazard Quotients for all mammalian and avian receptors (including the identified SAR) exposed to COPC were less than 1.0 under these scenarios, and therefore no unacceptable risks were predicted from exposure to environmental concentrations of COPC. For community-based receptors (i.e., terrestrial plants and soil invertebrates), an HQ greater than 1.0 was estimated as a result of exposure to manganese; no potential risk was predicted under the Project Alone scenario and estimated COPC contributions from the proposed JACOS facility expansion were deemed to be negligible compared to background concentrations. Risk estimated for community-based receptor is solely the result of existing background soil concentrations in the LSA, which, following the conservative methodology employed in this ERA are biased high. In reality, background soil concentrations within the LSA are not expected to differ from other rural areas in Alberta or result in risk to vegetation or invertebrate communities, a conclusion that is supported by the evidence of healthy and diverse vegetation communities observed within the LSA.


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Table of Contents

APPENDIX 19A HUMAN HEALTH AND ECOLOGICAL RISK ASSESSMENT – TECHNICAL REPORT

19A.1 INTRODUCTION .......................................................................................................................19A-1 19A.1.1 The Environmental Impact Assessment Process .....................................................19A-1 19A.1.2 Regulatory Guidance for HHERA .............................................................................19A-2 19A.1.3 Purpose of the HHERA Report .................................................................................19A-2 19A.1.4 Risk Assessment Framework ...................................................................................19A-3

19A.2 STUDY AREA, RECEPTOR LOCATIONS, RECEPTORS .......................................................19A-8 19A.2.1 Study Areas ..............................................................................................................19A-8 19A.2.2 Receptor Locations ................................................................................................ 19A-11 19A.2.3 Receptors ............................................................................................................... 19A-13

19A.3 CHEMICALS OF POTENTIAL CONCERN AND ASSESSMENT SCENARIOS ................... 19A-15 19A.3.1 Identification of Chemical Emission Sources ......................................................... 19A-15 19A.3.2 Screening of COPC by Pathway............................................................................ 19A-17 19A.3.3 Assessment Scenarios .......................................................................................... 19A-22

19A.4 BASELINE CONDITIONS ...................................................................................................... 19A-25 19A.4.1 Baseline Sampling Program .................................................................................. 19A-25 19A.4.2 Baseline Human Health Status .............................................................................. 19A-26 19A.4.3 Species at Risk ...................................................................................................... 19A-28

19A.5 FATE AND TRANSPORT MODELLING ................................................................................ 19A-29 19A.5.1 Ambient Air Exposure Point Concentrations ......................................................... 19A-29 19A.5.2 Surface Water and Fish Exposure Concentrations ............................................... 19A-30 19A.5.3 Soil Exposure Point Concentrations ...................................................................... 19A-30 19A.5.4 Vegetation .............................................................................................................. 19A-33 19A.5.5 Country Foods (Hunting) ....................................................................................... 19A-37 19A.5.6 Breast Milk ............................................................................................................. 19A-38 19A.5.7 Other Media Associated with Ecological Receptors .............................................. 19A-38

19A.6 HUMAN HEALTH RISK ASSESSMENT ................................................................................ 19A-39 19A.6.1 Problem Formulation ............................................................................................. 19A-39 19A.6.2 Exposure Assessment ........................................................................................... 19A-42 19A.6.3 Toxicity Assessment .............................................................................................. 19A-48 19A.6.4 Risk Characterization ............................................................................................. 19A-62 19A.6.5 Uncertainty Analysis .............................................................................................. 19A-98 19A.6.6 Human Health Conclusions ................................................................................. 19A-101

19A.7 ECOLOGICAL RISK ASSESSMENT ................................................................................... 19A-103 19A.7.1 Ecological Risk Assessment Framework ............................................................. 19A-103 19A.7.2 Problem Formulation ........................................................................................... 19A-104 19A.7.3 Exposure Assessment ......................................................................................... 19A-116 19A.7.4 Toxicity Assessment ............................................................................................ 19A-118 19A.7.5 Risk Characterization ........................................................................................... 19A-123 19A.7.6 ERA Uncertainty Analysis .................................................................................... 19A-147 19A.7.7 ERA Conclusions ................................................................................................. 19A-150

19A.8 FOLLOW-UP WORK AND MONITORING .......................................................................... 19A-151 19A.9 REFERENCES ..................................................................................................................... 19A-152

19A.9.1 Literature Cited .................................................................................................... 19A-152 19A.9.2 Internet Sites ........................................................................................................ 19A-154



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APPENDIX 19A-1 COPC SCREENING

APPENDIX 19A-2 PREDICTIVE ASSESSMENT METHODS

APPENDIX 19A-3 MODEL PHYSICAL CHEMICAL DATA

APPENDIX 19A-4 EXPOSURE POINT CONCENTRATIONS

APPENDIX 19A-5 HUMAN RECEPTOR CHARACTERISTICS AND HUMAN HEALTH EXPOSURE CALCULATIONS

APPENDIX 19A-6 TOXICOLOGICAL PROFILES FOR HUMAN HEALTH

APPENDIX 19A-7 HUMAN HEALTH RISK ASSESSMENT RESULTS

APPENDIX 19A-8 PARAMETERS FOR KEY INDICATOR RESOURCES

APPENDIX 19A-9 TOXICOLOGICAL REFERENCE VALUES (ECOLOGICAL HEALTH)

APPENDIX 19A-10 BIOLOGICAL UPTAKE FACTORS

APPENDIX 19A-11 ERA EXPOSURE POINT CONCENTRATIONS

APPENDIX 19A-12 ERA HAZARD QUOTIENTS

APPENDIX 19A-13 HQ DERIVATION: WORKED EXAMPLE

List of Tables

Table 2-1 Human and Ecological Receptor Locations .............................................................. 19A-11 Table 3-1 Chemicals of Potential Concern Evaluated in the Human and Ecological Health

Assessment ............................................................................................................... 19A-19 Table 3-2 Human and Ecological Receptor Locations and Type of HHERA Conducted.......... 19A-21 Table 3-3 Summary of Phases and Cases Assessed in the HHERA ....................................... 19A-23 Table 4-1 Health Statistics Comparison historical Region 7 (Northern Lights) and the

Province of Alberta .................................................................................................... 19A-26 Table 5-1 Measured Background Inorganic COPC concentrations in Soil and Predicted Soil

Loading for each Case .............................................................................................. 19A-32 Table 5-2 Predicted Aboveground Traditional Plants Loading over a 30 year period in the

LSA ........................................................................................................................... 19A-35 Table 5-3 Predicted Belowground Traditional Plants Loading over a 30 year period in the

LSA ........................................................................................................................... 19A-36 Table 6-1 General Receptor Characteristics ............................................................................. 19A-44 Table 6-2 Summary of Wein (1989) 24-hour Recall Data ......................................................... 19A-45 Table 6-3 Summary of Leaf and Root Consumption Data ........................................................ 19A-45 Table 6-4 Consumption/use quantities used in the assessment ............................................... 19A-46 Table 6-5 Food Ingestion Rates for the Aboriginal and AENV/AHW AR Toddler Receptor

(g/day) ....................................................................................................................... 19A-46 Table 6-6 Food Ingestion Rates for the Aboriginal and AENV/AHW AR Adult Receptor

(g/day) ....................................................................................................................... 19A-47 Table 6-6 Acute Exposure Limits for COPC (μg/m3) – 1-hour Exposures ................................ 19A-50


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Table 6-7 Acute Exposure Limits for COPC (μg/m3) – 24-hour Exposures .............................. 19A-52 Table 6-8 Chronic Non-carcinogenic Exposure Limits (μg/m3) ................................................. 19A-54 Table 6-9 Chronic Carcinogenic Exposure Limits (μg/m3)-1 ...................................................... 19A-56 Table 6-10 Chronic Non-carcinogenic Exposure Limits (μg/kg-day) .......................................... 19A-57 Table 6-11 Chronic Carcinogenic Exposure Limits (μg/kg-day)-1 ............................................... 19A-58 Table 6-12 Relative Dermal Bioavailability Factors..................................................................... 19A-59 Table 6-13 Toxic Equivalence Factors ........................................................................................ 19A-60 Table 6-14 Odour-Based Guidelines ........................................................................................... 19A-61 Table 6-15 Concentration Ratios for 1-hour Exposures .............................................................. 19A-68 Table 6-16 Concentration Ratios for 24-hour Exposures ............................................................ 19A-71 Table 6-17 Observed Responses in Humans to Short-Term Exposure to Acrolein ................... 19A-75 Table 6-18 Concentration Ratios for Annual Average Exposures .............................................. 19A-77 Table 6-19 Incremental Lifetime Cancer Risks (ILCRs) via Inhalation ....................................... 19A-81 Table 6-20 Non-Carcinogenic Human Health Risks from Exposure to Multi-Media – Resident . 19A-83 Table 6-21 Non-Carcinogenic Human Health Risks from Exposure to Multi-Media – Hunter .... 19A-84 Table 6-22 Non-Carcinogenic Human Health Risks from Exposure to Multi-Media – Camper .. 19A-85 Table 6-23 Non-Carcinogenic Human Health Risks from Exposure to Multi-Media –

Aboriginal Resident ................................................................................................... 19A-86 Table 6-24 Non-Carcinogenic Human Health Risks from Exposure to Multi-Media –

AENV/AHW AR ......................................................................................................... 19A-87 Table 6-25 Carcinogenic Human Health Risks from Exposure to Multi-Media ........................... 19A-95 Table 6-26 Concentration Ratios for Odour Exposures .............................................................. 19A-97 Table 7-1 COPC Included for Assessment in the ERA ........................................................... 19A-105 Table 7-2 Key Indicator Resource Locations .......................................................................... 19A-106 Table 7-3 Rationale for Inclusion/Exclusion of Species at Risk from ERA ............................. 19A-112 Table 7-4 Rationale for Exposure Pathways Evaluated for Avian and Mammalian

Receptors ................................................................................................................ 19A-114 Table 7-5 Summary of Maximum Hazard Quotients for Community-Based Receptors for

the Baseline Case Assessment .............................................................................. 19A-125 Table 7-6 Summary of Maximum Hazard Quotients for Avian Receptors for the Baseline

Case Assessment ................................................................................................... 19A-127 Table 7-7 Summary of Maximum Hazard Quotients for Mammalian receptors for the

Baseline Case Assessment .................................................................................... 19A-128 Table 7-8 Summary of Maximum Hazard Quotients for Community-Based Receptors for

the Project Alone Scenario Assessment ................................................................. 19A-129 Table 7-9 Summary of Maximum Hazard Quotients for Avian Receptors for the Project

Alone Scenario Assessment ................................................................................... 19A-131 Table 7-10 Summary of Maximum Hazard Quotients for Mammalian Receptors for the

Project Alone Scenario Assessment ....................................................................... 19A-133 Table 7-11 Summary of Maximum Hazard Quotients for Community-Based Receptors for

the Application Case Assessment .......................................................................... 19A-134 Table 7-12 Summary of Maximum Hazard Quotients for Avian Receptors for the

Application Case Assessment ................................................................................ 19A-136 Table 7-13 Summary of Maximum Hazard Quotients for Mammalian Receptors for the

Application Case Assessment ................................................................................ 19A-137 Table 7-14 Summary of Maximum Hazard Quotients for Community-Based Receptors for

the Planned Development Case Assessment ........................................................ 19A-138 Table 7-15 Summary of Maximum Hazard Quotients for Avian Receptors for the Planned

Development Case Assessment ............................................................................. 19A-140 Table 7-16 Summary of Maximum Hazard Quotients for Mammalian Receptors for the

Planned Development Case Assessment............................................................... 19A-141 Table 7-17 Summary of Maximum Hazard Quotients for Species at Risk Surrogates for the

Baseline Case Assessment .................................................................................... 19A-143



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Table 7-18 Summary of Maximum Hazard Quotients for Species at Risk Surrogates for the Project Alone Scenario Assessment ....................................................................... 19A-144

Table 7-19 Summary of Maximum Hazard Quotients for Species at Risk Surrogates for the Application Case Assessment ................................................................................ 19A-145

Table 7-20 Summary of Maximum Hazard Quotients for Species at Risk Surrogates for the Planned Development Case Assessment............................................................... 19A-146

List of Figures

Figure 1-1 Human Health and Ecological Risk Assessment Framework ......................................19A-4 Figure 2-1 Local Study Area ..........................................................................................................19A-9 Figure 2-2 Regional Study Area ................................................................................................. 19A-10 Figure 5-1 Modelling Soil Concentrations .................................................................................. 19A-30 Figure 5-2 Modelling Backyard Garden / Farm Produce ............................................................ 19A-33 Figure 5.3 Modelling Wild Game ................................................................................................ 19A-37 Figure 6-1 Relevant Pathway Breakdown for Oral/Dermal Exposures to Chromium –

AENV/AHW AR Toddler Receptor ............................................................................ 19A-88 Figure 6-2 Relevant Pathway Breakdown for Oral/Dermal Exposures to Cobalt –

AENV/AHW AR Toddler Receptor ............................................................................ 19A-90 Figure 6-3 Relevant Pathway Breakdown for Oral/Dermal Exposures to Lead – AENV/AHW

AR Toddler Receptor ................................................................................................ 19A-91 Figure 6-4 Relevant Pathway Breakdown for Oral/Dermal Exposures to Manganese –

AENV/AHW AR Toddler Receptor ............................................................................ 19A-93 Figure 6-5 Relevant Pathway Breakdown for Oral/Dermal Exposures to Zinc – AENV/AHW

AR Toddler Receptor ................................................................................................ 19A-94 Figure 7-1 Conceptual Site Model for ERA .............................................................................. 19A-115 Figure 7-2 Tiered Approach for the Application of Uncertainty Factors in ERA ....................... 19A-120


19A-1

19A.1 Introduction

Japan Canada Oil Sands Limited (JACOS) currently operates a Steam Assisted Gravity Drainage (SAGD) demonstration project (the Demonstration Project) at Legal Site Description 34/27/26-84-11-W4M, approximately 50 km south-southwest of Fort McMurray, Alberta. The Demonstration Project was previously approved to produce up to 11 000 barrels per day of bitumen and currently produces 8000 barrels per day. The JACOS Hangingstone Expansion Project (the Expansion Project, the Project subject to this EIA and Application) involves the expansion of this facility by up to 35 000 barrels per day of bitumen. The Expansion Project will require additional facilities, including new wellpads, seven steam boilers, two medium heaters, electrical generators, storage tanks, a high pressure flare, and a low pressure flare.

This Human Health and Ecological Risk Assessment (HHERA) technical study report (the Report) has been prepared by Stantec and describes the results of the human health and ecological risk assessment, which makes up one of several studies conducted as part of the overall Environmental Impact Assessment (EIA) process.

19A.1.1 The Environmental Impact Assessment Process

The purpose of conducting an EIA is to explain the potential environmental and socio-economic impacts of the construction, operation, and decommissioning of the Expansion Project. The EIA will examine alternatives, establish the environmental baseline conditions in the area, assess potential local and regional effects of the project, evaluate cumulative effects and provide monitoring and management plans to mitigate any identified potential adverse effects.

The approved terms of reference (ToR) sets out the overall framework for carrying out the EIA including the methodology, scope, assessment areas, evaluations and assessments of “alternatives to” and “alternative methods”, as well as the periods (construction, operation, and decommissioning) to be considered and assessed.

The EIA process has been prepared and conducted in accordance with the Alberta Environmental Protection and Enhancement Act (EPEA), and in accordance with the Japan Canada Oil Sands Hangingstone SAGD Project Public Disclosure Document (May 7th, 2008) and Final ToR (February 2, 2009). A requirement of the latter document is an assessment of the potential health effects to humans and wildlife, including cumulative health effects, as a result of changes to the quality of environmental media (e.g., air, soil, water, vegetation) as a result of Expansion Project-related activities. Section 3.8 and Section 6 of the Final ToR stipulate that health effects to humans and wildlife from both acute and chronic exposures be included in the environmental assessment.

An HHERA is the most appropriate mechanism to assess the potential environmental effects on the health of people and wildlife. Any chemical, from the least toxic to the most toxic, to which humans and ecological receptors can be exposed has the potential to cause environmental effects: it is the concentration, duration of exposure, and route by which receptors come into contact with a particular chemical that determines if it may cause harm to their health.



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19A.1.2 Regulatory Guidance for HHERA

Neither federal nor provincial regulatory authorities have published guidance for conducting a facility emission risk assessment in support of an EIA such as that required for the Expansion Project. Rather, Canadian risk assessment guidance and regulatory benchmarks for assessing contaminated sites were supplemented by methodologies developed by the United States Environmental Protection Agency (US EPA) or other agencies for the HHERA conducted for the Expansion Project. This methodology is consistent with previously submitted HHERAs conducted in support of EIA studies for facility emissions projects in Ontario and Alberta and reviewed/accepted by Health Canada.

The final protocols were adopted from published guidance, including:

• Federal Contaminated Sites Risk Assessment in Canada, Part I: Guidance on Human Health Risk Preliminary Quantitative Risk Assessment (PQRA), Version 2.0 (Health Canada 2004)

• A Framework for Ecological Risk Assessment – Canadian Council of Ministers of the Environment (CCME 1996)

• U.S. EPA. Human Health Risk Assessment Protocol for Hazardous Waste Combustion Facilities (US EPA 2005)

Environmental quality guidelines for chemical concentrations in soil and air were also used in the assessment, including:

• Alberta Air Quality Objectives (AAQO) (AENV 2009)

• Alberta Environment Tier 1 Soil and Groundwater Remediation Guidelines (AENV 2009)

• National Ambient Air Quality Objectives (NAAQO) (CCME 1999)

• Canada-wide Standard for Respirable Particulate Matter (PM2.5) (CCME 2000)

• Canadian Environmental Quality Guidelines (CCME 2009)

19A.1.3 Purpose of the HHERA Report

The purpose of the HHERA technical study was to evaluate the potential for adverse health outcomes from both short-term (acute) exposures and long-term (chronic) exposures resulting from Expansion Project-related activities in the study area. In addition, the HHERA was conducted to assess the potential cumulative effects of the Expansion Project in combination with other existing, approved and proposed projects in the area over the lifetime of the Expansion Project.

The potential health and ecological risks of Expansion Project-related emissions during the various phases of the Expansion Project were considered in the HHERA. This report focuses on the quantification of potential risk of adverse environmental effects, including cumulative environmental effects, from exposure to airborne chemical emissions from the Expansion Project. It includes the evaluation of direct inhalation of chemicals in air and the exposure of humans and ecological receptors to those chemicals that deposit into the environment and are taken up into other environmental media such as soil, plants, and game.


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Findings of other technical studies were incorporated in the HHERA to ensure that the assessment is an accurate reflection of the literature reviews and data gathering completed for the EIA. The HHERA relies on predictions of the anticipated concentrations of chemicals released by the Expansion Project as determined by analyses conducted for other technical studies, mainly from the outputs of air quality dispersion and deposition modelling conducted to characterize the potential environmental effects to the atmospheric environment (Volume 2, Section 5: Air Quality). Data gathered and assessed to characterize hydrology, hydrogeology, surface water quality, terrain and soils, wildlife, and land and resources were used to provide needed information for the HHERA.

The human health component examines the existing human health status of the region and assesses how project emissions may affect human health, including important resources such as traditional food consumption by First Nation and Métis persons in the area. The ecological health component focuses on terrestrial and avian wildlife receptors evaluated as key indicator resources.

The HHRA component is presented in Section 19A.6 with technical supporting information in Appendix 19A-1 through 19A-7. The ERA component is presented in Section 19A.7 with technical supporting information in Appendix 19A-8 through 19A-13.

19A.1.4 Risk Assessment Framework

All chemicals (from both anthropogenic and natural sources) have the potential to cause environmental effects. However, the level of environmental effect (i.e., risk) depends on the receptor (i.e., person or wildlife) being exposed, the route and duration of exposure, and the hazard (i.e., inherent toxicity) of the chemical. As illustrated in the diagram to the right, if all three components are present (i.e., where the three circles intersect), the possibility of a risk exists. If one or more of these three components is missing, then there would be no risk. For example, a receptor could be exposed to a chemical, but if that chemical is essentially hazardless (low toxicity) and present at only very low levels, then no unacceptable risk would be expected. Alternatively, an extremely hazardous chemical may be present, but if there is no way for a receptor to be exposed (i.e., no route of exposure), then that receptor is not at risk for contact with the chemical.

The risk assessment framework used in the HHERA followed a standard paradigm that progressed from a qualitative initial Problem Formulation step, through Exposure and Toxicity Assessment, and concluded with a quantitative Risk Characterization. The HHERA framework is depicted in Figure 1-1.

Receptor

Exposure HazardRisk



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Problem FormulationAre there Project-related chemicals in the environment that could cause health effects? Who could be exposed? How would these people or wildlife come into

contact with the chemicals?

Toxicity AssessmentWhat amount of these chemicals is

linked to health effects?

Exposure AssessmentTo what degree are people and

wildlife exposed to these chemicals?

Risk CharacterizationWhen predicted exposure levels are compared to exposure limits, is a health

risk predicted? If so, how could the identified risks be reduced?

Publ

ic C

onsu

ltatio

nU

ncertainty Analysis

Figure 1-1 Human Health and Ecological Risk Assessment Framework

19A.1.4.1 Problem Formulation

The problem formulation stage is an information gathering and interpretation stage that focuses the study on the primary areas of concern for the project. Problem formulation defines the nature and scope of the risk assessment, permits practical boundaries to be placed on the overall scope of work, and ensures that the HHERA is directed at the key areas and issues of concern related to the Expansion Project emissions. The gathered data provides information regarding the physical layout and characteristics of the study area, possible exposure pathways, potential human and ecological receptors, chemicals of concern (COPC) and any other specific areas or issues of concern to be addressed.

The key tasks requiring evaluation within the problem formulation step include:

• characterization of the Expansion Project and the study area, including habitat and land use

• identification of COPC (i.e., the hazards) associated with Expansion Project-related emissions

• identification of the potentially affected environmental media

• receptor identification and characterization

• identification of exposure pathways and routes


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An important component of these tasks was the engagement of the public and stakeholder groups to inform them of the HHERA process and to ensure that the problem formulation captured their views and concerns at the outset of the HHERA. In order to enhance Aboriginal involvement and to manage any “consultation or survey/study fatigue” in the JACOS Hangingstone Expansion Project, the JACOS Project team facilitated the development of an Aboriginal Review Group (ARG) involving representatives from the Chipewyan Prairie First Nation, the Fort McMurray First Nation and the Mikasew Cree First Nation. The ongoing interaction of the project team with the ARG replaced the traditional Open House consultation and provided a valuable opportunity to work directly with members of the Aboriginal populations who then relayed and obtained information from their respective communities.

Specific information that was required as an outcome of the consultation included:

• settlement, community and land use areas

• key wildlife and unique ecological areas

• key harvesting, hunting and fishing and resources

• local consumption information

• key species of traditional vegetation

All of the information collected was used to generate data inputs for the HHERA.

19A.1.4.2 Exposure Assessment

People and ecological receptors can come into contact with chemicals in their environment in a variety of ways depending on their daily activities and land use patterns. The means by which receptors contact a chemical in an environmental medium is referred to as an exposure pathway. The means by which a chemical enters the body from the environmental medium is referred to as an exposure route. The exposure assessment incorporates information about Expansion Project-related chemical emissions, activities and land use in the area, receptor characteristics, and the exposure pathways identified during the problem formulation phase of the HHERA.

Generally, receptors (human or ecological) can be exposed to chemicals in the environment by:

• directly inhaling them

• coming into direct dermal contact with them

• ingesting them along with food

The exposure assessment predicts the rate of exposure (i.e., the quantity and rate at which a chemical is received) of the selected receptors to the COPC via the various exposure scenarios and pathways identified in the problem formulation step. The rate of exposure to chemicals from many pathways is usually expressed as the amount of chemical taken in per body weight per unit time (e.g., microgram (µg) chemical/kilogram (kg) body weight/day).



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The magnitude of the exposure of receptors to chemicals in the environment depends on the interaction of a number of variables, including the:

• concentration of chemicals in various environmental media

• physical-chemical characteristics of the COPC, which affect their environmental fate and transport and determine such factors as efficiency of absorption into the body

• influence of site-specific environmental characteristics, such as geology, soil type, topography, hydrology, hydrogeology, local meteorology, and climatology on a chemical’s behaviour within environmental media

• physiological and behavioural characteristics of the receptors (e.g., respiration rate, soils/dusts intake, time spent at various activities and in different areas)

19A.1.4.3 Toxicity Assessment

The toxicity assessment involves the selection of toxicity reference values (TRVs), also referred to as exposure limits, for COPC. Toxicity is the potential for a chemical to produce any type of damage, permanent or temporary, to the structure or functioning of any part of the receptor’s body. The toxicity of a chemical depends on the amount of chemical taken into the body (referred to as the “dose”) and the duration of exposure (i.e., the length of time the receptor is exposed to the chemical). For each COPC, there is a specific dose and duration of exposure necessary to produce a toxic environmental effect in a given receptor. This is referred to as the “dose-response relationship” of a chemical. The toxic potency of a chemical (i.e., its ability to produce any type of damage to the structure or function of any part of the body), is dependent on the inherent properties of the chemical itself (i.e., its ability to cause a biochemical or physiological response at the site of action), as well as the ability of the chemical to reach the site of action. This dose-response principle is central to the HHERA methodology.

19A.1.4.4 Risk Characterization

The risk characterization step integrates the exposure and hazard assessments to provide a conservative estimate of health risk for the receptors assessed in the various exposure scenarios. Potential risks were characterized through a comparison of the estimated or predicted exposures from all pathways (from the exposure assessment) with the identified exposure limits (from the toxicity assessment) for COPC.

If the results of the risk assessment indicate the potential for adverse health risks related to Expansion Project emissions, this may lead to the requirement for the development of site-specific, facility-specific or study area-specific risk management options and/or criteria.

Limitations and uncertainties associated with the administrative and technical boundaries of the risk assessment, in addition to conservative assumptions used in the assessment, are identified and discussed in order to provide perspective on the assessment results.


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19A.1.4.5 Uncertainty Analysis

Uncertainties are inherent in every aspect of the risk assessment process. Generally, these technical boundaries are addressed by incorporating conservative assumptions in the analysis. As a result, risk assessments tend to overstate the actual risk. Although many factors are considered in preparation of a risk analysis, analysis results are generally only sensitive to very few of these factors. The uncertainty analysis is included to demonstrate that assumptions used are conservative, or that the analysis result is not sensitive to the key assumptions.

A risk assessment containing a high degree of confidence is based on the following factors:

• conditions where the nature and scope of the risk assessment is defined with a high level of certainty based on data and physical observations

• an acceptable and reasonable level of conservatism in assumptions that will ensure that risks are overstated and an appreciation of the bounds and limitations of the HHERA conclusions

The exposure assessment performed as part of this study was based on:

• available data to describe existing media conditions (e.g., soil, surface water, terrestrial plant and sediment)

• sound conservative assumptions for certain parameters, as required

• well understood and generally accepted methods for risk prediction

Throughout the entire HHERA, the use of the term conservatism is meant to convey a preference for erring on the side of overstating, as opposed to understating, risk under conditions of uncertainty. For example, analytical values or approaches were selected that would result in an overestimation of exposure or potential risk to humans and the environment, as opposed to understating the risk. A number of specific conservative assumptions are presented in both the HHRA and ERA.

The uncertainty associated with HHRA and those associated with ERA, although similar in nature, are distinct and will be addressed in Sections 19A.6.5 and 19A.7.6, respectively. Each of these sections details how this HHERA report meets the critical factors described above.



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19A.2 Study Area, Receptor Locations, Receptors

The study area for the HHERA was established to evaluate the potential for emissions to result in changes to the quality of the environmental media (i.e., air, soil, vegetation, game). The primary means for human and ecological health to be affected by the Expansion Project is via direct and indirect changes in environmental quality due to air emissions, opposed to Project-related releases of COPC to surface water or groundwater (as discussed in Section 19A.3.1.1 to 19A.3.1.3). Therefore, the study area for the HHERA is based on the boundaries of the air quality model.

19A.2.1 Study Areas

The Expansion Project is located in the Lower Athabasca Planning Region (LAPR), which is one of the seven land-use regions in Alberta. The LAPR includes the Wood Buffalo Environmental Association (WBEA) airshed located around and to the north of Fort McMurray, and a large portion of the Lakeland Industry and Community Association (LICA) airshed located in the Cold Lake area. The Expansion Project, specifically, is located within the WBEA airshed.

In recognition of the Expansion Project location relative to the LAPR, emissions were defined and modelled for a 290 km by 700 km area as part of the air quality assessment. However, smaller areas (see Figures 2-1 and 2-2) were selected to examine the effect of the Expansion Project emissions on the quality of environmental media. These smaller areas include:

Local Study Area: The local study area (LSA) is the area within which potential Expansion Project environmental effects can be predicted with a reasonable degree of accuracy and confidence and where impacts are likely to be most concentrated. For the HHERA, the LSA focuses on a 110 km x 110 km area centered on the Expansion Project (see Figure 2-1). This smaller study area allows the air quality changes due to the Expansion Project to be examined in the context of other emission sources and nearby areas of interest. Within the LSA are the cities of Fort McMurray and Anzac, and Clearwater Indian Reserve 175, Gregoire Lake Indian Reserve 176, and Janvier Indian Reserve 194. There are also several provincial wildlife parks, campgrounds, and trapper cabins located within the LSA.

Regional Study Area: The RSA (see Figure 2-2) consists of an area that is beyond the limits of the LSA that may potentially be affected by the Expansion Project. For the purposes of this technical study, the RSA is defined as a 2º latitude (approximately 220 km) by 2º longitude (approximately 130 km) area surrounding the Expansion Project. The RSA is defined in this manner to coincide with the RSA defined by the air quality team.


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Figure 2-1 Local Study Area



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Figure 2-2 Regional Study Area


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19A.2.2 Receptor Locations

The Expansion Project will be located along a roadway, 50 km to the south of the city of Fort McMurray, Alberta (approximate population 100 000). Surrounding land uses include hunting and trapping, recreation including camping, natural parklands, and wildlife preserves. Additional nearby areas of interest include the town of Anzac (population approximately 550) which lies 40 kilometers to the east of the Expansion Project and three First Nations communities (Clearwater Indian Reserve 175, Gregoire Lake Indian Reserve 176, and Janvier Indian Reserve 194). For the location of the Expansion Project and other regional features, see Figure 2-2.

An HHERA cannot be conducted adequately to be protective of human and ecological health for the entire LSA/RSA as a whole because average COPC concentrations used in the calculation of risk would minimize exposure. Rather, 45 specific locations within the LSA/RSA were selected as part of the HHRA and 35 locations selected as part of the ERA based on:

• incorporated land use

• preliminary air modelling results

• input from consultation

• valuable wildlife habitat

• wildlife parks

• eco-tourism areas

• Aboriginal communities

• the assessment of maximum predicted air concentrations at the fenceline of the central processing facility (CPF)

A summary of the receptor locations selected for the HHRA and the ERA is provided in Table 2-1.

Table 2-1 Human and Ecological Receptor Locations

Location Number Receptor Location Name UTM (E) UTM (N)

Human Health Risk

Assessment

Ecological Risk

Assessment 1 Fort McMurray 476552 6288534

2 Fort McMurray 472867 6287888





7 Forestry Station South of Ft. McMurray

480289 6281579



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Table 2-1 Human and Ecological Receptor Locations (cont’d)


Human Health Risk

Assessment

Ecological Risk

Assessment 8 Campground West of

Clearwater Indian Reserve 175 496005 6281535

9 Campground East of Clearwater Indian Reserve 175

503998 6278529

10 Anzac 497342 6255952

11 Gregoire Lake Indian Reserve 176

493698 6254467


493689 6248946


488471 6255225


488454 6248958

15 Gregoire Lake Indian Reserve 176A

489008 6255479

16 Gregoire Lake Provincial Park Campground

488217 6259244

17 Stony Mountain Fire Lookout 482685 6248732

18 Campground South of Stony Mountain Fire Lookout

481735 6245977

19 Campground Northwest of Stony Mountain Fire Lookout

476127 6253027

20 Engstrom Lake Campground 507822 6229404

21 Trapper Cabin 1 463446 6244697

22 Trapper Cabin 2 454208 6238030

23 Trapper Cabin 3 458615 6232724

24 Trapper Cabin 4 454790 6229095

25 Grande Fire Lookout 423040 6239608

26 Algar Fire Lookout 449182 6219916

27 Janvier Indian Reserve 194 510594 6199570

28 Mariana Settlement 435384 6201299

29 Fort Chipewyan 487123 6509003

30 Fort McKay 462059 6337184

31 Janvier 516265 6197290

32 Conklin Fire Lookout 489596 6163979

33 Conklin 494774 6164893

34 Trapper Cabin 5 454187 6238019


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Table 2-1 Human and Ecological Receptor Locations (cont’d)


Human Health Risk

Assessment

Ecological Risk

Assessment 35 Grand Rapids Wildland

Provincial Park 446893 6271313

36 36 - Grand Rapids Wildland Provincial Park

399899 6245063

37 Grand Rapids Wildland Provincial Park

410874 6265388


460873 6277378


432994 6269425

40 Stony Mountain Wildland Provincial Park

446893 6271313


480994 6225349


488920 6239373


486888 6225349


485021 6233424

45 The maximum concentration observed within the boundaries of the central processing facility (CPF).

Varies Varies

19A.2.3 Receptors

Five distinct groups of people were assessed in the HHRA, including:

• Resident: local residents and recreational users who live in the LSA, and enjoy recreational activities within the LSA

• Hunter: local residents who are hunt and eat local wild game, all from within the LSA

• Camper: visitors who camp at the local campgrounds

• Aboriginal Resident (AR): First Nations or Aboriginal resident in the LSA who rely exclusively on local wild game for their meat/poultry from the LSA and obtain traditional foods from the LSA

• AENV/AHW AR: although the Aboriginal resident represents the best available, current research regarding the current practices of First Nations and Aboriginal groups within Alberta, at the request of AENV, consideration was given for a potential, future scenario in which First Nations receptors would also rely exclusively on fruit and produce from the LSA for their fruit and vegetable consumption needs



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With the large number of wildlife species present in and around the LSA, it is neither practical nor necessary to conduct an assessment for each individual species. Rather, after reviewing the known species inventories of the LSA a carefully selected, representative subset of receptors was selected as the basis for the ERA:





• woodland caribou (Rangifer tarandus) (Species at Risk in Alberta)



• short-eared owl (Asio flammeus) (Species at Risk in Alberta)


• terrestrial plants and invertebrates

Additional details on the human and ecological receptors are provided in Section 19A.6.1 and 19A.7.2, respectively.


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19A.3 Chemicals of Potential Concern and Assessment Scenarios

19A.3.1 Identification of Chemical Emission Sources

The identification of chemicals of potential concern (COPC) for a Project that has yet to be built involves the review of several sources of information to determine what relevant chemical emissions can be expected from a SAGD project. Potential emissions to the various environmental media were considered in order to develop an appropriate list of COPC.

19A.3.1.1 Consideration of Emissions to Air

The Expansion Project requires facilities such as steam generators that will result in the release of combustion products to the atmosphere. The main combustion products are water vapour and carbon dioxide, with trace amounts of SO2, NOX, PM2.5, VOC, PAH and metals. The following combustion sources are associated with the Expansion Project:

• Steam Generators: JACOS plans to fire seven once-through steam generators (OTSG). Two of the seven OTSGs will be fired with a blend of produced gas and fuel gas, while five of the seven will be fired with fuel gas

• Heaters: Two heaters will be fired with natural gas

• Flare Stacks: Under normal operating conditions, small volumes of purge and pilot gases are directed to the flare stack

Under plant upset conditions, which are expected to be infrequent and of a short-term nature, larger volumes of gas will be directed to the flare stacks. The upset scenarios include:

• Flaring fuel gas in the event of a control failure - this scenario is expected to be rare, occurring less than five times during the life of the facility and no appreciable SO2 emissions are expected

• Flaring of solution gas – this scenario is expected to be occasional, less than 5 times per year, with each event expected to be up to a few hours in duration. The produced gas may contain up to 1.19% hydrogen sulfide, which would result in SO2 emissions

• Vapour Recovery Unit (VPU) compressor outage – this scenario would result in the flaring of vapours that are recovered from the various product tanks in the event of a VRU failure and is expected to occur occasionally, less than five times per year, with each event being up to a few hours in duration. As the recovered vapours can contain up to 0.08% hydrogen sulfide, this flaring will result in SO2 emissions

There are also 30 storage tanks associated with the Expansion Project where fugitive emissions could occur. Nine of the proposed tanks are in hydrocarbon service, which can result in the release of product due to emptying and filling operations (referred to as working losses) and from diurnal heating and cooling of the tanks (referred to as breathing losses). Gas streams that are handled at the central facility will result in fugitive emissions from the numerous valves, flanges, rotating seals, and drains.



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Emissions to air would also occur during construction. Construction emissions associated with the Expansion Project will occur largely between late 2011 and 2014. Construction of the central processing facility and infrastructure, including pipelines, will occur during this period. Sources of emissions include both on-road and off-road vehicular traffic, construction and abandonment heavy equipment, drilling rigs, and temporary power generation. However, these emissions will be less than the emissions associated with the operations.

Based on the above, COPC associated with air emissions are SO2, NOX, PM2.5, VOC, PAHs, and metals. Additional details of the specific emission rates associated with these COPC are provided in the Air Quality Assessment (Volume 2, Section 5).

19A.3.1.2 Consideration of Emissions to Surface Water

Activities associated with the Expansion Project, including construction, operations and decommissioning, have the potential to affect aquatic resources present in watercourses and waterbodies within the study area. Expansion Project activities have been identified as having the potential to cause changes to surface water through:

• increase in sedimentation (due to surface disturbances and changes in runoff)

• change in water levels and flows (due to groundwater withdrawals and changes in runoff)

• changes in riparian habitat (associated with road and pipeline crossing construction)

• changes in benthic invertebrate community abundance and composition (associated with road and pipeline crossing construction and acid deposition)

• changes in pH (associated with acid deposition)

The Surface Water Quality Assessment (Volume 2, Section 9) concluded that, in consideration of the planned mitigation, the potential changes in surface water quality from the Expansion Project activities are negligible.

Since there are no planned direct discharges of COPC to surface water, and changes in surface water quality have been determined to be negligible, chemicals potentially released to surface water from the Expansion Project were not included in the COPC list.

19A.3.1.3 Consideration of Emissions to Groundwater

US EPA (2005) guidance on evaluating the changes in environmental media from air emissions states that groundwater is not a substantive exposure pathway for combustion emissions. Aerial deposition of COPC are expected to occur in surficial soil layers of the LSA. Given the concentration of COPC emitted, leaching of these chemicals into groundwater is not considered a feasible pathway.

As noted in the Hydrogeology Assessment (Volume 2, Section 7), the Expansion Project may affect groundwater within the LSA and RSA through activities such as groundwater withdrawals, dewatering of Expansion Project Area for development, use of spent steam chambers for waste disposal, drilling,


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installation and operation of SAGD wells (including thermal heating and casing failures), and/or operation of production facilities (including accidental releases or leaks from ponds, tanks or other vessels).

The Hydrogeology assessment determined that given the Expansion Project mitigation measures and the Site characteristics, all effects to groundwater quantity, quality and groundwater-surface water interactions, as a result of Expansion Project activities, are not expected to be significant. As well, the Expansion Project’s contribution to cumulative effects within the area, are also not expected to be significant or negatively affect groundwater resources in the area.

Based on the above, the potential for the Expansion Project to result in measurable changes to the potable groundwater aquifers is considered very low. As a result, chemicals potentially released to groundwater from the Expansion Project were not included in the COPC list.

19A.3.1.4 Consideration of Accidental Spills/Releases to Soil, Surface Water, and Groundwater

Expansion Project activities will be conducted in a manner as to minimize the potential for adverse environmental effects from a hazardous material spill. Preventive programs and policies, and a well developed emergency response plan, will be developed for the Expansion Project. As conceived, planned and designed, the Expansion Project will inherently provide a high level of mitigation for the potential environmental effects caused by a hazardous material spill.

Based on the above, the potential environmental effects on soil, surface water, and groundwater from accidental spills or releases do not require further consideration in the HHERA.

19A.3.1.5 Summary

A review of the potential sources of chemical releases from the Expansion Project determined that emissions of COPC to the atmosphere would be the primary source and pathway for human and wildlife exposure to releases from the Expansion Project. Other potential releases (e.g., leakage of well fluids into potable aquifers) were considered to have a low potential to result in measurable changes to the environmental media. The chemicals identified as emissions as part of the Air Quality Assessment were included as COPC for the HHERA and are listed in Table 3-1.

19A.3.2 Screening of COPC by Pathway

19A.3.2.1 Inhalation Pathway Assessment

Total air concentrations for each of the chemicals included in Table 3-1 were predicted for 1-hour, 24-hour, and annual averaging periods. For the inhalation pathway, the COPC were modelled without deposition or plume depletion to consider worst-case maximum gorund level concentration GLC. The concentrations were reported for each of the receptor points in the LSA and RSA (shown on Figures 2-1 and 2-2), as well as for the location of the maximum concentrations occurring at the fenceline of the central processing facility over the five year model period. These air concentrations were used to evaluate the health risks to receptors from the direct inhalation of the COPC emitted from the Expansion Project, alone and in combination with other existing, approved, and planned projects in the RSA.



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19A.3.2.2 Multi-Media Pathway Assessment

In addition to the total air concentrations, total deposition into the environment (e.g., soil) was provided in total, wet, and dry deposition per year for the receptor locations. These deposition fluxes were subsequently used to estimate the concentrations in multiple environmental media (e.g., soil, vegetation) as described in Section 19A.5 below. These environmental media concentrations were used to estimate the health risks to receptors from oral and dermal contact with these media in a multiple pathway risk assessment.

Not all COPC presented in Table 3-1 were considered relevant to the multiple pathway assessment. This is due to the physical-chemical properties of the COPC; specifically that not all COPC released from the Expansion Project will persist or accumulate in the environment. To identify the COPC that were considered in the multiple pathway risk assessment, the physical-chemical properties of each of the COPC in Table 3-1 were compared to accepted national and international criteria for the classification of persistent and bio-accumulative substances (Environment Canada 2006; Rodan et al. 1999).

The characterization of persistence and bio-accumulation is provided in detail within Environment Canada’s Existing Substances Program and the Health Canada and Environment Canada’s Domestic Substances List Categorization, under the Canadian Environmental Protection Act (CEPA) (Environment Canada 2007).

Persistence refers to the length of time a chemical resides in the environment and is measured by its half-life. This is the time required for the quantity of a chemical to diminish or degrade to half of its original amount within a particular environment or medium. For the purposes of this HHERA, a chemical was considered persistent if its half-life in soil was greater than or equal to (≥) six months (182 days).

Bio-accumulation is a general term used to describe the process by which chemicals are accumulated in an organism directly from exposure to water, soil, or through consumption of food containing the substances. A chemical’s potential to bio-accumulate is related to its octanol-water partition coefficient (Kow). The Kow refers to the ratio of distribution of a substance in octanol compared to that in water. For the purposes of this HHERA, a chemical was considered bio-accumulative if its Log Kow was greater than or equal to five.

Therefore, COPC retained for full multi-pathway assessment in both the HHRA and ERA had:

• A half-life in soil greater than or equal to six months and/or

• An octanol-water partition coefficient (Log Kow) greater than or equal to five

The rationale behind this exercise was that if a chemical released to the air does not meet either of these criteria, only a limited opportunity exists for human or ecological exposure via secondary exposure pathways (i.e., those other than inhalation), as the potential for that chemical to persist and/or accumulate in the environment is negligible. However, if a chemical meets one or both of these criteria, sufficient opportunity could be present for human or ecological exposure. The screening completed on the COPC to evaluate persistence and bio-accumulation is provided in Appendix 19A-1.

The exposure pathways evaluated for each COPC assessed in the HHERA are shown in Table 3-1.


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Table 3-1 Chemicals of Potential Concern Evaluated in the Human and Ecological Health Assessment

COPC

Pathways Evaluated Inhalation

(Air) Oral/Dermal

(Multi-media) Criteria Air Contaminants (CAC) Sulphur Dioxide (SO2)

Nitrogen Dioxide (NO2)

PM2.5

Carbon Monoxide (CO) Petroleum Hydrocarbons Benzene

Toluene

Ethylbenzene

Xylenes

Aliphatic C5-C8

Aliphatic C9-C16

Aromatic C9-C16

Aromatic C17-C34

PAHs Anthracene

Benz(a)anthracene

Benzo(a)pyrene (BaP)

Benzo(e)pyrene

Benzo(b)fluoranthene

Benzo(g,h,i)perylene

Benzo(k)fluoranthene

Chrysene

Dibenzo(a,h)anthracene

Fluorene

Fluoranthene

Indeno(1,2,3-cd)pyrene

Naphthalene

Phenanthrene

Pyrene

Perylene

VOCs Acetaldehyde

Acrolein

Benzaldehyde



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Table 3-1 Chemicals of Potential Concern Evaluated in the Human and Ecological Health Assessment (cont’d)

COPC

Pathways Evaluated Inhalation

(Air) Oral/Dermal

(Multi-media) VOCs (cont’d) Carbon disulfide

Dichlorobenzene

Formaldehyde

Hexane

Hydrogen sulfide

Thiophene Metals Aluminum (Al)

Chromium (Total)

Cobalt (Co)

Copper (Cu)

Lead (Pb)

Manganese (Mn)

Molybdenum (Mo)

Nickel (Ni)

Strontium (Sr)

Vanadium (V)

Zinc (Zn)

For the HHERA, the multi-media assessment was only conducted at receptor locations where human receptors were expected to live but not for locations of high urban density (e.g., cities and communities) greater than 40 km away from the Expansion Project. For the ERA, the multi-media assessment was conducted at receptor locations that were identified as valuable wildlife habitat, wildlife parks, unique ecoregions and habitat, eco-tourism areas and Aboriginal communities. Where multiple receptors locations were near one another, a location grouping was formed, and the maximum concentration observed at any of the locations within the grouping was evaluated (Figure 2-1 and 2-2). An example of this would be receptor locations 11 through 15, all located near the Gregoire Lake Indian Reserve 176. Receptor locations and groupings where the inhalation and multi-media HHERA took place are listed in Table 3-2.


