Phase 5
Human Health Risk Assessment of
Air Emissions from the
Toronto Pearson International Airport
(TPIA)
FINAL REPORT
Date:
September 10, 2004
Submitted By: Cantox Environmental Inc.
Submitted To: Greater Toronto Airport Authority©
Rowan Williams Davies & Irwin Inc.
1900 Minnesota Court. Suite 130.
Mississauga, Ontario L5N 3C9
Tel: 905-814-7800
Fax: 905-814-4954
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HUMAN HEALTH RISK ASSESSMENT OF PREDICTED EMISSIONS FROM
THE TORONTO PEARSON INTERNATIONAL AIRPORT (TPIA)
Table of Contents
Page
EXECUTIVE SUMMARY ....................................................................................................................... i
1.0
BACKGROUND AND METHODOLOGY ...............................................................................1
1.1
Background ...............................................................................................................................1
1.2
Methodology ..............................................................................................................................5
1.2.1
Risk Assessment Approaches for Systemic and Point-of-Contact Chemicals.....................6
1.2.2
Problem Formulation........................................................................................................10
1.2.2.1 Chemicals of Concern...................................................................................................10
1.2.2.2
Exposure Scenarios and Pathways................................................................................11
1.2.2.3
Selection of Receptors and Receptor Locations ...........................................................12
1.2.3
Exposure Assessment ........................................................................................................12
1.2.4
Hazard Assessment ...........................................................................................................13
1.2.5
Risk Characterization .......................................................................................................13
2.0
HHRA OF VOCs, CARBONYLS AND PAHs.........................................................................15
2.1
Predicted Emissions from TPIA and Off-site Sources ........................................................15
2.2
Human Health Risk Assessment............................................................................................21
2.2.1
Problem Formulation.......................................................................................................21
2.2.1.1
Selection of Receptors .................................................................................................21
2.2.1.2
Selection of Chemicals of Concern..............................................................................23
2.2.1.3
Selection of Exposure Scenarios..................................................................................24
2.2.2
Exposure Assessment .......................................................................................................27
2.2.3
Hazard Assessment ..........................................................................................................27
2.2.4
Risk Characterization .......................................................................................................31
2.3
Results of the HHRA .............................................................................................................34
2.3.1
TPIA Emissions Only .......................................................................................................34
2.3.2
Off-site Sources Only .......................................................................................................35
2.3.3
TPIA and Off-site Sources Combined ...............................................................................35
2.4
Data Tables ..............................................................................................................................35
3.0
HHRA FOR CO, NO2 and SO2..................................................................................................66
3.1
HHRA for Carbon Monoxide ................................................................................................66
3.1.1
Sources of CO ...................................................................................................................66
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Page
3.1.2
Predicted CO Concentrations