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Table 3-2 Human and Ecological Receptor Locations and Type of HHERA Conducted

Location Number Receptor Location Name

Human Health Ecological Risk

Assessment Inhalation

Assessment Multimedia

Assessment 1 Fort McMurray

2 Fort McMurray

3 Fort McMurray

4 Fort McMurray

5 Fort McMurray

6 Fort McMurray

7 Forestry Station South of Ft. McMurray

8 Campground West of Clearwater Indian Reserve 175

9 Campground East of Clearwater Indian Reserve 175

10 Anzac





15 Gregoire Lake Indian Reserve 176A

16 Gregoire Lake Provincial Park Campground

17 Stony Mountain Fire Lookout

18 Campground South of Stony Mountain Fire Lookout

19 Campground Northwest of Stony Mountain Fire Lookout

20 Engstrom Lake Campground

21 Trapper Cabin 1

22 Trapper Cabin 2

23 Trapper Cabin 3

24 Trapper Cabin 4

25 Grande Fire Lookout

26 Algar Fire Lookout

27 Janvier Indian Reserve 194 (Grouped with 31)

(Grouped with 31)

28 Mariana Settlement

29 Fort Chipewyan

30 Fort McKay



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Table 3-2 Human and Ecological Receptor Locations and Type of HHERA Conducted (cont’d)

Location Number Receptor Location Name

Human Health Ecological Risk

Assessment Inhalation

Assessment Multimedia

Assessment 31 Janvier

(Grouped with 27)

(Grouped with 27) 32 Conklin Fire Lookout

33 Conklin

34 Trapper Cabin 5


36 36 - Grand Rapids Wildland Provincial Park









45 The maximum concentration observed within the boundaries of the central processing facility (CPF).

19A.3.3 Assessment Scenarios

Four main Expansion Project phases were assessed as part of the HHERA:

• Baseline – existing developments and those that have been approved but are not yet operational, incorporating existing background or natural conditions

• Construction – the time during which the Expansion Project would be constructed, expected to last about 3 years

• Operation – the time after the construction during which the Expansion Project would be operated, expected to be 25 years

• Decommissioning – the after which the Expansion Project would cease to operate

The emissions that people would be exposed to during Construction would be from combustion gas emissions from heavy equipment (including earth movers, excavation equipment, and grading equipment) as well as from fugitive dust (particulate matter) generated during the earth-moving activities associated with the site and right-of-way preparation. On-road vehicle traffic associated with the site activities will also generate emissions. Construction-related emissions can interact with other projects such as the local operation of the JACOS Demonstration Project and the operation of other SAGD projects. However,


19A-23

these interactions result in a smaller incremental addition relative to operation activities. The interaction of the Expansion Project operation emissions with other projects is assessed quantitatively through dispersion modelling owing to their greater quantity. Construction emissions interactions with other projects are not quantitatively assessed.

Chemical emissions and discharges during Operations will typically be the highest of the three Project phases, and will therefore pose the greatest potential for human exposure. The main sources of air emissions associated with the Expansion Project operations are the central processing facility, bitumen storage, and diluent storage and management processes. All of these sources produce direct (i.e., stack) and fugitive (i.e., tank, valves, flanges) air emissions that can result in changes to the quality of the environmental media to which people and wildlife are exposed, potentially affecting their health. As indicated in Table 3-3, three different cases were quantitatively assessed as part of the Operations phase: the Expansion Project alone, the Application Case (the Expansion Project in combination with existing developments and those that have been approved but are not yet operational), and the Planned Development Case (the Expansion Project in combination with existing developments, those that have been approved but are not yet operational, as well as planned sources).

Table 3-3 Summary of Phases and Cases Assessed in the HHERA

Project Phase Case Description Existing Conditions Baseline Case Evaluation of the Baseline Case includes quantitative

assessment of the potential health risks associated with existing developments and those that have been approved but are not yet operational. Existing concentrations in the environment were incorporated into the assessment.

Construction Construction Case As noted in text, evaluation of construction involved a qualitative assessment of the potential health risks associated with air emissions during construction of the Expansion Project.

Operation Project Alone Scenario Evaluation of the Expansion Project alone during operations involved a quantitative assessment of the potential health risks associated with air emissions from the Expansion Project in isolation from all other sources of COPC.

Application Case (Baseline Case + Project Alone Scenario)

Quantitative evaluation of the Expansion Project during operations in combination with existing developments and those that have been approved but are not yet operational.

Planned Development Case Quantitative evaluation of the Expansion Project during operations in combination with existing developments, those that have been approved but are not yet operational, as well as planned sources in the assessment area.

Decommissioning Decommissioning As noted in the text, evaluation of decommissioning involved the qualitative assessment if air emissions associated with decommissioning activities. It is expected that a separate assessment would take place prior to decommissioning activities in the future, based on legislative requirements of the day. Emissions associated with decommissioning activities are expected to be similar to or less than those during construction.



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As potential exposures and risks associated with Decommissioning will be considerably less than those during Operations (as air emissions will cease), the potential human health risks associated with Decommissioning are discussed qualitatively, in light of the HHRA results and conclusions for Operations.

It is important to recognize that this HHRA does not specifically assess human work-place related exposures and risks. All phases of the Expansion Project as currently planned will be carried out in compliance with the applicable occupational health and safety as well as public safety legislation of the Province of Alberta and the Government of Canada. Extensive mitigation, planning, and environmental management measures developed in support of the Expansion Project will assist in minimizing the risks with regard to health and safety. Though the current HHRA does not specifically assess human work-place related exposures and risks, it does evaluate those people living, working or enjoying recreational activities in the vicinity of the Expansion Project, including workers employed by the Expansion Project that live or enjoy recreational activities near the Expansion Project.


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19A.4 Baseline Conditions

19A.4.1 Baseline Sampling Program

Limited existing studies concerning baseline soil, vegetation, surface water and sediment conditions within 20 km of the site were identified. As a result, field sampling programs were initiated in order to better characterize baseline conditions at the site. Baseline sampling consisted of the evaluation of three types of media: air, soil and traditional edible vegetation.

Baseline air quality was assessed by reviewing data collected from continuous monitoring stations located within the Regional Municipality of Wood Buffalo. A quality assurance and quality control program involving routine audits, monthly calibrations and daily zero and span calibrations has been put in place by the WBEA to ensure the quality and accuracy of data received. Three of the 15 monitoring stations that currently make up the monitoring network are located within the Expansion Project LSA (2 in the Fort McMurray and 1 in Anzac), while the remaining 12 are located within the Expansion Project RSA. Results of the monitoring indicate that ambient air quality in the LSA and RSA is influenced by both industry and non-industry emissions. Maximum ambient criteria air contaminant concentrations in the RSA periodically exceed the Alberta Ambient Air Quality Objectives (AAAQOs); however, analysis of the data indicates that these exceedances are typically outliers, and the 99th percentile ambient air concentrations are generally less than the applicable AAAQOs. Further information on the ambient air quality program can be found in Volume 2, Section 5.

Soil was chosen as a media of interest as both human and ecological receptors are subject to direct exposure with soil and the models used in the risk assessment (chemical fate and transport models, human and ecological risk models) rely on soil concentrations to predict the uptake of chemicals into various other media. Baseline soil conditions were characterized through the sampling of 10 sites located within the LSA. Samples were analyzed for polycyclic aromatic hydrocarbons (PAHs) and inorganic compounds due to their high degree of persistence in the environment (e.g., greater than 182 days).

Baseline vegetation conditions were characterized through the sampling of 17 sites located within the LSA. Sites were selected in the field that had good populations of the target collection species (e.g., blueberry (Vaccinium myrtilloides) and Labrador tea (Ledum groenlandicum). Companion soil samples were also collected at each site. Like soils, vegetation samples were analyzed for PAHs and inorganics. Further information on the vegetation sampling program, including the location of the sampling sites, can be found in the Vegetation Baseline Report (Volume 2, Appendix 12C).

For both soils and vegetation, provided that the COPC was detected in at least 3 samples, statistical evaluation of the 95th upper confidence limit of the arithmetic mean of the concentrations was conducted and used to represent baseline conditions in LSA. Where all samples resulted in non-detectable values, the maximum detection limit was taken as the baseline concentration. Where the total number of detectable values was only one or two, the maximum concentration was selected. Due to laboratory restrictions, aluminum and manganese were only analyzed in a limited number (2-3) of blueberry samples – in this case, the arithmetic mean of the results was selected as the baseline concentration.

Using baseline soil concentrations, the risk assessment chemical fate and transport model was used to predict baseline concentrations in other media relevant to the assessment, such as small mammals, wild



19A-26

game, and garden produce. Such predictions are based on both the physical and chemical properties of the COPC in question, and site specific data such as climate, topographical and hydrological characteristics. As measured soil data was used to make the predictions, the data are viewed as being representative of baseline conditions in the LSA. The full suite of data (both measured and modelled) was then incorporated into the human health and ecological risk assessments. Further details on the baseline concentrations used for assessment as well as the chemical fate and transport modelling methods can be found in Appendix 19A-3 and 19A-4.

Activities associated with the Expansion Project have the potential to affect aquatic watercourses and waterbodies within the study area, and baseline sampling of the water quality was completed. However, a conclusion of the Surface Water Quality Assessment (see Volume 2, Section 9) was that given planned mitigation and the absence of planned direct discharges of COPC to surface water, the potential changes in surface water quality from Expansion Project activities are negligible. As such, chemicals potentially released to surface water from the Expansion Project were not included in the quantitative HHERA.

19A.4.2 Baseline Human Health Status

The health of Northern Albertans has been addressed by Alberta Health and Wellness (2006) in a report called “Report on the Health of Albertans”. The report addresses by historical (mid-2000s) health region the determinants of health, mental health, injury, and non-communicable diseases. Cancer incidence and mortality, the incidence of communicable disease and some of the demographic statistics (e.g., life expectancy, age specific fertility) are reported on a province wide basis as rate per 100 000. The Expansion Project area was included in historical Health Region 7 – Northern Lights which had a head office located in Fort McMurray. A comparison of the historical Region 7 data to the provincial averages are included in Table 4-1 and shows that the people in the historical Region 7 have comparable determinants of health quality to people in the rest of the province; however, certain health indicators are higher or lower than the provincial average.

Table 4-1 Health Statistics Comparison historical Region 7 (Northern Lights) and the Province of Alberta

Health Indicator Provincial average Northern Lights average Determinants of health

Percent of the population rating their health as good or excellent

64% 58%

Percent of population reporting smoking either daily or occasionally

23% 30%

Percentage of women (age 50-69) reporting they received a screening mammogram within the previous 2 years

52% 49.5%

Percentage of the population with a body mass index in the overweight or obese category

34% overweight 15% obese

35% overweight 22% obese

Percentage of the population reporting consumption of 5 or more servings of fruit and vegetables daily

36% 27%

Percentage of the population reporting activity limitation 24% 19.5%


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Table 4-1 Health Statistics Comparison historical Region 7 (Northern Lights) and the Province of Alberta (cont’d)

Health Indicator Provincial average Northern Lights average Determinants of health (cont’d)

Percentage of the population reporting consumption of 5 or more drinks on one occasion 12 or more times per year

22% 28%

Percent of the population reporting being active or moderately active during leisure time

54% 52%

Mental Health

Age standardized treated prevalence of mental health disorders

15.4% 14.5%

Age standardized treated prevalence of anxiety disorders or depression

11.9% 11.2%

Age standardized treated prevalence of substance abuse disorders

0.7% 1.00%

Non-Communicable diseases

Age standardized treated prevalence of ischemic heart disease

2.1% 2.4%

Age standardized treated prevalence of cerebrovascular disease

0.63% 0.46%

Age standardized treated prevalence of hypertension 9.8% 10.2%

Age standardized treated prevalence of asthma 4.2% 3.4%

Age standardized treated prevalence of chronic bronchitis 2.0% 3.0%

Age standardized treated prevalence of COPD 2.7% 3.9%

Age standardized treated prevalence of diabetes 3.4% 4.3%

Age standardized treated prevalence of chronic renal failure

0.37% 0.31%

Age standardized treated prevalence of arthritis 4.2% 4.6%

Injury Age standardized treated prevalence of injury 25.7% 21%

Age standardized suicide mortality per 100 000 14.4 10.1

Age standardized homicide mortality per 100 000 2.1 5.8

Of note in the health statistics are that the Northern Lights average for obesity, tobacco use and percentage of the population reporting consumption of 5 or more drinks on one occasion 12 or more times per year were the highest in the province. The age standardized prevalence of substance abuse disorders, hypertension, prevalence of COPD, arthritis and diabetes were statistically higher than the provincial average. The prevalence of mental health and anxiety disorders, cerebrovascular disease and asthma were statistically lower than the provincial average.



19A-28

19A.4.3 Species at Risk

Species at Risk (SAR) in this assessment are defined as any wildlife species listed as “Endangered”, “Threatened”, or “May be at Risk” under the federal Species at Risk Act (SARA) or noted by the Government of Alberta as being "At Risk" (formerly "Red List") or "May Be At Risk" (formerly "Blue List") of extinction. Only "At Risk" species are afforded legislative protection as "Endangered" or "Threatened" under Alberta's Wildlife Act (Alberta Sustainable Resource Development (ASRD) 2006). Detailed status reports have been published by the Government of Alberta for those species classified as "At Risk" or "May Be At Risk". The ranges of seven SAR are expected to overlap the borders of the LSA;

• three birds (Barred Owl - Strix varia; Peregrine Falcon - Falco peregrines; Short-eared Owl - Asio Flammeus)

• three mammals (Northern Long-eared Bat - Myotis septentrionalis; Woodland Caribou - Rangifer larandus; Wolverine - Gulo gulo)

• one amphibian (Canadian Toad - Bufo hemiophrys)


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19A.5 Fate and Transport Modelling

This section describes the methodologies used to estimate exposure point concentrations (EPCs) of COPCs in each exposure pathway. The equations and references used to calculate COPC-specific EPCs are presented in Appendix 19A-4, with a brief description provided in the following sections.

In accordance with US EPA (2005), COPCs are grouped into three broad categories for the assessment of potential exposure pathways:

• organics (e.g., polycyclic aromatic hydrocarbons [PAHs])

• metals

• volatile organic compounds

One of the cornerstones of risk assessment is the concept of conservatism. Throughout this section and the entire HHERA, the use of the term conservatism is meant to convey a preference for erring on the side of caution, as opposed to understating risk under conditions of uncertainty. For example, the HHERA study team selected analytical values or approaches that would result in an overestimation of exposure or potential risk to humans and the environment, as opposed to understating the risk. A number of specific conservative assumptions are presented in both the HHRA and ERA.

19A.5.1 Ambient Air Exposure Point Concentrations

When emitted from the Expansion Project, COPC will mix with the surrounding air or fall to the ground over time (on their own or mixed with precipitation), known respectively as dispersion and deposition. The COPC concentration in ambient air is directly inhaled and absorbed through the skin of a receptor, and deposition of the COPC affects the concentration of the COPC in the other environmental media that is ingested or absorbed through the skin of a receptor.

The CALPUFF transport and dispersion model (Appendix 5D), and the associated CALMET meteorology model (Appendix 5C) were the primary tools used to assess the air concentrations and deposition of the Expansion Project. Air modelling results included 1-hour, 24-hour, and annual average COPC concentrations for each of the receptor locations shown on Figure 2-2. In addition, the maximum air concentration at the fenceline of the central processing facility was also assessed for air quality.

The air modelling results also included annual average total, wet, and dry deposition rates. These rates were used to predict COPC concentrations in other environmental media, as described in the subsequent sections. For receptor locations represented by multiple receptor points, the maximum was selected as representative of the wet and dry deposition rates within the receptor location.

For the purposes of the human health risk assessment, it was assumed that the outdoor and indoor concentrations are equal; this is likely a conservative assumption.



19A-30

19A.5.2 Surface Water and Fish Exposure Concentrations

Concentrations of the COPCs in local sediment and surface water, and subsequently fish tissue, were not predicted to change as a result of the Expansion Project emissions (Appendix 19A, Section 19A.3.1).

19A.5.3 Soil Exposure Point Concentrations

The first step in determining COPC uptake is to estimate COPC concentrations in soil, based on results from the dispersion and deposition modelling. The COPC soil concentrations are used along with the air concentrations to calculate COPC intakes resulting from all other exposure pathways, as each pathway is influenced by the initial concentration of COPCs in soil and air (Figure 5-1). Receptors are directly exposed to soil through inhalation of soil-derived dust, dermal contact with soil and soil-derived dust, and incidental ingestion.

Figure 5-1 Modelling Soil Concentrations


19A-31

For the purposes of this assessment, there are two main classes of chemicals, carcinogenic and non-carcinogenic. Each class of chemicals can be treated differently in the calculation of COPC soil concentrations in the default US EPA model. However, for the purposes of this assessment soil concentrations for both non-carcinogens and carcinogens were conservatively calculated as the single highest annual soil concentration throughout the operating lifetime of the Expansion Project and loaded into the soil over the operating lifetime of the Expansion Project (assumed to be 30 years of operation1

When calculating potential risk in human and ecological receptors from exposure to these COPC in soil, the soil concentration used in the risk models was the background measured concentration plus the expected increase for each Case, rather than the background concentration alone (e.g., for the Baseline Case, soil concentration was background + expected Baseline Case increase; for the Planned Development Case, soil concentration was background + Planned Development Case increase).

).

Changes to COPC concentrations in soil were calculated by summing the vapour and particle phase deposition to the soil. Wet and dry deposition of particles was considered, with dry deposition of vapours calculated from the vapour air concentration and the dry deposition velocity. The calculation of soil concentration also incorporated a term (ks) that accounts for loss of COPC by several mechanisms, including leaching, erosion, runoff, degradation (biotic and abiotic), and volatilization. For inorganic COPCs (metals), it is assumed that soil losses due to abiotic degradation and volatilization are zero as these elements are not biodegradable, nor volatile. The US EPA model allows for variation of the soil mixing zone through which the chemicals would be deposited and then distributed. For all land uses and ecosystems, a 2 cm mixing zone was employed to estimate soil concentrations and subsequent fate and transport of chemicals in the environment.

Measured inorganic COPC soil concentrations, as well as the maximum expected increase in soil inorganic COPC concentration for each of the four case scenarios (Baseline Case, Project Alone Scenario, Application Case, and Planned Development Case), are provided in Table 5-1. Table 5-1 is limited to inorganic COPC as measured background data were not available for PHCs or VOCs, while concentrations of PAHs in all media never exceeded the laboratory detection limit. The percent loading is the expected increase over current conditions (as measured) based on model predictions. Loading of COPC over the 30 year operational period for the Expansion Project in all scenarios resulted in soil loadings of less than 0.15% of measured background concentrations, or only a minor contribution to existing conditions in the LSA.

1 30 years was selected as the operating life of the facility and conservatively assumes that no updates to pollution

control systems or operations would occur.



19A-32

Table 5-1 Measured Background Inorganic COPC concentrations in Soil and Predicted Soil Loading for each Case

COPC

Background Measured Soil Concentration

(mg/kg)

Baseline Case Project Alone Scenario Application Case Planned Development Case

Maximum Increase in

Soil Concentration

(mg/kg)

% Loading

Maximum Increase in

Soil Concentration

(mg/kg)

% Loading

Maximum Increase in

Soil Concentration

(mg/kg)

% Loading

Maximum Increase in

Soil Concentration

(mg/kg)

% Loading

Inorganics Aluminum 4177 0.030 7.29E-04 0.034 8.10E-04 0.048 0.0012 0.050 0.0012 Chromium (Total) 11 0.0017 0.016 2.69E-04 0.0025 0.0017 0.016 0.0018 0.017 Cobalt 6.2 1.98E-04 0.0032 1.48E-04 0.0024 2.44E-04 0.0039 2.56E-04 0.0041 Copper 2.5 9.40E-04 0.038 5.08E-04 0.020 9.43E-04 0.038 0.0010 0.041 Lead 6.2 0.0061 0.100 6.05E-04 0.0098 0.0061 0.100 0.0067 0.11 Manganese 967 0.0037 3.84E-04 5.45E-04 5.64E-05 0.0037 3.84E-04 0.0037 3.87E-04 Molybdenum 0.55 2.71E-04 0.049 8.03E-05 0.015 2.71E-04 0.049 2.96E-04 0.054 Nickel 6.0 0.0072 0.12 5.17E-04 0.0086 0.0072 0.12 0.0078 0.13 Strontium 5.0 6.83E-05 0.0014 1.59E-04 0.0032 1.89E-04 0.0038 1.94E-04 0.0039 Vanadium 15 0.0061 0.040 4.80E-04 0.0032 0.0061 0.040 0.0066 0.044 Zinc 21 0.028 0.13 0.0020 0.0093 0.028 0.13 0.030 0.14


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19A.5.4 Vegetation

Indirect exposure resulting from ingestion of produce, fruit and traditional vegetation depends on the total concentration of COPCs in the edible portions of the plant. Because differences exist in contamination mechanisms, consideration of indirect vegetation exposure was separated into two broad categories – aboveground plants (e.g., lettuce) and belowground plants (e.g., potatoes). In addition, the aboveground plants category was further subdivided into exposed (e.g. beans), protected (e.g., corn) and fruit (e.g., blueberries) subcategories.

Depending on the receptor under evaluation, ingestion of vegetation was evaluated as both typical home garden/farm produce and traditional plants. Consumption of home garden/farm produce applies to all receptors exposed to vegetation via ingestion, while traditional plants apply solely to Aboriginal receptors.

Figure 5-2 Modelling Backyard Garden / Farm Produce

Deposition of Particles

CoPC Concentration in Exposed Aboveground

Produce

Vapour Transfer Root Uptake from Soil

CoPC Concentration in Protected Aboveground and Belowground Produce

Deposition of Particles

COPC Concentration in Exposed Aboveground

Vegetation

Vapour Transfer Root Uptake from Soil

COPC Concentration in Protected Aboveground and Belowground Vegetation

COPC Concentration In Garden Fruit



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The modelling of COPC uptake to vegetation was weighted based on the possible uptake pathways and the characteristics of the vegetation under consideration. In doing so, receptors ingesting vegetation are exposed to COPC that may have arrived by all possible pathways. Direct deposition of particles onto the surface of the plant was modelled via COPC uptake to aboveground exposed vegetation. Root uptake was considered for aboveground protected and belowground vegetation while vapour transfer was considered for fruits.

For the purpose of the assessment, it is assumed that backyard garden produce grown in the summer is preserved or frozen and is consumed year-round, though it is also recognized that an individual’s annual intake of produce is typically not entirely supplied from their garden and this conservative assumption may overestimate potential risk to receptors. Resident, hunter and Aboriginal receptors were assumed to obtain 10% of their produce and fruit from their garden, while AENV/AHW AR receptor is assumed to obtain the entirety of their produce from the garden. With regards to traditional plants, it was assumed that both Aboriginal and AENV/AHW AR receptors obtain the entirety of their intake from the LSA.

Background concentrations of inorganics in aboveground and belowground traditional plants are presented in Tables 5-2 and 5-3. In addition, modelled COPC loading on these media over the operational period of the Expansion Project are provided, along with the percent change from the background concentrations. Maximum modelled values among all Aboriginal and AENV/AHW AR receptors evaluated for either human health were presented for each case scenario. As evidenced, loading of COPC over the 30 year operational period for the Expansion Project in all scenarios resulted in aboveground traditional plant loadings of less than 0.0025% of measured background concentrations, or only a minor contribution to existing conditions in the LSA. Loading of COPC in belowground traditional plants was higher as the dominant uptake pathway was through the roots planted within background soil concentrations.


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Table 5-2 Predicted Aboveground Traditional Plants Loading over a 30 year period in the LSA

COPC

Background Measured

Aboveground Traditional

Plants Concentration

(mg/kg)


Maximum Increase in



(mg/kg)

% Loading

Maximum Increase in



(mg/kg)

% Loading

Maximum Increase in



(mg/kg)

% Loading

Maximum Increase in



(mg/kg)

% Loading

Inorganics Aluminum 230 1.79E-04 7.79E-05 4.52E-06 1.96E-06 1.81E-04 7.85E-05 1.99E-04 8.63E-05 Chromium (Total) 5.0 5.80E-05 0.0012 1.88E-07 3.75E-06 5.80E-05 0.0012 6.28E-05 0.0013 Cobalt 2.0 3.20E-06 1.60E-04 4.91E-08 2.46E-06 3.22E-06 1.61E-04 3.53E-06 1.76E-04 Copper 33 1.67E-05 5.03E-05 2.06E-07 6.20E-07 1.67E-05 5.03E-05 1.83E-05 5.50E-05 Lead 6.0 4.08E-05 6.81E-04 8.26E-08 1.38E-06 4.08E-05 6.81E-04 4.43E-05 7.40E-04 Manganese 162 4.37E-05 2.70E-05 1.41E-07 8.74E-08 4.38E-05 2.70E-05 4.41E-05 2.73E-05 Molybdenum 0.90 9.12E-06 0.0010 5.41E-08 6.02E-06 9.14E-06 0.0010 9.89E-06 0.0011 Nickel 4.4 9.23E-05 0.0021 1.32E-07 3.02E-06 9.23E-05 0.0021 9.97E-05 0.0023 Strontium 12 1.12E-06 9.30E-06 6.46E-08 5.39E-07 1.14E-06 9.47E-06 1.28E-06 1.07E-05 Vanadium 2.4 4.06E-05 0.0017 6.40E-08 2.67E-06 4.06E-05 0.0017 4.39E-05 0.0018 Zinc 38 3.44E-04 9.04E-04 5.28E-07 1.39E-06 3.44E-04 9.04E-04 3.74E-04 9.83E-04



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Table 5-3 Predicted Belowground Traditional Plants Loading over a 30 year period in the LSA

COPC

Background Measured

Belowground Traditional


(mg/kg)


Maximum Increase in



(mg/kg)

% Loading

Maximum Increase in



(mg/kg)

% Loading

Maximum Increase in



(mg/kg)

% Loading

Maximum Increase in



(mg/kg)

% Loading

Inorganics Aluminum 131 2.7 2.1 4.26E-07 3.26E-07 2.7 2.1 2.7 2.1 Chromium (Total) 5.2 0.048 0.93 2.35E-08 4.51E-07 0.048 0.93 0.048 0.93 Cobalt 3.0 0.043 1.4 2.01E-08 6.69E-07 0.043 1.4 0.043 1.4 Copper 10 0.63 6.3 2.46E-06 2.46E-05 0.63 6.3 0.63 6.3 Lead 4.0 0.055 1.4 1.06E-07 2.64E-06 0.055 1.4 0.055 1.4 Manganese 102 48 48 5.28E-07 5.21E-07 48 48 48 48 Molybdenum 0.80 0.033 4.1 9.34E-08 1.17E-05 0.033 4.1 0.033 4.1 Nickel 16 0.048 0.29 8.02E-08 4.90E-07 0.048 0.29 0.048 0.29 Strontium 10 1.3 13 7.74E-07 7.74E-06 1.3 13 1.3 13 Vanadium 3.6 0.045 1.2 2.79E-08 7.66E-07 0.045 1.2 0.045 1.2 Zinc 31 19 62 3.45E-05 1.11E-04 19 62 19 62


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19A.5.5 Country Foods (Hunting)

For the purposes of this assessment wild game includes animals such as deer, turkey, and ducks. Wild game is assumed to forage and consume incidental COPC-affected soil in the vicinity of the Expansion Project. Wild game is assumed to spend its entire lifetime in the vicinity of the Project and not range into other regions that would be subject to different regimes of deposition, resulting in a conservative (i.e., protective) overestimation of wild game tissue concentrations for those animals with a large home range.

Figure 5.3 Modelling Wild Game

It is conservatively assumed that all COPCs are 100% bioavailable to wild game. In addition, it is assumed that they are not able to metabolize any of their COPC intakes. Both of these assumptions would tend to overestimate the uptake of COPCs through the food chain, as there is no mechanism to offset the amount of bioaccumulation suggested by the biotransfer factors.

For modelling purposes, primary literature uptake factors for predicting animal tissue concentrations are available for beef. In accordance with US EPA (2005) guidance, to predict the uptake of COPCs into wild game, the beef uptake factor is adjusted based on the relative lipid content of the game animal or pig. Whole body lipid contents for representative game species were obtained from Stephenson (2003), Wirsing et al. (2002), Stephenson et al. (1999), and Knott et al. (2005).



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19A.5.6 Breast Milk

This pathway is typically evaluated for highly bioaccumulative and lipophilic COPCs such as dioxins and PCBs, which are not being emitted from the Expansion Facility. In particular, metals do not bind to fat and so do not usually accumulate to higher concentrations in breast milk than in blood (Golding 1997). As a result, children are likely to be exposed to higher levels of metals in utero and as a toddler (7 months to 4 years old), than as an infant from breast-feeding.

Therefore, the potential for COPCs to accumulate in breast milk, and be transferred to infants, was not evaluated as part of the HHRA.

19A.5.7 Other Media Associated with Ecological Receptors

The estimation of additional EPC were necessary for aquatic plants, aquatic invertebrates and terrestrial invertebrates, biota relevant to the ERA only. Consumption of these biota were considered relevant exposure pathways for various ecological receptors, but do not contribute to human exposure.

EPCs for these biota were estimated for each COPC using compound-specific uptake factors (UPs) that describe the relationship between a specified chemical in a given abiotic media to various types of biota (e.g., the uptake of benzene from sediment by aquatic plants). A description of these UP are found in Appendix 19A-10.

The generalized equation used to calculate a COPC concentration in a biotic tissue (such as soil invertebrates) from a soil concentration is as follows:

EPCi = EPCsoil x UPi

where: EPCi = Exposure point concentration in target biotic tissue i (mg/kg wet weight);

EPCsoil = Exposure point concentration in soil (mg/kg dry weight); and

UPi = uptake factor from soil to wet weight target biotic tissue i (dimensionless).

An analogous equation is used to calculate EPCs for aquatic plants and invertebrates (on a mg/kg wet tissue basis) using water (mg/L) and sediment (mg/kg dry wt) EPC respectively.


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19A.6 Human Health Risk Assessment

An HHRA is a scientific study that estimates the nature and likelihood of the occurrence of potential adverse health risks in humans following chemical exposures. The fundamental purpose of such a study is to evaluate whether people working, living or visiting a given location are being exposed, or will be exposed, to concentrations of chemicals that have the potential to result in adverse risks to their health.

This HHRA examines potential human health risks to individuals living and visiting within the LSA and RSA at key human receptor locations due to short-term (acute) and long-term (chronic) exposures to COPC, for each assessment case as described in Section 19A.3.3 (i.e., Baseline Case, Project Alone Scenario, Application Case, and Planned Development Case). In addition to the evaluation of risks related to inhalation of COPC, assessments of certain COPC are conducted to evaluate potential oral and dermal exposures and related chronic human health risks resulting from long-term exposures to COPC present in a number of different local environmental media including soil, vegetation, and game.

This HHRA was conducted in accordance with current regulatory guidance documents, including:

• Federal Contaminated Sites Risk Assessment in Canada. PART I: Guidance on Human Health Risk Preliminary Quantitative Risk Assessment (PQRA), Version 2.0 (Health Canada 2004a)

• The US EPA Human Health Risk Assessment Protocol (HHRAP) for Hazardous Waste Combustion Facilities (US EPA 2005)

The prediction of people’s exposure to specific chemicals in the environment and the potential risks resulting from such exposures can be determined through the completion of a quantitative HHRA. The HHRA has been completed in five main steps or phases, as outlined in Section 19A.1.4:

• Problem Formulation

• Exposure Assessment

• Toxicity Assessment

• Risk Characterization

• Uncertainty Analysis

19A.6.1 Problem Formulation

Problem formulation is the first step in the risk assessment process. Information is gathered on the proposed operation and its potential interactions with the environment to provide focus for the subsequent phases of the risk assessment. Key factors that are evaluated include:

• potential emissions from the operations

• screening of COPC to focus on those chemicals that are most likely to contribute the greatest risk

• screening and assessment of potential exposure pathways



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• characterization of potential receptors who may be exposed to emissions

• development of a conceptual model that describes the potential interactions between the operation and the surrounding communities and environment

As stated, the primary objective of the HHRA is to evaluate the likelihood of adverse health effects due to Expansion Project operations. The focus of the assessment is the effects of emissions to air and food on communities in the region, including traditional use of the land by First Nations and Métis peoples.

19A.6.1.1 Chemicals of Potential Concern

COPCs are chemicals that are expected to be released from the Expansion Project that have the potential to cause adverse effects on human health. The process for COPC identification and selection is discussed in Section 19A.3.

19A.6.1.2 People Evaluated in Risk Assessment

The Expansion Project is to be located adjacent to the existing Demonstration Project Legal Site Description 34/27/26-84-11-W4M, approximately 50 km south-southwest of Fort McMurray, Alberta. Surrounding land uses include hunting and trapping, recreation including camping, natural parklands, and wildlife preserves. Additional nearby areas of interest include the town of Anzac (population approximately 550), which lies 40 kilometers to the east of the Expansion Project and three First Nations communities (Clearwater Indian Reserve 175, Gregoire Lake Indian Reserve 176, and Janvier Indian Reserve 194). For the location of the Expansion Project and other regional features, see Figure 2-2.

Within these study boundaries, airborne emissions from the operations would be dispersed over the region. Specific receptor locations were identified at which to quantitatively predict the potential effects of project activities. The following assumptions were made when selecting receptor locations:

• concentrations and deposition rates of COPC from the Expansion Project are greatest closest to the operation and diminish with distance within the study area

• receptor locations must account for occupancy and activity patterns of the regional population, including traditional use of the land by First Nations and Métis peoples

The receptor locations at which air concentrations and deposition rates were specifically identified are shown on Figure 2-2 and listed in Table 2-1.

Five distinct groups of people were assessed.

• Resident: An individual living year-round in the study area who grows a vegetable garden but does not hunt or spend any appreciable amount of time on the land.

• Hunter: An individual living in the study area who grows a vegetable garden and also traps and hunts in the vicinity of the Expansion Project. Their diet includes locally caught country foods (e.g., wild game).

• Camper: An individual using the area within the study region for camping and recreation use.


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• Aboriginal Resident (AR): First Nations or Aboriginal resident in the LSA living in the study area who grows a garden, relies exclusively on local wild game from the LSA, and obtains traditional foods from the LSA.

• AENV/AHW AR: although the First Nations receptor represents the best available, current research regarding the current practices of First Nations and Aboriginal groups within Alberta, at the request of AENV, consideration was given for a potential, future scenario in which First Nations receptors would also rely exclusively on fruit and produce from the LSA for their fruit and vegetable consumption needs.

It is important that conservative assumptions are made about the potential human receptors. In accordance with Health Canada guidance, carcinogenic and non-carcinogenic COPC are evaluated differently. Non-carcinogenic COPCs are assumed to act via a threshold mechanism and exposures are assessed within specific life stages. Generally, the toddler life stage, defined as 6 months to 4 years, is considered the most sensitive life stage based on receptor characteristics (e.g., lower body weights) combined with behavioural patterns (e.g., higher soil ingestion rates). Both a toddler receptor and an adult receptor were evaluated for the non-carcinogenic COPCs.

Carcinogenic COPCs are assumed to act via a non-threshold mechanism and exposures are assessed over a lifetime. Health Canada recommends that a full lifetime of exposure be adopted as the most sensitive approach, based on combining exposures from five individual life stages:

• Infant: 0 to 6 months

• Toddler: 6 months – 4 years

• Child: 5 years – 11 years

• Teen: 12 years – 19 years

• Adults: 20 years – 75 years

This combination of multiple life stages is referred to as a “composite” or “lifetime” receptor.

19A.6.1.3 Exposure Pathways

Human receptors may come into contact with chemicals present in the environment in different ways, depending on lifestyle and local resource utilization. Paths that chemicals may travel to reach environmental media such as air, soil, water and food and subsequently can lead to human exposure are termed exposure pathways.

An exposure pathway must exist from the point of chemical emission (e.g. release of chemical into air from Expansion Project) to the point of contact with humans in order for human exposure to take place. To adequately determine the relevant exposure pathways, all appropriate affected environmental media must be examined. For this HHERA, the environmental media considered include:

• air

• soil

• food



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How a chemical travels from environmental media into systemic circulation is called an exposure route. There are three major exposure routes, which include: inhalation, ingestion and dermal absorption.

In this quantitative HHRA, people were assumed to be exposed to chemicals present in Expansion Project emissions via the following exposure routes.

• Inhalation: Expansion Project-related air emissions will result in direct exposure to vapour and particulate form COPCs by local residents.

• Inhalation and Ingestion of Soil and Indoor Dust: Airborne chemicals deposit onto soil and other surfaces. Subsequent disturbance of soil may re-suspend COPCs bound to soil and lead to incidental inhalation exposure. Additionally, incidental ingestion exposure of contaminated fine soil particles or dust may occur via hand-to-mouth transfer. This is particularly the case with children as their behaviour lends itself to frequent mouth contact with non-food-related articles.

• Dermal (Skin) Exposure to Soil and Indoor Dust: Humans may come into contact with COPCs adsorbed onto soil and dust particles through direct skin contact.

• Consumption of Locally Grown Produce: Vegetables and fruits grown locally may be a source of indirect COPC exposure via ingestion. Fruits and vegetables grown in the area may contain deposited COPCs on leaf surfaces and absorbed fractions within the plant from root zone uptake.

• Consumption of Traditional Foods: It is anticipated that Aboriginal peoples would obtain all of their traditional foods from the local study area.

• Consumption of Wild Game: Exposure to COPCs sequestered in wild game tissue may be a source of exposure to certain population groups. Specifically, First Nations peoples as well as hunters may augment their diets with locally derived wild food sources.

As noted in Section 19A.3.1, Expansion Project emissions are expected to have a negligible effect on the quality of surface water and groundwater. As a result, consumption of surface water or groundwater as a drinking water source was not evaluated in the HHRA.

19A.6.2 Exposure Assessment

Exposure assessment involves estimating the amount of a COPC a person may take into his or her body (i.e., a dose) through all applicable exposure pathways. For the purposes of this assessment, the dose of a COPC depends on the concentration in air, soil, plants and wild game; the amount of time a person is in contact with these media; and the characteristics of the receptor (e.g., ingestion rate, inhalation rate, body weight, food preferences).

Input values, equations, and exposure assumptions are provided in Appendix 19A-2.

19A.6.2.1 Receptor Characteristics

The contribution of a particular route of exposure (e.g., inhalation, ingestion) to total exposure is determined by COPC fate and behaviour in the environment, as well as by the receptor characteristics relevant to each route of exposure (e.g., breathing rate, food consumption rate, area of skin exposed).


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To select the most appropriate receptor characteristics of typical people at each life stage, a number of different guidance documents were reviewed. The HHRA uses current guidance documents to define each receptor characteristic, including:

• Federal Contaminated Sites Risk Assessment in Canada. PART I: Guidance on Human Health Risk Preliminary Quantitative Risk Assessment (PQRA). (Health Canada 2004)

• Compendium of Canadian Human Exposure Factors for Risk Assessment. O’Connor Associates Environmental Inc. 1155-2720 Queensview Dr., Ottawa, Ontario. (Richardson, G. M. 1997)

• Health Canada (1994). Human Health Risk Assessment for Priority Substances: Canadian Environmental Protection Act: ISBN 0-662-22126-5

• Risk Assessment Guidance for Superfund Volume I: Human Health Evaluation Manual (Part E, Supplemental Guidance for Dermal Risk Assessment) Final. EPA/540//R/99/005. July, 2004. (US EPA 2004)

• The US EPA Human Health Risk Assessment Protocol (HHRAP) for Hazardous Waste Combustion Facilities. (US EPA 2005)

Canadian guidance documents (e.g. Health Canada 2004) were given priority when possible. However, Canadian directives containing receptor characterization data are currently not available. Accordingly, the US EPA (2005) is used as the primary source for exposure scenario development and the fate and transport methods. Furthermore, the receptor data published in the HHRAP (US EPA 2005) are intended for the fate and transport methods and therefore were used to help characterize human receptors.

A toddler and an adult were used to characterize risks to receptors associated with non-carcinogenic COPCs, and a composite lifetime receptor (consisting of infant, toddler, child, youth and adult life stages) was used to assess risk to carcinogenic COPCs. General receptor characteristics for each specific age group are presented in Table 6-1. Specific receptor characteristics and exposure variables used in the current assessment for each exposure scenario are summarized in Appendix 19A-5.

In order to adequately characterize the potential exposure to the Aboriginal population who live in the vicinity of the Expansion Project, two exposure scenarios were modelled with receptors labelled as Aboriginal receptor and the AENV/AHW AR receptor, respectively.

The Aboriginal receptor is a local Aboriginal resident who is assumed to harvest, hunt and fish for the majority of their food. Wild game is assumed to be the sole meat source. The receptor is also assumed to collect and harvest locally available traditional vegetation for consumption and medicinal purposes. It is also assumed that the Aboriginal receptor has a garden from which 10% of their produce and garden fruit is grown. The remaining 90% of the fruit and produce and the consumed dairy products are assumed to be commercially acquired and not impacted by the Expansion Project and therefore not included in the assessment.



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Table 6-1 General Receptor Characteristics

Characteristic Receptor Values

Reference Infant Toddler Child Teen Adult Age 0-6 mo. 7 mo.–4 yr 5-11 yr 12 – 19 yr 20 – 75 yr Health Canada (2004) AT (years) 0.5 4.5 7 8 56 Health Canada (2004) BW (kg) 8.2 16.5 32.9 59.7 70.7 Health Canada (2004) IRsoil (mg/d) 20 80 20 20 20 Health Canada (2004) IRair (m3/hr) 2.1 9.3 14.5 15.8 15.8 Health Canada (2004) SAhand (cm2) 320 430 590 800 890 Richardson (1997) SAbody (cm2) 1780 3010 5140 8000 9110 Richardson (1997)

The receptor identified as the AENV/AHW AR receptor is assumed to be an Aboriginal receptor that not only follows a lifestyle of traditional hunting, harvesting and fishing but also grows their annual supply of fruit and produce in the LSA. The receptor is also assumed to collect and harvest locally available traditional vegetation for consumption and medicinal purposes. The dairy products consumed by this receptor are assumed to be commercially acquired and therefore not impacted by the proposed Expansion Project. Accordingly, consumption of dairy products was not included in the assessment, consistent with the Aboriginal land use practices in the area and reflecting the absence of dairy cows.

The only difference between the Aboriginal receptor and the AENV/AHW AR receptor is in the assumption of the consumption of 100% of locally grown produce and garden fruit. All other consumption exposures and quantities are equivalent. The AENV/AHW AR receptor was included to fulfil information requirements of AHW and AENV, and is not based on current land use or practices. This artificial receptor has increased exposure to chemicals in the LSA through food consumption. The receptor modelled as a “Aboriginal receptor” provides a conservative and protective assessment of exposure to COPCs through food and is the best representation of the Aboriginal diet for local receptors.

Traditional vegetation is consumed by members of local First Nations and Métis groups. No consumption estimates were obtained specifically for this HHRA, therefore, available literature values were used in the assessment of exposure for Aboriginal and AENV/AHW AR receptors. The consumption of traditional vegetation was modelled through the analysis of data obtained by the collection of three representative species: blueberry (Vaccinium myrtilloides) (berry), Labrador tea (Ledum groenlandicum) (leaf) and blueberry (Vaccinium myrtilloides) (root). Fifteen distinct samples of Labrador tea and fourteen distinct samples of blueberry were collected from 17 geographic locations within the study area.

In 1989, Wein published a doctoral dissertation, which included the details of a food frequency and consumption study completed in the area of the Regional Municipality of Wood Buffalo. This study followed the traditional food consumption patterns of 178 subjects over one year. The consumption frequencies were calculated based on occasions of traditional food consumption. For a total of 319 occasions on which traditional foods were consumed over one year 63±10 (calculated as ((63/319)*100%) = 17%) occasions of consumption were berries and 7±2 (2%) occasions of consumption of traditional tea plants (Wein 1989).

Wein then applied these consumption frequencies to a Health and Welfare Canada 1977 survey to determine the potential daily consumption quantities. Reports from the Health and Welfare Canada 1977


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survey indicate that the average fruits consumption estimate was 134 g/day; from this survey and the frequency data, Wein estimated that 23 g/day of berries would be consumed (calculated as 17% of 134). Tea and root plant consumption has historically been estimated. While the survey included questions regarding the tea plants as a beverage, no consumption frequencies were obtained for the medicinal roots. On page 63 of the thesis it is indicated that “Wild roots, leaves and birch sap were very seldom used and do not appear in the table at all”. (The equivalent calculation for roots and plants = ((7/365)*100%*134) = 2.6 g/day).

Wein then completed four 24-hour dietary recall assessments in which participants identified the quantity of traditional foods consumed. Berries were considered a group and were not further distinguished by type. Plants and roots were not identified as a group.

In the absence of community specific consumption data, the data collected by Wein in the 24-hour recall analysis are used as representative of the consumption quantities for berries. For the purpose of this study, it is assumed that all of the berries consumed are blueberries. A summary of the Wein berry consumption data is included as Table 6-2. Wein did not calculate the quantity of Labrador or mint tea consumed, rather the frequency was recorded by season.

Table 6-2 Summary of Wein (1989) 24-hour Recall Data

Receptor Berry Consumption Quantity Reference Adolescent 4 g/day male; 2g/day female Wein (1989), page 105 Adult 15g/day max; 3g/day min Wein (1989), page 105 Entire sample (Adolescent and adult) 5g/day average Wein (1989)

A traditional food study including both food frequency surveys and 24-hour recalls for five Aboriginal communities in the Regional Municipality of Wood Buffalo was completed on behalf of CEMA in 2009. The study examined the consumption of traditional foods by adults. The average berry consumption estimated across the study population was 5.9±1.5 g/day. The consumption estimates of all traditional plants for tea (mint, Labrador tea and pine needle) ranged between 1.5 and 2.9 g/day for adult consumers and the maximum rat root consumption was noted at 1.6 g/day (CEMA 2009).

As the Wein (1989) study did not calculate an average plant or root intake, the adopted approach has been to estimate the root and tea plant consumption from the combination of the Wein food frequency data and the Health and Welfare Canada 1977 survey data (134 g fruit/day) to yield an average consumption estimate of 3 g/day for root and leaf consumption. A summary of the leaf and root consumption data is included as Table 6-3.

Table 6-3 Summary of Leaf and Root Consumption Data

Receptor Tea leaf use

data Rat Root Consumption

Quantity Reference Adult (maximum) 2.9 g/day 1.6 g/day CEMA (2009) Adult (average estimate) 3 g/day 3 g/day Wein (1989) and HWC (1977)



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The consumption or use quantity estimates used in the calculation of exposure to traditional vegetation in this assessment are included in Table 6-4. The maximum tea leaf use data and quantities from CEMA 2009 (2.9 g/day) compare to the Wein calculation and the data that has been used in recent risk assessments in this geographic area (3 g/day). The maximum root consumption quantities from CEMA 2009 (1.6 g/day) are considered appropriate for this HHRA.

Table 6-4 Consumption/use quantities used in the assessment

Receptor

Blueberry consumption quantities

(g/day)

Labrador Tea consumption/use quantities

(g/day)

Medicinal root consumption quantities

(g/day) Infant 0 0 0 Toddler 5 (Wein adolescent) 1 (assumed) 1 (assumed) Child 5 (Wein adolescent) 1 (assumed) 1 (assumed) Adolescent 5 (Wein adolescent) 1 (assumed) 1 (assumed) Adult 15 (Wein adult) 3 (CEMA, Wein) 1.6 (CEMA)

All of the consumption and use data for leaves and roots were provided for adult consumers. The infant is assumed to consume only breast milk for the first 6 months. The toddler, child and adolescent are assumed to consume less based on tea preference (cold drinks versus hot drinks). For the purposes of this study the adolescent, toddler and child are assumed to consume or use a maximum of 1 g/day of medicinal root and 1 g/day of tea leaf.

A summary of the receptor consumption characteristics for both the First Nation Receptor and the AENV/AHW AR receptor are included in Tables 6-5 and 6-6.

Table 6-5 Food Ingestion Rates for the Aboriginal and AENV/AHW AR Toddler Receptor (g/day)

Receptor Characteristic Aboriginal Receptor

AENV/AHW AR Receptor Reference

Aboveground Exposed Garden Producea

2.8 28 Health Canada (2004) – Other Vegetables

Aboveground Protected Garden Producea


Belowground Produce 10.5 105 Health Canada (2004) – Root Vegetables

Garden Fruit 11.2 112 US EPA (1997) Aboveground Exposed Traditional Plants

1 1 CEMA (2009) and Wein (1989)

Belowground Traditional Plants 1 1 CEMA (2009) and Wein (1989) Wild Fruit 5 5 Wein (1989) Wild Game 31 31 Alberta Health (1997) NOTE: a Health Canada values for other vegetables were distributed between aboveground exposed and protected garden

produce based on a ratio of ingestion rates as per US EPA Exposure Factors Handbook (1997) Table 13-63


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Table 6-6 Food Ingestion Rates for the Aboriginal and AENV/AHW AR Adult Receptor (g/day)

Receptor Characteristic Aboriginal Receptor

AENV/AHW AR Receptor Reference

Aboveground Exposed Garden Producea


Aboveground Protected Garden Producea


Belowground Produce 18.8 188 Health Canada (2004) – Root Vegetables

Garden Fruit 70.2 702 US EPA (1997) Aboveground Exposed Traditional Plants

3 3 CEMA (2009) and Wein (1989)

Belowground Traditional Plants 1.6 1.6 CEMA (2009) and Wein (1989) Wild Fruit 15 15 Wein (1989) Wild Game 126 126 US EPA (1997) – Sum of Beef

and Pork Ingestion Rates for Subsistence Farmerb

NOTES: a Health Canada values for other vegetables were distributed between aboveground exposed and protected garden

produce based on a ratio of ingestion rates as per US EPA Exposure Factors Handbook (1997) Table 13-63 b US EPA (1997) consumption rate used as the Alberta Health (1997) reported ingestion rate of 67 g/day was lower

than that reported for a subsistence farmer

19A.6.2.2 Predicting Human Intakes

Daily intakes from all sources are discussed by scenario in the following sections and presented for individual COPCs. Ingestion rates and receptor characteristics (e.g., body weight) were obtained from a variety of sources, including Health Canada (2004a), the Exposure Factors Handbook (US EPA 1997) or from Richardson (1997) and are briefly discussed in Section 19A.6.3.1.

Daily intakes are calculated in the form of chronic daily intakes (CDIs) (to assess non-carcinogenic endpoints) and lifetime average daily doses (LADDs) (to assess carcinogenic endpoints), using the equations presented below:

Where:

CDIi = chronic daily intake via pathway i mg/kg bw-day

LADDi = lifetime average daily dose via pathway i mg/kg bw-day

Intake nc = intake rate for medium i (e.g., game) (non-carcinogenic) kg medium/kg bw-day

inci C x IntakeCDI =

ici C xIntakeLADD =



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Intake c = intake rate for medium i (e.g., game)(carcinogenic) kg medium/kg bw-day

Ci = concentration of chemical in medium i (e.g., game) mg COPC/kg medium

Tables of all CDIs and LADDs by scenario and receptor for all COPCs are presented in Appendix 19A-7.

19A.6.3 Toxicity Assessment

The objective of the toxicity assessment is to identify the potential adverse health effects associated with each COPC as a consequence of acute and chronic exposures. Using this knowledge, a Toxicity Reference Value (TRV) is generated, which defines the chronic daily dose of a COPC below which unacceptable adverse effects are not expected to occur. TRVs are specific to each COPC evaluated in the HHRA.

TRVs used in this risk assessment were determined from studies where endpoints were derived from the administered dose, rather than the absorbed dose (i.e., absorbed / retained concentration of contaminant in the organ or body). This is a conservative approach because compounds are often administered in a more available form than would be found in the environment and via an exposure route that over estimates a real-world exposure scenario (e.g. gastric lavage vs. incidental ingestion).

Two distinct patterns of dose-response relationships have been observed: threshold behaviour and non-threshold behaviour. In the first pattern, threshold behaviour, a specific dose level can be identified at which no adverse effects are observed. This dose, known as a No Observed Adverse Effects Level (NOAEL), adjusted by uncertainty factors, serves as the basis for many TRVs. Alternatively, if a NOAEL cannot be identified, a lowest observed adverse effects level (LOAEL), being the minimum dose, at which (usually minor) adverse effects are observed, may be used to derive a TRV instead; the application of an extra uncertainty factor to a LOAEL is warranted when deriving a TRV, since the “safe” dose level below that LOAEL may not have been identified.

Many dose-response relationships, however, do not show threshold behaviour, and no NOAEL or LOAEL can be clearly identified. Such cases arise when studying carcinogenic effects of chemicals, and for these effects, it is not practical to propose a TRV based on the NOAEL/LOAEL approach, since no dose can be designated as having zero risk. For chemicals that induce cancer, a slope factor or unit risk factor is used as a TRV; usually based on statistical measures of incidence of or mortality due to cancer in cohorts of individuals exposed to the chemicals in question.

In addition to the TRVs, relative oral, inhalation, and dermal bioavailability values are also part of the toxicity assessment. Bioavailability refers to the amount of a chemical that reaches the bloodstream, once it has entered the body through a specific route. Oral bioavailability, then, refers to the fraction of a chemical that reaches the bloodstream after ingestion and its partial passage through the gastrointestinal tract. Similarly, inhalation bioavailability refers to the fraction of inhaled chemical that reaches the bloodstream after absorption in the lungs, and dermal bioavailability refers to the fraction of chemical that reaches the bloodstream after being applied to the skin. Bioavailability factors used in the risk assessment are summarized in Section 19A.6.3.2.


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19A.6.3.1 Selection of TRVs

The toxicity reference values used in this risk assessment may be divided into two categories: those for acute, or short-term exposures and chronic, or long-term exposures. For acute exposures, concentrations of COPC in air were compared to health-based benchmarks established by the following regulatory agencies:

• Alberta Environment (AENV) – as the Expansion Project is located in northern Alberta and is subject to Provincial jurisdiction, criteria published by AENV were included in the review

• Ontario Ministry of the Environment (OMOE) – the OMOE represents another Canadian provincial jurisdiction that has the most complete listing of acute screening criteria for air pollutants

• Agency for Toxic Substances and Disease Registry (ATSDR) – the ATSDR is a recognized source agency recommended by Health Canada

• California Environmental Protection Agency (CalEPA) – the CalEPA Office of Environmental Health Hazard Assessment (OEHHA) developed health-based reference exposure levels for acute exposures and has been accepted as an appropriate source of toxicological values by AENV

In instances where more than one of the above-noted agencies provided an acute health-based benchmark, the most stringent exposure limit was typically selected. In instances where none of the above-noted agencies provided an acute health-based benchmark, the following additional sources were considered:

• Texas Commission on Environmental Quality (TCEQ) - The TCEQ effects screening levels database has been cited as a source of acute exposure limits by AENV

• Total Petroleum Hydrocarbon Criteria Working Group (TPHCWG) – The TPHCWG was the primary source of toxicological information used in the development of the Canada Wide Standards for TPH

A summary of the TRV selection for acute 1-hour and 24-hour exposure periods is provided in Table 6-6 and 6-7, respectively. Additional details are provided in the toxicological profiles in Appendix 19A-6.

For chronic exposures, concentrations of COPC were compared to health-based benchmarks established by the following regulatory agencies:

• Alberta Environment (AENV) – as the Expansion Project is located in northern Alberta and is subject to Provincial jurisdiction, criteria published by AENV were included in the review

• Health Canada (HC) – Alberta is subject to federal jurisdiction and Health Canada is the federal agency responsible for the development of TRVs

• US Environmental Protection Agency (US EPA) – The US EPA Integrated Risk Information System (IRIS) provides the best source of extensively peer-reviewed TRVs published by another North American jurisdiction



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• Agency for Toxic Substances and Disease Registry (ATSDR) – the ATSDR is a recognized source agency recommended by Health Canada

• Netherlands (RIVM) – The Netherlands is a recognized source agency recommended by Health Canada

Table 6-6 Acute Exposure Limits for COPC (μg/m3) – 1-hour Exposures

COPC Primary Regulatory Agencies Reviewed Value

Selected Critical Effect AENV OMOE ATSDR CalEPA Criteria Air Contaminants SO2 450 690 - 660 450 Pulmonary function NO2 400 400 - 470 400 Health Effects PM2.5 - - - - NV -- CO 15,000 36,200 - 23,000 15,000 Oxygen carrying capacity of

blood Petroleum hydrocarbons Benzene 30 - 30 1,300 30 Health Effects Toluene 1,880 - 3,800 37,000 1,880 Health Effects Ethylbenzene - - 43,350 - 43,350 Significant deterioration in

CAP auditory thresholds and significant OHC losses

Xylenes 2,300 - 8,670 22,000 2,300 Neurological effects Aliphatic C5-C8 - - - - 3,500 Health effects (based on

heptane as surrogate) 1 Aliphatic C9-C16 - - - - 2,600 Neurological effects 2 Aromatic C9-C16 - - - - 9,000 No significant adverse

effect3 Aromatic C17-C34 - - - - 0.5 Health effects 1 Carcinogenic PAHs Benz(a)anthracene - - - - 0.5 Health effects 1 Benzo(a)pyrene (BaP) - - - - 0.03 Health effects 1 Benzo(e)pyrene - - - - 0.5 Health effects 1 Benzo(b)fluoranthene - - - - 0.5 Health effects 1 Benzo(g,h,i)perylene - - - - 0.5 Health effects 1 Benzo(k)fluoranthene - - - - 0.5 Health effects 1 Chrysene - - - - 0.5 Health effects 1 Dibenzo(a,h)anthracene - - - - 0.5 Health effects 1 Fluoranthene - - - - 0.5 Health effects 1 Indeno(1,2,3-cd)pyrene - - - - 0.5 Health effects 1 Phenanthrene - - - - 0.5 Health effects 1 Pyrene - - - - 0.5 Health effects 1 Perylene - - - - 0.5 Health effects 1


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Table 6-6 Acute Exposure Limits for COPC (μg/m3) – 1-hour Exposures (cont’d)


Selected Critical Effect AENV OMOE ATSDR CalEPA Non-carcinogenic PAHs Anthracene - - - - 0.5 Health effects 1 Fluorene - - - - 10 Health effects 1 Naphthalene - - - - NV -- VOCs Acetaldehyde - - - 470 470 Respiratory effects Acrolein - - 6.9 2.3 2.3 Eye irritation Benzaldehyde - - - - NV -- Carbon disulfide - - - 6,200 6,200 Reproductive/developmental

effects Dichlorobenzene - 30,500 12,000 - 12,000 Eye/nose irritation Formaldehyde 65 - 50 55 50 Respiratory effects Hexane 21,000 - - - 21,000 Neurotoxicity Hydrogen sulfide - - 100 42 42 Headache, nausea Thiophene - - - - NV -- Metals Aluminum (Al) - - - - 50 Health effects 1 Chromium (Total) 1 - - - 1 Health effects Cobalt (Co) - - - - 0.2 Health effects 1 Copper (Cu) - - - 100 100 Detectable by taste Lead (Pb) 1.5 - - - 1.5 Hemopoietic system

impairment Manganese (Mn) 2 - - - 2 Health effects Molybdenum (Mo) - - - - 50 Health effects 1 Nickel (Ni) 6 - - 6 6 Respiratory effects Strontium (Sr) - - - - 20 Health effects 1 Vanadium (V) - - - - 0.5 Health effects 1 Zinc (Zn) - - - - 50 Health effects 1 NOTES: 1 Value obtained from TCEQ effects screening levels database 2 Value obtained from Massachusetts Department of Environmental Protection 3 Value obtained from TPHCWG NV – No value identified



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Table 6-7 Acute Exposure Limits for COPC (μg/m3) – 24-hour Exposures


Selected Critical Effect AENV OMOE ATSDR CalEPA Criteria Air Contaminants SO2 150 275 - - 150 Vegetation NO2 - 200 - - 200 Health effects PM2.5 30 30 - - 30 Health effects CO - - - - NV -- Petroleum hydrocarbons Benzene - - 30 - 30 Reduced lymphocyte

proliferation following mitogen stimulation

Toluene 400 - - - 400 Health effects Ethylbenzene - 1,000 - - 1,000 Dizziness, throat and eye

irritation Xylenes 700 730 - - 700 Nervous system and

respiratory effects Aliphatic C5-C8 - 11,000 - - 11,000 Health effects (based on

heptane as surrogate) Aliphatic C9-C16 - - - - NV -- Aromatic C9-C16 - - - - NV -- Aromatic C17-C34 - - - - NV -- Carcinogenic PAHs Benz(a)anthracene - - - - NV -- Benzo(a)pyrene (BaP) - 0.0011 - - 0.0011 Health effects Benzo(e)pyrene - - - - NV -- Benzo(b)fluoranthene - - - - NV -- Benzo(g,h,i)perylene - - - - NV -- Benzo(k)fluoranthene - - - - NV -- Chrysene - - - - NV -- Dibenzo(a,h)anthracene - - - - NV -- Fluoranthene - - - - NV -- Indeno(1,2,3-cd)pyrene - - - - NV -- Phenanthrene - - - - NV -- Pyrene - - - - NV -- Perylene - - - - NV --


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Table 6-7 Acute Exposure Limits for COPC (μg/m3) – 24-hour Exposures (cont’d)


Selected Critical Effect AENV OMOE ATSDR CalEPA Non-carcinogenic PAHs Anthracene - - - - NV -- Fluorene - - - - NV -- Naphthalene - 22.5 - - 22.5 Health effects VOCs Acetaldehyde - 500 - - 500 Tissue damage Acrolein - 0.08 - - 0.08 Nasal lesions Benzaldehyde - - - - NV -- Carbon disulfide - - - - NV -- Dichlorobenzene - 95 - - 95 Eye and nasal irritation Formaldehyde - 65 - - 65 Health effects Hexane 7,000 7,500 - - 7,000 Nervous system effects Hydrogen sulfide - 7 - - 7 Health effects Thiophene - - - - NV -- Metals Aluminum (Al) - - - - NV -- Chromium (Total) - - - - NV -- Cobalt (Co) - 0.1 - - 0.1 Respiratory effects Copper (Cu) - 50 - - 50 Respiratory irritation Lead (Pb) - 0.5 - - 0.5 Adverse effects on liver and

kidney Manganese (Mn) - 2.5 - - 2.5 Central nervous system

effects Molybdenum (Mo) - 120 - - 120 Particulate Nickel (Ni) - 2 0.2 - 0.2 Respiratory effects Strontium (Sr) - 120 - - 120 Particulate Vanadium (V) - 2 - - 2 Health effects Zinc (Zn) - 120 - - 120 Particulate NOTE: NV – No value identified



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The World Health Organizations (WHO) air quality guidelines for Europe were also consulted for chronic exposures via inhalation. In instances where more than one of the above-noted agencies provided a TRV, the most stringent exposure limit was typically selected.

A summary of the TRV selection for chronic inhalation of non-carcinogenic and carcinogenic COPC is provided in Tables 6-8 and 6-9, respectively. A summary of the oral TRVs for non-carcinogenic and carcinogenic COPC is provided in Tables 6-10 and 6-11, respectively. Additional details are provided in the toxicological profiles in Appendix 19A-6.

Table 6-8 Chronic Non-carcinogenic Exposure Limits (μg/m3)

COPC

Primary Regulatory Agencies Reviewed Value

Selected Critical Effect AENV HC US

EPA ATSDR RIVM Criteria Air Contaminants SO2 30 30 79 - - 30 Environment NO2 60 60 , - - 60 Health PM2.5 - - - - - NV -- CO - - - - - NV -- Petroleum hydrocarbons Benzene - - 30 98 - 30 Decreased lymphocyte

count Toluene 3,800 3,800 5,000 300 400 300 Vision impairment Ethylbenzene 1,000 1,000 1,000 1,300 770 770 Liver and kidney

effects Xylenes 180 180 100 200 870 100 Impaired motor

coordination, decreased rotarod performance

Aliphatic C5-C8 - - - - - 18,400 Neurotoxicity Aliphatic C9-C16 - - - - - 1,000 Hepatic and

hematological changes Aromatic C9-C16 - - - - - 200 Decreased body

weight Aromatic C17-C34 - - - - - NV Not sufficiently volatile Carcinogenic PAHs Benz(a)anthracene - - - - - 0.05 Health effects 1 Benzo(a)pyrene (BaP) 0.0003 - - - - 0.0003 Chronic and

carcinogenic human health effects

Benzo(e)pyrene - - - - - 0.05 Health effects 1


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Table 6-8 Chronic Non-carcinogenic Exposure Limits (μg/m3) (cont’d)

COPC



EPA ATSDR RIVM Carcinogenic PAHs (cont’d) Benzo(b)fluoranthene - - - - - 0.05 Health effects 1 Benzo(g,h,i)perylene - - - - - 0.05 Health effects 1 Benzo(k)fluoranthene - - - - - 0.05 Health effects 1 Chrysene - - - - - 0.05 Health effects 1 Dibenzo(a,h)anthracene - - - - - 0.05 Health effects 1 Fluoranthene 180 - - - - 180 Route-to-route

extrapolation 2 Indeno(1,2,3-cd)pyrene - - - - - 0.05 Health effects 1 Phenanthrene - - - - - 0.05 Health effects 1 Pyrene 130 - - - - 130 Route-to-route

extrapolation 2 Perylene - - - - - 0.05 Health effects 1 Non-carcinogenic PAHs Anthracene 1,340 - - - - 1,340 Route-to-route

extrapolation 2 Fluorene 180 - - - - 180 Route-to-route

extrapolation 2 Naphthalene 3 - 3 4 - 3 Nasal effects,

hyperplasia and metaplasia in respiratory and olfactory epithelium

VOCs Acetaldehyde - - 9 - - 9 Degeneration of

olfactory epithelium Acrolein - - 0.02 - - 0.02 Nasal lesions Benzaldehyde - - - - - NV -- Carbon disulfide - - 700 800 - 700 Peripheral nervous

system dysfunction Dichlorobenzene 95 95 800 60 600 60 Moderate to severe

eosinophilic changes in the nasal olfactory epithelium

Formaldehyde - - - 10 10 10 Eye and respiratory tract irritation; damage to the nasal epithelium

Hexane - 700 700 2,000 - 700 Peripheral neuropathy Hydrogen sulfide - - 2 - - 2 nasal lesions of the

olfactory mucosa Thiophene



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Table 6-8 Chronic Non-carcinogenic Exposure Limits (μg/m3) (cont’d)

COPC



EPA ATSDR RIVM Metals Aluminum (Al) - - - - - 5 Health effects 1 Chromium (Total) - - - - 60 60 Kidney effects in

humans Cobalt (Co) - - - 0.1 0.5 0.1 Respiratory irritation 3 Copper (Cu) - - - - 1 1 Lung, immune system Lead (Pb) - - - - - 0.5 Blood lead levels 3 Manganese (Mn) - - 0.05 0.3 - 0.05 Impairment of

neurobehavioral function

Molybdenum (Mo) - - - - 12 12 Body weight Nickel (Ni) - 0.018 - 0.09 0.05 0.018 Respiratory effects,

morphological and biological effects

Strontium (Sr) - - - - - 2 Health effects 1 Vanadium (V) - - - - - 1 Chronic upper

respiratory tract symptoms 3

Zinc (Zn) - - - - - 5 Metal fume fever 1 NOTES: 1 Value obtained from TCEQ effects screening levels database 2 Route-to-route extrapolation from oral TDI assuming body weight of 70.7 kg and inhalation rate of 15.8 m3/day 3 Value obtained from WHO (2000) NV – No value identified

Table 6-9 Chronic Carcinogenic Exposure Limits (μg/m3)-1

COPC



EPA ATSDR RIVM Benzene 3.3E-06 3.3E-06 7.8E-06 - 5.0E-06 7.8E-06 Leukemia Benzo(a)pyrene (BaP) - 3.1E-05 - - - 3.1E-05 Respiratory Tract

Tumours Acetaldehyde - - 2.2E-06 - - 2.2E-06 nasal squamous cell

carcinoma Formaldehyde - - 1.3E-05 - - 1.3E-05 squamous cell

carcinoma Chromium (Total) - 0.0109 - - - 0.0109 lung carcinogen NOTES: COPC not shown in Table 6-9 do not have a carcinogenic TRV. Carcinogenic PAHs were assessed as a mixture, as discussed in Section 19A.6.3.3.


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Table 6-10 Chronic Non-carcinogenic Exposure Limits (μg/kg-day)

COPC 1



EPA ATSDR RIVM Petroleum hydrocarbons Aliphatic C5-C8 - - - - - 5,000 Neurotoxicity 2 Aliphatic C9-C16 - - - - - 100 Hepatic and

hematological changes2

Aromatic C9-C16 - - - - - 40 Decreased body weight2

Aromatic C17-C34 - - - - - 30 Nephrotoxicity 2 PAHs Anthracene 300 - 300 - - 300 No observed effects Fluoranthene 40 - 40 - - 40 Nephopathy, increased

liver weight, hematological alterations and clinical effects

Fluorene 40 - 40 - - 40 Decreased rbc, packed cell volume and hemoglobin

Pyrene 30 30 30 - - 30 Kidney effects VOCs Dichlorobenzene 110 110 90 70 190 110 3 Nephrotoxic,

nepropathy and parathyroid hyperplasia

Metals Aluminum (Al) - - - 1,000 - 1,000 Neurological Chromium (Total) - 1 - - - 1 Hepatotoxicity, irritation

or corrosion of the gastrointestinal mucosa encephalitis

Cobalt (Co) - - - - 1.4 1.4 Cardiomyopathy Copper (Cu) - 90 - - 140 90 0-4 years of age;

hepatotoxicity, gastrointestinal effects

Lead (Pb) - 3.6 - - 3.6 3.6 Net retention of Pb in blood of infants

Manganese (Mn) - 100 140 - - 100 0-19 years of age; Parkinsonian-like neurotoxicity

Molybdenum (Mo) - 23 5 - 10 5 Increased serum uric acid levels

Nickel (Ni) - - 20 - 50 20 Decreased body and organ weight



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Table 6-10 Chronic Non-carcinogenic Exposure Limits (μg/kg-day) (cont’d)

COPC 1



EPA ATSDR RIVM Metals (cont’d) Strontium (Sr) - - 600 - - 600 Rachitic bone Vanadium (V) - - 9 - - 9 Decreased hair cystine Zinc (Zn) - 500 300 300 500 300 Decreased EROD

activity NOTES: 1 COPC not shown in Table 6-10 either do not have a non-carcinogenic TRV or have negligible potential to persist

or bioaccumulate in the environment (see Section 19A.3.2.2). 2 Value selected from Canada Wide Standards technical document (CCME 2008). 3 The Alberta Environment (2009; based on Health Canada, 2009) TDI of 110 μg/kg-day for 1,4-dichlorobenzene

was selected for use in this risk assessment. The lower US EPA RfD (for 1,2-dichlorobenzene) was not selected based on the questionable significance of the health effects observed in the basis study, as well as the uncertainty involved with the derivation of the RfD. The lower ATSDR MRL (for 1,4-dichlorobenzene) was not selected as the confidence in the measured critical health effects is lower. Effects such as changes in liver weight are subject to a greater variety of confounding factors and the direct cause of such changes can be more difficult to isolate.

NV – No value identified

Table 6-11 Chronic Carcinogenic Exposure Limits (μg/kg-day)-1

COPC



EPA ATSDR RIVM Benzo(a)pyrene (BaP) - 3.1E-05 - - - 3.1E-05 Respiratory Tract

Tumours NOTES: Carcinogenic PAHs were assessed as a mixture, as discussed in Section 19A.6.3.3. COPC not shown in Table 6-11 either do not have a carcinogenic TRV or have negligible potential to persist or bioaccumulate in the environment (see Section 19A.3.2.2).

19A.6.3.2 Bioavailability

Bioavailability of a contaminant can be defined as the total dose, administered by any route, which makes it to systemic circulation in an unchanged form. The bioavailability will vary depending on the pathway of exposure (i.e., ingestion, inhalation, or dermal contact), the form of the contaminant (e.g., dissolved in water versus adsorbed to fine soil), and the physiological characteristics of the receptor at the time of exposure (e.g., absorption may be higher if the receptor is malnourished, or has a specific nutritional requirement, such as toddlers). Bioaccessibility is the fraction of a contaminant in an environmental medium that is available for absorption based on laboratory extraction, but it is not necessarily absorbed.

The process of a contaminant entering the body can be described in two steps – contact with an outer boundary (exposure or intake), followed by actual entry into the bloodstream (uptake). Intake is typically defined as the process by which a contaminant crosses the outer surface of a receptor without passing an absorption barrier (such as through ingestion, inhalation, or dermal contact), while uptake is the process


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by which a contaminant crosses an absorption barrier (such as the lining of the gastrointestinal tract, the outer layer of skin, or the lining of the lungs) into the receptor.

All oral and inhalation bioavailability factors have been conservatively set to 1.0, meaning each COPC is 100% bioavailable via the oral and inhalation routes of exposure. The dermal bioavailability factors used in this assessment are provided in Table 6-12.

Table 6-12 Relative Dermal Bioavailability Factors

COPC Relative Dermal Bioavailability

Factor Source Petroleum Hydrocarbons Aliphatic C5-C8 0.2 Health Canada (2004) Aliphatic C9-C16 0.2 Health Canada (2004) Aromatic C9-C16 0.2 Health Canada (2004) Aromatic C17-C34 0.2 Health Canada (2004) PAHs Anthracene 0.29 Health Canada (2004) Benz(a)anthracene 0.2 Health Canada (2004) Benzo(a)pyrene (BaP) 0.2 Health Canada (2004) Benzo(e)pyrene 0.2 Health Canada (2004) Benzo(b)fluoranthene 0.2 Health Canada (2004) Benzo(g,h,i)perylene 0.2 Health Canada (2004) Benzo(k)fluoranthene 0.2 Health Canada (2004) Chrysene 0.2 Health Canada (2004) Dibenzo(a,h)anthracene 0.2 Health Canada (2004) Fluoranthene 0.2 Health Canada (2004) Fluorene 0.2 Health Canada (2004) Indeno(1,2,3-cd)pyrene 0.2 Health Canada (2004) Phenanthrene 0.2 Health Canada (2004) Pyrene 0.2 Health Canada (2004) Perylene 0.2 Health Canada (2004) VOCs Dichlorobenzene 1 assumed Inorganics Aluminum 1 assumed Chromium (Total) 0.04 Health Canada (2004) Cobalt 0.1 Health Canada (2004) Copper 0.1 Health Canada (2004) Lead 0.006 Health Canada (2004) Manganese 1 assumed Molybdenum 0.1 Health Canada (2004)



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Table 6-12 Relative Dermal Bioavailability Factors (cont’d)

COPC Relative Dermal Bioavailability

Factor Source Inorganics (cont’d) Nickel 0.35 RAIS (2006) Strontium 1 assumed Vanadium 0.1 Health Canada (2004) Zinc 0.02 Health Canada (2004)

19A.6.3.3 Chemical Mixtures

In order to properly assess health risks to the human receptors, certain groups of chemicals were assessed as mixtures. For the purposes of this assessment, the carcinogenic PAHs have been assessed as a mixture, the TRVs for which are based benzo[a]pyrene. The modes of cancer induction of these PAHs are all similar; their carcinogenic potencies are; however, different. In this risk assessment, each of the carcinogenic PAHs has been assigned a toxic equivalency factor (TEF), relative to benzo(a)pyrene, to represent this differing potency. The TEFs were chosen based on the recommendations of the World Health Organization (WHO 1998), with benzo(a)pyrene being assigned a TEF of 1. These TEFs are summarized in the table below.

Table 6-13 Toxic Equivalence Factors

Chemical CAS# TEF Source Agency Anthracene 120-12-7 NA Non-carcinogenic

Benzo(a)anthracene 56-55-3 0.1 Health Canada 2007

Benzo(b)fluoranthene 205-99-2 0.1 Health Canada 2007

Benzo(k)fluoranthene 207-08-9 0.1 Health Canada 2007

Benzo(ghi)perylene 191-24-2 0.01 Health Canada 2007

Benzo(a)pyrene 50-32-8 1 NA

Benzo(e)pyrene 192-97-2 0.01 IPCS 1998

Chrysene 218-01-9 0.01 Health Canada 2007

Dibenzo(a,h)anthracene 53-70-3 1 Health Canada 2007

Fluoranthene 206-44-0 0.001 Health Canada 2007

Fluorene 86-73-7 NA Non-carcinogenic

Indeno(1,2,3 – cd)pyrene 193-39-5 0.1 Health Canada 2007

Naphthalene 91-20-3 NA Non-carcinogenic

Perylene 198-55-0 0.001 IPCS 1998

Phenanthrene 85-01-8 0.001 Health Canada 2007

Pyrene 129-00-0 0.001 RIVM 2001


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19A.6.3.4 Additivity of Risks

In the assessment of toxic effects of a mixture, it is generally assumed that each component of the mixture causes the same type of adverse effects (i.e. similar mechanism of action) in a receptor, albeit perhaps at different potencies. It should be noted that combined toxic effects may also be produced in a receptor due to exposure to interacting COPCs. Such combined effects may be additive, synergistic (greater than additive), or antagonistic (less than additive). These combined effects could arise because two or more COPC target the same organs or tissues in the body, affect each others’ bioavailabilities, or disturb biological processes in a similar manner. In order to assess these combined effects quantitatively, however, detailed studies of the interactions between COPC are required, and little information is available in this regard. This risk assessment assesses risks from individual COPC.

19A.6.3.5 Assessment of Odour

The inhalation TRVs selected for use in the HHRA were limited to health-based effects. However, for a number of parameters, regulatory guidelines are based on odour. Odour is defined as a property of a substance affecting the sense of smell in humans. In this case, reference is made specifically to any Expansion Project-related odour that is potentially unpleasant to humans. Odour-causing compounds may cause loss of enjoyment of property; however, this is not considered a health effect.

Recent research suggests that the exposure to nuisance factors, such as odour, may cause anxiety in some individuals, affect stress levels, and result in a perception of risk (Shusterman 1999; Schiffman and Williams 2005). While it is not possible to predict the associated potential psychosocial responses in exposed residents, due to the individuality and variability of the human detection and reaction to odours as well as other contributing factors that could lead to a psychosocial response in individuals (e.g., stress occurring from other life events or factors), comparison of regulatory guidelines that are based on odour are useful indicators of exposure.

Table 6-14 provides a summary of odour-causing compounds and the associated regulatory guidelines used to assess the potential for human exposure.

Table 6-14 Odour-Based Guidelines

COPC

Odour-Based Regulatory Guidelines 1-Hour (μg/m3)

24-Hour (μg/m3)

Value Source Value Source Criteria Air Contaminants NO2 400 AENV 2009a 200 AENV 2009a Petroleum Hydrocarbons Ethylbenzene 2,000 AENV 2009a NV -- Non-carcinogenic PAHs Naphthalene 440 TCEQ 2009 NV --



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Table 6-14 Odour-Based Guidelines (cont’d)

COPC

Odour-Based Regulatory Guidelines 1-Hour (μg/m3)

24-Hour (μg/m3)

Value Source Value Source VOCs Acetaldehyde 90 AENV 2009a NV -- Benzaldehyde 22 TCEQ 2009 NV -- Carbon disulfide 30 AENV 2009a NV -- Hydrogen sulfide 14 AENV 2009a 4 AENV 2009a

Thiophene 2.6 TCEQ 2009 NV --

NOTE: COPC not shown in Table 6-14 do not have an odour-based guideline

19A.6.4 Risk Characterization

The purpose of the risk characterization is to combine the information from the exposure assessment (Section 19A.6.2) and the results of the toxicity assessment (Section 19A.6.3) to estimate the potential risks to human health from the COPC evaluated. This section briefly summarizes the general approach to the risk characterization for non-carcinogenic and carcinogenic COPC, respectively.

19A.6.4.1 Approach

Risk characterization is essentially a comparison of the predicted human intake of a COPC to the TRV for that COPC. Evaluation of potential chronic and potential acute risks is completed separately; potential chronic health risks are evaluated using chronic daily intakes or lifetime average daily doses, based on annual average air concentrations and depositions rates. Potential inhalation acute health risks are evaluated using short-term intakes, based on 1-hour and 24-hour air concentrations, compared with acute TRVs. Chronic risk is assessed both through inhalation and multiple pathway exposure. Therefore, risk estimates were separated as follows:

• Acute inhalation (1-hour and 24-hour durations)

• Chronic inhalation (annual average durations)

• Chronic multiple pathways

The potential health effects associated with contaminants with non-carcinogenic endpoints are assessed differently than those for carcinogenic contaminants. Non-carcinogenic contaminants are generally considered to act through a threshold mechanism where it is assumed that there is a dose (or concentration) that does not produce any adverse effect. As the dose or concentration increases to the point where the body can no longer process or excrete the chemical, an adverse effect may occur. This point is termed the threshold and is different for every chemical.

For contaminants for which the critical effect is assumed to have no threshold (i.e., carcinogens), it is assumed that there is some probability of harm to human health at any level of exposure. There is a


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dose-response relationship that converts estimated daily intakes averaged over a lifetime of exposure directly to an incremental risk of an individual developing cancer.

NON-CARCINOGENS – INHALATION

Concentration ratios (CR) are used to evaluate acute and chronic non-carcinogenic health risks from direct exposure to chemicals in air. CR values are calculated by dividing the predicted air concentration (1-hour, 24-hour, or annual average) by the appropriate exposure limit (i.e., ambient air quality guideline or reference concentration) as follows:

Where:

CR = the exposure-duration specific concentration ratio (unitless)

[Air] = the predicted air concentration (μg/m3) for a specific exposure duration (i.e., 1-hour, 24-hour, or annual average)

Exposure Limit = the exposure-duration specific exposure limit (μg/m3)

If the CR is less than 1.0, the air concentration does not exceed the regulatory exposure limit and adverse health effects are not expected. However, a CR greater than 1.0 does not necessarily imply that action is required to mitigate unacceptable risks; rather, an exceedance is an indication that the data and assumptions used to estimate the risks should be more closely examined.

NON-CARCINOGENS – MULTIPLE PATHWAY EXPOSURE

The potential for adverse non-carcinogenic health effects for each COPC is estimated by the hazard quotient (HQ), calculated by dividing the chronic daily intake (CDI) for each route of exposure (e.g., soil contact, food chain uptakes) by the reference dose (RfD) as follows:

Where:

HQ = the hazard quotient for chronic exposures resulting from multiple exposure pathways (unitless)

CDI = the total chronic daily intake from via multiple pathways in (μg/kg body weight/day)

RfD = the COPC-specific chronic reference dose in (μg/kg body weight/day)

RfDCDIHQ =

Limit Exposure[Air]CR =



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If the HQ is less than 1.0, the intake of the COPC by all routes of exposure does not exceed the tolerable intake and no adverse health effects are expected. However, a HQ greater than 1.0 does not necessarily imply that action is required to mitigate risks; rather, an exceedance is an indication that the data and assumptions used to estimate the risks should be more closely examined.

CARCINOGENS

For non-threshold carcinogenic chemicals, potential risks are expressed as incremental lifetime cancer risks (ILCRs) and lifetime cancer risks (LCRs), which represents the risk of an individual within a given population developing cancer over his or her lifetime (increased risk, in the case of the ILCR). For the current assessment, ILCRs consider the increase in risk over and above the probability of developing cancer due to background exposures while LCRs represent total lifetime cancer risks.

ILCR and LCR estimates were used to evaluate the increased cancer risk resulting from a lifetime of exposure to non-threshold genotoxic carcinogenic chemicals. ILCR estimates provided the incremental lifetime cancer risk resulting from emissions from the proposed Expansion Project (i.e., Project Alone Scenario), while LCR estimates provide the overall background lifetime cancer risk associated with typical concentrations of the COPC within the Assessment Area (i.e., Baseline Case, Application Case and Planned Development Case).

DIRECT AIR INHALATION

ILCR and LCR estimates from direct air inhalation were calculated as follows:

Where:

ILCR = the incremental (or additional) lifetime cancer risk (unitless)

[AIR]project alone = the predicted annual average ground-level air concentration (μg/m3) from only the Expansion Project emissions

UR = the COPC-specific unit risk (μg/m3)-1

Where:

LCR = the lifetime cancer risk (unitless)

[AIR]all sources = the predicted annual average ground-level air concentration (μg/m3) from all sources, including the Expansion Project

UR = the COPC-specific unit risk (μg/m3)-1

UR X ILCR aloneprojectAIR][=

UR X LCR sourcesallAIR][=


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MULTIPLE PATHWAY EXPOSURE

For those carcinogenic chemicals evaluated as part of the multi-media pathway assessment, ILCR and LCR estimates resulting from a lifetime of exposure through multiple pathways were calculated as follows:

Where:

ILCR = the incremental (or additional) lifetime cancer risk (unitless)

LADDproject alone = the incremental Lifetime Average Daily Dose via multiple pathways resulting from only the Expansion Project emissions in (μg/kg body weight/day)

CSF = the cancer slope factor (μg/kg body weight/day)-1

Where:

LCR = the lifetime cancer risk (unitless)

LADDall sources = The Lifetime Average Daily Dose via multiple pathways resulting from all sources, including the Expansion Project emissions in (μg/kg body weight/day)

CSF = the cancer slope factor (μg/kg body weight/day)-1

Non-threshold chemicals that can alter genetic material (i.e., genotoxic) are capable of producing cancer. Regulatory agencies such as Health Canada and the US EPA have therefore assumed that any level of long-term exposure to a carcinogenic compound is associated with some “hypothetical cancer risk”. As a result, regulatory agencies have typically employed acceptable ILCR levels (i.e., incremental cancer risks over and above background cancer incidence) between 1-in-100 000 and 1-in-1 000 000. ILCRs generally consider risks related to a particular facility (facility alone) in that the cancer risks are expressed on an incremental or additional basis as compared to cancer risks related to all sources.

As this HHRA is being conducted as part of the EIA process for in Alberta, the ILCR benchmark used to predict risk from the Project Alone Scenario is 1-in-100 000 or 1E-05; this value is equivalent to the Health Canada benchmark. Any ILCR estimate less than 1E-05 indicates that predicted exposures are considered negligible. Conversely, a ILCR greater than 1E-05 does not necessarily imply that action is required to mitigate risks; rather, an exceedance is an indication that the data and assumptions used to estimate the risks should be more closely examined.

In the case of LCR estimates, there are no accepted regulatory benchmarks by which to evaluate an acceptable level of lifetime cancer risk. Unlike ILCRs, LCRs include the consideration of cancer risks from all sources. As such, LCRs are expressed on a total or all sources basis. Since regulators have not

CSF X LADDILCR aloneproject=

CSF X LADDLCR all sources=



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recommended an acceptable benchmark LCR for exposure to carcinogens associated with background or baseline conditions, interpretation of the significance of the LCR values is difficult. The only comparison one could make would be to the typical observed cancer incidence in the Canadian population. Each year, approximately 145 000 Canadians are diagnosed with cancer. Based on current cancer incidence and mortality rates, the lifetime probability of developing cancer is 38% for women and 44% for men (Canadian Cancer Society 2007).

ODOUR

Concentration ratios (CR) are used to evaluate potential exposure to odour-causing chemicals. CR values are calculated by dividing the predicted air concentration (1-hour or 24-hour) by the appropriate exposure limit (i.e., odour-based ambient air quality guideline) as follows:

Where:

CR = the exposure-duration specific concentration ratio (unitless)

[Air] = the predicted air concentration (μg/m3) for a specific exposure duration (i.e., 1-hour or 24-hour)

Exposure Limit = the odour-based ambient air guideline (μg/m3)

If the CR is less than 1.0, the air concentration does not exceed the odour-based regulatory exposure limit. However, a CR greater than 1.0 does not necessarily imply that action is required to reduce odours; rather, an exceedance is an indication that odours may be present and that the data and assumptions used should be more closely examined.

19A.6.4.2 Results – Non-carcinogenic Human Health Risks via Inhalation

As discussed in Section 19A.6.4.1, the CR represents the relationship between the magnitude of exposure to the contaminant in air relative to a regulatory exposure limit. The CR indicates the probability of occurrence of adverse health effects. The benchmark CR value for inhaled exposures is 1.0. If the CR is greater than 1.0, then there may be potential for adverse health effects and further assessment or monitoring would be required. Conversely, a CR of less than 1.0 indicates that the intake of the contaminant from inhalation exposure does not exceed the tolerable intake and no adverse health effects are expected.

1-HOUR EXPOSURES

The CR values associated with the maximum predicted 1-hour exposure concentrations at each of the receptor locations identified in Table 2-1 were determined for the Baseline Case, the Expansion Project alone (Project Alone Scenario), the Application Case, and the Planned Development Case. The results

Limit Exposure[Air]CR =


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are provided in Appendix 19A-7. The maximum CR values at the fenceline of the central processing facility (CPF), as well as the maximum CR value of the other 44 discrete receptor locations evaluated, are provided in Table 6-15.

The acute health risks from exposure to the 1-hour maximum predicted air concentrations at each of the human health receptor locations, where people might be exposed for any appreciable length of time, were below the benchmark criteria (i.e., CR values less than 1.0). The contribution of the Expansion Project to the total health risks at the human health receptor locations were negligible, and evidenced by the CR values for the Project Alone Scenario, which were all well below 1.0.

The acute health risks at the fenceline of the CPF were all less than the benchmarks, with the exception of the 1-hour exposure to SO2. To put the risks associated with this short term (1-hour) exposure to SO2 into context, it is important to evaluate the toxicological basis of the risk predictions, the likelihood of exposure, and the frequency of exposure. Studies have shown that SO2 in air acts primarily as a respiratory tract irritant in humans following short-term exposures (WHO 2000). The maximum modelled 1-hour concentration of SO2 is 490 μg/m3, which was compared to the AAQO of 450 μg/m3. The basis for the selection of 450 μg/m3 is reported as pulmonary function (AENV 2009). Exposure limits greater than the AENV limits of (660 μg/m3 to 690 μg/m3) have been used in other jurisdictions (CalEPA 2007; MOE 2008)). These exposure limits are based on a 1-hour no observed adverse effect level from multiple studies of healthy, asthmatic, and atopic volunteers (CalEPA 2007b). The maximum ground level concentration of SO2 is less than this 660 μg/m3 exposure limit.

The 1-hour maximum concentration of SO2 is the highest 1-hour concentration from the five years of modelling; the next highest 1-hour concentration is 361 μg/m3, which indicates that 99.99% of the time the concentration of SO2 in air near the fenceline meets the AAQO. As noted previously, the Expansion Project is located in a relatively remote area; human receptors would not likely be found at this location of any appreciable length of time. Based on these results, the likelihood that a person would be exposed to concentrations of SO2 that are greater than the AAQO is very low.

24-HOUR EXPOSURES

The CR values associated with the maximum predicted 24-hour exposure concentrations at each of the receptor locations identified in Table 2-1 were determined for the Baseline Case, the Expansion Project alone (Project Alone Scenario), the Application Case, and the Planned Development Case. The results are provided in Appendix 19A-7. The maximum CR values at the fenceline of the central processing facility (CPF), as well as the maximum CR value of the other 44 receptor locations evaluated, are provided in Table 6-16.

The acute health risks from exposure to the 24-hour maximum predicted air concentrations were all less than 1.0, with the following exceptions:

• PM2.5

• Acrolein

• Hydrogen sulfide



19A-68

Table 6-15 Concentration Ratios for 1-hour Exposures

COPC

Central Processing Facility (CPF) Local Study Area (LSA) Maximum 1-Hour Concentration Ratio (CR) 1-Hour Concentration Ratio (CR)

Baseline Case

Project Alone

Scenario Application

Case

Planned Development

Case Baseline

Case

Project Alone


Case

Planned Development

Case Criteria Air Contaminants SO2 0.34 1.1 1.1 1.1 0.44 0.076 0.44 0.46 NO2 0.2 0.36 0.36 0.36 0.47 0.087 0.47 0.47 PM2.5 - - - - - - - - CO 0.018 0.15 0.16 0.16 0.12 0.0099 0.12 0.12 Petroleum Hydrocarbons Benzene 0.26 0.027 0.27 0.31 0.47 0.0012 0.47 0.55 Toluene 0.029 3.70E-04 0.03 0.038 0.07 1.70E-05 0.07 0.093 Ethylbenzene 3.90E-04 2.40E-06 3.90E-04 5.00E-04 9.50E-04 1.00E-07 9.50E-04 0.0013 Xylenes 0.042 1.30E-04 0.042 0.054 0.1 7.80E-06 0.1 0.14 Aliphatic C5-C8 0.16 0.052 0.2 0.25 0.4 0.0023 0.4 0.54 Aliphatic C9-C16 0.3 3.30E-04 0.3 0.35 0.53 2.00E-05 0.53 0.59 Aromatic C9-C16 0.0028 4.70E-05 0.0028 0.0034 0.0062 1.70E-06 0.0062 0.0078 Aromatic C17-C34 0.0046 2.20E-04 0.0047 0.0045 0.091 1.40E-05 0.091 0.085 Carcinogenic PAHs Benz(a)anthracene 0.0018 2.30E-04 0.0018 0.0019 0.0038 5.60E-06 0.0038 0.0042 Benzo(a)pyrene (BaP) 0.024 0.0037 0.024 0.024 0.016 9.10E-05 0.016 0.016 Benzo(e)pyrene 7.30E-06 7.30E-07 7.40E-06 7.90E-06 4.20E-06 1.80E-08 4.20E-06 4.60E-06 Benzo(b)fluoranthene 0.0014 2.20E-04 0.0014 0.0014 9.80E-04 5.50E-06 9.80E-04 9.80E-04 Benzo(g,h,i)perylene 0.0014 2.20E-04 0.0014 0.0015 9.80E-04 5.50E-06 9.80E-04 9.80E-04 Benzo(k)fluoranthene 0.0014 2.20E-04 0.0014 0.0014 9.80E-04 5.50E-06 9.80E-04 9.80E-04 Chrysene 0.0018 2.30E-04 0.0018 0.0019 0.0043 5.50E-06 0.0043 0.0047


19A-69

Table 6-15 Concentration Ratios for 1-hour Exposures (cont’d)

COPC


Baseline Case

Project Alone


Case

Planned Development

Case Baseline

Case

Project Alone


Case

Planned Development

Case Criteria Air Contaminants (cont’d) Dibenzo(a,h)anthracene 0.0014 2.20E-04 0.0014 0.0015 9.80E-04 5.50E-06 9.80E-04 9.80E-04 Fluoranthene 0.012 2.40E-04 0.012 0.014 0.068 1.10E-05 0.068 0.075 Indeno(1,2,3-cd)pyrene 0.0014 2.20E-04 0.0015 0.0015 9.80E-04 5.50E-06 9.80E-04 9.80E-04 Phenanthrene 0.02 4.10E-04 0.02 0.024 0.12 2.80E-05 0.12 0.13 Pyrene 0.015 2.40E-04 0.015 0.018 0.092 6.10E-06 0.092 0.1 Perylene 7.40E-06 7.30E-07 7.50E-06 8.10E-06 4.30E-06 1.80E-08 4.30E-06 4.80E-06 Benzo(a)pyrene TEQ - - - - - - - - Non-carcinogenic PAHs Anthracene 0.0037 2.30E-04 0.0037 0.0042 0.016 5.80E-06 0.016 0.018 Fluorene 4.10E-04 1.30E-05 4.10E-04 4.90E-04 0.0022 3.80E-07 0.0022 0.0024 Naphthalene - - - - - - - - VOCs Acetaldehyde 0.0088 2.00E-04 0.0089 0.011 0.057 1.30E-05 0.057 0.063 Acrolein 0.15 0.049 0.18 0.21 0.95 0.0031 0.95 1 Benzaldehyde - - - - - - - - Carbon disulfide 0.015 1.60E-06 0.015 0.019 0.038 5.40E-08 0.038 0.051 Dichlorobenzene 1.10E-07 6.10E-07 7.10E-07 7.40E-07 7.20E-07 3.80E-08 7.20E-07 7.30E-07 Formaldehyde 0.06 0.027 0.077 0.085 0.29 0.0017 0.29 0.31 Hexane 0.0022 0.0025 0.0041 0.0042 0.005 1.10E-04 0.005 0.005 Hydrogen sulfide 0.39 0.47 0.8 0.89 0.79 0.02 0.79 1 Thiophene - - - - - - - -



19A-70


COPC


Baseline Case

Project Alone


Case

Planned Development

Case Baseline

Case

Project Alone


Case

Planned Development

Case Metals Aluminum (Al) 5.60E-04 4.40E-04 0.001 0.001 7.40E-04 2.70E-05 7.40E-04 7.50E-04 Chromium (Total) 0.011 7.50E-04 0.011 0.012 0.0096 4.70E-05 0.0096 0.01 Cobalt (Co) 0.0032 0.0012 0.0044 0.0045 0.0029 7.50E-05 0.0029 0.003 Copper (Cu) 1.60E-05 9.90E-06 2.60E-05 2.70E-05 4.40E-05 6.30E-07 4.40E-05 4.30E-05 Lead (Pb) 0.0016 2.70E-04 0.0018 0.0019 0.0066 1.70E-05 0.0066 0.0063 Manganese (Mn) 0.0038 3.40E-04 0.0041 0.0041 0.013 2.10E-05 0.013 0.013 Molybdenum (Mo) 3.90E-05 5.20E-06 4.40E-05 4.60E-05 3.60E-05 3.30E-07 3.60E-05 3.70E-05 Nickel (Ni) 0.0028 8.60E-05 0.0029 0.003 0.0026 5.40E-06 0.0026 0.0027 Strontium (Sr) 6.00E-06 1.60E-05 2.20E-05 2.20E-05 1.60E-05 9.80E-07 1.60E-05 1.70E-05 Vanadium (V) 0.015 5.00E-04 0.015 0.016 0.014 3.10E-05 0.014 0.014 Zinc (Zn) 0.0012 5.10E-05 0.0012 0.0013 0.001 3.20E-06 0.001 0.0011 NOTES: Highlighted values (grey) indicate CR value greater than benchmark of 1.0 (CR > 1.0) “—“ indicates that a health-based regulatory TRV was not located for this COPC.


19A-71

Table 6-16 Concentration Ratios for 24-hour Exposures

COPC


Baseline Case

Project Alone


Case

Planned Development

Case Baseline

Case

Project Alone


Case

Planned Development

Case Criteria Air Contaminants SO2 0.3 0.85 0.88 0.88 0.47 0.035 0.48 0.51 NO2 0.21 0.43 0.44 0.44 0.45 0.027 0.45 0.45 PM2.5 0.44 0.34 0.47 0.52 1.5 0.02 1.5 1.6 CO - - - - - - - - Petroleum Hydrocarbons Benzene 0.019 0.014 0.033 0.034 0.17 4.10E-04 0.17 0.18 Toluene 0.0082 8.00E-04 0.0086 0.011 0.056 2.70E-05 0.056 0.068 Ethylbenzene 9.50E-04 4.60E-05 9.70E-04 0.0012 0.0064 1.50E-06 0.0064 0.0081 Xylenes 0.0078 1.90E-04 0.0078 0.01 0.051 6.10E-06 0.051 0.066 Aliphatic C5-C8 0.003 0.0074 0.01 0.012 0.025 2.50E-04 0.025 0.03 Aliphatic C9-C16 - - - - - - - - Aromatic C9-C16 - - - - - - - - Aromatic C17-C34 - - - - - - - - Carcinogenic PAHs Benz(a)anthracene - - - - - - - - Benzo(a)pyrene (BaP) 0.1 0.017 0.11 0.11 0.074 6.10E-04 0.074 0.075 Benzo(e)pyrene - - - - - - - - Benzo(b)fluoranthene - - - - - - - - Benzo(g,h,i)perylene - - - - - - - - Benzo(k)fluoranthene - - - - - - - - Chrysene - - - - - - - - Dibenzo(a,h)anthracene - - - - - - - -



19A-72


COPC


Baseline Case

Project Alone


Case

Planned Development

Case Baseline

Case

Project Alone


Case

Planned Development

Case Carcinogenic PAHs (cont’d) Fluoranthene - - - - - - - - Indeno(1,2,3-cd)pyrene - - - - - - - - Phenanthrene - - - - - - - - Pyrene - - - - - - - - Perylene - - - - - - - - Benzo(a)pyrene TEQ - - - - - - - - Non-carcinogenic PAHs Anthracene - - - - - - - - Fluorene - - - - - - - - Naphthalene 0.0046 5.10E-04 0.0047 0.0051 0.016 1.90E-05 0.016 0.018 VOCs Acetaldehyde 0.0021 4.10E-05 0.0021 0.0025 0.028 2.00E-06 0.028 0.031 Acrolein 1.1 0.3 1.4 1.6 14.0 0.014 14.0 16.0 Benzaldehyde - - - - - - - - Carbon disulfide - - - - - - - - Dichlorobenzene 3.80E-06 1.70E-05 1.90E-05 2.00E-05 2.40E-05 7.90E-07 2.40E-05 2.90E-05 Formaldehyde 0.012 0.0045 0.015 0.018 0.12 2.20E-04 0.12 0.13 Hexane 6.10E-04 0.0033 0.0038 0.0038 0.0061 1.10E-04 0.0061 0.0062 Hydrogen sulfide 0.15 1.2 1.4 1.4 1.1 0.039 1.1 1.3 Thiophene - - - - - - - -


19A-73


COPC


Baseline Case

Project Alone


Case

Planned Development

Case Baseline

Case

Project Alone


Case

Planned Development

Case Metals Aluminum (Al) - - - - - - - - Chromium (Total) - - - - - - - - Cobalt (Co) 0.0016 5.10E-04 0.002 0.0021 0.0019 2.40E-05 0.0019 0.0021 Copper (Cu) 9.10E-06 4.30E-06 1.30E-05 1.30E-05 3.50E-05 2.00E-07 3.50E-05 3.50E-05 Lead (Pb) 0.0014 1.70E-04 0.0016 0.0017 0.0096 8.20E-06 0.0096 0.01 Manganese (Mn) 7.80E-04 5.90E-05 8.30E-04 8.30E-04 9.80E-04 2.80E-06 9.80E-04 9.80E-04 Molybdenum (Mo) 3.90E-06 4.70E-07 4.30E-06 4.60E-06 5.00E-06 2.20E-08 5.00E-06 5.30E-06 Nickel (Ni) 0.02 5.60E-04 0.021 0.022 0.026 2.60E-05 0.026 0.027 Strontium (Sr) 2.90E-07 5.60E-07 7.60E-07 7.90E-07 1.10E-06 2.70E-08 1.10E-06 1.20E-06 Vanadium (V) 8.90E-04 2.70E-05 9.10E-04 9.60E-04 0.0011 1.30E-06 0.0011 0.0012 Zinc (Zn) 1.20E-04 4.60E-06 1.30E-04 1.30E-04 1.80E-04 2.20E-07 1.80E-04 1.70E-04 NOTES: Highlighted values (grey) indicate CR value greater than benchmark of 1.0 (CR > 1.0) “—“ indicates that a health-based regulatory TRV was not located for this COPC.



19A-74

PM2.5

Particulate matter can cause serious health problems when fine particles get deep into the lungs. The AAQO for 24-hour PM2.5 is 30 μg/m3, and references the Canada Wide Standard (CWS). This Canada-Wide Standard is based on 98th percentile ambient measurements conducted annually and averaged over 3 years. The Ontario Ministry of the Environment (MOE 2008) Ambient Air Quality Criteria is also 30 μg/m3 for PM2.5 and is based on the critical effect of respiratory irritation.

Two of the discrete receptor locations evaluated had maximum modelled 24-hour concentrations higher than 30 μg/m3 – Fort McKay (CR = 1.6) and Fort McMurray (CR = 1.2). Neither of these cities are proximal to the Expansion Project, with Fort McMurray located 50 km north of the Expansion Project and Fort McKay located 100 km north of the Expansion Project. The maximum 24-hour concentrations of PM2.5 at all other receptor locations are less than 30 μg/m3.

The Planned Development Case CR values for Fort McKay and Fort McMurray are about 10% higher than they were for the Application Case, indicating that other planned projects will contribute to PM2.5

concentrations at these locations. However, the CR values for Fort McKay and Fort McMurray were the same for the Baseline Case and the Application Case, indicating that Expansion Project contributions to the PM2.5 concentrations are negligible.

ACROLEIN

Throughout most of the LSA, the maximum 24-hour acrolein concentrations associated with the Baseline Case range from 0.04 μg/m3 (e.g., Marianna Settlement, Conklin) to 0.18 μg/m3 (e.g., Anzac, Gregoire Lake), with higher CR values associated with Fort McMurray (0.61 μg/m3) and Fort McKay (1.12 μg/m3). These results for the Application Case were the same as the Baseline Case, with the exception of the fenceline of the central processing facility, where concentrations increased about 30% over Baseline Case. These results indicate that, with the exception of the fenceline of the central processing facility, the contributions of the Expansion Project to acrolein concentrations are negligible.

The CR values for the Planned Development Case are 10 to 15% higher than the Application Case, indicating that planned projects will contribute to increases in the maximum acrolein concentrations; however, with the exception of the fenceline of the central processing facility, the contributions of the Expansion Project to acrolein concentrations are negligible. As noted previously, the Expansion Project is in a relatively remote area, and there is a low likelihood that people would be exposed to this 24-hour concentration of acrolein at the fenceline.

Since the CR values for acrolein within the LSA are higher than 1.0, it is important to understand the toxicological basis for the risk predictions. The maximum predicted 24-hour concentration of acrolein is 1.3 μg/m3, at Fort McKay under the Planned Development Case. The acrolein concentrations were compared to a 24-hour exposure limit of 0.08 µg/m3 (MOE 2008).

Studies have shown that acrolein (in air) acts primarily as an eye and upper respiratory tract irritant in humans (WHO 2002). Exposure to concentrations as low as 140 µg/m3 for five minutes may elicit subjective complaints of irritation, with increasing concentrations leading to more intense eye, nose and respiratory symptoms. In a study that exposed 36 healthy volunteers for five minutes to 140 µg/m3, mild


19A-75

eye irritation was observed (Darley et al. 1960). This study formed the basis of the acute airborne exposure limit used in this assessment.

In a clinical study by Weber-Tschopp et al. (1977), which provides one of the most comprehensive descriptions of health risks of acrolein in humans following short-term exposures, three experiments were performed using male and female student volunteers. These involved:

• Continuous exposure at constantly increasing acrolein concentrations

• Short exposures to successively increasing acrolein concentrations

• A single hour of exposure to a constant concentration

The investigators concluded that the average threshold of health-related environmental effects for acrolein is between 210 µg/m3 (eye irritation) and 700 µg/m3 (throat irritation and decreased respiration rate), with nasal irritation at 350 µg/m3.

As shown in Table 6-17, the lowest concentration at which mild eye irritation has been observed in humans (i.e., 140 µg/m3) is more than 100-times higher than the maximum modelled 24-hour air concentration of acrolein at the receptor locations (i.e., 1.3 µg/m3 at Fort McKay). As such, it is unlikely that concentrations of acrolein would result in a substantive health risk.

Table 6-17 Observed Responses in Humans to Short-Term Exposure to Acrolein

Air concentration (a) (µg/m3)

Acute Health Endpoints

Reference

140(b) to 210 mild eye irritation (Note that this study formed the basis of the acute inhalation exposure limit for acrolein of 0.19 µg/m3).

Darley et al. (1960); Weber Tschopp et al. (1977)

230(c) lacrimation and irritation of the eyes, nose and throat Fassett (1962) 350 nasal irritation Weber-Tschopp et al. (1977) 700 decreased respiratory rate and throat irritation Weber-Tschopp et al. (1977)

350,000(b) lethality Prentiss (1937) NOTES: (a) On an acute basis, the toxicity of acrolein is determined to a greater extent by the exposure concentration than

by duration. As such, the air concentrations were not duration-adjusted. Unless stated otherwise, the air concentrations are based on 1-hour exposure duration.

(b) Air concentration based on 5-minute exposure duration. (c) Air concentration based on 10-minute exposure duration.



19A-76

HYDROGEN SULFIDE

The predicted 24-hour maximum concentration of hydrogen sulfide within the LSA is generally less than 2 µg/m3 for all cases, and only two locations, Fort McKay and the fenceline of the central processing facility, having concentrations that exceed the exposure limit of 7 µg/m3 (8.8 and 9.9 µg/m3, respectively).

The health-based benchmark of 7 µg/m3 was derived by the MOE (2006) by adapting the scientific rationale used by the US EPA IRIS (2003) to derive the chronic reference concentration. The health endpoint in the study used by US EPA IRIS (2003) was nasal irritation. This is considered a reversible effect.

The Expansion Project contributions to health risks at each of the human health receptor locations, where people might be exposed to Expansion Project-related emissions for any appreciable length of time, were well below the benchmark criteria (i.e., CR values much less than 1.0). The maximum 24-hour concentrations of hydrogen sulfide at the receptor locations for the Planned Development Case increased up to 20% from the Application Case, indicating that planned projects will contribute to increases in the maximum acrolein concentrations.

The only location where the Expansion Project has a substantive contribution to the concentrations of hydrogen sulphide in air is at the fenceline of the central processing facilty. The 24-hour maximum concentration of hydrogen sulfide evaluated in the HHRA is the highest 24-hour concentration from the five years of modelling; the next highest 24-hour concentration is 7.6 μg/m3 while all other 24-hour fenceline concentrations are less than the benchmark. This indicates that 99.9% of the time the concentration of hydrogen sulphide in air near the fenceline meets the benchmark. As noted previously, the Expansion Project is located in a relatively remote area; human receptors would not likely be found at this location of any appreciable length of time (i.e., a 24-hour period). Based on these results, the likelihood that a person would be exposed to concentrations of hydrogen sulfide at the fenceline that are greater than the benchmark is very low.

CHRONIC (ANNUAL AVERAGE) EXPOSURE

The CR values associated with the annual average exposure concentrations at each of the receptor locations identified in Table 2-1 were determined for the Baseline Case, the Expansion Project alone (Project Alone Scenario), the Application Case, and the Planned Development Case. The results are provided in Appendix 19A-7. The maximum CR values at the fenceline of the central processing facility (CPF), as well as the maximum CR value of the other 44 receptor locations evaluated, are provided in Table 6-18.

The chronic health risks from exposure to the annual average predicted air concentrations were all less than 1.0, with the exception of acrolein.


19A-77

Table 6-18 Concentration Ratios for Annual Average Exposures

COPC

Central Processing Facility (CPF) Local Study Area (LSA) Maximum Chronic (Annual Average) Concentration Ratio (CR) Chronic (Annual Average) Concentration Ratio (CR)

Baseline Case

Project Alone


Case

Planned Development

Case Baseline

Case

Project Alone


Case

Planned Development

Case Criteria Air Contaminants SO2 0.073 0.34 0.41 0.41 0.17 0.0078 0.17 0.17 NO2 0.071 0.12 0.18 0.18 0.47 0.0043 0.47 0.49 PM2.5 - - - - - - - - CO - - - - - - - - Petroleum Hydrocarbons Benzene 0.0015 0.0014 0.0029 0.0032 0.032 1.80E-05 0.032 0.034 Toluene 6.00E-04 1.10E-04 7.00E-04 8.30E-04 0.014 1.70E-06 0.014 0.016 Ethylbenzene 6.20E-05 4.90E-06 6.50E-05 8.00E-05 0.0014 8.60E-08 0.0014 0.0018 Xylenes 0.0027 1.20E-04 0.0027 0.0034 0.061 2.30E-06 0.061 0.077 Aliphatic C5-C8 1.40E-04 4.30E-04 5.60E-04 6.20E-04 0.0036 6.60E-06 0.0036 0.0044 Aliphatic C9-C16 0.0051 3.30E-05 0.0051 0.0068 0.091 6.60E-07 0.091 0.11 Aromatic C9-C16 5.00E-04 6.30E-05 5.50E-04 6.60E-04 0.0099 1.10E-06 0.0099 0.012 Aromatic C17-C34 - - - - - - - - Carcinogenic PAHs Benz(a)anthracene 2.10E-04 3.10E-05 2.30E-04 2.50E-04 0.0032 5.60E-07 0.0032 0.0034 Benzo(a)pyrene (BaP) 0.018 0.0051 0.021 0.021 0.016 8.40E-05 0.016 0.016 Benzo(e)pyrene 5.40E-07 9.70E-08 6.00E-07 6.60E-07 6.00E-07 1.50E-09 6.10E-07 6.80E-07 Benzo(b)fluoranthene 1.00E-04 3.10E-05 1.20E-04 1.30E-04 9.40E-05 5.10E-07 9.40E-05 9.70E-05 Benzo(g,h,i)perylene 1.00E-04 3.10E-05 1.20E-04 1.30E-04 9.40E-05 5.20E-07 9.40E-05 9.70E-05 Benzo(k)fluoranthene 1.00E-04 3.10E-05 1.20E-04 1.30E-04 9.30E-05 5.00E-07 9.30E-05 9.50E-05 Chrysene 2.30E-04 3.10E-05 2.50E-04 2.70E-04 0.0036 5.30E-07 0.0036 0.0038 Dibenzo(a,h)anthracene 1.00E-04 3.00E-05 1.20E-04 1.30E-04 9.30E-05 5.00E-07 9.30E-05 9.60E-05



19A-78

Table 6-18 Concentration Ratios for Annual Average Exposures (cont’d)

COPC


Baseline Case

Project Alone


Case

Planned Development

Case Baseline

Case

Project Alone


Case

Planned Development

Case Carcinogenic PAHs (cont’d) Fluoranthene 5.90E-07 1.30E-08 6.00E-07 6.80E-07 1.60E-05 3.20E-10 1.60E-05 1.70E-05 Indeno(1,2,3-cd)pyrene 1.00E-04 3.10E-05 1.20E-04 1.30E-04 9.40E-05 5.10E-07 9.50E-05 9.70E-05 Phenanthrene 0.0038 1.20E-04 0.0038 0.0043 0.099 2.50E-06 0.099 0.11 Pyrene 8.40E-07 1.30E-08 8.40E-07 1.00E-06 2.90E-05 3.00E-10 2.90E-05 3.10E-05 Perylene 5.50E-07 9.80E-08 6.20E-07 6.80E-07 6.20E-07 1.50E-09 6.20E-07 7.10E-07 Benzo(a)pyrene TEQ - - - - - - - - Non-carcinogenic PAHs Anthracene 2.60E-08 1.20E-09 2.60E-08 2.90E-08 5.00E-07 2.10E-11 5.00E-07 5.40E-07 Fluorene 4.90E-07 1.30E-08 5.00E-07 5.50E-07 1.00E-05 2.80E-10 1.00E-05 1.10E-05 Naphthalene 0.0023 3.20E-04 0.0025 0.0027 0.027 5.70E-06 0.027 0.031 VOCs Acetaldehyde 0.0091 2.70E-04 0.0092 0.01 0.25 5.70E-06 0.25 0.27 Acrolein 0.37 0.14 0.44 0.49 9.1 0.003 9.1 9.7 Benzaldehyde - - - - - - - - Carbon disulfide 3.50E-04 7.10E-07 3.50E-04 4.70E-04 0.0078 6.90E-09 0.0078 0.01 Dichlorobenzene 3.60E-07 3.10E-06 3.40E-06 3.50E-06 1.20E-05 6.60E-08 1.20E-05 1.40E-05 Formaldehyde 0.0059 0.0035 0.0078 0.0086 0.12 7.40E-05 0.12 0.13 Hexane 3.60E-04 0.0031 0.0035 0.0035 0.0095 5.10E-05 0.0095 0.0097 Hydrogen sulfide 0.029 0.32 0.35 0.36 0.72 0.0058 0.72 0.83 Thiophene - - - - - - - -


19A-79

Table 6-18 Concentration Ratios for Annual Average Exposures (cont’d)

COPC


Baseline Case

Project Alone


Case

Planned Development

Case Baseline

Case

Project Alone


Case

Planned Development

Case Metals Aluminum (Al) 6.20E-05 1.10E-04 1.60E-04 1.60E-04 8.80E-04 2.30E-06 8.80E-04 9.20E-04 Chromium (Total) 1.30E-06 3.20E-07 1.40E-06 1.60E-06 3.80E-06 6.70E-09 3.80E-06 4.10E-06 Cobalt (Co) 5.20E-05 6.00E-05 1.00E-04 1.00E-04 3.50E-04 1.30E-06 3.50E-04 3.80E-04 Copper (Cu) 2.60E-05 2.50E-05 4.50E-05 4.60E-05 4.80E-04 5.30E-07 4.80E-04 4.80E-04 Lead (Pb) 1.10E-04 2.00E-05 1.20E-04 1.20E-04 0.0021 4.30E-07 0.0021 0.0021 Manganese (Mn) 0.0012 3.50E-04 0.0014 0.0014 0.0044 7.30E-06 0.0044 0.0045 Molybdenum (Mo) 1.20E-06 5.50E-07 1.50E-06 1.70E-06 6.00E-06 1.20E-08 6.00E-06 6.20E-06 Nickel (Ni) 0.0066 7.30E-04 0.007 0.0076 0.016 1.50E-05 0.016 0.017 Strontium (Sr) 9.50E-07 4.00E-06 4.70E-06 4.80E-06 2.00E-05 8.40E-08 2.00E-05 2.20E-05 Vanadium (V) 5.20E-05 6.40E-06 5.60E-05 6.00E-05 1.20E-04 1.30E-07 1.20E-04 1.20E-04 Zinc (Zn) 1.10E-04 1.30E-05 1.20E-04 1.30E-04 0.0012 2.70E-07 0.0012 0.0011 NOTES: Highlighted values (grey) indicate CR value greater than benchmark of 1.0 (CR > 1.0) “—“ indicates that a health-based regulatory TRV was not located for this COPC.



19A-80

Throughout most of the LSA, the predicted annual average concentrations of acrolein for the Baseline Case are generally about 0.01 μg/m3, with the exception of the concentrations in Fort McMurray (0.11 μg/m3) and Fort McKay (0.18 μg/m3). The concentrations for the Application Case remain unchanged from the Baseline Case, while results for the Planned Development Case are about 5 to 8% higher. These findings indicate that planned projects will contribute to increases in the maximum acrolein concentrations; however, the contributions of the Expansion Project to acrolein concentrations are negligible.

As with the health risks related to short-term acrolein exposures, the concern with acrolein is specifically nasal irritation potentially leading to nasal lesions due to continuous long-term exposures to this irritant. A detailed review of the scientific and regulatory literature indicated that no studies detailing long-term toxicity to people from inhalation were available (Appendix 19A-6).

As such, the inhalation exposure limit used in the current assessment was established by the US EPA IRIS (2003), based upon observations from a sub-chronic inhalation study of rats exposed to acrolein. In the underlying study used to develop this limit (Feron et al. 1978), the selected concentrations (900 µg/m3) resulted in slight nasal irritation in 1 of the 12 studied rats and was adjusted for a human equivalent concentration (HEC) of 20 µg/m3. Though the same study was also conducted in hamsters and rabbits, none of these health-related environmental effects were observed at this exposure concentration (i.e., rats were the most sensitive species). A 1000-fold uncertainty factor (to account for the considerable uncertainty inherent within the derived exposure limit) was applied to derive the ultimate reference concentration of 0.02 µg/m3. It is these uncertainty factors that account for a great deal of conservatism in HHRA.

Given that concentrations measured within the LSA meet the benchmark, the 1000-fold conservative safety factors built into the reference concentration, and the fact this regulatory limit is based upon minor nasal irritation for a very sensitive test species (i.e., in only 1 of 12 studied rats), it is unlikely that prolonged exposure to this ambient concentration of acrolein would result in any appreciable health risk to the overall population.

19A.6.4.3 Results – Carcinogenic Human Health Risks via Inhalation

This section addresses the risks of adverse health effects from long-term (chronic) inhalation exposure to carcinogenic COPCs under the Baseline Case, Project Alone Scenario, Application Case, and Planned Development Case. Carcinogenic health risks, expressed as ILCRs, assume that individuals would be continuously exposed to the predicted annual average air concentration over the course of a lifetime.

Results of the carcinogenic inhalation risk characterization are presented in Appendix 19A-7 by scenario and receptor, for all COPC. The maximum predicted ILCRs/LCRs are presented in Table 6-19.

Results of the assessment indicate that none of the ILCR values predicted for the carcinogenic COPC under the Project Alone Scenario exceeded the recommend regulatory acceptable cancer risk level of 1-in-100 000. LCR values were calculated for the other cases for information purposes; however, as previously discussed, there are currently no regulatory benchmarks for LCR values.


19A-81

Table 6-19 Incremental Lifetime Cancer Risks (ILCRs) via Inhalation

COPC

Central Processing Facility (CPF) Local Study Area (LSA) Maximum

Baseline Case (LCR)

Project Alone

Scenario (ILCR)

Application Case (LCR)

Planned Development

Case (LCR)

Baseline Case (LCR)

Project Alone

Scenario (ILCR)


Planned Development

Case (LCR)

Petroleum Hydrocarbons Benzene 3.54E-07 3.39E-07 6.80E-07 7.47E-07 7.43E-06 4.31E-09 7.43E-06 7.92E-06 Carcinogenic PAHs Benzo(a)pyrene TEQ 4.23E-10 1.15E-10 4.96E-10 5.09E-10 1.05E-09 1.90E-12 1.05E-09 1.12E-09 VOCs Acetaldehyde 1.80E-07 5.35E-09 1.82E-07 2.07E-07 4.88E-06 1.13E-10 4.88E-06 5.25E-06 Formaldehyde 7.64E-07 4.56E-07 1.01E-06 1.12E-06 1.56E-05 9.63E-09 1.56E-05 1.67E-05 Metals Chromium (Total) 8.32E-07 2.07E-07 9.46E-07 1.03E-06 2.51E-06 4.37E-09 2.51E-06 2.66E-06 NOTES: Highlighted values (grey) indicate ILCR value greater than benchmark of 1-in-100 000 (ILCR > 1.0E-05) . There are no established benchmarks for LCR. COPC not shown in Table 6-18 do not have an inhalation carcinogenic TRV.



19A-82

19A.6.4.4 Results – Non-carcinogenic Human Health Risks via Multiple Pathways

The HQ values for long-term exposure to chemicals via multiple exposure pathways for each of the receptor types (i.e., Resident, Hunter, Camper, Aboriginal, and AENV/AHW AR) are summarized in Tables 6-20 to 6-24. The HQ value for each non-carcinogenic chemical is less than the benchmark of 1.0 for each receptor, for each case, with the following exceptions:

• Chromium – Aboriginal receptor, AENV/AHW AR Receptor

• Cobalt – AENV/AHW AR receptor

• Lead - AENV/AHW AR receptor

• Manganese – Resident, Hunter, Aboriginal receptor, AENV/AHW AR receptor

• Zinc - AENV/AHW AR receptor

For each of the above-noted metals, the exceedance occurs at all receptor-specific locations assessed, and for each of the Base, Application, and Planned Development Cases. Contributions of the Expansion Project to the health risk estimates are negligible, as indicated by the extremely low HQ values for the Project Alone Scenario (i.e., less than 1E-06).

Additional discussion of the potential health risks associated with each of these metals is provided below.


19A-83

Table 6-20 Non-Carcinogenic Human Health Risks from Exposure to Multi-Media – Resident

COPC

Resident – Toddler Resident – Adult

Baseline Case

Project Alone


Case

Planned Development

Case Baseline

Case

Project Alone


Case

Planned Development

Case Petroleum Hydrocarbons Aliphatic C5-C8 8.08E-09 9.58E-12 8.09E-09 1.07E-08 3.43E-09 4.07E-12 3.44E-09 4.53E-09 Aliphatic C9-C16 5.31E-07 4.37E-12 5.31E-07 6.84E-07 1.85E-07 1.52E-12 1.85E-07 2.39E-07 Aromatic C9-C16 6.10E-05 2.42E-09 6.10E-05 6.99E-05 2.58E-05 1.03E-09 2.58E-05 2.96E-05 Aromatic C17-C34 3.16E-07 2.22E-11 3.16E-07 3.00E-07 1.39E-07 9.72E-12 1.39E-07 1.32E-07 PAHs Anthracene 1.71E-06 1.62E-12 1.71E-06 1.71E-06 9.09E-07 7.24E-13 9.09E-07 9.10E-07 Fluoranthene 8.71E-06 1.73E-11 8.71E-06 8.74E-06 4.52E-06 7.49E-12 4.52E-06 4.53E-06 Fluorene 2.33E-05 3.68E-12 2.33E-05 2.33E-05 1.26E-05 1.68E-12 1.26E-05 1.26E-05 Pyrene 1.44E-05 7.12E-11 1.44E-05 1.47E-05 7.39E-06 3.06E-11 7.39E-06 7.52E-06 VOCs Dichlorobenzene 1.23E-09 2.36E-11 1.25E-09 1.47E-09 5.18E-10 9.94E-12 5.27E-10 6.18E-10 Metals Aluminum (Al) 0.036 1.40E-09 0.036 0.036 0.012 4.66E-10 0.012 0.012 Chromium (Total) 0.16 1.89E-08 0.16 0.16 0.064 7.08E-09 0.064 0.064 Cobalt (Co) 0.10 7.41E-09 0.10 0.10 0.042 2.71E-09 0.042 0.042 Copper (Cu) 0.018 7.6E-09 0.018 0.018 0.0087 3.3E-09 0.0087 0.0087 Lead (Pb) 0.14 1.28E-08 0.14 0.14 0.092 4.72E-09 0.092 0.092 Manganese (Mn) 1.5 1.89E-09 1.5 1.5 0.72 8.19E-10 0.72 0.72 Molybdenum (Mo) 0.020 6.38E-09 0.020 0.020 0.0093 2.77E-09 0.0093 0.0093 Nickel (Ni) 0.012 1.94E-09 0.012 0.012 0.0066 7.26E-10 0.0066 0.0066 Strontium (Sr) 0.0076 5.00E-10 0.0076 0.0076 0.0037 2.25E-10 0.0037 0.0037 Vanadium (V) 0.019 2.06E-09 0.019 0.019 0.0069 6.05E-10 0.0069 0.0069 Zinc (Zn) 0.10 1.98E-08 0.10 0.10 0.051 8.32E-09 0.051 0.051 NOTES: Highlighted values (grey) indicate HQ value greater than benchmark of 1.0 (HQ > 1.0) COPC not shown in Table 6-20 either do not have a non-carcinogenic TRV or have negligible potential to persist or bioaccumulate in the environment (see Section 19A.3.2.2).



19A-84

Table 6-21 Non-Carcinogenic Human Health Risks from Exposure to Multi-Media – Hunter

COPC

Hunter – Toddler Hunter – Adult

Baseline Case

Project Alone


Case

Planned Development

Case Baseline

Case

Project Alone


Case

Planned Development

Case Petroleum Hydrocarbons Aliphatic C5-C8 8.09E-09 3.73E-11 8.09E-09 1.07E-08 3.44E-09 1.59E-11 3.44E-09 4.53E-09 Aliphatic C9-C16 5.37E-07 1.22E-11 5.37E-07 6.91E-07 1.91E-07 4.64E-12 1.91E-07 2.46E-07 Aromatic C9-C16 6.10E-05 1.10E-08 6.10E-05 6.99E-05 2.59E-05 4.67E-09 2.59E-05 2.96E-05 Aromatic C17-C34 3.20E-07 4.53E-11 3.20E-07 3.04E-07 1.43E-07 2.11E-11 1.43E-07 1.36E-07 PAHs Anthracene 1.71E-06 3.56E-12 1.71E-06 1.71E-06 9.13E-07 1.61E-12 9.13E-07 9.14E-07 Fluoranthene 8.74E-06 3.74E-11 8.74E-06 8.77E-06 4.55E-06 1.72E-11 4.55E-06 4.56E-06 Fluorene 2.34E-05 8.54E-12 2.34E-05 2.34E-05 1.26E-05 3.95E-12 1.26E-05 1.26E-05 Pyrene 1.44E-05 1.53E-10 1.44E-05 1.47E-05 7.44E-06 6.73E-11 7.44E-06 7.57E-06 VOCs Dichlorobenzene 1.23E-09 4.60E-11 1.25E-09 1.47E-09 5.21E-10 1.96E-11 5.29E-10 6.22E-10 Metals Aluminum (Al) 0.037 3.27E-09 0.037 0.037 0.013 1.45E-09 0.013 0.013 Chromium (Total) 0.18 1.10E-07 0.18 0.18 0.076 8.71E-08 0.076 0.076 Cobalt (Co) 0.13 6.84E-08 0.13 0.13 0.069 5.93E-08 0.069 0.069 Copper (Cu) 0.019 1.80E-08 0.019 0.019 0.0096 9.73E-09 0.0096 0.0096 Lead (Pb) 0.14 2.55E-08 0.14 0.14 0.092 9.85E-09 0.092 0.092 Manganese (Mn) 1.5 3.74E-09 1.5 1.5 0.73 1.67E-09 0.73 0.73 Molybdenum (Mo) 0.021 1.87E-08 0.021 0.021 0.011 1.17E-08 0.011 0.011 Nickel (Ni) 0.012 7.06E-09 0.012 0.012 0.0073 4.70E-09 0.0073 0.0073 Strontium (Sr) 0.0077 9.86E-10 0.0077 0.0077 0.0037 4.53E-10 0.0037 0.0037 Vanadium (V) 0.020 5.46E-09 0.020 0.020 0.0077 2.64E-09 0.0077 0.0077 Zinc (Zn) 0.10 3.84E-08 0.10 0.10 0.051 1.61E-08 0.051 0.051 NOTES: Highlighted values (grey) indicate HQ value greater than benchmark of 1.0 (HQ > 1.0) COPC not shown in Table 6-21 either do not have a non-carcinogenic TRV or have negligible potential to persist or bioaccumulate in the environment (see Section 19A.3.2.2).


19A-85

Table 6-22 Non-Carcinogenic Human Health Risks from Exposure to Multi-Media – Camper

COPC

Camper – Toddler Camper – Adult

Baseline Case

Project Alone


Case

Planned Development

Case Baseline

Case

Project Alone


Case

Planned Development

Case Petroleum Hydrocarbons Aliphatic C5-C8 6.32E-12 2.56E-14 6.32E-12 8.46E-12 8.81E-13 3.57E-15 8.83E-13 1.18E-12 Aliphatic C9-C16 1.13E-07 3.66E-12 1.13E-07 1.48E-07 1.58E-08 5.11E-13 1.58E-08 2.06E-08 Aromatic C9-C16 4.83E-08 6.42E-12 4.83E-08 5.64E-08 6.74E-09 8.96E-13 6.74E-09 7.87E-09 Aromatic C17-C34 1.05E-09 2.67E-13 1.05E-09 1.02E-09 1.47E-10 3.73E-14 1.47E-10 1.43E-10 PAHs Anthracene 3.60E-08 3.44E-13 3.60E-08 3.61E-08 6.04E-09 5.79E-14 6.04E-09 6.06E-09 Fluoranthene 3.30E-07 6.61E-12 3.30E-07 3.34E-07 4.61E-08 9.22E-13 4.61E-08 4.66E-08 Fluorene 3.06E-07 5.31E-13 3.06E-07 3.07E-07 4.28E-08 7.41E-14 4.28E-08 4.28E-08 Pyrene 5.66E-07 2.40E-11 5.66E-07 5.97E-07 7.90E-08 3.35E-12 7.90E-08 8.32E-08 VOCs Dichlorobenzene 1.17E-13 1.38E-14 1.20E-13 1.42E-13 1.20E-14 1.41E-15 1.23E-14 1.46E-14 Metals Aluminum (Al) 0.017 2.86E-09 0.017 0.017 0.0051 8.70E-10 0.0051 0.0051 Chromium (Total) 0.024 1.26E-08 0.024 0.024 0.0023 1.24E-09 0.0023 0.0023 Cobalt (Co) 0.0099 4.97E-09 0.0099 0.0099 0.0010 5.09E-10 0.0010 0.0010 Copper (Cu) 6.20E-05 2.66E-10 6.20E-05 6.20E-05 6.35E-06 2.72E-11 6.35E-06 6.35E-06 Lead (Pb) 0.0035 7.25E-09 0.0035 0.0035 2.14E-04 4.44E-10 2.14E-04 2.14E-04 Manganese (Mn) 0.039 4.61E-10 0.039 0.039 0.012 1.40E-10 0.012 0.012 Molybdenum (Mo) 2.45E-04 7.55E-10 2.45E-04 2.45E-04 2.52E-05 7.74E-11 2.52E-05 2.52E-05 Nickel (Ni) 8.20E-04 1.49E-09 8.20E-04 8.20E-04 1.52E-04 2.75E-10 1.52E-04 1.52E-04 Strontium (Sr) 3.34E-05 2.25E-11 3.34E-05 3.34E-05 1.02E-05 6.84E-12 1.02E-05 1.02E-05 Vanadium (V) 0.0038 2.51E-09 0.0038 0.0038 3.85E-04 2.57E-10 3.85E-04 3.85E-04 Zinc (Zn) 1.47E-04 2.88E-10 1.47E-04 1.47E-04 9.97E-06 1.96E-11 9.97E-06 9.97E-06 NOTES: Highlighted values (grey) indicate HQ value greater than benchmark of 1.0 (HQ > 1.0) COPC not shown in Table 6-22 either do not have a non-carcinogenic TRV or have negligible potential to persist or bioaccumulate in the environment (see Section 19A.3.2.2).



19A-86

Table 6-23 Non-Carcinogenic Human Health Risks from Exposure to Multi-Media – Aboriginal Resident

COPC

Aboriginal – Toddler Aboriginal – Adult

Baseline Case

Project Alone


Case

Planned Development

Case Baseline

Case

Project Alone


Case

Planned Development

Case Petroleum Hydrocarbons Aliphatic C5-C8 1.28E-08 2.19E-10 1.28E-08 1.68E-08 5.41E-09 9.28E-11 5.42E-09 7.13E-09 Aliphatic C9-C16 8.84E-07 4.28E-11 8.84E-07 1.18E-06 3.30E-07 1.63E-11 3.30E-07 4.40E-07 Aromatic C9-C16 8.29E-05 7.12E-08 8.29E-05 9.83E-05 3.51E-05 3.01E-08 3.51E-05 4.16E-05 Aromatic C17-C34 2.79E-07 1.03E-10 2.79E-07 2.71E-07 1.26E-07 4.73E-11 1.26E-07 1.23E-07 PAHs Anthracene 9.96E-05 1.16E-11 9.96E-05 9.96E-05 6.62E-05 5.76E-12 6.62E-05 6.62E-05 Fluoranthene 9.34E-04 1.01E-10 9.34E-04 9.34E-04 6.22E-04 5.02E-11 6.22E-04 6.22E-04 Fluorene 9.50E-04 2.95E-11 9.50E-04 9.50E-04 6.30E-04 1.50E-11 6.30E-04 6.30E-04 Pyrene 0.0012 4.45E-10 0.0012 0.0013 8.31E-04 2.16E-10 8.31E-04 8.31E-04 VOCs Dichlorobenzene 8.65E-10 1.04E-10 9.18E-10 1.12E-09 3.65E-10 4.40E-11 3.88E-10 4.72E-10 Metals Aluminum (Al) 0.087 7.25E-09 0.087 0.087 0.046 3.27E-09 0.046 0.046 Chromium (Total) 1.4 2.40E-07 1.4 1.4 0.86 1.77E-07 0.86 0.86 Cobalt (Co) 0.62 1.38E-07 0.62 0.62 0.37 1.12E-07 0.37 0.37 Copper (Cu) 0.085 4.14E-08 0.085 0.085 0.053 2.21E-08 0.053 0.053 Lead (Pb) 0.49 9.12E-08 0.49 0.49 0.31 4.67E-08 0.31 0.31 Manganese (Mn) 2.0 8.91E-09 2.0 2.0 1.1 4.17E-09 1.1 1.1 Molybdenum (Mo) 0.11 4.23E-08 0.11 0.11 0.072 2.54E-08 0.072 0.072 Nickel (Ni) 0.11 1.67E-08 0.11 0.11 0.057 1.06E-08 0.057 0.057 Strontium (Sr) 0.013 2.35E-09 0.013 0.013 0.0074 1.13E-09 0.0074 0.0074 Vanadium (V) 0.10 1.24E-08 0.10 0.10 0.058 5.94E-09 0.058 0.058 Zinc (Zn) 0.14 9.26E-08 0.14 0.14 0.073 4.04E-08 0.073 0.073 NOTES: Highlighted values (grey) indicate HQ value greater than benchmark of 1.0 (HQ > 1.0) COPC not shown in Table 6-23 either do not have a non-carcinogenic TRV or have negligible potential to persist or bioaccumulate in the environment (see Section 19A.3.2.2).


19A-87

Table 6-24 Non-Carcinogenic Human Health Risks from Exposure to Multi-Media – AENV/AHW AR

COPC

AENV/AHW AR – Toddler AENV/AHW AR – Adult

Baseline Case

Project Alone


Case

Planned Development

Case Baseline

Case

Project Alone


Case

Planned Development

Case Petroleum Hydrocarbons Aliphatic C5-C8 1.17E-07 2.00E-09 1.17E-07 1.54E-07 4.96E-08 8.50E-10 4.96E-08 6.53E-08 Aliphatic C9-C16 5.74E-06 2.75E-10 5.74E-06 7.65E-06 2.53E-06 1.21E-10 2.53E-06 3.37E-06 Aromatic C9-C16 7.58E-04 6.51E-07 7.58E-04 8.99E-04 3.21E-04 2.76E-07 3.21E-04 3.81E-04 Aromatic C17-C34 2.46E-06 8.95E-10 2.46E-06 2.39E-06 1.09E-06 3.96E-10 1.09E-06 1.06E-06 PAHs Anthracene 1.15E-04 8.73E-11 1.15E-04 1.15E-04 7.43E-05 4.18E-11 7.43E-05 7.43E-05 Fluoranthene 0.0010 7.11E-10 0.0010 0.0010 6.62E-04 3.47E-10 6.62E-04 6.62E-04 Fluorene 0.0012 2.28E-10 0.0012 0.0012 7.43E-04 1.10E-10 7.43E-04 7.43E-04 Pyrene 0.0014 3.23E-09 0.0014 0.0014 9.01E-04 1.54E-09 9.01E-04 9.03E-04 VOCs Dichlorobenzene 7.90E-09 9.50E-10 8.39E-09 1.02E-08 3.34E-09 4.01E-10 3.54E-09 4.31E-09 Metals Aluminum (Al) 0.16 1.92E-08 0.16 0.16 0.083 8.86E-09 0.083 0.083 Chromium (Total) 2.6 7.55E-07 2.6 2.6 1.4 4.17E-07 1.4 1.4 Cobalt (Co) 1.4 3.39E-07 1.4 1.4 0.74 2.03E-07 0.74 0.74 Copper (Cu) 0.25 3.09E-07 0.25 0.25 0.13 1.41E-07 0.13 0.13 Lead (Pb) 1.7 4.56E-07 1.7 1.7 1.1 2.11E-07 1.1 1.1 Manganese (Mn) 15 7.05E-08 15 15 7.4 3.18E-08 7.4 7.4 Molybdenum (Mo) 0.29 2.62E-07 0.29 0.29 0.16 1.24E-07 0.16 0.16 Nickel (Ni) 0.20 6.68E-08 0.20 0.20 0.11 3.32E-08 0.11 0.11 Strontium (Sr) 0.082 2.00E-08 0.082 0.082 0.040 9.11E-09 0.040 0.040 Vanadium (V) 0.22 5.35E-08 0.22 0.22 0.12 2.46E-08 0.12 0.12 Zinc (Zn) 1.1 8.00E-07 1.1 1.1 0.53 3.39E-07 0.53 0.53 NOTES: Highlighted values (grey) indicate HQ value greater than benchmark of 1.0 (HQ > 1.0) COPC not shown in Table 6-24 either do not have a non-carcinogenic TRV or have negligible potential to persist or bioaccumulate in the environment (see Section 19A.3.2.2).



19A-88

CHROMIUM

Chromium is a naturally-occurring element found in rocks, animals, plants, and soil. The general population is most likely to be exposed to trace levels chromium in the food that is eaten (ATSDR 2008).

Both the Aboriginal receptor and the AENV/AHW AR receptor had predicted health risks that were greater than 1.0 (i.e., CR values of 1.4 and 2.6, respectively).

The breakdown of the relevant pathways for the multimedia assessment is illustrated in Figure 6-1. The predominant source of chromium to the various receptor groups is though ingestion of: aboveground produce, belowground produce, and fruit for all receptors; and traditional plants (Labrador tea, and blueberries) for Aboriginal and AENV/AHW AR receptors. Modelled air concentrations from the Baseline Case had no effect on the predicted concentrations of chromium in the vegetation samples hence the vegetation exposure concentrations were the same at all receptor locations, as they were based on the results of the baseline sampling program (see Section 19A.4).

Soil/Dust Dermal Contact/Ingestion

Ingestion -Aboveground

Garden Produce


Protected Garden Produce

Ingestion -Belowground

Garden Produce

Ingestion - Home Grown Fruit


Traditional Plant


Traditional Plant

Ingestion - Wild Fruit

Ingestion - Wild Game

Total Chromium

Figure 6-1 Relevant Pathway Breakdown for Oral/Dermal Exposures to Chromium – AENV/AHW AR Toddler Receptor


19A-89

As indicated previously, the baseline concentrations of traditional foods were based on a 95% upper confidence limit on the mean on the observed concentrations in the samples of traditional foods. The baseline concentrations of other fruit and vegetables were based on applying conservative uptake factors to the 95% upper confidence limit on the mean on the observed concentrations in the soil samples.

In addition, the food consumption rates used for the receptors are very conservative. It has been assumed that First Nation receptors, in addition to their use of traditional foods, are harvesting 10% of their total fruit and vegetable consumption from local gardens. For the AENV/AHW AR receptor, 100% of their total fruit and vegetable consumption is assumed to come from local gardens.

The assessment takes a conservative approach to oral exposures to chromium. It is assumed that 100% of ingested chromium is bioavailable and is absorbed, thereby having the potential to produce health effects. However, actual absorption of chromium has been reported to be less than 10% (Health Canada 1986) of the ingested dose.

The oral exposure reference dose for chromium is meant to be protective of gastrointestinal effects. However, given the conservatism in the exposure assessment associated with food concentrations, ingestion rates, and bioavailability, and that the HQ values are only slightly above the benchmark of 1.0, it is unlikely that changes to public health would occur.

COBALT

Cobalt is naturally found in most rocks, soil, water, plants, and animals, typically in small amounts. For most people, food is the largest source of cobalt intake (ATSDR 2008).

Of the five receptor types, only the AENV/AHW AR receptor had predicted health risks that were greater than 1.0 (i.e., CR value of 1.4).

The breakdown of the relevant pathways for the multimedia assessment is illustrated in Figure 6-2. The predominant source of cobalt to the various receptor groups is though ingestion of: aboveground and belowground produce for all receptors; and traditional plants (Labrador tea, and blueberries) for Aboriginal and AENV/AHW AR receptors. Modelled air concentrations from the Baseline Case had no effect on the predicted concentrations of cobalt in the vegetation samples hence the vegetation exposure concentrations were the same at all receptor locations, as they were based on the results of the baseline sampling program (see Section 19A.4).




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Garden Produce




Garden Produce Ingestion - Home Grown Fruit


Traditional Plant


Traditional PlantIngestion - Wild FruitIngestion -Wild Game

Cobalt

Figure 6-2 Relevant Pathway Breakdown for Oral/Dermal Exposures to Cobalt – AENV/AHW AR Toddler Receptor


The assessment takes a conservative approach to oral exposures to cobalt. It is assumed that 100% of ingested cobalt is bioavailable and is absorbed, thereby having the potential to produce health effects. However, actual absorption of cobalt has been reported to range from 1-50% of the ingested dose (Nieboer and Fletcher 2001).

The oral exposure reference dose for cobalt is meant to be protective of cardiomyopathy (weakening of the heart muscle or a change in heart muscle structure). However, given the conservatism in the exposure assessment associated with food concentrations, ingestion rates, and bioavailability, and that the HQ values are only slightly above the benchmark of 1.0, it is unlikely that changes to public health would occur.


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LEAD

Lead occurs naturally in the earth’s crust; however, it is usually found combined with two or more other elements to form lead compounds (ATSDR 2007). Of the five receptor types, only the AENV/AHW AR receptor had predicted health risks that were greater than 1.0 (i.e., CR value of 1.7).

The breakdown of the relevant pathways for the multimedia assessment is illustrated in Figure 6-3. The predominant source of lead to the various receptor groups is though ingestion of: aboveground produce, belowground produce, and fruit for all receptors. Modelled air concentrations from the Baseline Case had no effect on the predicted concentrations of lead in the vegetation samples hence the vegetation exposure concentrations were the same at all receptor locations, as they were based on the results of the baseline sampling program (see Section 19A.4).



Garden Produce




Garden Produce



Traditional Plant


Traditional Plant


Ingestion -Wild Game

Lead

Figure 6-3 Relevant Pathway Breakdown for Oral/Dermal Exposures to Lead – AENV/AHW AR Toddler Receptor


In addition, the food consumption rates used for the receptors are very conservative. It has been assumed that First Nation receptors, in addition to their use of traditional foods, are harvesting 10% of



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their total fruit and vegetable consumption from local gardens. For the AENV/AHW AR receptor, 100% of their total fruit and vegetable consumption is assumed to come from local gardens.

The assessment takes a conservative approach to oral exposures to lead. It is assumed that 100% of ingested lead is bioavailable and is absorbed, thereby having the potential to produce health effects. However, actual absorption of lead by children through food has been reported to range from 40 to 53% of the ingested dose (Health Canada 1992).

The oral exposure reference dose for lead is meant to be protective of blood levels in infants. However, given the conservatism in the exposure assessment associated with food concentrations, ingestion rates, and bioavailability, and that the HQ values are only slightly above the benchmark of 1 for a receptor scenario that does not currently exist, it is unlikely that changes to public health would occur.

MANGANESE

Manganese is an element that occurs naturally within the earth’s crust. Food ingestion is the predominant route of exposure to manganese.

Of the five receptor types, only the Recreational Camper had predicted health risks that were less than 1.0. The CR values for Residents and Hunters were relatively low (1.5) as was the CR value for Aboriginal (2.0); however, the CR value for the AENV/AHW AR receptor was 15.

The breakdown of the relevant pathways for the multimedia assessment is illustrated in Figure 6-4. The predominant source of manganese to the various receptor groups is though ingestion of: garden produce and fruit for all receptors. Modelled air concentrations from the Baseline Case had no effect on the predicted concentrations of manganese in the vegetation samples hence the vegetation exposure concentrations were the same at all receptor locations, as they were based on the results of the baseline sampling program (see Section 19A.4).


In addition, the food consumption rates used for the receptors are very conservative. It has been assumed that First Nation receptors, in addition to their use of traditional foods, are harvesting 10% of their total fruit and vegetable consumption from local gardens. For the AENV/AHW AR receptor, 100% of their total fruit and vegetable consumption is assumed to come from local gardens. The high modelled concentrations of manganese in produce accounts for the considerably higher CR value for the AENV/AHW AR receptor.

Manganese is an essential element for plants and animals, and is therefore readily taken up and absorbed by most organisms (WHO 2004). Manganese is regarded as one of the least toxic elements (Health Canada 1987).


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Garden Produce




Garden Produce



Traditional Plant


Traditional Plant



Manganese

Figure 6-4 Relevant Pathway Breakdown for Oral/Dermal Exposures to Manganese – AENV/AHW AR Toddler Receptor

The oral exposure reference dose for manganese is meant to be protective of mild central nervous system outcomes. However, given the conservatism in the exposure assessment associated with food concentrations, ingestion rates, and bioavailability, and that with the exception of the AENV/AHW AR receptor, the HQ values are only slightly above the benchmark of 1, it is unlikely that changes to public health would occur.

ZINC

Zinc is one of the most common elements in the Earth's crust. For most people, food is the largest source of zinc intake (ATSDR 2005).

Of the five receptor types, only the AENV/AHW AR receptor had predicted health risks that were greater than 1.0 (i.e., CR value of 1.1).

The breakdown of the relevant pathways for the multimedia assessment is illustrated in Figure 6-5. The predominant source of zinc to the various receptor groups is though ingestion of garden produce and fruit. Modelled air concentrations from the Baseline Case had no effect on the predicted concentrations of zinc in the vegetation samples hence the vegetation exposure concentrations were the same at all receptor locations, as they were based on the results of the baseline sampling program (see Section 19A.4).



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Garden ProduceIngestion -

Aboveground Protected Garden

Produce


Garden Produce



Traditional Plant


Traditional Plant

Ingestion -Wild Fruit


Zinc

Figure 6-5 Relevant Pathway Breakdown for Oral/Dermal Exposures to Zinc – AENV/AHW AR Toddler Receptor



The assessment takes a conservative approach to oral exposures to zinc. It is assumed that 100% of ingested zinc is bioavailable and is absorbed, thereby having the potential to produce health effects. However, actual absorption of zinc is generally considered to be about 33% (Health Canada 1971).

The oral exposure reference dose for zinc is meant to be protective of erythrocyte copper-zinc-superoxide dismutase activity (reflects copper utilization and the risk of copper deficiency). However, given the conservatism in the exposure assessment associated with food concentrations, ingestion rates, and bioavailability, and that the HQ value is only slightly above the benchmark of 1, it is unlikely that changes to public health would occur.


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19A.6.4.5 Results –Carcinogenic Human Health Risks via Multiple Pathways

The ILCR values for long-term exposure to carcinogenic chemicals via multiple exposure pathways for the Project Alone Scenario are summarized in Table 6-25. Of the chemicals screened in for the multi-media assessment, only PAHs are considered carcinogenic via oral/dermal exposure. The cancer risk estimates for carcinogenic PAHs are expressed in terms of their toxic equivalency quotient (TEQ) relative to benzo(a)pyrene (see Section 19A.6.3.3 for additional details). The table provides the ILCR values for each of the human health receptor locations assessed based on exposure throughout a lifetime (i.e., infant through to adult). The ILCR value for each carcinogenic chemical for the Project Alone Scenario is less than the benchmark of 1-in-100 000.

Table 6-25 Carcinogenic Human Health Risks from Exposure to Multi-Media

Receptor Location

Benzo(a)pyrene TEQ Cancer Risk – Lifetime Exposure

Baseline Case (LCR)

Project Alone

Scenario (ILCR)


Planned Development

Case (LCR)

AENV/AHW AR - Clearwater Indian Reserve 175 4.25E-04 1.17E-09 4.25E-04 4.25E-04

Aboriginal - Clearwater Indian Reserve 175 4.18E-04 6.41E-10 4.18E-04 4.18E-04

Resident - Anzac 8.88E-07 9.82E-11 8.88E-07 8.92E-07

Hunter – Anzac 9.56E-07 4.22E-10 9.56E-07 9.61E-07

AENV/AHW AR - Gregoire Lake Indian Reserve 176 4.25E-04 2.50E-09 4.25E-04 4.25E-04

Aboriginal - Gregoire Lake Indian Reserve 176 4.18E-04 8.16E-10 4.18E-04 4.18E-04

Camper - Gregoire Lake Provincial Park Campground 4.46E-08 2.50E-13 4.46E-08 4.46E-08

Camper - South of Stony Mountain Fire Lookout 4.46E-08 7.41E-13 4.46E-08 4.46E-08

Camper - Northwest of Stony Mountain Fire Lookout 4.46E-08 3.57E-13 4.46E-08 4.46E-08

Camper - Engstrom Lake Campground 4.46E-08 2.53E-13 4.46E-08 4.47E-08

AENV/AHW AR - Trapper Cabins 4.26E-04 6.56E-09 4.26E-04 4.26E-04

Aboriginal - Trapper Cabins 4.18E-04 1.35E-09 4.18E-04 4.18E-04

AENV/AHW AR - Janvier Indian Reserve 4.25E-04 1.45E-09 4.25E-04 4.25E-04

Aboriginal - Janvier Indian Reserve 4.18E-04 6.78E-10 4.18E-04 4.18E-04

AENV/AHW AR - Mariana Settlement 4.25E-04 1.27E-09 4.25E-04 4.25E-04

Aboriginal - Mariana Settlement 4.18E-04 6.54E-10 4.18E-04 4.18E-04

Resident - Mariana Settlement 8.43E-07 6.85E-11 8.43E-07 8.45E-07

Hunter - Trapper Cabin 5 9.35E-07 5.39E-10 9.36E-07 9.40E-07

AENV/AHW AR - Trapper Cabin 5 4.25E-04 2.78E-09 4.25E-04 4.25E-04

Aboriginal - Trapper Cabin 5 4.18E-04 8.53E-10 4.18E-04 4.18E-04



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The LCR values for long-term exposure to chemicals via multiple exposure pathways for the Baseline Case, Application Case, and Planned Development Case are included in Table 6-24. The cancer risks associated with these cases are primarily associated with the consumption of fruit and produce from the LSA. The concentrations include the measured concentrations of PAHs in soil and plant samples obtained from the LSA. Although PAHs were not detected in the samples, the ½ detection limits were used in the risk estimates.

19A.6.4.6 Results - Odour

The CR values associated with the maximum predicted 1-hour exposure concentrations at each of the receptor locations identified in Table 2-1 were determined for the Baseline Case, the Expansion Project alone (Project Alone Scenario), the Application Case, and the Planned Development Case. The results are provided in Appendix 19A-7. The maximum CR values at the fenceline of the central processing facility (CPF), as well as the maximum CR value of the other 44 discrete receptor locations evaluated, are provided in Table 6-26.

The Project Alone Scenario CR values for hydrogen sulfide at the fenceline of the CPF were higher than the odour-based benchmarks for both the 1-hour and 24-hour maximum concentrations. Concentrations of carbon disulphide and thiophene at the fenceline of the CPF also higher than the odour-based guidelines; however, the contribution of the Expansion Project to these concentrations are negligible. The Expansion Project is located in a relatively remote area; human receptors would not likely be found at this location of any appreciable length of time and therefore the likelihood that a person would be exposed to concentrations of hydrogen sulfide that are greater than the odour-based guidelines is very low.

The concentrations of carbon disulfide, hydrogen sulfide, and thiophene at a number of the human health receptor locations, where people might be exposed for any appreciable length of time, were higher than the odour-based guidelines. These results indicate that people in the LSA may be exposed to unpleasant odours from industrial sources. However, the contribution of the Expansion Project to these concentrations is negligible, as indicated by the very low CR values for the Project Alone Scenario.


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Table 6-26 Concentration Ratios for Odour Exposures

COPC

Central Processing Facility (CPF) Local Study Area (LSA) Maximum

Baseline Case

Project Alone


Case

Planned Development

Case Baseline

Case

Project Alone


Case

Planned Development

Case 1-Hour Concentration Ratio NO2 0.2 0.36 0.36 0.36 0.47 0.087 0.47 0.47 Ethylbenzene 0.0084 5.10E-05 0.0084 0.011 0.021 2.20E-06 0.021 0.027 Naphthalene 0.0021 1.60E-04 0.0022 0.0025 0.003 3.90E-06 0.003 0.0037 Carbon disulfide 3.0 3.30E-04 3.0 4.0 7.9 1.10E-05 7.9 10 Hydrogen sulfide 1.2 1.4 2.4 2.7 2.4 0.059 2.4 3.1 Thiophene 20 0.0025 20 27 53 8.50E-05 53 70 24-Hour Concentration Ratio NO2 0.21 0.43 0.44 0.44 0.45 0.027 0.45 0.45 Hydrogen sulfide 0.26 2.2 2.4 2.5 2.0 0.069 2.0 2.2



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19A.6.5 Uncertainty Analysis

All risk estimates have inherent uncertainty. These uncertainties are addressed by incorporating conservative assumptions into every aspect of the risk assessment. Although many factors contribute to a risk estimate, analysis results are generally sensitive to only a few of these factors, which are described below.

19A.6.5.1 Uncertainties in Toxicological Information

There is limited toxicological information on the effects associated with low-level chemical exposures to humans. Most information available is based on epidemiological studies of occupationally exposed workers. These are usually based on an 8hr/day or 40hr/week, higher level exposure regimes and do not apply well to low-level, chronic exposures. Additionally reference doses and cancer potency estimates for many chemicals are based on laboratory dose-response estimates in animals. The use of animals requires certain assumptions be made, which introduces further uncertainty. Assumptions include:

• the toxicological effect in animals also occurs in humans

• the short-term exposures used in animal studies can be extrapolated to chronic or long term human exposures

• the toxicokinetic and toxicodynamic processes that occur in animals also occur in humans

• the uptake of the compound from the test vehicle (the medium within which the test compound is delivered to the animals, e.g. water, food) will be representative of the uptake of the chemical from real-world environmental media (e.g., soil, water, air)

• the assumption that extrapolation from high-dose laboratory studies low-dose environmental studies accurately reflects the shape of the dose response curve at the low dose-response range

To account for these and other related uncertainties regulatory agencies such as Health Canada and the US EPA adopt conservative assumptions to account for uncertainties. The use of Uncertainty Factors accounts for uncertainties by lowering the reference dose of the Hazard Quotient calculation well below the level where no effects were seen in animals. Uncertainty Factors are applied by factors of 10 to account for uncertainties such as, interspecies differences (e.g., physiology), individual variation (e.g., unusually sensitive individuals), limitations in toxicological information, and extrapolation from acute exposures to chronic exposures. Depending on the degree of uncertainty, typical factors will range from 100 to 10 000, with some being lower than 10 (in the case where solid human data is available). The incorporation of these factors results in risk estimates that are extremely conservative and ensure that limited exposures above reference does concentrations will not result in adverse human health effects.


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For the purposes of this assessment a toxic equivalency factor (TEF) approach was used for PAHs. Although Health Canada has recently commissioned a report summarizing the TEF approach regarding assessment of carcinogenic and non-carcinogenic PAHs, no Canadian or other international agency has developed cancer slope factors for any of the potentially carcinogenic PAH-containing mixtures based on oral exposures (CCME 2008). Agencies that have developed TEFs tend to have limited confidence in them. There are at least four factors that create uncertainty about TEFs:

• Prediction of mixture effects from single substance studies

• Prediction of potency from one exposure route based on experimental data from another exposure route

• Possible presence of carcinogens or carcinogenic promoters present in the mixture that are not measured/considered in the TEF scheme

• Uncertainty about the use of laboratory rodent models to predict human cancer potential

The TEF approach for PAHs is based on a whole mixture of PAH assuming that a combination is considered a dilution of a “surrogate” mixture of PAHs. The “surrogate” is generally considered a potent PAH mixture with well-defined chemistry and toxicology. The approach uses a single compound, benzo(a)pyrene (B[a]P), as the surrogate for the PAH fraction of other complex mixtures. Using this method, the risk from any PAH mixture of concern can be estimated as the product of the environmental levels of B[a]P and the estimate of risk attributable to mixtures per unit B[a]P. In general the approach does not predict the potency of an ambient complex mixture, only its PAH component.

The relative potencies, or TEFs, can be used in one of two ways:

• To modify the TRV for B[a]P for each carcinogenic PAH or

• To calculate B[a]P equivalent concentrations for each of the PAHs and evaluate the total B[a]P equivalent concentration against the B[a]P TRV

The two approaches are mathematically equivalent; however, the second method is commonly used and consistent with existing approaches. The second method was adopted for this assessment.

SENSITIVE POPULATIONS

A susceptible population will exhibit a different or enhanced response to a COPC than will most persons exposed to the same level of the contaminant in the environment. Reasons may be genetic makeup, age (e.g., children or seniors), health and nutritional status, behaviour and exposure to other toxic substances (e.g., cigarette smoke) (ATSDR 2002). Human receptors are selected such that the most sensitive individuals and individuals having the greatest potential for exposure to COPCs and adverse effects from such exposures are represented. For these reasons an Aboriginal Adult and Toddler receptor were selected. It is assumed that the Aboriginal receptor will rely heavily on local wild game to supplement their diets and therefore represent a high level exposure scenario. The Aboriginal Toddler will represent the most sensitive individual for reasons just mentioned plus the physiological (nutritional needs) and behavioural (frequent hand to mouth transfer) considerations associated with children of that age. The non-cancer TRVs used in this risk assessment are estimates of a continuous exposure to the human



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population, including sensitive subgroups, that are to be without appreciable risk of adverse non-cancer effects during a lifetime. Toxicity doses and cancer slope factors used in the assessment have accounted for sensitive populations by applying uncertainty factors (see toxicity assessment above).

19A.6.5.2 Uncertainties in Exposure Assessment

ESTIMATION OF DEPOSITION RATES AND AIR CONCENTRATIONS

As noted in Section 19A.5.1, the air concentrations and deposition rates are obtained directly from the air dispersion modelling results. Conservative assumptions were used in the development of the air model. Maximum predicted 1-hour and 24-hour concentrations in air at each receptor location were used to evaluate all acute inhalation risk estimates.

In reality, the frequency with which the maximum concentration would occur at any one receptor location is relatively low for most COPC. Therefore, the risk estimates tend to overestimate, rather than underestimate, health risks.

FOOD CHAIN UPTAKES

Estimation of COPC uptake through the food chain involves the use of assumptions regarding many factors, including root uptake factors, air to plant transfer factors, biotransfer and bioconcentration factors, and crop and soil ingestion rates (Health Canada 2004; US EPA 1997). Typically, these assumptions are conservative and tend to overestimate, rather than underestimate, risks.

RECEPTOR CHARACTERISTICS

For each receptor scenario, traditional knowledge and professional judgement was used in determining exposure durations, consumption patterns and ingestion rates (e.g., Wein 1999; Health Canada 2004; US EPA 1997).

19A.6.5.3 Uncertainties in Risk Characterization

The risk assessment of contaminants is complicated by the reality that most toxicological studies are on single chemicals but exposures are rarely to single chemicals. Exposures generally involve more than one contaminant. Although chemicals in the environment are most often present in some sort of mixture, guidelines for the protection of human health are almost exclusively based on exposure to single chemicals. The lack of approaches to evaluate biological effects of chemical mixtures and the use of single-compound toxicity data makes their use highly speculative.

Chemicals in a mixture may interact in four general ways to elicit a response:

• Non-interacting – chemicals have no effect in combination with each other; the toxicity of the mixture is the same as the toxicity of the most toxic component of the mixture

• Additive – chemicals have similar targets and modes of action but do not interact, the hazard for exposure to the mixture is simply the sum of hazards for the individual chemicals


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• Synergistic – there is a positive interaction among the chemicals such that the response is greater than would be expected if the chemicals acted independently

• Antagonistic – there is a negative interaction among chemicals such that the response is less than would be expected if the chemicals acted independently

For human health exposures, quantitative information on interactions among chemicals in mixtures is rarely available. In the absence of information on the mixture, risk is sometimes based on the addition of the risks of the individual mixture components, unless there is information indicating that the interaction is other than additive in nature. However, this practice is only appropriate if the COPC in question have similar modes of action and similar toxic endpoints in the human body. There is uncertainty associated with any of the above approaches in that risk may be overestimated or underestimated.

In this risk assessment, the COPC-specific HQs, ILCRs and LCRs for a receptor have been characterized for single COPCs only.

19A.6.6 Human Health Conclusions

The HHRA derived health risk estimates (i.e., HQ, and ILCR) associated with air emissions from the Expansion Project in combination with existing industrial sources (Application Case), and in combination emissions from planned sources in the RSA. The cumulative health risks estimates associated with acute and chronic exposures to emissions of COPC via inhalation and oral and dermal contact were less than the applicable benchmark for each of the COPC, with the exception of the:

• SO2 – 1-hour exposure period

• PM2.5 - 24-hour exposure period

• Acrolein – 24-hour exposure period and annual average exposure period

• Hydrogen sulfide – 24-hour exposure period

• Chromium – Aboriginal receptor, AENV/AHW AR receptor

• Cobalt – AENV/AHW AR receptor

• Lead - AENV/AHW AR receptor

• Manganese - Resident, Hunter, Aboriginal receptor, AENV/AHW AR receptor

• Zinc - AENV/AHW AR receptor

As previously discussed, the Expansion Project contributions to the 1-hour SO2 concentrations and the 24-hour hydrogen sulfide concentrations at the fenceline of the central processing facility are substantive; however, 99.9% of the time, the concentrations of these COPC at the fenceline would meet the health-based benchmarks. The types of effects associated with these short-term exposures (respiratory and nasal irritation) are reversible. As the Expansion Project is located in a relatively remote area; human receptors would not likely be found at this location of any appreciable length of time. Based on these results, the likelihood that a person would be exposed to concentrations of SO2 or hydrogen sulfide at the fenceline that are greater than the benchmark is very low.



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Elevated 24-hour exposures to PM2.5 and hydrogen sulfide, and annual average exposures to acrolein are generally limited to the cities of Fort McMurray and Fort McKay, each of which are located more than 50 km from the Expansion Project. The assessment demonstrated that the contribution of the Expansion Project to these elevated concentrations was negligible.

The CR values based on the maximum 24-hour concentrations of acrolein are higher than 1 throughout much of the LSA; however, the assessment indicates that the contributions of the Expansion Project to acrolein concentrations are negligible. The lowest concentration at which mild eye irritation has been observed in humans (i.e., 140 µg/m3) is more than 100-times higher than the maximum modelled 24-hour air concentration of acrolein at the receptor locations and as such, it is unlikely that the concentrations of acrolein would result in a substantive health risk.

The health risks associated with each of the metals (chromium, cobalt, lead, manganese, and zinc) did not change from the Baseline Case to Application Case to Planned Development Case, indicating that contributions from the Expansion Project and other planned projects are negligible. As indicated previously, given the conservatism in the exposure assessment associated with food concentrations, ingestion rates, and bioavailability, and that the HQ values are generally low, it is unlikely that multi-media exposures to these metals would result in a change in public health.


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19A.7 Ecological Risk Assessment

The purpose of an ecological risk assessment (ERA) is to evaluate the potential that ecological receptors (e.g., mammals, birds, plants, soil invertebrates) may experience adverse environmental effects as a result of exposure to chemical stressors. For this ERA, environmental effects refer to toxicologically-induced changes in the health of receptors that may be exposed to COPC released into the environment, specifically the local study area (LSA), as a result of Expansion Project related activities.

The potential for adverse environmental effects is quantified by comparing the amount of a substance that can be tolerated below which adverse environmental effects are not expected (e.g., toxicity reference value (TRV) or toxicity benchmark) to the amount of a COPC a receptor is expected to be exposed to, or come into contact with, on a daily basis. The quotient of the two and the magnitude by which values differ from parity (e.g., TRV = daily dose) is used to make inferences about the possibility of ecological risks. For this ERA the primary assessment endpoint was the protection of wildlife populations (i.e., the entity) based on predicted changes to growth, reproduction, or survival (i.e., the attribute) (Suter 2007) rather than at the individual level, with the notable exception being species protected under the Species at Risk Act or noted by the Government of Alberta as being “At Risk” (formerly "Red List") or "May Be at Risk" (formerly "Blue List"). Risk estimates were based on the use of several predictive models to estimate atmospheric Project emissions and the environmental fate and transport of COPC (see Section 19A.5). Additional assumptions and modelling were also necessary for the quantification of exposure, derivation of appropriate toxicity thresholds, and characterization of potential ecological risk. These are discussed in detail in the following sections.

In addition to COPC exposure, receptors in the LSA may encounter non-chemical stressors like noise and habitat alteration. The potential environmental effects of these stressors on ecological health was not evaluated in this ERA but has been discussed elsewhere in the EIA report.

19A.7.1 Ecological Risk Assessment Framework

This ERA followed a recognized framework (Figure 1-1) that progressed from a qualitative initial Problem Formulation step, through Exposure and Toxicity Assessment, and concluded with a quantitative Risk Characterization. Following this, a discussion of the uncertainties inherent to ERA, and conclusions and recommendations stemming from the assessment are discussed.

The risk assessment methodology for this ERA is based on a number of guidance documents including but not limited to:

• A Framework for Ecological Risk Assessment (General Guidance) (CCME 1996)

• Guidelines for Ecological Risk Assessment (US EPA 1998)

• US EPA Screening Level Ecological Risk Assessment Protocol for Hazardous Waste Combustion Facilities (US EPA 1999)



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19A.7.2 Problem Formulation

The nature, scope, and goals of the risk assessment are defined in the Problem Formulation stage and established by addressing a series of key planning tasks. In the context of an ERA, the Problem Formulation stage serves to develop a focused understanding of how COPC could affect the health of receptors in the LSA.

The four key points addressed in the Problem Formulation are as follows.

• Chemical Screening: Identification of the COPC evaluated in the ERA. This was achieved by comparing all chemicals in the emission inventory against specific physical and chemical property criteria (Section 19A.7.2.1).

• Identification of Key Indicator Resources Locations and Key Indicator Resources: A representative number of floral and faunal species (i.e.,receptors) were selected from numerous locations within and near the LSA (discussed in Sections 19A.7.2.2 and 19A.7.2.3).

• Exposure Pathway Screening: Identification of the potential pathways and routes of receptor exposure to COPC that need to be evaluated in the ERA (Section 19A.7.2.4).

Results of the above points are illustrated in a conceptual site model, which provides a visual depiction of the relevant pathways linking COPC in various environmental media and biota to the receptor of interest.

19A.7.2.1 Chemical Screening

A variety of sources were used to develop an expected atmospheric emissions inventory for the Expansion Project. This inventory underwent subsequent screening (in Section 19A.3) following nationally and internationally accepted criteria for the categorization of persistent and bio-accumulative chemicals (Environment Canada 2006; Rodan et al. 1999). Briefly, chemicals having a soil half-life greater than or equal to 182 days (6 months) and/or a log octanol-water partition coefficient (log Kow) greater than or equal to five were considered persistent, and carried forward as COPC for evaluation in the ERA. COPC evaluated in the ERA are listed in Table 7-1.

Unlike for the HHERA, gaseous COPC were not retained for evaluation in the ERA. Though wildlife may inhale airborne COPC emissions from the Expansion Project, this pathway of exposure is considered negligible and the current state of knowledge on inhalation toxicity of the COPC carried forward for assessment does not permit a quantitative and ecologically relevant evaluation. However, a qualitative assessment of receptor exposure to COPC through the inhalation pathway was conducted by using human receptors as a surrogate assuming that if humans are adequately protected against inhalation, so too will ecological receptors (Section 19A.7.5.7).

Similarly, though vegetation in the LSA may be exposed to sulphur dioxide (SO2) and nitrogen dioxide (NO2), both of which are known to produce adverse effects in exposed foliage (e.g., foliar necrosis, marginal or interveinal chlorosis in broad leaf plants, premature fall colouration and premature leaf abscission (Legge et al. 1998; Malhotra and Blauel 1980)), a quantitative evaluation was not conducted as part of the ERA. Rather, the effects of SO2 and NO2 have been assessed in the Vegetation and Wetlands section of the EIA report (Volume 2, Section 12).


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Table 7-1 COPC Included for Assessment in the ERA

Petroleum Hydrocarbons

Polycyclic Aromatic Hydrocarbons

Chlorinated Monocyclic Aromatics Inorganics

Aliphatic C5-C8 Anthracene Dichlorobenzene Aluminum Aliphatic C9-C16 Benzo(a)anthracene Chromium (total) Aromatic C9-C16 Benzo(a)pyrene Cobalt Aromatic C17-C34 Benzo(e)pyrene Copper Benzo(b)fluoranthene Lead Benzo(g,h,i)perylene Manganese Benzo(k)fluoranthene Molybdenum Chrysene Nickel Dibenzo(a,h)anthracene Strontium Fluoranthene Vanadium Fluorene Zinc Indeno(1,2,3-cd)pyrene Phenanthrene Pyrene Perylene

19A.7.2.2 Key Indicator Resource Locations

The LSA lies within the Athabasca Oil Sands area of northeastern Alberta, and is situated approximately 50 km southwest of Fort McMurray and 39 km southwest of the community of Anzac, in township 84, ranges 10, 11, & 12 W4M. The area falls within the central mixedwood sub region of the boreal forest natural region, and is characterized by low, rolling lands with a wide diversity of soils, deciduous and coniferous forests, and small lakes and wetlands. The major water bodies are the Hangingstone River and Horse Creek (JACOS 2002a-c). The wide variety of habitat available to wildlife means that many species may be found in the area year-round, with others using the habitat seasonally or as part of their yearly migration (Appendix 13c; JACOS 2002a-c).

The quantitative assessment of risk to receptors exposed to Expansion Project-related COPC was conducted at 13 discrete receptor locations within or near the LSA (Table 7-2, Figure 2-1). Receptor locations were selected based on proximity to:

• identified valuable wildlife habitat

• wildlife parks

• watersheds and watercourses

• unique ecoregions and habitat

• eco-tourism areas

• Aboriginal communities



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Table 7-2 Key Indicator Resource Locations

Site # Location Name 8-9 Campgrounds West and East of Clearwater Indian Reserve 175 11-15 Gregoire Lake Indian Reserve 176 16 Gregoire Lake Provincial Park Campground 18 Campground South of Stony Mountain Fire Lookout 19 Campground Northwest of Stony Mountain Fire Lookout 20 Engstrom Lake Campground 21-24 Trapper Cabins 1-4 27 and 31 Janvier Indian Reserve 194/Janvier 28 Mariana Settlement 35-39 Grand Rapids Wildland Provincial Park 40-44 Stony Mountain Provincial Park 34 Trapper Cabin 5 45 Overall Maximum Predicted within LSA (modelled as adjacent to the Central Processing

Facility)

Where more than one Site # has been given (e.g., 8-9) the maximum modelled COPC concentrations from the specified locations were used in the ERA to represent each of the sites.

19A.7.2.3 Identification of Key Indicator Resources

With the large number of wildlife species present in and around the LSA, it is neither practical nor necessary to conduct an assessment for each individual species. Rather, after reviewing the known species inventories of the LSA (Appendix 13c; JACOS 2002a-c) a carefully selected, representative subset of receptors was selected as the basis for this ERA. Key Indicator Resources were chosen for the ERA by focusing on wildlife species that were:

• indigenous to the area

• most likely to receive the greatest exposure to contaminant releases due to their habitat and home range

• representative of various levels in the terrestrial trophic web (e.g., carnivore, herbivore, insectivore)

• of cultural, economic, or social significance

Each selected receptor is considered representative of other species occupying a similar position in the food web. In other words, results of the Risk Characterization stage for a selected receptor can be used to make inferences about risk to other species occupying a similar level in the food web. For example, if results of the ERA indicate that no unacceptable risk is expected for American robin, a species that relies heavily on a diet of terrestrial invertebrates, then it can be expected that other invertivore bird species will be protected. Using these criteria, the receptors assessed in the ERA are expected to provide adequate and conservative representation of the species diversity in the LSA.


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AVIAN AND MAMMALIAN KEY INDICATOR RESOURCES

Since Expansion Project activities are expected to have a negligible effect of the aquatic environment (Section 19A.3.1.2 and 19A.3.1.3), only receptors part of the terrestrial food web were included in the ERA. The following mammalian species, listed in alphabetical order, were identified as receptors for quantitative risk evaluation in the ERA:





• woodland caribou (Rangifer tarandus)

The following bird species, listed in alphabetical order, were identified as receptors for quantitative risk evaluation in the ERA:



• short-eared owl (Asio flammeus)


The following community receptors were identified as receptors for quantitative risk evaluation in the ERA:

• terrestrial plants

• soil invertebrates

A description of the ecology, dietary behaviour and life history parameters for each receptor is provided below. A detailed summary of parameters used for modelling each receptor (e.g., body weight, water ingestion rate, dietary composition, and food intake rate) is provided in Appendix 19A-8. Briefly, for avian and mammalian receptors, food ingestion rates were calculated according to Nagy 1987, water ingestion rates from Calder and Braun (1983) and soil ingestion rates as modified from Beyer et al. (1994).

MAMMALS

Canada Lynx (Lynx canadensis) is a secretive, medium-sized member of the cat family, with major populations inhabiting much of Canada and the northern US (CWS & CWF 2009). The Canada lynx prefers to inhabit old growth boreal forest with dense thickets, but adapts easily to other types of land so long as adequate cover is available for prey species. Populations of the Canada lynx are closely tied to those of the snowshoe hare, the prey item upon which the lynx almost exclusively feeds, and crashes in snowshoe hare populations are



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generally followed by reductions in lynx populations (CWS & CWF 2009). The Canada lynx weighs approximately 11 kg, though males may weigh as much as 17 kilograms (CWS & CWF 2009; Fox and Murphy 2002). Home ranges in Alberta have been recorded at 1500 to 4700 ha, varying in size with the abundance and effort required to track snowshoe hares (CWS & CWF 2009). When snowshoe hares are scarce, the Canada lynx will hunt and kill voles, mice, grouse, squirrels and foxes (CWS & CWF 2009). The pelt of the Canada lynx is sought by trappers in many provinces, and demand for this commodity has increased steadily since the 1970s (CWS & CWF 2009). In this ERA, the Canada lynx is modelled as consuming 1.5 kg of wet-weight food per day, 100% of which is small mammal and bird prey. The Canada lynx may be classified as a tertiary/quaternary consumer within the ecosystem (CCME 1997).

Masked Shrew (Sorex cinereus) is the most widely distributed shrew in North America, and is found throughout most of Canada (Lee 2001). It is common in moist environments and inhabits open and closed forests, meadows, riverbanks, lakeshores, and willow thickets (Lee 2001). The masked shrew weighs approximately 0.005 kg (US EPA 1993) and has home ranges varying from 0.2 to 0.6 ha in size (Saunders 1988). Masked shrews are preyed upon by many small predators such as weasels, hawks, falcons, owls, domestic cats, foxes, snakes, and short-tailed shrews (Lee 2001). The masked shrew does not hibernate (NWF 2003) and feeds year-round on insect larvae (dormant insects in winter), ants, beetles, crickets, grasshoppers, spiders, harvestmen, centipedes, slugs, snails, and seeds and fungi (NWF 2003; Lee 2001). It consumes approximately 0.003 kg of wet-weight food per day. In this ERA, the shrew’s diet is modelled as including 2.5% terrestrial plant material and 97.5% terrestrial invertebrates. Insectivores such as the masked shrew may be classified as secondary/tertiary consumers within the ecosystem (CCME 1997).

Meadow Vole (Microtus pennsylvanicus) is a small rodent (approximately 0.042 kg), which makes its burrows along surface runways in grasses or other herbaceous vegetation (US EPA 1993). It is active year-round and is the most widely distributed small grazing herbivore in North America, inhabiting moist to wet habitats including grassy fields, marshes, and bogs (US EPA 1993). Meadow voles are found throughout Canada, roughly to the limit of the tree line in the north. Home ranges vary considerably, from less than 0.0002 ha to greater than 0.083 ha (US EPA 1993). Meadow voles are a major prey item for predators such as hawks and foxes, and they feed primarily on vegetation such as grasses, leaves, sedges, seeds, roots, bark, fruits, and fungi, but will occasionally feed on insects and animal matter (US EPA 1993, Neuburger 1999). It consumes approximately 0.011 kg of wet-weight food per day. The meadow vole's diet is modelled as including 98% terrestrial plant material and 2% terrestrial invertebrates. Herbivores such as the meadow vole are classified as a primary consumer within the ecosystem (CCME 1997).

Snowshoe Hare (Lepus americanus) uses many forest types and are present in all provinces and territories in Canada (CWS & CWF 2008). They prefer forested areas with a dense understory of seedlings and tall shrubs. The understory cover helps to protect them from predators and provides them with food. The snowshoe hare is the primary prey item of the Canada lynx, and population numbers of the snowshoe hare are tightly linked to Canada lynx


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numbers. Female snowshoe hares are often slightly larger than males, and adults typically weigh 1.2 to 1.6 kg. The home range of a snowshoe hare is approximately 6 to 10 ha. Snowshoe hares consume a variety of herbaceous plants during the summer, including strawberry, fireweed, lupine, bluebell, and some grasses. They will also eat many leaves from shrubs. Their winter diet consists of small twigs, buds, and bark from many coniferous and deciduous species, and they have been known to scavenge meat from carcasses when available (CWS & CWF 2008). In this ERA the snowshoe hare is modelled as consuming 0.26 kg of wet-weight food per day, 95% of which is terrestrial vegetation, and 5% scavenged meat. The snowshoe hare is classified as a primary consumer within the ecosystem (CCME 1997).

Woodland Caribou (Rangifer tarandus) is a medium-sized member of the Cervidae family, which includes four other species native to Canada: moose, elk,

white-tailed deer, and mule deer (CWS & CWF 2008). The woodland caribou is an ungulate, meaning, a cloven-hoofed cud-chewing animal. It is found throughout most of the boreal forests across Canada. In the mountainous regions of western Canada the woodland caribou make seasonal movements from winter range on forested mountainsides to summer range on higher, alpine tundra habitats (CWS & CWF 2008). During the winter months, caribou consume primarily ground and tree lichens, which provide an energy-rich food source (SARA 2008). In the spring and summer months the caribou switch to fresh green vegetation, and so is considered to be a primary consumer. The adult woodland caribou is 1.0 to 1.2 m high at the shoulder and weighs 110 to 210 kg. The average weight for bulls is 180 kg and for cows, 135 kg (SARA 2008). In this ERA the woodland caribou is modelled as consuming 8.2 kg of wet-weight food per day, 100% of which is terrestrial vegetation. Woodland caribou is considered a “Threatened species” in Alberta and is given legislative protection under Alberta's Wildlife Act (http://www.srd.alberta.ca/BioDiversityStewardship/SpeciesAtRisk/GeneralStatus/Default.aspx and http://www.srd.alberta.ca/BioDiversityStewardship/SpeciesAtRisk/Default.aspx).

BIRDS

American Robin (Turdus migratorius) is a medium-sized bird (weighing approximately 0.08 kg; US EPA 1993) that occurs throughout most of Canada during the breeding season and overwinters in mild areas of Canada (CWS & CWF 2008). Access to fresh water, protected nesting habitat, and foraging areas are important to the American robin. Nesting habitat includes moist forest, swamps, open woodlands, orchards, parks, and lawns (US EPA 1993). The diet of the American robin typically consists of fruits, seeds, soil invertebrates (i.e., earthworms) and insects. Foraging home range sizes are approximately 0.15 ha to 0.81 ha (US EPA 1993). In this ERA, the American robin is modelled as consuming approximately 0.065 kg of wet weight food per day, 52.3% of which is terrestrial vegetation and 47.8% soil invertebrates. The American robin is an omnivore and as such is classified as a primary/secondary consumer within the ecosystem (CCME 1997).



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Red-Tailed Hawk (Buteo jamaicensis) are found as far south as Panama and as far north as the tree line in northern Canada and Alaska (Alberta Gov. 2007). Spring and summer are generally spent in the northern part of this range and winters in the southern states and Central America. In Alberta, this hawk prefers habitat in parkland and mixedwood zones and will also nest in wooded areas on the prairies. Red-tailed hawk home ranges vary in size from approximately 85 ha to greater than 2400 ha, depending on the habitat (US EPA 1993; Arnold and Dewey 2002). They generally hunt from an elevated perch, feeding primarily (approximately 80% to 85% of diet) on small rodents such as mice, voles, shrews, rabbits, and squirrels, as well as birds and reptiles (Arnold and Dewey 2002). Small mammals including rodents and rabbits comprise the largest portion of prey with birds and reptiles supplementing the diet (Alberta Gov. 2007). The red-tailed hawk weighs approximately 0.7 to 1.5 kg (Cornell Lab of Ornithology 2003). In this ERA, the red-tailed hawk is modelled as consuming 0.19 kg of wet weight food per day, 100% of which is terrestrial prey items. The red-tailed hawk is a carnivore and as such is classified as a tertiary consumer within the ecosystem (CCME 1997).

Short-eared Owl (Asio flammeus) is a medium sized owl weighing approximately 0.32 to 0.38 kg (Clayton 2000). Deriving its name from the inconspicuous tufts of feathers on its head, the short-eared owl is widespread throughout most of the world. The short-eared owl is listed as “May Be at Risk” (formerly “Blue Listed”) in Alberta (Clayton 2000; http://www.srd.alberta.ca/BioDiversityStewardship/SpeciesAtRisk/DetailedStatus/Birds.aspx). Within Alberta the short-eared owl is typically found inhabiting grasslands, marshes, clear cuts, and other open terrain, and requires a perch from which to spot prey items (Clayton 2000). Territories of this species range from 18 to 240 ha. Nesting location of this species is highly dependent on prey availability, and this species is one of the few species of owl that routinely builds nests on the ground (Clayton 2000). Sexual dimorphism is typically not pronounced in this species and males and females are similar in size and plumage, although males may be paler. The primary prey item of the short-eared owl is the vole, and in a similar fashion to the Canada lynx-snowshoe hare dynamic, short-eared owl populations respond synchronously to vole populations (Clayton 2000). In this ERA, the short-eared owl is modelled as consuming 0.09 kg of wet-weight food per day, 95% of which is small mammal prey, and 5% terrestrial invertebrates. The short-eared owl is a carnivore and as such is classified as a tertiary consumer within the ecosystem (CCME 1997).

Spruce Grouse (Falcipennis canadensis) is a favoured woodland gamebird by hunters, and is well known for its unique “drumming’ sound made by cupping and beating its wings against its body. They are a medium-sized bird, weighing approximately 0.5 kg (Terres 1995). Its preferred habitat is coniferous forest and it can be found throughout most of Canada wherever these forests exist (Alberta Gov. 2007). Spruce grouse are a non-migratory species, and once mature, generally occupy a relatively large area; typical home ranges are approximately 27 hectares (Environment Canada 2005). Adults are entirely herbivorous during the winter/non-breeding season, but will consume small amounts of


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animal food (i.e., insects, invertebrates) when breeding and rearing young (Alberta Gov. 2007). Spruce grouse are predominantly browsers, relying heavily on a diet of conifer needles, berries, and leaves. Young grouse consume an insect-rich diet at first, but quickly transition to plant food (Alberta Gov. 2007). Spruce grouse are estimated to consume approximately 0.22 kg of wet-weight food per day, 95% of which is terrestrial vegetation, and 5% terrestrial invertebrates. The spruce grouse is an omnivore and is classified as a primary/secondary consumer within the ecosystem (CCME 1997).

COMMUNITY-BASED KEY INDICATOR RESOURCES

The primary exposure pathway for some flora and fauna is from direct contact with a single abiotic environmental medium (e.g., soil). Accordingly, toxicity benchmarks are commonly derived based on COPC media concentrations and the adverse environmental effects thresholds for organisms that reside/rely on those media. Additionally, these benchmarks are typically generated using toxicity data for not one, but several species that rely on that medium, and are intended to represent a COPC concentration that will be protective of most, if not all species associated with that medium. For these reasons, the following receptors were evaluated in this ERA at the community level, rather than as individual species:

• Terrestrial plants

• Soil invertebrates

AMPHIBIANS AND REPTILES

Two amphibian and one reptile species were identified in the LSA during recent field surveys: boreal chorus frog (Pseudacris maculate); wood frog (Rana sylvatica); and red-sided garter snake (Thamnophis sirtalis) (Appendix 13c). Historically, the Canadian toad (Bufo hemiophrys), has also been identified as potentially occurring within the LSA, although it has not been recently sighted (JACOS 2002a-c).

To date, the current state of knowledge on toxicology and exposure characterization are simply not adequate to permit an assessment of risk to amphibians and reptiles exposed to the COPC released to the environment as a result of Expansion Project-related activities. Toxicological information for amphibians and reptiles is available from several publications including:

• Ecotoxicology of Amphibians and Reptiles (Sparling et al. 2000)

• RATL: A Database of Reptile and Amphibian Toxicity Literature (Pauli et al. 2000) that updates the older Canadian Wildlife Service report, A Review and Evaluation of the Amphibian Toxicological Literature (1989): Technical Report Series No. 61

• Ecotoxicity of Chemicals to Amphibians (Devillers and Exbrayat 1992)

• The US EPA’s ECOTOX database (http://cfpub.epa.gov/ecotox/)

• California Wildlife Biology, Exposure Factor, and Toxicity Database (Cal/Ecotox http://oehha.ca.gov/cal_ecotox/)



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A review of these sources confirms that for most organic contaminants, with the possible exception of polychlorinated biphenyls (PCBs), organochlorine pesticides (OCs) and some metals, there is a lack of information on chronic toxicology and bioavailability of the COPC assessed in this ERA. Mainly body burden and acute toxicity (exposure durations of 96 hours or less) data are available, and the vast majority of laboratory amphibian toxicity tests have focused on changes to embryonic and larval life stages occurring from water-borne contaminant exposure only. Species-specific chronic toxicity information is rarely available. Current research is being conducted on the environmental effects of specific chemical stresses on amphibians and reptiles, however, individual studies are not generally acceptable as the basis of toxicity data for quantitative ERA. Refer to Appendix 19A-9 for further discussion regarding amphibian and reptilian toxicology.

SPECIES AT RISK

Species at Risk (SAR) in this ERA are defined as any wildlife species listed as “Endangered”, “Threatened”, or “May be at Risk” under the federal Species at Risk Act (SARA) or noted by the Government of Alberta as being "At Risk" (formerly "Red List") or "May Be At Risk" (formerly "Blue List") of extinction. Only "At Risk" species are afforded legislative protection as "Endangered" or "Threatened" under Alberta's Wildlife Act (Alberta Sustainable Resource Development (ASRD) 2006).

Detailed status reports have been published by the Government of Alberta for those species classified as "At Risk" or "May Be At Risk" (Government of Alberta: http://www.srd.alberta.ca/BioDiversityStewardship/SpeciesAtRisk/SpeciesSummaries/SpeciesAtRiskFactSheets.aspx). Detailed information about the life history, ranges, habitat, and population size trends of each species is provided in the status reports, and these were reviewed in order to determine the likelihood that a species may fall within the LSA at any point during its life, including migration.

The ranges of seven SAR are expected to overlap the borders of the LSA (Table 7-3); three birds, three mammals, and one amphibian. It is difficult in ERA to quantitatively address COPC risk to SAR because quantitative information is often lacking on diet, inadvertent soil ingestion and toxicological reference data. To accommodate SAR in this ERA, receptors found within the same class and within a similar trophic level were used as surrogates to assess risk when SAR-specific information was scarce and explicit modelling was not performed. This information is also summarized in Table 7-3.

Table 7-3 Rationale for Inclusion/Exclusion of Species at Risk from ERA

Species Scientific name Rationale for Inclusion/Exclusion from ERA Assessed in ERA

(surrogate species) Barred Owl Strix varia According to information from the Government

of Alberta this species may be found within the LSA and was observed by project biologists during field surveys.

(Short-eared Owl)

Canadian Toad Bufo hemiophrys According to information from the Government of Alberta this species may be found within the LSA but difficulty with assessing amphibians and reptiles in ERA precludes the evaluation of this receptor.


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Table 7-3 Rationale for Inclusion/Exclusion of Species at Risk from ERA (cont’d)

Species Scientific name Rationale for Inclusion/Exclusion from ERA Assessed in ERA

(surrogate species) Northern Long-eared Bat

Myotis septentrionalis

According to information from the Government of Alberta this species may be found within the LSA and was observed by project biologists during field surveys. As with all bats in Canada, this species feeds exclusively on insects caught “on the wing”. As such, incidental soil ingestion rates are expected to be lower for this species than for ground dwelling receptors such as shrews. Therefore, protection of smaller mammals such as shrews (also an invertivore) was deemed to afford this species an adequate level of protection.

(Masked Shrew)

Peregrine Falcon

Falco peregrinus According to information from the Government of Alberta, the anatum subspecies is a possible breeder within the LSA.

(Red-tailed Hawk)

Short-eared Owl Asio Flammeus According to information from the Government of Alberta this species may be found within the LSA. Sufficient information was available to model this species in the ERA.

Woodland Caribou

Rangifer larandus According to information from the Government of Alberta this species may be found within the LSA and was observed by project biologists during field surveys. Sufficient information was available to model this species in the ERA.

Wolverine Gulo gulo According to information from the Government of Alberta this species may be found within the LSA and was observed by project biologists during field surveys. This species feeds on small mammals and birds, and may occasionally bring down deer and caribou.

(Canada Lynx)

19A.7.2.4 Exposure Pathway Identification

An exposure pathway identifies the potential routes of receptor exposure to COPC. Potential exposure media and the routes of exposure for receptors, and a rationale for the inclusion or exclusion from this ERA, are presented in Table 7-4.

For terrestrial wildlife receptors (i.e., birds and mammals), exposure to COPC may occur through the following routes:

• ingestion of soil (i.e., as a result of feeding and grooming)

• ingestion of plants or prey species that have accumulated chemicals from the soil, and other media

• dermal contact with soils

• inhalation



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Table 7-4 Rationale for Exposure Pathways Evaluated for Avian and Mammalian Receptors

Exposure Pathway Inclusion in ERA Rationale Soil Ingestion During Expansion Project related activities, air emissions will deposit

directly onto soil. Wildlife species inadvertently consume soil during foraging, preening and grooming. Therefore, this exposure pathway will be evaluated in the ERA for wildlife receptors.

Ingestion of Terrestrial Vegetation, Soil Invertebrates and Small Mammal Prey

During Expansion Project related activities, air emissions will deposit directly onto plant surfaces. Chemicals may subsequently be taken up into plants from the soil in which they are rooted. Consumption of plants could expose herbivorous wildlife to COPC. Therefore, this exposure pathway will be evaluated for herbivorous wildlife receptors. Carnivorous and omnivorous animals have the potential to be exposed to COPC via ingestion of exposed prey. For this reason, ingestion of prey will be evaluated in the ERA for these receptors.

Dermal Contact Although wildlife may be exposed by direct contact with soil, absorption of COPC through the skin is not generally considered a major route of exposure, especially for the COPC assessed herein. Therefore, the dermal exposure route will not be evaluated in the ERA.

Inhalation During Expansion Project related activities, wildlife may inhale airborne COPC resulting from emissions. The current state of knowledge on inhalation toxicity does not permit a quantitative, ecologically relevant assessment of this pathway for most COPC. As an alternative to conducting a quantitative risk assessment based on the inhalation pathway for ecological receptors, human receptor exposure to average annual COPC concentrations was used as a surrogate for ecological risk assuming that if humans are adequately protected against inhalation, so too will ecological receptors.

The principal exposure pathway for terrestrial plants and soil invertebrates is from direct contact with their associated media (i.e., soil).

Evaluation of surface water exposure pathways was not considered in the assessment given that potential Expansion Project related impacts to groundwater and surface water were considered to be negligible and dominant exposure pathways for wildlife are from soil and food item ingestion (Sections 19A.3.1.2 and 19A.3.1.3).

19A.7.2.5 Conceptual Site Model (CSM)

The Conceptual Site Model (CSM) constructed for this ERA provides a simplified representation of the exposure pathways linking COPC emitted from Expansion Project related activities to each identified receptor (see Figure 7-1). Exposure pathways are designated in the CSM by arrows leading from one compartment to another compartment, and boxes with an “” denote relevance to a particular receptor.


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19A.7.3 Exposure Assessment

The purpose of the Exposure Assessment component of the ERA is to develop a quantitative estimate of exposure to each COPC for each receptor for four assessment cases.

• Baseline Case: Includes industrial facilities that are currently operating and those that have regulatory approval and not yet operating, as well as non industry sources such as communities and traffic.

• Application Case: Includes emissions from existing and approved regional sources (i.e. Baseline Case) in combination with Expansion Project emissions (Project Alone Scenario).

• Planned Development Case: Includes emissions from the Application Case in combination with emissions from publicly disclosed future planned facilities. For the purpose of this assessment, the publically disclosed facilities only include those facilities for which a regulatory application has been submitted.

An additional scenario was considered as part of the assessment. A “Project” scenario was included to allow identification of potential project effects for the Expansion Project only.

This task was accomplished by determining the concentrations of COPC in relevant environmental abiotic media (i.e., soil). For each case involving Expansion Project emissions (i.e., Project Alone Scenario, Application Case and Planned Development Case), environmental fate and transport models were used to describe the movement of COPC from the emission source(s) through various environmental processes (e.g., deposition, leaching) to the potential exposure sources (e.g., plant tissue, soil). Fate and transport modelling was applied for the Baseline Case to estimate COPC concentrations in biota on top of empirical measurements (obtained for food basket assessment, Section 19A.4) where available. Following this, exposure for each receptor was quantified via all applicable exposure pathways by incorporating receptor-specific information such as dietary composition and ingestion rates (Appendix 19A-8).

19A.7.3.1 Exposure Point Concentrations

Using modelled air contaminant emission and deposition rates for each COPC, environmental fate modelling was used to generate COPC concentrations (referred to as exposure point concentrations; EPCs) in soil and terrestrial biota (vegetation and small animals) for all assessment cases. Additionally, background soil COPC concentrations were measured at select locations within the LSA (Section 19A.4 and 19A.5) for use in the Baseline Case Assessment. Background EPCs used in the ERA were the upper concentration limits of the mean (UCLM) obtained using ProUCL v4.0 software (US EPA 2009).

EPCs for soil invertebrates were estimated independently of the fate and transport model using COPC-specific uptake factors called bioaccumulation factors (BAF), which describe the relationship between a specified chemical in a given abiotic medium to various types of biota (e.g., the uptake of vanadium from soil by earthworms). A detailed description of uptake factors may be found in Appendix 19A-10.


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Briefly, the equation used to calculate a COPC concentration in a biotic tissue (such as soil invertebrates) from a soil concentration is as follows:

EPCi = EPCsoil x UPi

Where: EPCi = Exposure point concentration in target biotic tissue i (mg/kg wet weight);

EPCsoil = Exposure point concentration in soil (mg/kg dry weight); and

UPi = Uptake Factor from soil to wet weight target biotic tissue i (dimensionless).

19A.7.3.2 Calculation of the Average Daily Dose for Avian and Mammalian Receptors

For mammalian and avian receptors, exposure was calculated as the average ingested daily dose (ADD). The ADD can be defined as the amount of a COPC a receptor might be exposed to on a mg/kg-bw/day basis. For each receptor and COPC, the ADD was calculated by summing the intake from each applicable exposure pathway. The generalized equation for ADD is as follows:

ADDj = IFj x AFj x EPCj

For exposure pathway ‘j’, where:

IFj = Intake Factor (kg contaminated medium/kg body weight - day),

AFj = Absorption Factor (default value of 1), and

EPCj = Exposure Point Concentration (mg chemical/kg medium)

The Intake Factor (IF) is not specific to each COPC, but is a characteristic of the receptor being evaluated. The IF was calculated for each exposure pathway using the receptor’s medium-specific ingestion rate (IR), the fraction of the time spent on site (fsite, as a conservative measure assumed to equal 100% for this ERA) and the receptor’s body weight (BW) as follows:

IFj = (IRj x fsite)/BW

The assumption of 100% time spent on site means that exposure to COPC from emission sources is assumed to occur continuously throughout the life of the receptor. It is acknowledged that certain receptor move in and out of the LSA (e.g., for migration), thereby reducing their exposure, but this conservative assumption is meant to be a protective measure. For details related to the body weight, dietary composition (plant, insect, prey), and soil ingestion rates for each of the receptor evaluated in the ERA, refer to Appendix 19A-8, where details and results of all ADD calculations are summarized.

19A.7.3.3 Exposure Estimation for Community – Based Receptors

The exposure assessment for community-based receptors does not require the use of UP or ADD calculations. Since terrestrial plants and soil invertebrates are primarily associated with a single environmental media (e.g., soil) and the potential for adverse environmental effects can be characterized by comparing COPC concentrations in each media with corresponding toxicity benchmarks. Therefore, the EPC associated with the relevant environmental media for each community-based receptors is used as the exposure estimate in this ERA (relevant media are identified in the conceptual site model).



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19A.7.4 Toxicity Assessment

The objective of the Toxicity Assessment is to identify the potential adverse environmental effects associated with chronic exposure of receptors to each COPC. A Hazard Assessment is the basis for evaluating what might be an acceptable exposure level and what level may result in adverse environmental effects due to chronic exposure to COPC. The amount of a substance that can be tolerated, below which adverse environmental effects are not expected to be observed in a population, is referred to as the Toxicity Reference Value (TRV) for mammalian and avian species and generally referred to as toxicity benchmarks or guidelines for community-based receptors.

19A.7.4.1 Derivation of Oral Toxicity Reference Values for Mammalian and Avian Receptors

The toxicological database in support of a TRV preferably includes a number of chronic or multi-generational exposure studies involving exposure of relevant test species (i.e., the receptors of interest) to appropriate chemical forms of the substance of interest. Ideally, one or more relevant biological endpoints such as growth, reproductive outcomes, or survival were measured in the study. Databases that meet this requirement are available for some chemicals, but in most cases, available toxicity data is limited to studies conducted with laboratory animals (e.g., mice, rats, rabbits, quail, chicken, ducks).

Toxicity Reference Values for this ERA are based on dose response studies, typically conducted with laboratory animals where the lowest observed adverse effects level (LOAEL) or no observed adverse effects level (NOAEL) has been quantified. Toxicity Reference Values used in this ERA were determined from studies in which endpoints were derived from the administered dose, rather than the absorbed dose. This is a conservative approach because compounds are often administered in a more available form than would be found in the environment.

The preferred toxicity measure used for derivation of TRVs in this ERA is the LOAEL; however, in the absence of a suitable LOAEL, NOAEL-based TRVs were used. Generally, LOAELs used towards TRV derivation are based on long-term growth or survival, or sub-lethal reproductive outcomes determined from chronic exposure studies. As such, these endpoints are relevant to the maintenance of wildlife populations. The LOAEL represents a threshold dose at which adverse outcomes are likely to become evident (Sample et al. 1996). This threshold is considered an appropriate endpoint for ERA since TRVs are used as the denominator in the hazard quotient (HQ) calculation (see Section 19A.7.5), and HQ values greater than one may be considered indicative of potential adverse environmental effects. Hazard quotients calculated with NOAEL-based TRVs are more conservative since NOAELs relate to the threshold at which no individual environmental effects from COPC exposure are observed.

Numerous sources were reviewed to obtain the most relevant TRVs for receptors. Information sources included, but were not limited to:

• Oak Ridge National Laboratory Toxicity Benchmarks for Wildlife (Sample et al. 1996)

• US Environmental Protection Agency’s Ecological Soil Screening (Eco-SSL) documents (US EPA 2007)

• Agency for Toxic Substances and Disease Registry (ATSDR)


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• Canadian Environmental Protection Act (CEPA), Priority Substance List Assessment Reports

• primary scientific literature

Toxicological testing of environmental contaminants is not nearly as extensive for avian species as it is for mammalian species. As a result, avian TRVs for many COPC are unavailable. This disparity is primarily due to the widely accepted practice of applying mammalian toxicity data for use in human health risk assessments and establishing other human health-based guidelines (e.g., tolerable intake levels). Cross-class extrapolation for TRVs is not advised (Ohio EPA 2003, 2008) and the possible uncertainty associated with the extrapolation of mammalian toxicity data for the purpose of generating avian TRVs was considered unacceptable for this ERA. The exception to this is with the case of PAHs. The US EPA (2007) identified nearly 5500 papers with possible toxicity data for either birds or mammals exposed to high and low molecular weight PAHs. Of those meeting the Eco-SSL acceptability criteria (46 papers), only two contained data concerning avian species and Eco-SSLs were not derived for birds due to data limitations. However, during the Eco-SSL literature review it was observed that for the compounds that had toxicological results for bird species, mammals were always more sensitive (Kapustka 2004). On the basis of this observation, it has been suggested that mammalian TRVs for PAHs can be assumed to be protective of avian species (Kapustka 2004); this approach has been followed herein.

UNCERTAINTY FACTORS

The LOAEL-based benchmark represents a threshold level at which adverse health outcomes are likely to become evident (Sample et al. 1996). The use of the LOAEL is appropriate since a TRV based on the LOAEL is used as the denominator in the HQ calculation, and an HQ greater than 1 is considered indicative of potential adverse environmental effects. In cases where no chronic LOAEL is available, a NOAEL toxicity value may be selected, or UFs may be applied to other existing exposure and toxicological data using a tiered process to derive suitable ecological TRVs. When TRVs are based on US EPA Ecological Soil Screening Levels (Eco-SSLs), NOAELs are often the selected endpoint, but can vary depending on the chemical (Appendix 19A-9). The UF scheme outlined here (Figure 7-2) is based on guidance provided by Ohio EPA (2003, 2008), US EPA (2002), Sample and Arenal (1999) and the professional judgment of Stantec scientists.



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NOTES: * A NOAEL can be used if no appropriate LOAEL is available but the resultant RfD should be considered more conservative than

if it was derived using the LOAEL. Refer to document text for details. ** No inter-class UF is used to derive TRVs (i.e., mammalian data are not used as the basis to derive avian TRVs). *** An UF (“Sensitive Species Factor”) of 3 is not required if the RfD for an endangered species is based on a NOAEL. Refer to

document text for details.

Figure 7-2 Tiered Approach for the Application of Uncertainty Factors in ERA


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UNCERTAINTY FACTORS FOR EXPOSURE DURATION

In cases where a search of scientific data indicates a lack of chronic studies for a particular contaminant, UFs may be applied to adjust toxicity data to a chronic exposure basis. Acute studies are those that are of short duration, generally less than one week. Sub-chronic exposures are of longer duration (generally less than 90 days), but may be considered equivalent to a chronic study if a critical life stage (such as the gestational period) is included. Chronic exposures would generally be greater than 90 days in length, exceed 50% of the animal’s lifespan, or include a reproductive period. An UF of 3 (half an order of magnitude on a log scale) is applied to adjust from sub-chronic to chronic, and 10 to adjust from acute to chronic. Preference is given to longer duration exposure assessments in cases where published data are available, and acute data are relied on only when absolutely necessary.

UNCERTAINTY FACTORS FOR TOXICITY ENDPOINT

In cases where a search of scientific data indicates the absence of reproductive or other performance-based toxicity endpoints that would indicate a potential for adverse environmental effects at the population level, other less sensitive toxicity endpoints may be considered. Where only a lethal dose (LD50) is available, an UF of 10 (an order of magnitude) is applied to derive a LOAEL from LD50 data. Again, preference is always given to sub-lethal data, and lethal data are relied on only when absolutely necessary.

NOAELs were not adjusted upwards to estimate LOAELs. Where the only chronic endpoint available is a NOAEL, it is used directly and reported as such in the discussion of uncertainties. Hazard quotients based on the NOAEL may be permitted to exceed a value of 1 since the NOAEL is not an endpoint that signifies toxicological outcomes.

UNCERTAINTY FACTORS FOR INDIVIDUAL RISK

In ERA the focus of the assessment is normally to provide protection for receptors at the population level. This is in contrast to human toxicology and human health risk assessment where protection of individuals is of paramount concern. For this ERA, an exception is species protected under the Species at Risk Act or noted by the Government of Alberta as being “At Risk” (formerly "Red List") or "May Be at Risk" (formerly "Blue List").

To ensure that SAR are afforded an appropriate level of protection in ERA, TRVs are preferentially based on the NOAEL, or if not available, a LOAEL adjusted with an UF of 3 (half order of magnitude). This is an arbitrary value based on professional judgment and is expected to be protective yet realistic. This approach is intended to ensure that receptors are not exposed to doses of contaminants that would cause an adverse effect at the individual level.



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BODY MASS SCALING FACTORS

Aside from the use of UFs, a number of other methods have been used to extrapolate toxicity data between species with different body masses. The application of acute-based extrapolation factors (derived using LD50, HD5 and standard deviation) to reproductive toxicity data (e.g., Luttik et al. 2005), interspecies correlation estimation (ICE) models (Raimondo et al. 2007) and allometric scaling (Travis and White 1988; Chappell 1992; Mineau et al. 1996, Sample and Arenal 1999) have all been used in ERA. Each of these methods has positive and negative attributes, and none is without its drawbacks for extrapolating toxicity data between laboratory and wildlife species. Ultimately, the choice in method for use in ERA comes to scientific defensibility, practicality, and professional judgment. In this ERA, an allometric scaling factor of 0.75 both mammalian and avian receptors was used (Knopper et al. 2009). Details of the rationale for this scaling factor are in Appendix 19A-9.

INHALATION TOXICITY ASSESSMENT

The inhalation pathway as an exposure pathway for wildlife receptors is rarely considered in ERA since wildlife exposures to COPC in air are usually considered to be negligible in comparison with their exposure from soil and dietary pathways (including pathways associated with grooming). An alternative to conducting a quantitative risk assessment based on the inhalation pathway for receptors is to examine potential risk to human health via the chronic inhalation pathway (annual average concentrations). It is reasonable to suggest that human exposure TRVs for airborne contaminants are likely to be lower than equivalent TRVs for receptors given that:

• there is an extensive body of literature and regulations to protect humans against adverse health from air pollutants

• the level of protection afforded to humans focuses on the health of individuals, and often sensitive health outcomes (such as childhood asthma) and is therefore more protective than what is generally afforded to ecological receptors

• the exposure durations that are considered for human receptors are often longer (i.e., up to 70 years) than would be considered usual for ecological receptors

• the health outcomes for human receptors often include considerations such as whether a potential for cancer exists, for which very low ambient air concentrations may be required, which is generally not considered for ecological receptors

Therefore, provided that human receptors are adequately protected against inhalation exposures to annual average air concentrations, then it follows that receptors should also be protected.


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19A.7.4.2 Toxicity Values for Community-Based Receptors

PHYTOTOXICITY ASSESSMENT

Individual plant species were not evaluated in the ERA; rather toxicity assessments were based on phytotoxicity benchmarks that are protective of plant life for each COPC. Phytotoxicity benchmarks used in this ERA are found in Appendix 19A-9.

SOIL INVERTEBRATE TOXICITY ASSESSMENT

Soil invertebrates were not evaluated for individual species in the ERA; rather toxicity assessments were based on soil screening benchmarks that are protective of terrestrial invertebrate life for each COPC. For the soil screening benchmarks used in this ERA refer to Appendix 19A-9.

19A.7.5 Risk Characterization

The purpose of the Risk Characterization step in ERA is to evaluate the evidence linking COPC with adverse environmental effects by combining information from the Exposure and Toxicity Assessments. The potential for adverse environmental effects is quantified by comparing the dose of a substance that can be tolerated, or below which adverse environmental effects are not expected (i.e., TRV), to the expected daily dose, the amount of a COPC an organism is expected to be exposed to on a daily basis (i.e., ADD). The quotient of the two is referred to as an HQ and the magnitude by which values differ from parity (i.e., TRV = daily dose) is used to make inferences about the possibility of ecological risks. For the assessment of potential risk to community-based receptors (e.g., terrestrial plants and soil invertebrates), the EPC of the associated environmental media is divided by a toxicological benchmark (rather than dividing an ADD by a TRV, as was done for birds and mammals).

An HQ less than or equal to 1 indicates that the exposure concentration is less than or meets the threshold of toxicity for the COPC being evaluated (but does not exceed it), and given the conservative approach to the estimation of exposure and selection of TRVs, adverse environmental effects are not expected. On the other hand, an HQ of greater than 1 does not necessarily indicate an unacceptable level of risk. In these cases, values greater than 1 indicate that there is a possibility of adverse environmental effects and indicates a need for more careful review of both predicted exposure levels and TRVs. As a result, HQ greater than 1 should be interpreted carefully, and further, more focused investigations may be required to reduce conservatism and provide a more realistic assessment of the actual level of risk. A worked example of HQ derivation may be found in Appendix 19A-13.



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19A.7.5.1 Chemical Interactions and Additivity of Hazard Quotients

Risk assessments are complicated by the fact that most toxicological studies are conducted using a single chemical whereas environmental exposures generally involve more than one COPC. Calculating an HQ for exposure to mixtures of COPC is problematic because all COPC do not have the same modes of action, target endpoints, or magnitudes of toxicity. Chemicals in a mixture may interact in four general ways to elicit a response:

• Non-interacting – chemicals have no effect in combination with each other; the toxicity of the mixture is the same as the toxicity of the most toxic component of the mixture

• Additive – chemicals have similar targets and modes of action but do not interact, the hazard for exposure to the mixture is simply the sum of hazards for the individual chemicals

• Synergistic – there is a positive interaction among the chemicals such that the response is greater than would be expected if the chemicals acted independently or in an additive manner

• Antagonistic – there is a negative interaction among the chemicals such that the response is less than would be expected if the chemicals acted independently or in an additive manner

There are chemical classes that have similar modes of action and target organs, and in these cases, a more appropriate characterization of risk is achieved by summing the HQ for each compound. In this ERA, HQs for PHCs as well as PAHs were summed to derive a single conservative HQ index for each respective chemical class. In cases where toxicity data was unavailable for any component of the class (e.g., terrestrial plants and some PAHs), a summation was not performed due uncertainty associated with the potential toxicity of the entire mixture. However, it was assumed that the soil invertebrate HQ index for PAHs is applicable to terrestrial plants given that in all cases where data were available, soil invertebrate benchmarks were either the same or lower than those for plants.

Hazard quotients for inorganic COPC were evaluated independently because unlike PHCs or PAHs, they generally have specific toxicities, different modes of action, and different target organs.

19A.7.5.2 Baseline Case

Baseline Case HQs provide an indication of potential adverse environmental effects (i.e., risk) to receptors resulting from exposure to COPC released to the atmosphere from industrial facilities that are currently operating, those that have regulatory approval but are not yet operating, as well as non industry sources such as nearby communities and traffic. Emissions from the proposed JACOS facility expansion are not included in this assessment.

The Baseline Case assessment includes both modelled and measured background soil COPC concentrations, as well as modelled COPC concentrations in terrestrial biota (e.g., vegetation, terrestrial invertebrates, and small mammals). Maximum Baseline Case HQs for each COPC and receptor, and the receptor location number (from Table 2-1) at which each maximum HQ occurs, are summarized in Tables 7-5 to 7-7.

Hazard Quotients for avian and mammalian receptors were well below 1.0 for all COPC. Hazard Quotients for community-based receptors were well below 1.0 for all COPC with the exception of


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manganese, where the 95th UCLM EPC concentration (~967 mg/kg) at the Gregoire Lake Provincial Park (Site 16) resulted in HQs of 4.4 and 2.1 for terrestrial plant and soil invertebrate communities, respectively. A closer examination of the baseline data (Appendix 19A-11) reveals that at all 13 receptor locations the baseline manganese soil concentration is approximately 967 mg/kg, and this concentration is almost entirely based on existing concentrations in soil (i.e., measured from field samples). Manganese in soil sampled from various locations within the LSA (n=10) ranged from a minimum concentration of 24 mg/kg to a maximum concentration of 1400 mg/kg, however, in all sampling locations plant communities (and by extension the soil invertebrate communities closely associated with them) appeared healthy and showed no visible evidence of manganese related stress (i.e., leaf margin chlorosis/necrosis). Additionally, during field vegetation surveys all plants appeared healthy. Therefore it can reasonably be concluded that the elevated HQs in this scenario are wholly the result of the very conservative methodology employed in this ERA and not an indication of actual risk.

Detailed HQ results for the Baseline Case are provided in Appendix 19A-12.

Table 7-5 Summary of Maximum Hazard Quotients for Community-Based Receptors for the Baseline Case Assessment

Constituent HQ for Phytotoxicity HQ for Soil Invertebrates Petroleum Hydrocarbons Aliphatic C5-C8 1.6E-07 (Max of Sites 35-39) 1.6E-07 (Max of Sites 35-39) Aliphatic C9-C16 1.0E-04 (Max of Sites 35-39) 1.0E-04 (Max of Sites 35-39) Aromatic C9-C16 7.0E-05 (Max of Sites 35-39) 7.0E-05 (Max of Sites 35-39) Aromatic C17-C34 7.2E-08 (Site 16) 7.2E-08 (Site 16)

Total PHC HQ = 1.7E-04 (Max of Sites 35-39) 1.7E-04 (Max of Sites 35-39) Polycyclic Aromatic Hydrocarbons Low Molecular Weight PAHs Anthracene 1.7E-03 (Max of Sites 8&9) 1.7E-03 (Max of Sites 8&9) Fluoranthene 1.1E-04 (Max of Sites 8&9) 1.1E-04 (Max of Sites 8&9) Fluorene -- 1.7E-04 (Max of Sites 8&9) Phenanthrene 1.4E-04 (Max of Sites 8&9) 1.9E-04 (Max of Sites 8&9)

Total LMW PAH HQ = -- a 2.1E-03 (Max of Sites 8&9) High Molecular Weight PAHs

Benz(a)anthracene 1.3E-04 (Max of Sites 8&9) 2.8E-04 (Max of Sites 8&9) Benzo(a)pyrene 2.5E-04 (Site 45) 2.5E-04 (Site 45) Benzo(e)pyrene -- 2.8E-04 (Site 20) Benzo(b)fluoranthene -- 2.8E-04 (Site 45) Benzo(g,h,i)perylene 1.3E-04 (Site 45) 2.8E-04 (Site 45) Benzo(k)fluoranthene 1.3E-04 (Site 45) 2.8E-04 (Site 45)



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Table 7-5 Summary of Maximum Hazard Quotients for Community-Based Receptors for the Baseline Case Assessment (cont’d)

Constituent HQ for Phytotoxicity HQ for Soil Invertebrates High Molecular Weight PAHs (cont’d) Chrysene 1.3E-04 (Max of Sites 8&9) 2.8E-04 (Max of Sites 8&9) Dibenz(a,h)anthracene -- 2.8E-04 (Site 45) Indeno(1,2,3-cd)pyrene 1.3E-04 (Site 45) 2.8E-04 (Site 45) Perylene -- 2.8E-04 (Site 20) Pyrene -- 4.5E-04 (Max of Sites 8&9)

Total HMW PAH HQ = -- a 3.2E-03 (Max of Sites 8&9) Total LMW + HMW PAH HQ = -- a 5.3E-03 (Max of Sites 8&9)

Chlorinated Monocyclic Aromatics

Dichlorobenzene 1.9E-10 (Site 16) 2.9E-10 (Site 16) Inorganics Aluminum -- -- Chromium (Total) 1.7E-01 (Site 20) 1.7E-01 (Site 20) Cobalt 3.1E-01 (Site 20) 3.1E-01 (Site 20) Copper 4.0E-02 (Site 16) 4.0E-02 (Site 16) Lead 2.1E-02 (Site 16) 2.1E-02 (Site 16) Manganese 4.4E+00 (Site 16) 2.1E+00 (Site 16) Molybdenum 1.4E-01 (Site 20) 1.4E-01 (Site 20) Nickel 1.2E-01 (Max of Sites 40-44) 1.2E-01 (Max of Sites 40-44) Strontium -- -- Vanadium 1.2E-01 (Site 20) 1.2E-01 (Site 20) Zinc 1.1E-01 (Site 16) 1.1E-01 (Site 16) NOTES: "--" - Quantitative assessment of COPC could not be performed due to lack of suitable toxicity data Bold – Value exceeds maximum acceptable HQ of 1.0 a Sum cannot be calculated due to uncertainty associated with contributions from COPC lacking suitable toxicity data


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Table 7-6 Summary of Maximum Hazard Quotients for Avian Receptors for the Baseline Case Assessment

Constituent American Robin Red-tailed Hawk Short-eared Owl Spruce Grouse Petroleum Hydrocarbons Aliphatic C5-C8 1.3E-07 (Max of Sites 35-39) 5.0E-10 (Max of Sites 35-39) 4.0E-09 (Max of Sites 35-39) 9.1E-08 (Max of Sites 35-39) Aliphatic C9-C16 4.5E-06 (Max of Sites 35-39) 3.3E-08 (Max of Sites 35-39) 2.2E-07 (Max of Sites 35-39) 3.1E-06 (Max of Sites 35-39) Aromatic C9-C16 6.6E-06 (Max of Sites 35-39) 3.1E-08 (Max of Sites 35-39) 2.1E-07 (Max of Sites 35-39) 4.8E-06 (Max of Sites 35-39) Aromatic C17-C34 3.9E-06 (Site 16) 4.8E-09 (Site 16) 7.6E-08 (Site 16) 2.7E-06 (Site 16)

Total PHC HQ = 1.2E-05 (Max of Sites 35-39) 6.6E-08 (Max of Sites 35-39) 4.6E-07 (Max of Sites 35-39) 8.7E-06 (Max of Sites 35-39) Polycyclic Aromatic Hydrocarbons Low Molecular Weight PAHs Anthracene -- -- -- -- Fluoranthene -- -- -- -- Fluorene -- -- -- -- Phenanthrene -- -- -- --

Total LMW PAH HQ = -- -- -- -- High Molecular Weight PAHs Benz(a)anthracene -- -- -- -- Benzo(a)pyrene -- -- -- -- Benzo(e)pyrene -- -- -- -- Benzo(b)fluoranthene -- -- -- -- Benzo(g,h,i)perylene -- -- -- -- Benzo(k)fluoranthene -- -- -- -- Chrysene -- -- -- -- Dibenz(a,h)anthracene -- -- -- -- Indeno(1,2,3-cd)pyrene -- -- -- -- Perylene -- -- -- -- Pyrene -- -- -- --

Total HMW PAH HQ = -- -- -- -- Total LMW + HMW PAH HQ = -- -- -- --

Chlorinated Monocyclic Aromatics Dichlorobenzene -- -- -- -- Inorganics Aluminum -- -- -- -- Chromium (Total) 1.2E-01 (Site 20) 6.9E-03 (Site 20) 1.3E-02 (Site 20) 3.5E-02 (Site 20) Cobalt 6.3E-02 (Site 20) 1.4E-02 (Site 20) 2.1E-02 (Site 20) 3.3E-02 (Site 20) Copper 5.7E-02 (Site 16) 2.5E-03 (Site 16) 4.1E-03 (Site 16) 3.2E-02 (Site 16) Lead 3.7E-02 (Site 16) 4.0E-04 (Site 16) 1.3E-03 (Site 16) 1.4E-02 (Site 16) Manganese 7.7E-02 (Site 16) 4.1E-04 (Site 16) 6.6E-04 (Site 16) 6.1E-02 (Site 16) Molybdenum 3.2E-03 (Site 20) 1.2E-04 (Site 20) 6.0E-04 (Site 20) 1.9E-03 (Site 20) Nickel 8.0E-02 (Max of Sites 40-44) 2.1E-03 (Max of Sites 40-44) 5.2E-03 (Max of Sites 40-44) 1.9E-02 (Max of Sites 40-44) Strontium -- -- -- -- Vanadium 8.2E-01 (Site 20) 1.2E-01 (Site 20) 4.7E-01 (Site 20) 6.7E-01 (Site 20) Zinc 2.7E-01 (Site 16) 2.3E-04 (Site 16) 2.3E-02 (Site 16) 4.9E-02 (Site 16) NOTE: "--" - Quantitative assessment of COPC could not be performed due to lack of suitable toxicity data



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Table 7-7 Summary of Maximum Hazard Quotients for Mammalian receptors for the Baseline Case Assessment

Constituent Canada Lynx Masked Shrew Meadow Vole Snowshoe Hare Woodland Caribou Petroleum Hydrocarbons Aliphatic C5-C8 5.5E-10 (Max of Sites 35-39) 2.0E-08 (Max of Sites 35-39) 4.3E-08 (Max of Sites 35-39) 4.1E-08 (Max of Sites 35-39) 1.2E-07 (Max of Sites 35-39) Aliphatic C9-C16 3.6E-08 (Max of Sites 35-39) 8.5E-07 (Max of Sites 35-39) 1.5E-06 (Max of Sites 35-39) 1.4E-06 (Max of Sites 35-39) 4.0E-06 (Max of Sites 35-39) Aromatic C9-C16 3.4E-08 (Max of Sites 35-39) 8.8E-07 (Max of Sites 35-39) 2.3E-06 (Max of Sites 35-39) 2.2E-06 (Max of Sites 35-39) 6.1E-06 (Max of Sites 35-39) Aromatic C17-C34 5.3E-09 (Site 16) 5.8E-07 (Site 16) 1.2E-06 (Site 16) 1.2E-06 (Site 16) 3.4E-06 (Site 16)

Total PHC HQ = 7.2E-08 (Max of Sites 35-39) 1.9E-06 (Max of Sites 35-39) 4.2E-06 (Max of Sites 35-39) 4.0E-06 (Max of Sites 35-39) 1.1E-05 (Max of Sites 35-39) Polycyclic Aromatic Hydrocarbons Low Molecular Weight PAHs Anthracene 1.5E-08 (Max of Sites 8&9) 6.7E-07 (Max of Sites 8&9) 1.4E-06 (Max of Sites 8&9) 9.2E-07 (Max of Sites 8&9) 2.7E-07 (Max of Sites 8&9) Fluoranthene 2.0E-08 (Max of Sites 8&9) 1.1E-06 (Max of Sites 8&9) 1.3E-06 (Max of Sites 8&9) 8.2E-07 (Max of Sites 8&9) 2.4E-07 (Max of Sites 8&9) Fluorene 1.9E-08 (Max of Sites 8&9) 1.1E-06 (Max of Sites 8&9) 2.4E-06 (Max of Sites 8&9) 1.7E-06 (Max of Sites 8&9) 4.7E-07 (Max of Sites 8&9) Phenanthrene 2.0E-08 (Max of Sites 8&9) 8.3E-07 (Max of Sites 8&9) 1.9E-06 (Max of Sites 8&9) 1.2E-06 (Max of Sites 8&9) 3.6E-07 (Max of Sites 8&9) Total LMW PAH HQ = 7.4E-08 (Max of Sites 8&9) 3.7E-06 (Max of Sites 8&9) 7.0E-06 (Max of Sites 8&9) 4.6E-06 (Max of Sites 8&9) 1.3E-06 (Max of Sites 8&9) High Molecular Weight PAHs Benz(a)anthracene 1.6E-07 (Max of Sites 8&9) 5.1E-06 (Max of Sites 8&9) 7.0E-06 (Max of Sites 8&9) 4.2E-06 (Max of Sites 8&9) 1.3E-06 (Max of Sites 8&9) Benzo(a)pyrene 1.6E-07 (Site 45) 1.1E-05 (Site 45) 6.5E-06 (Site 45) 3.8E-06 (Site 45) 1.2E-06 (Site 45) Benzo(e)pyrene 1.5E-07 (Site 20) 5.9E-05 (Site 20) 4.3E-06 (Site 20) 2.0E-06 (Site 20) 6.5E-07 (Site 20) Benzo(b)fluoranthene 1.5E-07 (Site 45) 4.7E-06 (Site 45) 3.8E-06 (Site 45) 2.0E-06 (Site 45) 6.4E-07 (Site 45) Benzo(g,h,i)perylene 2.1E-07 (Site 45) 1.1E-05 (Site 45) 4.2E-05 (Site 45) 2.9E-05 (Site 45) 8.3E-06 (Site 45) Benzo(k)fluoranthene 1.6E-07 (Site 45) 4.9E-06 (Site 45) 7.5E-06 (Site 45) 4.6E-06 (Site 45) 1.4E-06 (Site 45) Chrysene 1.6E-07 (Max of Sites 8&9) 4.8E-06 (Max of Sites 8&9) 5.2E-06 (Max of Sites 8&9) 3.0E-06 (Max of Sites 8&9) 9.2E-07 (Max of Sites 8&9) Dibenz(a,h)anthracene 3.2E-07 (Site 45) 2.3E-05 (Site 45) 1.1E-04 (Site 45) 7.7E-05 (Site 45) 2.2E-05 (Site 45) Indeno(1,2,3-cd)pyrene 1.5E-07 (Site 45) 1.3E-05 (Site 45) 3.4E-06 (Site 45) 1.6E-06 (Site 45) 5.3E-07 (Site 45) Perylene 1.5E-07 (Site 20) 2.1E-05 (Site 20) 6.7E-06 (Site 20) 3.9E-06 (Site 20) 1.2E-06 (Site 20) Pyrene 2.6E-07 (Max of Sites 8&9) 7.8E-06 (Max of Sites 8&9) 1.7E-05 (Max of Sites 8&9) 1.1E-05 (Max of Sites 8&9) 3.2E-06 (Max of Sites 8&9)

Total HMW PAH HQ = 2.0E-06 (Site 45) 1.6E-04 (Site 45) 2.1E-04 (Site 45) 1.4E-04 (Site 45) 4.0E-05 (Site 45) Total LMW + HMW PAH HQ = 2.0E-06 (Site 45) 1.7E-04 (Site 45) 2.1E-04 (Site 45) 1.4E-04 (Site 45) 4.1E-05 (Site 45)

Chlorinated Monocyclic Aromatics Dichlorobenzene 7.6E-12 (Site 16) 6.3E-12 (Site 16) 1.8E-11 (Site 16) 3.0E-11 (Site 16) 8.4E-11 (Site 16) Inorganics Aluminum 5.0E-03 (Site 16) 2.1E-02 (Site 16) 9.5E-03 (Site 16) 1.3E-02 (Site 16) 3.9E-02 (Site 16) Chromium (Total) 6.1E-03 (Site 20) 1.7E-01 (Site 20) 4.9E-02 (Site 20) 2.2E-02 (Site 20) 7.6E-03 (Site 20) Cobalt 3.8E-03 (Site 20) 1.8E-02 (Site 20) 1.3E-02 (Site 20) 6.9E-03 (Site 20) 2.1E-03 (Site 20) Copper 3.9E-03 (Site 16) 5.9E-02 (Site 16) 4.8E-02 (Site 16) 3.4E-02 (Site 16) 3.2E-02 (Site 16) Lead 7.3E-04 (Site 16) 8.2E-02 (Site 16) 3.0E-02 (Site 16) 1.8E-02 (Site 16) 5.3E-03 (Site 16) Manganese 1.1E-03 (Site 16) 2.2E-02 (Site 16) 1.6E-01 (Site 16) 1.1E-01 (Site 16) 3.2E-02 (Site 16) Molybdenum 5.5E-03 (Site 20) 2.2E-02 (Site 20) 2.2E-02 (Site 20) 3.5E-02 (Site 20) 9.9E-02 (Site 20) Nickel 3.4E-03 (Max of Sites 40-44) 2.0E-01 (Max of Sites 40-44) 3.5E-02 (Max of Sites 40-44) 1.9E-02 (Max of Sites 40-44) 1.7E-02 (Max of Sites 40-44) Strontium 1.3E-04 (Site 16) 1.2E-03 (Site 16) 1.5E-02 (Site 16) 1.5E-02 (Site 16) 1.4E-02 (Site 16) Vanadium 6.0E-03 (Site 20) 3.8E-02 (Site 20) 2.9E-02 (Site 20) 1.8E-02 (Site 20) 6.3E-02 (Site 20) Zinc 1.6E-04 (Site 16) 2.9E-01 (Site 16) 3.0E-02 (Site 16) 1.9E-02 (Site 16) 1.6E-02 (Site 16) NOTE: "--" - Quantitative assessment of COPC could not be performed due to lack of suitable toxicity data


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19A.7.5.3 Project Alone Scenario

Project Alone Scenario HQs provide an indication of potential adverse environmental effects (i.e., risk) to receptors resulting from exposure to COPC released to the atmosphere from the proposed JACOS facility expansion over a 30 year period.

Hazard Quotients for community-based, avian, and mammalian receptors were well below 1.0 for all COPC, and for all receptors, the maximum HQ is expected to occur adjacent to the Central Processing Facility (Site 45). No potential risk is expected from project related emissions.

Maximum Project Alone Scenario HQs for each COPC and receptors, and the receptor location number (from Table 2-1) at which each maximum HQ occurs, are summarized in Tables 7-8 to 7-10.

Detailed HQ results for the Project Alone Scenario are provided in Appendix 19A-12.

Table 7-8 Summary of Maximum Hazard Quotients for Community-Based Receptors for the Project Alone Scenario Assessment

Constituent HQ for Phytotoxicity HQ for Soil Invertebrates Petroleum Hydrocarbons Aliphatic C5-C8 1.7E-07 (Site 45) 1.7E-07 (Site 45) Aliphatic C9-C16 2.4E-07 (Site 45) 2.4E-07 (Site 45) Aromatic C9-C16 2.9E-06 (Site 45) 2.9E-06 (Site 45) Aromatic C17-C34 8.6E-10 (Site 45) 8.6E-10 (Site 45)

Total PHC HQ = 3.3E-06 (Site 45) 3.3E-06 (Site 45) Polycyclic Aromatic Hydrocarbons Low Molecular Weight PAHs Anthracene 1.4E-06 (Site 45) 1.4E-06 (Site 45) Fluoranthene 1.0E-07 (Site 45) 1.0E-07 (Site 45) Fluorene -- 2.4E-08 (Site 45) Phenanthrene 1.4E-07 (Site 45) 2.0E-07 (Site 45)

Total LMW PAH HQ = -- a 1.8E-06 (Site 45) High Molecular Weight PAHs Benz(a)anthracene 1.4E-07 (Site 45) 3.0E-07 (Site 45) Benzo(a)pyrene 2.8E-07 (Site 45) 2.8E-07 (Site 45) Benzo(e)pyrene -- 1.3E-09 (Site 45) Benzo(b)fluoranthene -- 3.7E-07 (Site 45) Benzo(g,h,i)perylene 1.7E-07 (Site 45) 3.7E-07 (Site 45) Benzo(k)fluoranthene 5.5E-07 (Site 45) 1.2E-06 (Site 45) Chrysene 2.0E-07 (Site 45) 4.4E-07 (Site 45) Dibenz(a,h)anthracene -- 5.7E-07 (Site 45) Indeno(1,2,3-cd)pyrene 2.0E-07 (Site 45) 4.4E-07 (Site 45)



19A-130

Table 7-8 Summary of Maximum Hazard Quotients for Community-Based Receptors for the Project Alone Scenario Assessment (cont’d)

Constituent HQ for Phytotoxicity HQ for Soil Invertebrates High Molecular Weight PAHs (cont’d) Perylene -- 1.7E-09 (Site 45) Pyrene -- 9.3E-07 (Site 45)

Total HMW PAH HQ = -- a 4.9E-06 (Site 45) Total LMW + HMW PAH HQ = -- a 6.7E-06 (Site 45)

Chlorinated Monocyclic Aromatics Dichlorobenzene 1.1E-09 (Site 45) 1.6E-09 (Site 45) Inorganics Aluminum -- -- Chromium (Total) 4.2E-06 (Site 45) 4.2E-06 (Site 45) Cobalt 7.4E-06 (Site 45) 7.4E-06 (Site 45) Copper 8.1E-06 (Site 45) 8.1E-06 (Site 45) Lead 2.0E-06 (Site 45) 2.0E-06 (Site 45) Manganese 2.5E-06 (Site 45) 1.2E-06 (Site 45) Molybdenum 2.0E-05 (Site 45) 2.0E-05 (Site 45) Nickel 1.0E-05 (Site 45) 1.0E-05 (Site 45) Strontium -- -- Vanadium 3.7E-06 (Site 45) 3.7E-06 (Site 45) Zinc 9.9E-06 (Site 45) 9.9E-06 (Site 45) NOTES: "--" - Quantitative assessment of COPC could not be performed due to lack of suitable toxicity data a Sum cannot be calculated due to uncertainty associated with contributions from COPC lacking suitable toxicity data


19A-131

Table 7-9 Summary of Maximum Hazard Quotients for Avian Receptors for the Project Alone Scenario Assessment

Constituent American Robin Red-tailed Hawk Short-eared Owl Spruce Grouse Petroleum Hydrocarbons Aliphatic C5-C8 1.4E-07 (Site 45) 5.3E-10 (Site 45) 4.2E-09 (Site 45) 9.6E-08 (Site 45) Aliphatic C9-C16 1.0E-08 (Site 45) 7.5E-11 (Site 45) 5.0E-10 (Site 45) 7.0E-09 (Site 45) Aromatic C9-C16 2.7E-07 (Site 45) 1.3E-09 (Site 45) 8.7E-09 (Site 45) 2.0E-07 (Site 45) Aromatic C17-C34 4.7E-08 (Site 45) 5.8E-11 (Site 45) 9.1E-10 (Site 45) 3.3E-08 (Site 45) Total PHC HQ = 4.7E-07 (Site 45) 1.9E-09 (Site 45) 1.4E-08 (Site 45) 3.3E-07 (Site 45) Polycyclic Aromatic Hydrocarbons Low Molecular Weight PAHs Anthracene -- -- -- -- Fluoranthene -- -- -- -- Fluorene -- -- -- -- Phenanthrene -- -- -- --





19A-132

Table 7-9 Summary of Maximum Hazard Quotients for Avian Receptors for the Project Alone Scenario Assessment (cont’d)

Constituent American Robin Red-tailed Hawk Short-eared Owl Spruce Grouse Chlorinated Monocyclic Aromatics Dichlorobenzene -- -- -- -- Inorganics Aluminum -- -- -- -- Chromium (Total) 1.6E-05 (Site 45) 4.0E-07 (Site 45) 6.4E-07 (Site 45) 1.1E-05 (Site 45) Cobalt 4.8E-06 (Site 45) 4.6E-07 (Site 45) 6.8E-07 (Site 45) 3.4E-06 (Site 45) Copper 1.1E-05 (Site 45) 3.4E-07 (Site 45) 6.1E-07 (Site 45) 5.6E-06 (Site 45) Lead 4.9E-06 (Site 45) 3.8E-08 (Site 45) 1.3E-07 (Site 45) 2.2E-06 (Site 45) Manganese 4.8E-08 (Site 45) 1.8E-10 (Site 45) 3.2E-10 (Site 45) 3.8E-08 (Site 45) Molybdenum 6.7E-07 (Site 45) 1.6E-08 (Site 45) 8.2E-08 (Site 45) 4.3E-07 (Site 45) Nickel 1.0E-05 (Site 45) 2.0E-07 (Site 45) 4.7E-07 (Site 45) 4.2E-06 (Site 45) Strontium -- -- -- -- Vanadium 7.3E-05 (Site 45) 3.9E-06 (Site 45) 1.5E-05 (Site 45) 7.8E-05 (Site 45) Zinc 3.4E-05 (Site 45) 2.0E-08 (Site 45) 3.0E-06 (Site 45) 5.1E-06 (Site 45) NOTE: "--" - Quantitative assessment of COPC could not be performed due to lack of suitable toxicity data


19A-133

Table 7-10 Summary of Maximum Hazard Quotients for Mammalian Receptors for the Project Alone Scenario Assessment

Constituent Canada Lynx Masked Shrew Meadow Vole Snowshoe Hare Woodland Caribou Petroleum Hydrocarbons Aliphatic C5-C8 5.9E-10 (Site 45) 2.1E-08 (Site 45) 4.5E-08 (Site 45) 4.4E-08 (Site 45) 1.2E-07 (Site 45) Aliphatic C9-C16 8.2E-11 (Site 45) 1.9E-09 (Site 45) 3.4E-09 (Site 45) 3.2E-09 (Site 45) 9.1E-09 (Site 45) Aromatic C9-C16 1.4E-09 (Site 45) 3.6E-08 (Site 45) 9.3E-08 (Site 45) 8.9E-08 (Site 45) 2.5E-07 (Site 45) Aromatic C17-C34 6.4E-11 (Site 45) 7.0E-09 (Site 45) 1.5E-08 (Site 45) 1.5E-08 (Site 45) 4.1E-08 (Site 45)

Total PHC HQ = 2.1E-09 (Site 45) 6.6E-08 (Site 45) 1.6E-07 (Site 45) 1.5E-07 (Site 45) 4.3E-07 (Site 45) Polycyclic Aromatic Hydrocarbons Low Molecular Weight PAHs Anthracene 1.2E-11 (Site 45) 5.6E-10 (Site 45) 8.1E-10 (Site 45) 5.2E-10 (Site 45) 1.5E-10 (Site 45) Fluoranthene 2.1E-11 (Site 45) 1.1E-09 (Site 45) 2.9E-09 (Site 45) 2.0E-09 (Site 45) 5.6E-10 (Site 45) Fluorene 2.4E-12 (Site 45) 1.5E-10 (Site 45) 2.6E-10 (Site 45) 1.8E-10 (Site 45) 5.1E-11 (Site 45) Phenanthrene 2.1E-11 (Site 45) 9.0E-10 (Site 45) 2.3E-09 (Site 45) 1.5E-09 (Site 45) 4.3E-10 (Site 45)

Total LMW PAH HQ = 5.6E-11 (Site 45) 2.7E-09 (Site 45) 6.2E-09 (Site 45) 4.2E-09 (Site 45) 1.2E-09 (Site 45) High Molecular Weight PAHs Benz(a)anthracene 5.8E-10 (Site 45) 1.7E-08 (Site 45) 2.0E-07 (Site 45) 1.4E-07 (Site 45) 4.0E-08 (Site 45) Benzo(a)pyrene 1.6E-09 (Site 45) 5.4E-08 (Site 45) 7.1E-07 (Site 45) 5.1E-07 (Site 45) 1.4E-07 (Site 45) Benzo(e)pyrene 2.0E-10 (Site 45) 7.0E-09 (Site 45) 1.1E-07 (Site 45) 8.2E-08 (Site 45) 2.3E-08 (Site 45) Benzo(b)fluoranthene 2.5E-10 (Site 45) 7.9E-09 (Site 45) 3.5E-08 (Site 45) 2.4E-08 (Site 45) 6.9E-09 (Site 45) Benzo(g,h,i)perylene 1.9E-08 (Site 45) 6.8E-07 (Site 45) 1.1E-05 (Site 45) 8.1E-06 (Site 45) 2.3E-06 (Site 45) Benzo(k)fluoranthene 2.7E-09 (Site 45) 8.4E-08 (Site 45) 1.1E-06 (Site 45) 7.8E-07 (Site 45) 2.2E-07 (Site 45) Chrysene 2.7E-10 (Site 45) 8.5E-09 (Site 45) 2.7E-08 (Site 45) 1.8E-08 (Site 45) 5.2E-09 (Site 45) Dibenz(a,h)anthracene 5.2E-08 (Site 45) 1.9E-06 (Site 45) 3.1E-05 (Site 45) 2.2E-05 (Site 45) 6.2E-06 (Site 45) Indeno(1,2,3-cd)pyrene 3.7E-10 (Site 45) 2.6E-08 (Site 45) 1.0E-07 (Site 45) 7.1E-08 (Site 45) 2.0E-08 (Site 45) Perylene 9.2E-10 (Site 45) 2.9E-08 (Site 45) 4.9E-07 (Site 45) 3.5E-07 (Site 45) 9.9E-08 (Site 45) Pyrene 5.4E-10 (Site 45) 1.6E-08 (Site 45) 3.8E-08 (Site 45) 2.5E-08 (Site 45) 7.2E-09 (Site 45)


Chlorinated Monocyclic Aromatics Dichlorobenzene 4.2E-11 (Site 45) 3.5E-11 (Site 45) 1.0E-10 (Site 45) 1.7E-10 (Site 45) 4.7E-10 (Site 45) Inorganics Aluminum 4.0E-08 (Site 45) 2.0E-07 (Site 45) 6.0E-07 (Site 45) 1.0E-06 (Site 45) 2.8E-06 (Site 45) Chromium (Total) 3.5E-07 (Site 45) 4.7E-06 (Site 45) 9.6E-06 (Site 45) 6.6E-06 (Site 45) 1.9E-06 (Site 45) Cobalt 1.3E-07 (Site 45) 4.6E-07 (Site 45) 9.9E-07 (Site 45) 6.6E-07 (Site 45) 1.9E-07 (Site 45) Copper 5.3E-07 (Site 45) 1.2E-05 (Site 45) 8.5E-06 (Site 45) 5.9E-06 (Site 45) 5.6E-06 (Site 45) Lead 6.9E-08 (Site 45) 8.7E-06 (Site 45) 4.4E-06 (Site 45) 2.8E-06 (Site 45) 8.2E-07 (Site 45) Manganese 5.1E-10 (Site 45) 1.5E-08 (Site 45) 1.0E-07 (Site 45) 7.1E-08 (Site 45) 2.0E-08 (Site 45) Molybdenum 7.5E-07 (Site 45) 3.3E-06 (Site 45) 4.9E-06 (Site 45) 8.1E-06 (Site 45) 2.3E-05 (Site 45) Nickel 3.2E-07 (Site 45) 1.7E-05 (Site 45) 6.9E-06 (Site 45) 4.4E-06 (Site 45) 3.9E-06 (Site 45) Strontium 2.5E-09 (Site 45) 3.5E-08 (Site 45) 4.2E-07 (Site 45) 4.2E-07 (Site 45) 3.9E-07 (Site 45) Vanadium 1.9E-07 (Site 45) 1.3E-06 (Site 45) 2.2E-06 (Site 45) 1.9E-06 (Site 45) 5.5E-06 (Site 45) Zinc 1.4E-08 (Site 45) 3.9E-05 (Site 45) 3.0E-06 (Site 45) 1.8E-06 (Site 45) 1.5E-06 (Site 45) NOTE: "--" - Quantitative assessment of COPC could not be performed due to lack of suitable toxicity data



19A-134

19A.7.5.4 Application Case

Application Case HQs provide an indication of potential adverse environmental effects (i.e., risk) to receptors resulting from exposure to COPC released to the atmosphere from the proposed JACOS facility expansion (i.e., Project Alone Scenario), in addition to measured and modelled existing concentrations (i.e., Baseline Case).

Hazard Quotients for avian and mammalian receptors were well below 1.0 for all COPC. Hazard Quotients for community-based receptors were well below 1.0 for all COPC with the exception of manganese, where a maximum soil concentration at Gregoire Lake Provincial Park (Site 16) resulted in HQs of 4.4 and 2.1 for terrestrial plant and soil invertebrate communities, respectively. Note that the predicted HQs are no different from those estimated in the Baseline Case, and, as the estimated input from the Project Alone (Section 19A.7.5.3) is negligible (plant HQ=2.5E-06; invertebrate HQ=1.2E-06), HQs exceeding 1.0 for these receptors can be entirely attributed to Base conditions. As discussed in Section 19A.7.5.2, these elevated HQs are not anticipated to translate into actual risk.

Maximum Application Case HQs for each COPC and receptors, and the receptor location number (from Table 2-1) at which each maximum HQ occurs, are summarized in Tables 7-11 to 7-13.

Detailed HQ results for the Application Case are provided in Appendix 19A-12.

Table 7-11 Summary of Maximum Hazard Quotients for Community-Based Receptors for the Application Case Assessment

Constituent HQ for Phytotoxicity HQ for Soil Invertebrates Petroleum Hydrocarbons Aliphatic C5-C8 2.2E-07 (Site 45) 2.2E-07 (Site 45) Aliphatic C9-C16 1.0E-04 (Max of Sites 35-39) 1.0E-04 (Max of Sites 35-39) Aromatic C9-C16 7.0E-05 (Max of Sites 35-39) 7.0E-05 (Max of Sites 35-39) Aromatic C17-C34 7.2E-08 (Site 16) 7.2E-08 (Site 16)


Total LMW PAH HQ = -- a 2.1E-03 (Max of Sites 8&9) High Molecular Weight PAHs Benz(a)anthracene 1.3E-04 (Max of Sites 8&9) 2.8E-04 (Max of Sites 8&9) Benzo(a)pyrene 2.5E-04 (Site 45) 2.5E-04 (Site 45) Benzo(e)pyrene -- 2.8E-04 (Site 20) Benzo(b)fluoranthene -- 2.8E-04 (Site 45)


19A-135

Table 7-11 Summary of Maximum Hazard Quotients for Community-Based Receptors for the Application Case Assessment (cont’d)

Constituent HQ for Phytotoxicity HQ for Soil Invertebrates High Molecular Weight PAHs (cont’d) Benzo(g,h,i)perylene 1.3E-04 (Site 45) 2.8E-04 (Site 45) Benzo(k)fluoranthene 1.3E-04 (Site 45) 2.8E-04 (Site 45) Chrysene 1.3E-04 (Max of Sites 8&9) 2.8E-04 (Max of Sites 8&9) Dibenz(a,h)anthracene -- 2.8E-04 (Site 45) Indeno(1,2,3-cd)pyrene 1.3E-04 (Site 45) 2.8E-04 (Site 45) Perylene -- 2.8E-04 (Site 20) Pyrene -- 4.5E-04 (Max of Sites 8&9)

Total HMW PAH HQ = -- a 3.2E-03 (Max of Sites 8&9) Total LMW + HMW PAH HQ = -- a 5.3E-03 (Max of Sites 8&9)

Chlorinated Monocyclic Aromatics Dichlorobenzene 1.2E-09 (Site 45) 1.7E-09 (Site 45) Inorganics Aluminum -- -- Chromium (Total) 1.7E-01 (Site 20) 1.7E-01 (Site 20) Cobalt 3.1E-01 (Site 45) 3.1E-01 (Site 45) Copper 4.0E-02 (Site 16) 4.0E-02 (Site 16) Lead 2.1E-02 (Site 16) 2.1E-02 (Site 16) Manganese 4.4E+00 (Site 16) 2.1E+00 (Site 16) Molybdenum 1.4E-01 (Site 20) 1.4E-01 (Site 20) Nickel 1.2E-01 (Max of Sites 40-44) 1.2E-01 (Max of Sites 40-44) Strontium -- -- Vanadium 1.2E-01 (Max of Sites 40-44) 1.2E-01 (Max of Sites 40-44) Zinc 1.1E-01 (Site 16) 1.1E-01 (Site 16) NOTES: "--" - Quantitative assessment of COPC could not be performed due to lack of suitable toxicity data Bold – Value exceeds maximum acceptable HQ of 1.0 a Sum cannot be calculated due to uncertainty associated with contributions from COPC lacking suitable toxicity data



19A-136

Table 7-12 Summary of Maximum Hazard Quotients for Avian Receptors for the Application Case Assessment

Constituent American Robin Red-tailed Hawk Short-eared Owl Spruce Grouse Petroleum Hydrocarbons Aliphatic C5-C8 1.8E-07 (Site 45) 7.0E-10 (Site 45) 5.5E-09 (Site 45) 1.3E-07 (Site 45) Aliphatic C9-C16 4.5E-06 (Max of Sites 35-39) 3.3E-08 (Max of Sites 35-39) 2.2E-07 (Max of Sites 35-39) 3.1E-06 (Max of Sites 35-39) Aromatic C9-C16 6.6E-06 (Max of Sites 35-39) 3.1E-08 (Max of Sites 35-39) 2.1E-07 (Max of Sites 35-39) 4.8E-06 (Max of Sites 35-39) Aromatic C17-C34 3.9E-06 (Site 16) 4.8E-09 (Site 16) 7.6E-08 (Site 16) 2.7E-06 (Site 16)




Chlorinated Monocyclic Aromatics Dichlorobenzene -- -- -- -- Inorganics Aluminum -- -- -- -- Chromium (Total) 1.2E-01 (Site 20) 6.9E-03 (Site 20) 1.3E-02 (Site 20) 3.5E-02 (Site 20) Cobalt 6.3E-02 (Site 45) 1.4E-02 (Site 45) 2.1E-02 (Site 45) 3.3E-02 (Site 45) Copper 5.7E-02 (Site 16) 2.5E-03 (Site 16) 4.1E-03 (Site 16) 3.2E-02 (Site 16) Lead 3.7E-02 (Site 16) 4.0E-04 (Site 16) 1.3E-03 (Site 16) 1.4E-02 (Site 16) Manganese 7.7E-02 (Site 16) 4.1E-04 (Site 16) 6.6E-04 (Site 16) 6.1E-02 (Site 16) Molybdenum 3.2E-03 (Site 20) 1.2E-04 (Site 20) 6.0E-04 (Site 20) 1.9E-03 (Site 20) Nickel 8.0E-02 (Max of Sites 40-44) 2.1E-03 (Max of Sites 40-44) 5.2E-03 (Max of Sites 40-44) 1.9E-02 (Max of Sites 40-44) Strontium -- -- -- -- Vanadium 8.2E-01 (Max of Sites 40-44) 1.2E-01 (Max of Sites 40-44) 4.7E-01 (Max of Sites 40-44) 6.7E-01 (Max of Sites 40-44) Zinc 2.7E-01 (Site 16) 2.3E-04 (Site 16) 2.3E-02 (Site 16) 4.9E-02 (Site 16) NOTE: "--" - Quantitative assessment of COPC could not be performed due to lack of suitable toxicity data


19A-137

Table 7-13 Summary of Maximum Hazard Quotients for Mammalian Receptors for the Application Case Assessment

Constituent Canada Lynx Masked Shrew Meadow Vole Snowshoe Hare Woodland Caribou Petroleum Hydrocarbons Aliphatic C5-C8 7.7E-10 (Site 45) 2.7E-08 (Site 45) 6.0E-08 (Site 45) 5.7E-08 (Site 45) 1.6E-07 (Site 45) Aliphatic C9-C16 3.6E-08 (Max of Sites 35-39) 8.5E-07 (Max of Sites 35-39) 1.5E-06 (Max of Sites 35-39) 1.4E-06 (Max of Sites 35-39) 4.0E-06 (Max of Sites 35-39) Aromatic C9-C16 3.4E-08 (Max of Sites 35-39) 8.8E-07 (Max of Sites 35-39) 2.3E-06 (Max of Sites 35-39) 2.2E-06 (Max of Sites 35-39) 6.1E-06 (Max of Sites 35-39) Aromatic C17-C34 5.3E-09 (Site 16) 5.8E-07 (Site 16) 1.2E-06 (Site 16) 1.2E-06 (Site 16) 3.4E-06 (Site 16)

Total PHC HQ = 7.2E-08 (Max of Sites 35-39) 1.9E-06 (Max of Sites 35-39) 4.2E-06 (Max of Sites 35-39) 4.0E-06 (Max of Sites 35-39) 1.1E-05 (Max of Sites 35-39) Polycyclic Aromatic Hydrocarbons Low Molecular Weight PAHs Anthracene 1.5E-08 (Max of Sites 8&9) 6.7E-07 (Max of Sites 8&9) 1.4E-06 (Max of Sites 8&9) 9.2E-07 (Max of Sites 8&9) 2.7E-07 (Max of Sites 8&9) Fluoranthene 2.0E-08 (Max of Sites 8&9) 1.1E-06 (Max of Sites 8&9) 1.3E-06 (Max of Sites 8&9) 8.2E-07 (Max of Sites 8&9) 2.4E-07 (Max of Sites 8&9) Fluorene 1.9E-08 (Max of Sites 8&9) 1.1E-06 (Max of Sites 8&9) 2.4E-06 (Max of Sites 8&9) 1.7E-06 (Max of Sites 8&9) 4.7E-07 (Max of Sites 8&9) Phenanthrene 2.0E-08 (Max of Sites 8&9) 8.3E-07 (Max of Sites 8&9) 1.9E-06 (Max of Sites 8&9) 1.2E-06 (Max of Sites 8&9) 3.6E-07 (Max of Sites 8&9)

Total LMW PAH HQ = 7.4E-08 (Max of Sites 8&9) 3.7E-06 (Max of Sites 8&9) 7.0E-06 (Max of Sites 8&9) 4.6E-06 (Max of Sites 8&9) 1.3E-06 (Max of Sites 8&9) High Molecular Weight PAHs Benz(a)anthracene 1.6E-07 (Max of Sites 8&9) 5.1E-06 (Max of Sites 8&9) 7.0E-06 (Max of Sites 8&9) 4.2E-06 (Max of Sites 8&9) 1.3E-06 (Max of Sites 8&9) Benzo(a)pyrene 1.6E-07 (Site 45) 1.1E-05 (Site 45) 7.0E-06 (Site 45) 4.2E-06 (Site 45) 1.3E-06 (Site 45) Benzo(e)pyrene 1.5E-07 (Site 20) 5.9E-05 (Site 20) 4.3E-06 (Site 20) 2.0E-06 (Site 20) 6.5E-07 (Site 20) Benzo(b)fluoranthene 1.5E-07 (Site 45) 4.7E-06 (Site 45) 3.8E-06 (Site 45) 2.0E-06 (Site 45) 6.4E-07 (Site 45) Benzo(g,h,i)perylene 2.2E-07 (Site 45) 1.1E-05 (Site 45) 5.0E-05 (Site 45) 3.5E-05 (Site 45) 9.8E-06 (Site 45) Benzo(k)fluoranthene 1.6E-07 (Site 45) 4.9E-06 (Site 45) 8.2E-06 (Site 45) 5.1E-06 (Site 45) 1.5E-06 (Site 45) Chrysene 1.6E-07 (Max of Sites 8&9) 4.8E-06 (Max of Sites 8&9) 5.2E-06 (Max of Sites 8&9) 3.0E-06 (Max of Sites 8&9) 9.2E-07 (Max of Sites 8&9) Dibenz(a,h)anthracene 3.5E-07 (Site 45) 2.4E-05 (Site 45) 1.3E-04 (Site 45) 9.1E-05 (Site 45) 2.6E-05 (Site 45) Indeno(1,2,3-cd)pyrene 1.5E-07 (Site 45) 1.3E-05 (Site 45) 3.4E-06 (Site 45) 1.6E-06 (Site 45) 5.5E-07 (Site 45) Perylene 1.5E-07 (Site 20) 2.1E-05 (Site 20) 6.7E-06 (Site 20) 3.9E-06 (Site 20) 1.2E-06 (Site 20) Pyrene 2.6E-07 (Max of Sites 8&9) 7.8E-06 (Max of Sites 8&9) 1.7E-05 (Max of Sites 8&9) 1.1E-05 (Max of Sites 8&9) 3.2E-06 (Max of Sites 8&9)


Chlorinated Monocyclic Aromatics Dichlorobenzene 4.6E-11 (Site 45) 3.9E-11 (Site 45) 1.1E-10 (Site 45) 1.9E-10 (Site 45) 5.1E-10 (Site 45) Inorganics Aluminum 5.0E-03 (Site 45) 2.1E-02 (Site 45) 9.5E-03 (Site 45) 1.3E-02 (Site 45) 3.9E-02 (Site 45) Chromium (Total) 6.1E-03 (Site 20) 1.7E-01 (Site 20) 4.9E-02 (Site 20) 2.2E-02 (Site 20) 7.6E-03 (Site 20) Cobalt 3.8E-03 (Site 45) 1.8E-02 (Site 45) 1.3E-02 (Site 45) 6.9E-03 (Site 45) 2.1E-03 (Site 45) Copper 3.9E-03 (Site 16) 5.9E-02 (Site 16) 4.8E-02 (Site 16) 3.4E-02 (Site 16) 3.2E-02 (Site 16) Lead 7.3E-04 (Site 16) 8.2E-02 (Site 16) 3.0E-02 (Site 16) 1.8E-02 (Site 16) 5.3E-03 (Site 16) Manganese 1.1E-03 (Site 16) 2.2E-02 (Site 16) 1.6E-01 (Site 16) 1.1E-01 (Site 16) 3.2E-02 (Site 16) Molybdenum 5.5E-03 (Site 20) 2.2E-02 (Site 20) 2.2E-02 (Site 20) 3.5E-02 (Site 20) 9.9E-02 (Site 20) Nickel 3.4E-03 (Max of Sites 40-44) 2.0E-01 (Max of Sites 40-44) 3.5E-02 (Max of Sites 40-44) 1.9E-02 (Max of Sites 40-44) 1.7E-02 (Max of Sites 40-44) Strontium 1.3E-04 (Site 45) 1.2E-03 (Site 45) 1.5E-02 (Site 45) 1.5E-02 (Site 45) 1.4E-02 (Site 45) Vanadium 6.0E-03 (Max of Sites 40-44) 3.8E-02 (Max of Sites 40-44) 2.9E-02 (Max of Sites 40-44) 1.8E-02 (Max of Sites 40-44) 6.3E-02 (Max of Sites 40-44) Zinc 1.6E-04 (Site 16) 2.9E-01 (Site 16) 3.0E-02 (Site 16) 1.9E-02 (Site 16) 1.6E-02 (Site 16) NOTE: "--" - Quantitative assessment of COPC could not be performed due to lack of suitable toxicity data



19A-138

19A.7.5.5 Planned Development Case

Planned Development Case HQs provide an indication of potential adverse environmental effects (i.e., risk) to receptors resulting from exposure to COPC released to the atmosphere from emissions from the Application Case in combination with emissions from publicly disclosed future planned facilities. Publically disclosed facilities only include those facilities for which a regulatory application has been submitted.

Hazard Quotients for avian and mammalian receptors were well below 1.0 for all COPC. Hazard Quotients for community-based receptors were well below 1.0 for all COPC with the exception of manganese, where a maximum soil concentration at Gregoire Lake Provincial Park (Site 16) resulted in HQs of 4.4 and 2.1 for terrestrial plant and soil invertebrate communities, respectively. Note that the predicted HQs are no different from those estimated in the Baseline Case or the Application Case, and, as the estimated input from the Project Alone (Section 19A.7.5.3) is negligible, HQs exceeding 1.0 for these receptors can be entirely attributed to existing Base conditions. Again, these elevated HQs are not anticipated to translate into actual risk.

Maximum Planned Development Case HQs for each COPC and receptors, and the receptor location number (from Table 2-1) at which each maximum HQ occurs, are summarized in Tables 7-14 to 7-16.

Detailed HQ results for the Planned Development Case are provided in Appendix 19A-12.

Table 7-14 Summary of Maximum Hazard Quotients for Community-Based Receptors for the Planned Development Case Assessment

Constituent HQ for Phytotoxicity HQ for Soil Invertebrates Petroleum Hydrocarbons Aliphatic C5-C8 2.4E-07 (Site 45) 2.4E-07 (Site 45) Aliphatic C9-C16 1.4E-04 (Max of Sites 35-39) 1.4E-04 (Max of Sites 35-39) Aromatic C9-C16 8.4E-05 (Max of Sites 35-39) 8.4E-05 (Max of Sites 35-39) Aromatic C17-C34 7.0E-08 (Site 16) 7.0E-08 (Site 16)


Total LMW PAH HQ = -- a 2.1E-03 (Max of Sites 8&9) High Molecular Weight PAHs Benz(a)anthracene 1.3E-04 (Max of Sites 8&9) 2.8E-04 (Max of Sites 8&9) Benzo(a)pyrene 2.5E-04 (Site 45) 2.5E-04 (Site 45) Benzo(e)pyrene -- 2.8E-04 (Site 20) Benzo(b)fluoranthene -- 2.8E-04 (Site 45) Benzo(g,h,i)perylene 1.3E-04 (Site 45) 2.8E-04 (Site 45)


19A-139

Table 7-14 Summary of Maximum Hazard Quotients for Community-Based Receptors for the Planned Development Case Assessment (cont’d)

Constituent HQ for Phytotoxicity HQ for Soil Invertebrates High Molecular Weight PAHs (cont’d) Benzo(k)fluoranthene 1.3E-04 (Site 45) 2.8E-04 (Site 45) Chrysene 1.3E-04 (Max of Sites 8&9) 2.8E-04 (Max of Sites 8&9) Dibenz(a,h)anthracene -- 2.8E-04 (Site 45) Indeno(1,2,3-cd)pyrene 1.3E-04 (Site 45) 2.8E-04 (Site 45) Perylene -- 2.8E-04 (Site 20) Pyrene -- 4.7E-04 (Max of Sites 35-39)

Total HMW PAH HQ = -- a 3.2E-03 (Max of Sites 35-39) Total LMW + HMW PAH HQ = -- a 5.4E-03 (Max of Sites 8&9)

Chlorinated Monocyclic Aromatics Dichlorobenzene 1.2E-09 (Site 45) 1.8E-09 (Site 45) Inorganics Aluminum -- -- Chromium (Total) 1.7E-01 (Site 20) 1.7E-01 (Site 20) Cobalt 3.1E-01 (Site 45) 3.1E-01 (Site 45) Copper 4.0E-02 (Site 16) 4.0E-02 (Site 16) Lead 2.1E-02 (Site 16) 2.1E-02 (Site 16) Manganese 4.4E+00 (Site 16) 2.1E+00 (Site 16) Molybdenum 1.4E-01 (Site 20) 1.4E-01 (Site 20) Nickel 1.2E-01 (Site 20) 1.2E-01 (Site 20) Strontium -- -- Vanadium 1.2E-01 (Site 20) 1.2E-01 (Site 20) Zinc 1.1E-01 (Site 16) 1.1E-01 (Site 16) NOTES: "--" - Quantitative assessment of COPC could not be performed due to lack of suitable toxicity data Bold – Value exceeds maximum acceptable HQ of 1.0 a Sum cannot be calculated due to uncertainty associated with contributions from COPC lacking suitable toxicity

data



19A-140

Table 7-15 Summary of Maximum Hazard Quotients for Avian Receptors for the Planned Development Case Assessment

Constituent American Robin Red-tailed Hawk Short-eared Owl Spruce Grouse Petroleum Hydrocarbons Aliphatic C5-C8 2.0E-07 (Site 45) 7.7E-10 (Site 45) 6.1E-09 (Site 45) 1.4E-07 (Site 45) Aliphatic C9-C16 5.8E-06 (Max of Sites 35-39) 4.3E-08 (Max of Sites 35-39) 2.9E-07 (Max of Sites 35-39) 4.0E-06 (Max of Sites 35-39) Aromatic C9-C16 7.9E-06 (Max of Sites 35-39) 3.7E-08 (Max of Sites 35-39) 2.5E-07 (Max of Sites 35-39) 5.7E-06 (Max of Sites 35-39) Aromatic C17-C34 3.8E-06 (Site 16) 4.7E-09 (Site 16) 7.4E-08 (Site 16) 2.6E-06 (Site 16)




Chlorinated Monocyclic Aromatics Dichlorobenzene -- -- -- -- Inorganics Aluminum -- -- -- -- Chromium (Total) 1.2E-01 (Site 20) 6.9E-03 (Site 20) 1.3E-02 (Site 20) 3.5E-02 (Site 20) Cobalt 6.3E-02 (Site 45) 1.4E-02 (Site 45) 2.1E-02 (Site 45) 3.3E-02 (Site 45) Copper 5.7E-02 (Site 16) 2.5E-03 (Site 16) 4.1E-03 (Site 16) 3.2E-02 (Site 16) Lead 3.7E-02 (Site 16) 4.0E-04 (Site 16) 1.3E-03 (Site 16) 1.4E-02 (Site 16) Manganese 7.7E-02 (Site 16) 4.1E-04 (Site 16) 6.6E-04 (Site 16) 6.1E-02 (Site 16) Molybdenum 3.2E-03 (Site 20) 1.2E-04 (Site 20) 6.0E-04 (Site 20) 1.9E-03 (Site 20) Nickel 8.0E-02 (Site 20) 2.1E-03 (Site 20) 5.2E-03 (Site 20) 1.9E-02 (Site 20) Strontium -- -- -- -- Vanadium 8.2E-01 (Site 20) 1.2E-01 (Site 20) 4.7E-01 (Site 20) 6.7E-01 (Site 20) Zinc 2.7E-01 (Site 16) 2.3E-04 (Site 16) 2.3E-02 (Site 16) 4.9E-02 (Site 16) NOTE: "--" - Quantitative assessment of COPC could not be performed due to lack of suitable toxicity data


19A-141

Table 7-16 Summary of Maximum Hazard Quotients for Mammalian Receptors for the Planned Development Case Assessment

Constituent Canada Lynx Masked Shrew Meadow Vole Snowshoe Hare Woodland Caribou Petroleum Hydrocarbons Aliphatic C5-C8 8.5E-10 (Site 45) 3.0E-08 (Site 45) 6.6E-08 (Site 45) 6.3E-08 (Site 45) 1.8E-07 (Site 45) Aliphatic C9-C16 4.7E-08 (Max of Sites 35-39) 1.1E-06 (Max of Sites 35-39) 2.0E-06 (Max of Sites 35-39) 1.8E-06 (Max of Sites 35-39) 5.3E-06 (Max of Sites 35-39) Aromatic C9-C16 4.1E-08 (Max of Sites 35-39) 1.1E-06 (Max of Sites 35-39) 2.7E-06 (Max of Sites 35-39) 2.6E-06 (Max of Sites 35-39) 7.3E-06 (Max of Sites 35-39) Aromatic C17-C34 5.2E-09 (Site 16) 5.6E-07 (Site 16) 1.2E-06 (Site 16) 1.2E-06 (Site 16) 3.3E-06 (Site 16)

Total PHC HQ = 9.0E-08 (Max of Sites 35-39) 2.4E-06 (Max of Sites 35-39) 5.1E-06 (Max of Sites 35-39) 4.9E-06 (Max of Sites 35-39) 1.4E-05 (Max of Sites 35-39) Polycyclic Aromatic Hydrocarbons Low Molecular Weight PAHs Anthracene 1.5E-08 (Max of Sites 8&9) 6.8E-07 (Max of Sites 8&9) 1.4E-06 (Max of Sites 8&9) 9.2E-07 (Max of Sites 8&9) 2.7E-07 (Max of Sites 8&9) Fluoranthene 2.0E-08 (Max of Sites 8&9) 1.1E-06 (Max of Sites 8&9) 1.3E-06 (Max of Sites 8&9) 8.5E-07 (Max of Sites 8&9) 2.5E-07 (Max of Sites 8&9) Fluorene 1.9E-08 (Max of Sites 8&9) 1.1E-06 (Max of Sites 8&9) 2.4E-06 (Max of Sites 8&9) 1.7E-06 (Max of Sites 8&9) 4.7E-07 (Max of Sites 8&9) Phenanthrene 2.0E-08 (Max of Sites 8&9) 8.4E-07 (Max of Sites 8&9) 1.9E-06 (Max of Sites 8&9) 1.3E-06 (Max of Sites 8&9) 3.6E-07 (Max of Sites 8&9)

Total LMW PAH HQ = 7.5E-08 (Max of Sites 8&9) 3.8E-06 (Max of Sites 8&9) 7.0E-06 (Max of Sites 8&9) 4.7E-06 (Max of Sites 8&9) 1.4E-06 (Max of Sites 8&9) High Molecular Weight PAHs Benz(a)anthracene 1.6E-07 (Max of Sites 8&9) 5.1E-06 (Max of Sites 8&9) 7.3E-06 (Max of Sites 8&9) 4.4E-06 (Max of Sites 8&9) 1.3E-06 (Max of Sites 8&9) Benzo(a)pyrene 1.6E-07 (Site 45) 1.1E-05 (Site 45) 7.0E-06 (Site 45) 4.2E-06 (Site 45) 1.3E-06 (Site 45) Benzo(e)pyrene 1.5E-07 (Site 20) 5.9E-05 (Site 20) 4.4E-06 (Site 20) 2.1E-06 (Site 20) 6.7E-07 (Site 20) Benzo(b)fluoranthene 1.5E-07 (Site 45) 4.7E-06 (Site 45) 3.8E-06 (Site 45) 2.0E-06 (Site 45) 6.4E-07 (Site 45) Benzo(g,h,i)perylene 2.2E-07 (Site 45) 1.1E-05 (Site 45) 5.0E-05 (Site 45) 3.5E-05 (Site 45) 9.9E-06 (Site 45) Benzo(k)fluoranthene 1.6E-07 (Site 45) 5.0E-06 (Site 45) 8.3E-06 (Site 45) 5.1E-06 (Site 45) 1.5E-06 (Site 45) Chrysene 1.6E-07 (Max of Sites 8&9) 4.8E-06 (Max of Sites 8&9) 5.3E-06 (Max of Sites 8&9) 3.0E-06 (Max of Sites 8&9) 9.3E-07 (Max of Sites 8&9) Dibenz(a,h)anthracene 3.6E-07 (Site 45) 2.5E-05 (Site 45) 1.3E-04 (Site 45) 9.3E-05 (Site 45) 2.6E-05 (Site 45) Indeno(1,2,3-cd)pyrene 1.5E-07 (Site 45) 1.3E-05 (Site 45) 3.4E-06 (Site 45) 1.6E-06 (Site 45) 5.5E-07 (Site 45) Perylene 1.5E-07 (Site 20) 2.1E-05 (Site 20) 7.2E-06 (Site 20) 4.3E-06 (Site 20) 1.3E-06 (Site 20) Pyrene 2.8E-07 (Max of Sites 35-39) 8.3E-06 (Max of Sites 35-39) 1.8E-05 (Max of Sites 35-39) 1.2E-05 (Max of Sites 35-39) 3.4E-06 (Max of Sites 35-39)


Chlorinated Monocyclic Aromatics Dichlorobenzene 4.7E-11 (Site 45) 3.9E-11 (Site 45) 1.1E-10 (Site 45) 1.9E-10 (Site 45) 5.2E-10 (Site 45) Inorganics Aluminum 5.0E-03 (Site 45) 2.1E-02 (Site 45) 9.5E-03 (Site 45) 1.3E-02 (Site 45) 3.9E-02 (Site 45) Chromium (Total) 6.1E-03 (Site 20) 1.7E-01 (Site 20) 4.9E-02 (Site 20) 2.2E-02 (Site 20) 7.6E-03 (Site 20) Cobalt 3.8E-03 (Site 45) 1.8E-02 (Site 45) 1.3E-02 (Site 45) 6.9E-03 (Site 45) 2.1E-03 (Site 45) Copper 3.9E-03 (Site 16) 5.9E-02 (Site 16) 4.8E-02 (Site 16) 3.4E-02 (Site 16) 3.2E-02 (Site 16) Lead 7.3E-04 (Site 16) 8.2E-02 (Site 16) 3.0E-02 (Site 16) 1.8E-02 (Site 16) 5.3E-03 (Site 16) Manganese 1.1E-03 (Site 16) 2.2E-02 (Site 16) 1.6E-01 (Site 16) 1.1E-01 (Site 16) 3.2E-02 (Site 16) Molybdenum 5.5E-03 (Site 20) 2.2E-02 (Site 20) 2.2E-02 (Site 20) 3.5E-02 (Site 20) 9.9E-02 (Site 20) Nickel 3.4E-03 (Site 20) 2.0E-01 (Site 20) 3.5E-02 (Site 20) 1.9E-02 (Site 20) 1.7E-02 (Site 20) Strontium 1.3E-04 (Site 45) 1.2E-03 (Site 45) 1.5E-02 (Site 45) 1.5E-02 (Site 45) 1.4E-02 (Site 45) Vanadium 6.0E-03 (Site 20) 3.8E-02 (Site 20) 2.9E-02 (Site 20) 1.8E-02 (Site 20) 6.3E-02 (Site 20) Zinc 1.6E-04 (Site 16) 2.9E-01 (Site 16) 3.0E-02 (Site 16) 1.9E-02 (Site 16) 1.6E-02 (Site 16) NOTE: "--" - Quantitative assessment of COPC could not be performed due to lack of suitable toxicity data



19A-142

19A.7.5.6 Species at Risk

In order to assess species at risk where explicit modelling could not be performed (e.g., peregrine falcon, barred owl, wolverine, and northern long-eared bat), surrogate species were identified and assessed based on an examination of their role in ecological food webs and their trophic relations (Section 19A.7.2.3). To ensure that species at risk are afforded an appropriate level of protection in ERA, TRVs based on NOAELs rather than LOAELs are preferred to characterize individual risk. An additional UF of 3 (defined as the “Sensitive Species Factor”, Figure 7-3) was applied to LOAEL based TRVs for species adopted as surrogates for SAR in this ERA. For example, where a LOAEL based zinc TRV of 66.5 mg/kg-bw/day is protective of a population of red-tailed hawks within the LSA, using this species as a surrogate for the protection of an individual peregrine falcon reduces the allowable TRV by a factor of three, to 22.2 mg/kg-bw/day. A Sensitive Species Factor has not been applied to PAHs, chromium, cobalt, lead, manganese, and strontium for mammalian species, and total chromium, cobalt, copper, lead, and nickel for avian species as NOAEL based TRVs were used for these COPC. Additionally, the assessment of the short-eared owl as a surrogate for the barred owl did not require an additional Sensitive Species Factor, as the former was already evaluated as a SAR.

Maximum HQs generated for each of the SAR surrogates for each assessment case are summarized in Tables 7-17 to 7-20, along with the receptor location number where the maximum value was predicted. Maximum HQs for all SAR surrogates were all below 1.0. The highest HQ was for the masked shrew as a surrogate for the northern long-eared bat (0.87 for zinc from Baseline Case, Application Case and Planned Development Case). The contribution to this HQ from exposure to COPC during Expansion Project related activities was very small at 1.2E-04. This HQ is very conservative given that the soil content of flying insects that bats exclusively feeds on is assumed to not be greater than 1% (Sample and Suter 1994; Appendix 19A-8) compared to the soil content of the masked shrew’s prey (approximately 5-6%), which is a conservative overestimate. In reality the zinc HQ for the northern long-eared bat is likely much lower than 0.87.


19A-143

Table 7-17 Summary of Maximum Hazard Quotients for Species at Risk Surrogates for the Baseline Case Assessment

Constituent Red-tailed Hawk

(as Surrogate for Peregrine Falcon) Short-eared Owl

(as Surrogate for Barred Owl) Canada Lynx

(as Surrogate for Wolverine)

Masked Shrew (as Surrogate for Northern Long-eared

Bat) Petroleum Hydrocarbons Aliphatic C5-C8 1.5E-09 (Max of Sites 35-39) 4.0E-09 (Max of Sites 35-39) 1.7E-09 (Max of Sites 35-39) 5.9E-08 (Max of Sites 35-39) Aliphatic C9-C16 9.9E-08 (Max of Sites 35-39) 2.2E-07 (Max of Sites 35-39) 1.1E-07 (Max of Sites 35-39) 2.5E-06 (Max of Sites 35-39) Aromatic C9-C16 9.3E-08 (Max of Sites 35-39) 2.1E-07 (Max of Sites 35-39) 1.0E-07 (Max of Sites 35-39) 2.6E-06 (Max of Sites 35-39) Aromatic C17-C34 1.5E-08 (Site 16) 7.6E-08 (Site 16) 1.6E-08 (Site 16) 1.7E-06 (Site 16)

Total PHC HQ = 2.0E-07 (Max of Sites 35-39) 4.6E-07 (Max of Sites 35-39) 2.2E-07 (Max of Sites 35-39) 5.8E-06 (Max of Sites 35-39) Polycyclic Aromatic Hydrocarbons Low Molecular Weight PAHs Anthracene -- -- 1.5E-08 (Max of Sites 8&9) 6.7E-07 (Max of Sites 8&9) Fluoranthene -- -- 2.0E-08 (Max of Sites 8&9) 1.1E-06 (Max of Sites 8&9) Fluorene -- -- 1.9E-08 (Max of Sites 8&9) 1.1E-06 (Max of Sites 8&9) Phenanthrene -- -- 2.0E-08 (Max of Sites 8&9) 8.3E-07 (Max of Sites 8&9)

Total LMW PAH HQ = -- -- 7.4E-08 (Max of Sites 8&9) 3.7E-06 (Max of Sites 8&9) High Molecular Weight PAHs Benz(a)anthracene -- -- 1.6E-07 (Max of Sites 8&9) 5.1E-06 (Max of Sites 8&9) Benzo(a)pyrene -- -- 1.6E-07 (Site 45) 1.1E-05 (Site 45) Benzo(e)pyrene -- -- 1.5E-07 (Site 20) 5.9E-05 (Site 20) Benzo(b)fluoranthene -- -- 1.5E-07 (Site 45) 4.7E-06 (Site 45) Benzo(g,h,i)perylene -- -- 2.1E-07 (Site 45) 1.1E-05 (Site 45) Benzo(k)fluoranthene -- -- 1.6E-07 (Site 45) 4.9E-06 (Site 45) Chrysene -- -- 1.6E-07 (Max of Sites 8&9) 4.8E-06 (Max of Sites 8&9) Dibenz(a,h)anthracene -- -- 3.2E-07 (Site 45) 2.3E-05 (Site 45) Indeno(1,2,3-cd)pyrene -- -- 1.5E-07 (Site 45) 1.3E-05 (Site 45) Perylene -- -- 1.5E-07 (Site 20) 2.1E-05 (Site 20) Pyrene -- -- 2.6E-07 (Max of Sites 8&9) 7.8E-06 (Max of Sites 8&9)

Total HMW PAH HQ = -- -- 2.0E-06 (Site 45) 1.6E-04 (Site 45) Total LMW + HMW PAH HQ = -- -- 2.0E-06 (Site 45) 1.7E-04 (Site 45)

Chlorinated Monocyclic Aromatics Dichlorobenzene -- -- 2.3E-11 (Site 16) 1.9E-11 (Site 16) Inorganics Aluminum -- -- 1.5E-02 (Site 16) 6.3E-02 (Site 16) Chromium (Total) 6.9E-03 (Site 20) 1.3E-02 (Site 20) 6.1E-03 (Site 20) 1.7E-01 (Site 20) Cobalt 1.4E-02 (Site 20) 2.1E-02 (Site 20) 3.8E-03 (Site 20) 1.8E-02 (Site 20) Copper 2.5E-03 (Site 16) 4.1E-03 (Site 16) 1.2E-02 (Site 16) 1.8E-01 (Site 16) Lead 4.0E-04 (Site 16) 1.3E-03 (Site 16) 7.3E-04 (Site 16) 8.2E-02 (Site 16) Manganese 4.1E-04 (Site 16) 6.6E-04 (Site 16) 1.1E-03 (Site 16) 2.2E-02 (Site 16) Molybdenum 3.5E-04 (Site 20) 6.0E-04 (Site 20) 1.7E-02 (Site 20) 6.5E-02 (Site 20) Nickel 2.1E-03 (Max of Sites 40-44) 5.2E-03 (Max of Sites 40-44) 1.0E-02 (Max of Sites 40-44) 5.9E-01 (Max of Sites 40-44) Strontium -- -- 1.3E-04 (Site 16) 1.2E-03 (Site 16) Vanadium 3.7E-01 (Site 20) 4.7E-01 (Site 20) 1.8E-02 (Site 20) 1.2E-01 (Site 20) Zinc 6.8E-04 (Site 16) 2.3E-02 (Site 16) 4.7E-04 (Site 16) 8.7E-01 (Site 16) NOTE: "--" - Quantitative assessment of COPC could not be performed due to lack of suitable toxicity data



19A-144

Table 7-18 Summary of Maximum Hazard Quotients for Species at Risk Surrogates for the Project Alone Scenario Assessment




(as Surrogate for Wolverine) Masked Shrew

(as Surrogate for Northern Long-eared Bat) Petroleum Hydrocarbons Aliphatic C5-C8 1.6E-09 (Site 45) 4.2E-09 (Site 45) 1.8E-09 (Site 45) 6.3E-08 (Site 45) Aliphatic C9-C16 2.2E-10 (Site 45) 5.0E-10 (Site 45) 2.5E-10 (Site 45) 5.8E-09 (Site 45) Aromatic C9-C16 3.8E-09 (Site 45) 8.7E-09 (Site 45) 4.2E-09 (Site 45) 1.1E-07 (Site 45) Aromatic C17-C34 1.7E-10 (Site 45) 9.1E-10 (Site 45) 1.9E-10 (Site 45) 2.1E-08 (Site 45)

Total PHC HQ = 5.8E-09 (Site 45) 1.4E-08 (Site 45) 6.4E-09 (Site 45) 2.0E-07 (Site 45) Polycyclic Aromatic Hydrocarbons Low Molecular Weight PAHs Anthracene -- -- 1.2E-11 (Site 45) 5.6E-10 (Site 45) Fluoranthene -- -- 2.1E-11 (Site 45) 1.1E-09 (Site 45) Fluorene -- -- 2.4E-12 (Site 45) 1.5E-10 (Site 45) Phenanthrene -- -- 2.1E-11 (Site 45) 9.0E-10 (Site 45)

Total LMW PAH HQ = -- -- 5.6E-11 (Site 45) 2.7E-09 (Site 45) High Molecular Weight PAHs Benz(a)anthracene -- -- 5.8E-10 (Site 45) 1.7E-08 (Site 45) Benzo(a)pyrene -- -- 1.6E-09 (Site 45) 5.4E-08 (Site 45) Benzo(e)pyrene -- -- 2.0E-10 (Site 45) 7.0E-09 (Site 45) Benzo(b)fluoranthene -- -- 2.5E-10 (Site 45) 7.9E-09 (Site 45) Benzo(g,h,i)perylene -- -- 1.9E-08 (Site 45) 6.8E-07 (Site 45) Benzo(k)fluoranthene -- -- 2.7E-09 (Site 45) 8.4E-08 (Site 45) Chrysene -- -- 2.7E-10 (Site 45) 8.5E-09 (Site 45) Dibenz(a,h)anthracene -- -- 5.2E-08 (Site 45) 1.9E-06 (Site 45) Indeno(1,2,3-cd)pyrene -- -- 3.7E-10 (Site 45) 2.6E-08 (Site 45) Perylene -- -- 9.2E-10 (Site 45) 2.9E-08 (Site 45) Pyrene -- -- 5.4E-10 (Site 45) 1.6E-08 (Site 45)


Chlorinated Monocyclic Aromatics Dichlorobenzene -- -- 1.3E-10 (Site 45) 1.1E-10 (Site 45) Inorganics Aluminum -- -- 1.2E-07 (Site 45) 5.9E-07 (Site 45) Chromium (Total) 4.0E-07 (Site 45) 6.4E-07 (Site 45) 3.5E-07 (Site 45) 4.7E-06 (Site 45) Cobalt 4.6E-07 (Site 45) 6.8E-07 (Site 45) 1.3E-07 (Site 45) 4.6E-07 (Site 45) Copper 3.4E-07 (Site 45) 6.1E-07 (Site 45) 1.6E-06 (Site 45) 3.6E-05 (Site 45) Lead 3.8E-08 (Site 45) 1.3E-07 (Site 45) 6.9E-08 (Site 45) 8.7E-06 (Site 45) Manganese 1.8E-10 (Site 45) 3.2E-10 (Site 45) 5.1E-10 (Site 45) 1.5E-08 (Site 45) Molybdenum 4.8E-08 (Site 45) 8.2E-08 (Site 45) 2.2E-06 (Site 45) 9.8E-06 (Site 45) Nickel 2.0E-07 (Site 45) 4.7E-07 (Site 45) 9.6E-07 (Site 45) 5.2E-05 (Site 45) Strontium -- -- 2.5E-09 (Site 45) 3.5E-08 (Site 45) Vanadium 1.2E-05 (Site 45) 1.5E-05 (Site 45) 5.7E-07 (Site 45) 3.9E-06 (Site 45) Zinc 6.0E-08 (Site 45) 3.0E-06 (Site 45) 4.1E-08 (Site 45) 1.2E-04 (Site 45) NOTE: "--" - Quantitative assessment of COPC could not be performed due to lack of suitable toxicity data


19A-145

Table 7-19 Summary of Maximum Hazard Quotients for Species at Risk Surrogates for the Application Case Assessment





(as Surrogate for Northern Long-eared Bat) Petroleum Hydrocarbons Aliphatic C5-C8 2.1E-09 (Site 45) 5.5E-09 (Site 45) 2.3E-09 (Site 45) 8.2E-08 (Site 45) Aliphatic C9-C16 9.9E-08 (Max of Sites 35-39) 2.2E-07 (Max of Sites 35-39) 1.1E-07 (Max of Sites 35-39) 2.5E-06 (Max of Sites 35-39) Aromatic C9-C16 9.3E-08 (Max of Sites 35-39) 2.1E-07 (Max of Sites 35-39) 1.0E-07 (Max of Sites 35-39) 2.6E-06 (Max of Sites 35-39) Aromatic C17-C34 1.5E-08 (Site 16) 7.6E-08 (Site 16) 1.6E-08 (Site 16) 1.7E-06 (Site 16)


Total LMW PAH HQ = -- -- 7.4E-08 (Max of Sites 8&9) 3.7E-06 (Max of Sites 8&9) High Molecular Weight PAHs Benz(a)anthracene -- -- 1.6E-07 (Max of Sites 8&9) 5.1E-06 (Max of Sites 8&9) Benzo(a)pyrene -- -- 1.6E-07 (Site 45) 1.1E-05 (Site 45) Benzo(e)pyrene -- -- 1.5E-07 (Site 20) 5.9E-05 (Site 20) Benzo(b)fluoranthene -- -- 1.5E-07 (Site 45) 4.7E-06 (Site 45) Benzo(g,h,i)perylene -- -- 2.2E-07 (Site 45) 1.1E-05 (Site 45) Benzo(k)fluoranthene -- -- 1.6E-07 (Site 45) 4.9E-06 (Site 45) Chrysene -- -- 1.6E-07 (Max of Sites 8&9) 4.8E-06 (Max of Sites 8&9) Dibenz(a,h)anthracene -- -- 3.5E-07 (Site 45) 2.4E-05 (Site 45) Indeno(1,2,3-cd)pyrene -- -- 1.5E-07 (Site 45) 1.3E-05 (Site 45) Perylene -- -- 1.5E-07 (Site 20) 2.1E-05 (Site 20) Pyrene -- -- 2.6E-07 (Max of Sites 8&9) 7.8E-06 (Max of Sites 8&9)


Chlorinated Monocyclic Aromatics Dichlorobenzene -- -- 1.4E-10 (Site 45) 1.2E-10 (Site 45) Inorganics Aluminum -- -- 1.5E-02 (Site 45) 6.3E-02 (Site 45) Chromium (Total) 6.9E-03 (Site 20) 1.3E-02 (Site 20) 6.1E-03 (Site 20) 1.7E-01 (Site 20) Cobalt 1.4E-02 (Site 45) 2.1E-02 (Site 45) 3.8E-03 (Site 45) 1.8E-02 (Site 45) Copper 2.5E-03 (Site 16) 4.1E-03 (Site 16) 1.2E-02 (Site 16) 1.8E-01 (Site 16) Lead 4.0E-04 (Site 16) 1.3E-03 (Site 16) 7.3E-04 (Site 16) 8.2E-02 (Site 16) Manganese 4.1E-04 (Site 16) 6.6E-04 (Site 16) 1.1E-03 (Site 16) 2.2E-02 (Site 16) Molybdenum 3.5E-04 (Site 20) 6.0E-04 (Site 20) 1.7E-02 (Site 20) 6.5E-02 (Site 20) Nickel 2.1E-03 (Max of Sites 40-44) 5.2E-03 (Max of Sites 40-44) 1.0E-02 (Max of Sites 40-44) 5.9E-01 (Max of Sites 40-44) Strontium -- -- 1.3E-04 (Site 45) 1.2E-03 (Site 45) Vanadium 3.7E-01 (Max of Sites 40-44) 4.7E-01 (Max of Sites 40-44) 1.8E-02 (Max of Sites 40-44) 1.2E-01 (Max of Sites 40-44) Zinc 6.8E-04 (Site 16) 2.3E-02 (Site 16) 4.7E-04 (Site 16) 8.7E-01 (Site 16) NOTE: "--" - Quantitative assessment of COPC could not be performed due to lack of suitable toxicity data



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Table 7-20 Summary of Maximum Hazard Quotients for Species at Risk Surrogates for the Planned Development Case Assessment





(as Surrogate for Northern Long-eared Bat) Petroleum Hydrocarbons Aliphatic C5-C8 2.3E-09 (Site 45) 6.1E-09 (Site 45) 2.5E-09 (Site 45) 9.1E-08 (Site 45) Aliphatic C9-C16 1.3E-07 (Max of Sites 35-39) 2.9E-07 (Max of Sites 35-39) 1.4E-07 (Max of Sites 35-39) 3.3E-06 (Max of Sites 35-39) Aromatic C9-C16 1.1E-07 (Max of Sites 35-39) 2.5E-07 (Max of Sites 35-39) 1.2E-07 (Max of Sites 35-39) 3.2E-06 (Max of Sites 35-39) Aromatic C17-C34 1.4E-08 (Site 16) 7.4E-08 (Site 16) 1.5E-08 (Site 16) 1.7E-06 (Site 16)


Total LMW PAH HQ = -- -- 7.5E-08 (Max of Sites 8&9) 3.8E-06 (Max of Sites 8&9) High Molecular Weight PAHs Benz(a)anthracene -- -- 1.6E-07 (Max of Sites 8&9) 5.1E-06 (Max of Sites 8&9) Benzo(a)pyrene -- -- 1.6E-07 (Site 45) 1.1E-05 (Site 45) Benzo(e)pyrene -- -- 1.5E-07 (Site 20) 5.9E-05 (Site 20) Benzo(b)fluoranthene -- -- 1.5E-07 (Site 45) 4.7E-06 (Site 45) Benzo(g,h,i)perylene -- -- 2.2E-07 (Site 45) 1.1E-05 (Site 45) Benzo(k)fluoranthene -- -- 1.6E-07 (Site 45) 5.0E-06 (Site 45) Chrysene -- -- 1.6E-07 (Max of Sites 8&9) 4.8E-06 (Max of Sites 8&9) Dibenz(a,h)anthracene -- -- 3.6E-07 (Site 45) 2.5E-05 (Site 45) Indeno(1,2,3-cd)pyrene -- -- 1.5E-07 (Site 45) 1.3E-05 (Site 45) Perylene -- -- 1.5E-07 (Site 20) 2.1E-05 (Site 20) Pyrene -- -- 2.8E-07 (Max of Sites 35-39) 8.3E-06 (Max of Sites 35-39)


Chlorinated Monocyclic Aromatics Dichlorobenzene -- -- 1.4E-10 (Site 45) 1.2E-10 (Site 45) Inorganics Aluminum -- -- 1.5E-02 (Site 45) 6.3E-02 (Site 45) Chromium (Total) 6.9E-03 (Site 20) 1.3E-02 (Site 20) 6.1E-03 (Site 20) 1.7E-01 (Site 20) Cobalt 1.4E-02 (Site 45) 2.1E-02 (Site 45) 3.8E-03 (Site 45) 1.8E-02 (Site 45) Copper 2.5E-03 (Site 16) 4.1E-03 (Site 16) 1.2E-02 (Site 16) 1.8E-01 (Site 16) Lead 4.0E-04 (Site 16) 1.3E-03 (Site 16) 7.3E-04 (Site 16) 8.2E-02 (Site 16) Manganese 4.1E-04 (Site 16) 6.6E-04 (Site 16) 1.1E-03 (Site 16) 2.2E-02 (Site 16) Molybdenum 3.5E-04 (Site 20) 6.0E-04 (Site 20) 1.7E-02 (Site 20) 6.5E-02 (Site 20) Nickel 2.1E-03 (Site 20) 5.2E-03 (Site 20) 1.0E-02 (Site 20) 5.9E-01 (Site 20) Strontium -- -- 1.3E-04 (Site 45) 1.2E-03 (Site 45) Vanadium 3.7E-01 (Site 20) 4.7E-01 (Site 20) 1.8E-02 (Site 20) 1.2E-01 (Site 20) Zinc 6.8E-04 (Site 16) 2.3E-02 (Site 16) 4.7E-04 (Site 16) 8.7E-01 (Site 16) NOTE: "--" - Quantitative assessment of COPC could not be performed due to lack of suitable toxicity data

Volume 2 EIA: JACOS Hangingstone Expansion Project Appendix 19A: Human Health and Ecological Risk Assessment – Techncial Report April 2010

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19A.7.5.7 Characterization for Inhalation Route of Exposure

As discussed in Section 19A.7.4.1 the current state of knowledge on inhalation toxicity does not permit an ecologically relevant quantitative assessment of this pathway for most COPC. As an alternative to conducting a quantitative risk assessment based on the inhalation pathway for ecological receptors, human receptor exposure to COPC concentrations was used as a surrogate for ecological risk assuming that if humans are adequately protected against inhalation risks, ecological receptors will also be protected.

Results of the HHRA suggest that non-chronic (1-hour and 24-hour averaging periods) exposure to airborne COPC, SO2 (1-hour), acrolein (24-hour), and PM2.5 (24-hour) exceeded an acceptable CR of 1.0, when compared against TRVs with health-based endpoints (Section 19A.6.4.2). Of these COPC, SO2 was the only one for which contributions from the Project (Project Alone Scenario) were expected to account for the majority of environmental input (CR = 1.1). Conversely, acrolein and PM2.5 exceedances only occurred for the Baseline Case, Project Alone Scenario, and Planned Development Case scenarios, with Expansion Project related sources estimated to be essentially negligible. In all instances of estimated non-chronic CRs greater than 1.0, exceedances were noted to occur in areas where adequate permanent habitat for receptors was not expected to be found. The SO2 exceedance occurs adjacent to the Central Processing Facility (CPF), and not anywhere else within the study area, while the acrolein and PM2.5 exceedances were localized near Fort McMurray and Fort McKay. Estimated CRs for these COPC decreased with increasing distance from densely populated areas. Furthermore, 1-hour and 24-hour exceedance of health-based criteria for these COPC is expected to occur very infrequently and air modelling assumed scenarios using the worst-case meteorological conditions.

Results of the HHRA (Section 19A.6.4.2) indicated that acrolein was the only COPC for which the acceptable Concentration Ratio (CR) of 1.0 was exceeded for chronic health risks, using a TRV with a health-based endpoint (as opposed to odour-based endpoints). However, the estimated exceedance only occurred for the Baseline Case, Project Alone Scenario, and Planned Development Case scenarios (estimated CRs = 9.1, 9.1, 9.7, respectively), whereas no exceedance was noted under the Project Alone Scenario (estimated CR = 0.003). Estimated contributions of acrolein from Expansion Project related sources are, therefore, considered to be negligible. Furthermore, a review of the receptor locations where elevated annual acrolein CRs are expected to occur reveals that exceedances are limited to areas within or very near to Fort McMurray and Fort McKay. These locations are not expected to provide adequate permanent habitat for receptors assessed in this ERA, and so, receptors are not expected to be at risk from acrolein over a chronic exposure period.

19A.7.6 ERA Uncertainty Analysis

Uncertainty is inherent to many aspects of predicting health risks to receptors. The level of uncertainty depends upon the availability and quality of information, as well as the variability associated with many of the processes and factors being considered. When conducting risk assessments, it is standard practice to implement conservative assumptions (i.e., to make assumptions that are biased towards safety) when uncertainty is encountered. This strategy generally results in an overestimation of actual risk, which helps



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ensure that the overall ERA conclusions would be protective of the health of ecological receptors. The following sections outline the main sources of uncertainty in this ERA.

19A.7.6.1 Food Chain Interactions

Limited "real world" data exist that allow quantification of the true relationship between a chemical in an environmental media and chemical transfer through the food chain. Only a few classes of chemicals appear to be magnified through the food chain. These substances include methyl mercury, PCBs, some chlorinated pesticides (such as DDT), and some PCDD/PCDF compounds. These substances all have a tendency to partition into fatty tissue rather than water. They are also resistant to natural degradation processes by metabolic enzymes. PHCs and PAHs are also classes of hydrophobic chemicals present in the environment. Although these hydrocarbons are hydrophobic, they can be metabolized and/or excreted by some invertebrates and most vertebrates. For this reason, food chain magnification does not tend to occur with PHCs or PAHs, although they can still be accumulated to some extent by many wildlife species. For other organic substances, such as dichlorobenzene, the extent of food chain magnification is not well understood. Among the inorganic chemicals, some, such as zinc are subject to biological regulation. Others, such as thallium and mercury, appear to have high potential for bioaccumulation, and still others, such as methyl mercury, undergo biomagnification in the food chain. The extent of food chain magnification is a source of uncertainty that is addressed by using a conservative approach to uptake of COPC.

19A.7.6.2 Selection of Chemicals of Potential Concern

COPC retained for multi-pathway analysis were compiled on the basis of their bioaccumulative potential and persistence in the environment. The list of COPC was extensive for a facility of this nature and it is unlikely that any additional COPC would be emitted from the Expansion Project that could affect ecological receptors.

19A.7.6.3 Inhalation Pathway

The current state of inhalation toxicology literature does not permit a quantitative assessment of risk for most COPC. Very little is known regarding species sensitivity relationships across taxonomic orders or classes for health outcomes from inhalation exposure. Consequently, the use of uptake factors or allometric scaling is not recommended because there is little assurance of what values will be protective. This ERA did not directly evaluate the potential risks to ecological receptors from exposure to COPC via the inhalation pathway even though, given the nature of the Expansion Project, it is assumed that terrestrial receptors would be exposed to certain COPC in this manner. Instead, potential risk to human health via the inhalation pathway was used as an indicator of ecological inhalation risk based on the ascertation that provided that human receptors are adequately protected against inhalation exposures to COPC, then receptors should be protected as well. Given that the level of protection afforded to humans focuses on the health of individuals and often sensitive health outcomes (such as childhood asthma), it is reasonable to assume that human exposure TRVs for airborne contaminants are likely to be lower than equivalent TRVs for ecological receptors. As such, using the results of the human health inhalation pathway assessment is a conservative and protective method of assessing inhalation risk to receptors.


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19A.7.6.4 Selection of Appropriate Receptors and Receptor Characterization

Key indicator resources evaluated in this ERA were carefully selected to include species that are present in the LSA, and could collectively provide a representation of vital components of the food web (i.e., omnivore, herbivore). As such, these receptors are expected to be representative of other species that may be present in the LSA and exposed to COPC. For this ERA it has been assumed that each receptor spends its entire life cycle (12 months of the year) within the LSA, even if life history traits suggest the receptor undertakes yearly migration.

The use of receptors is intended to limit the number of species to a reasonable number. The receptors selected are considered to be consistently present in the assessment areas and to be exposed to the COPC via relevant exposure pathways. Therefore, it is reasonable to assume that conclusions that are reached with respect of receptors can be generalized to other biota that might use the LSA, including species at risk.

For each receptor, the estimated exposure to COPC was dependent on attributes such as food and soil intake and dietary composition. These attributes were characterized through extensive reviews of the available scientific literature. Where receptor-specific values were unavailable, body weight based estimation was utilized (i.e., estimation of food requirements using Nagy’s (1987) equations).

19A.7.6.5 Uncertainty Factors Applied for TRV Derivation

For several COPC, the available toxicity database is very limited. Consequently, TRVs for these substances were occasionally based on less-than-optimal toxicological studies. These TRVs were not necessarily specific to the receptor assessed, based on reproductive or population-level endpoints, or of chronic duration. Uncertainty factors were, therefore, often necessary to modify available toxicological data for use in the ERA. The UF used were scientifically based and were applied conservatively in a manner that is consistent with regulatory guidance.

The preferred measure of toxicity for TRVs in this ERA is the chronic LOAEL. For certain COPC the only chronic endpoints available were NOAELs. In this situation, the NOAEL was used as the TRV (without the application of uncertainty factors). The decision not to apply uncertainty factors to translate a NOAEL to a LOAEL is a conservative measure to avoid overestimating the LOAEL (and consequently underestimating potential risks). For mammalian receptors, NOAEL-based TRVs were used for the following COPC: PAHs, chromium, cobalt, lead, manganese, and strontium. For avian receptors, a NOAEL based TRV was used for total chromium, cobalt, copper, lead, manganese, and nickel.

19A.7.6.6 Exposure Prediction Limitations

For all four assessment cases various models were used to estimate air emissions and environmental fate and transport of COPC for the purpose of generating EPCs. These modelling exercises were carried out in a way that is expected to result in conservative estimates that overstate actual levels of risk. Additionally, for the Baseline Case assessment, EPCs for soil were in part derived from empirical measurements where upper concentration limits were conservative chosen to represent existing



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background concentrations. Therefore, the calculated risks to receptors that result from these data are also highly conservative.

19A.7.6.7 Chemical Speciation

The fate, food chain interactions, and toxicity of a number of inorganic elements depend to a large extent upon their chemical form. As such, conservative assumptions about chemical form, bioavailability, and absorption across the gut were generally carried forward in the risk assessment, and the potential for exposure is likely to be overstated. For example, it was assumed that 100% of each ingested COPC is absorbed from ingested soil or food, and is available to the organism as a potentially toxic substance. This may be reasonable for some COPC but would be highly conservative for others.

19A.7.6.8 Environmental Fate and Transport

The environmental fate and transport of COPC was modelled following US EPA and similar fate and transport models. Although the overall model structures are reliable, the quality of many of the parameter values describing the environmental fate and partitioning of COPC varies. For some COPC and/or environmental media, the environmental fate and transport parameters are uncertain, and in the face of this, conservative assumptions were implemented that may overstate the likely environmental concentrations and exposure of wildlife to these and other substances.

19A.7.7 ERA Conclusions

The purpose of this ERA was to evaluate the potential ecological risk to receptors exposed to Expansion Project related COPC under four assessment scenarios. Hazard Quotients for all mammalian and avian receptors (including the identified SAR) exposed to COPC were less than 1.0 under all four scenarios, and therefore no unacceptable risks were predicted from exposure to environmental concentrations of COPC. For community-based receptors (i.e., terrestrial plants and soil invertebrates), an HQ greater than 1.0 was estimated as a result of exposure to manganese under the Baseline Case, Application Case, and Planned Development Case scenarios only. However, no potential risk was predicted under the Project Alone Scenario and estimated COPC contributions from the proposed JACOS facility expansion were deemed to be negligible compared to background concentrations. Risk estimated for community-based receptors is solely the result of existing background soil concentrations in the LSA, which, following the conservative methodology employed in this ERA are biased high. In reality, background soil concentrations within the LSA are not expected to differ from other rural areas in Alberta or result in risk to vegetation or invertebrate communities, a conclusion that is supported by the evidence of healthy and diverse vegetation communities observed within the LSA.


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19A.8 Follow-up Work and Monitoring

Although the multimedia exposures are not predicted to result in a either human or ecological health, if it is determined that persons in the LSA intend to grow and/or gather 100% of their produce from the LSA, monitoring to confirm actual produce concentrations is recommended. However, it is also noted that the Expansion Project will have a negligible effect on the produce concentrations (i.e., the potential exposures are related to the existing conditions).


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19A.9 References

19A.9.1 Literature Cited

Alberta Health and Wellness (2006) Report on the Health of Albertans. Edmonton: Alberta Health and Wellness. ISBN 0-7785-3477-4.

Alberta Sustainable Resource Development (ASRD). 2006. The General Status of Alberta Wild Species 2005. Edmonton, AB: Natural Resources Service, Wildlife Management Division. 46pp.

BC Gov (Government of British Columbia). Ministry of Environment, Lands and Parks. 2000. Mountain Goat in British Columbia: Ecology, Conservation and Management. MELP 851541.0300.

Beyer,W.N., S. Gerould and E.E. Connor. 1994. Estimates of Soil Ingestion by Wildlife. Journal of Wildlife Management, 58, 375-382.

Calder, W.A. and E.J. Braun. 1983. Scaling of osmotic regulation in mammals and birds. Am. J. Physiol. 224: R601-R606

Canadian Council of Ministers of the Environment (CCME). 1996. A Framework for Ecological Risk Assessment: General Guidance. Canadian Council of Ministers of the Environment. Winnipeg, Manitoba. En 108- 4-10-1996E.

CCME. 1997. A Framework for Ecological Risk Assessment: Technical Appendices. The National Contaminated Sites Program. Canadian Council of Ministers of the Environment. Winnipeg, Manitoba.

Chappell, W.R. 1992. Scaling toxicity data across species. Environmental Geochemistry and Health 14(3): 71-80.

Clayton, K. M. 2000. Status of the Short-eared Owl (Asio flammeus) in Alberta. Alberta Environment, Fisheries and Wildlife Management Division, and Alberta Conservation Association, Wildlife Status Report No. 28, Edmonton, AB. 15 pp.

Devillers, J. and J.M. Exbrayat (eds.) 1992. Ecotoxicity of chemicals to amphibians. Gordon and Breach Science Publishers. Philadelphia.

Government of British Columbia: Ministry of Lands, Environment and Parks. Mule and Black-Tailed Deer in British Columbia: Ecology, Conservation and Management. 2000. MELP 851538.0300

Grande Cache Coal Project. Environmental Impact Assessment. October 2001.

Jacques Whitford. 2008. Jacques Whitford Wildlife Technical Report.

Japan Canada Oil Sands Limited (JACOS). 2002a. JACOS Hangingstone SAGD Project Environmental Impact Assessment. Section 1: Baseline Overview. Report on file at JACOS, Calgary, Alberta. Prepared by AXYS Environmental Consulting Ltd. Calgary, Alberta

Japan Canada Oil Sands Limited (JACOS). 2002b. JACOS Hangingstone SAGD Project Environmental Impact Assessment. Section 3: Species List. Report on file at JACOS, Calgary, Alberta. Prepared by AXYS Environmental Consulting Ltd. Calgary, Alberta


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Japan Canada Oil Sands Limited (JACOS). 2002c. JACOS Hangingstone SAGD Project Environmental Impact Assessment. Section 10: Wildlife. Report on file at JACOS, Calgary, Alberta. Prepared by AXYS Environmental Consulting Ltd. Calgary, Alberta

Kapustka, L.A. 2004. Establishing Eco-SSLs for PAHs: Lessons Revealed from a Review of Literature in Exposure and Effects to Terrestrial Receptors. Human and Ecological Risk Assessment, 10:2, 185-205.

Knopper, L.D., Smith, G.K., Ollson, C.A., and Stephenson, M. 2009. Use of Body Mass Scaling of Dose in Ecological Risk Assessments. In: Ecotoxicology Research Developments, Santos, E.B. (ed). Nova Publishers, NJ.

Legge, A.H., Jager H. and S.V. Kruppa. 1998. Sulphur Dioxide. In: Recognition of Air Pollution injury to vegetation: A pictorial atlas, 2nd Edition (Eds. R.B. Flagler), pp.3-1-1-42. Air and Waste Management Association, Pittsburgh, PA.

Luttik, R., P. Mineau and W. Roelofs. 2005. A review of interspecies toxicity extrapolation in birds and mammals and a proposal for long-term toxicity data. Ecotoxicology 14: 817-832.

Malhotra, S.S.; Blauel, R.A. 1980. Diagnosis of air pollutant and natural stress symptoms on forest vegetation in western Canada. North. For. Res. Cent., Can. For. Serv., Environ. Can. Inf. Rep. NOR-X-228. 84 p.

Martin, A.C., Zim, H.S., Nelson, A.L. 1951. American Wildlife and Plants, A Guide to Wildlife Food Habits. Dover Publications Inc., New York.

Mineau, P., B.T. Collins and A. Baril. 1996. On the use of scaling factors to improve interspecies extrapolation of acute toxicity in birds. Regulatory Toxicology and Pharamacology 24: 24-29.

Nagy, K.A. 1987. Field metabolic rate and food requirement scaling inmammals and birds. Ecological Monographs. 57(2):111–128.

NWF (National Wildlife Federation). 2003. eNature. Accessed February 9, 2005 at http://www.enature.com /guides/select_group.asp.

Ohio EPA. 2003. Division of Emergency and Remedial Response. Ecological Risk Assessment Guidance Document. DERR - 00 - RR – 031.

Pauli, B.D., J.A. Perrault and S.L. Money. 2000. RATL: A Database of Reptile and Amphibian Toxicology Literature. Environment Canada. Canada Wildlife Service.

Raimondo, S., P. Mineau and M.G. Barron. 2007. Estimation of Chemical Toxicity to Wildlife Species Using Interspecies Correlation Models. Environmental Science and Technology 41: 5888-5894.

Rodan BD, Pennington DW, Eckley N, Boethling RS. 1999. Screening for persistent organic pollutants: techniques to provide a scientific basis for POPs criteria in international negotiations. Environ Sci Technol 33:3482–3488.

Sample, B. E. and C. A. Arenal, 1999. Allometric Models for Interspecies Extrapolation of Wildlife. Bull. Environ. Contam Toxicol. 62:653-663


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Sample, B.E. and G.W. Suter. 1994. Estimating exposure of terrestrial wildlife to contaminants. Oak Ridge National Laboratory Report ES/ER/TM-125.

Sample, B.E., D.M. Opresko and G.W. Suter II. 1996. Toxicological Benchmarks for Wildlife: 1996 Revision. Oak Ridge National Laboratory, Oak Ridge, TN. ES/ER/TM-86/

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Sparling, D.W., G. Linder and C.A. Bishop (eds.). 2000. Ecotoxicology of Amphibians and Reptiles. SETAC Press. Pensacola, Florida. 663-696.

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Terres, J.K. Audubon Society Encyclopedia of North American Birds. Wings. 1109 p.

Travis, C.C. and White R.K. 1988. Interspecific scaling of toxicity data. Risk Analysis. 8:119-125.

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19A.9.2 Internet Sites

Alberta Government (Alberta Gov), 2007. Alberta Government, Sustainable Resource Development: Fish and Wildlife. Accessed May 2008 at: http://www.srd.gov.ab.ca/fishwildlife/default.aspx

Arnold, D. and T. Dewey. 2002. Buteo jamaicensis. Animal Diversity Web. Accessed March 22, 2005 at http://animaldiversity.ummz.edu/site/accounts/information/Buteo_jamaicensis.html.

Canadian Wildlife Service & Canadian Wildlife Federation (CWS & CWF). 2005 to 2008. Hinterland Who’s Who. Accessed at various times from 2005 to 2008 at http://www.hww.ca.

Cornell Lab of Ornithology. 2003. All About Birds. Online Bird Guide. Accessed 2005 and 2008 at http://birds.cornell.edu/programs/AllAboutBirds/Bird Guide/.

CWS & CWF (Canadian Wildlife Service & Canadian Wildlife Federation). 2005 to 2008. Hinterland Who’s Who. Accessed at various times from 2005 to 2008 at http://www.hww.ca.

Environment Canada (EC). 2005. National Pollutant Release Inventory (NPRI) for 2005. Available at: http://www.ec.gc.ca/pdb/npri/npri_prev_dat_e.cfm.

Environment Canada. 2005. Canadian Wildlife Service, Ontario Region: Project WILDSPACE. Accessed November, 2009. Available at: http://wildspace.ec.gc.ca/life.cfm?Lang=e


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Environment Canada 2006. Priority Substance List Assessment Reports. Canadian Environmental Protection Act (CEPA) Environmental Registry. Environment Canada. Existing Substances Branch. Available at http://www.ec.gc.ca/CEPARegistry/subs_list/Priority.cfm

Fox, D. and T. Murphy. 2002. "Lynx canadensis" (On-line), Animal Diversity Web. Accessed November, 2009 at http://animaldiversity.ummz.umich.edu/site/accounts/information/Lynx_canadensis.html.

Lee, W. 2001. "Sorex cinereus". Animal Diversity Web. Accessed March 22, 2005 at http://animaldiversity.ummz.umich.edu/site/accounts/information/Sorex_cinereus.html

National Wildlife Federation (NWF). 2003. eNature. Accessed February 9, 2005 at http://www.enature.com /guides/select_group.asp.

Neuburger, T. 1999. Microtus pennsylvanicus. Animal Diversity Web. Accessed February 17, 2005 at http://animaldiversity.ummz.edu/site/accounts/information/Microtus_pennsylvanicus.html.

Ohio EPA. 2008. Division of Emergency and Remedial Response. Ecological Risk Assessment Guidance Document. April 2008 Revision. DERR - 00 - RR – 031. Available at: http://www.epa.state.oh.us/derr/rules/RR-031.pdf

SARA: Government of Canada. 2005 to 2008. Species at Risk Act Public Registry. Accessed at various times in 2005 to 2008 at http://www.sararegistry.gc.ca.

State of California. 2008.Cal/Ecotox Database. Available at: http://www.oehha.org/cal_ecotox/

U.S. EPA. 1999. Screening Level Ecological Risk Assessment Protocol for Hazardous Waste Combustion Facilities. Available at: http://www.epa.gov/combustion/ecorisk.htm

U.S. EPA. 2007. Ecological Soil Screening Levels. Online: http://www.epa.gov/ecotox/ecossl/

US EPA. 2008. Ecotox Database. Available at: http://cfpub.epa.gov/ecotox/

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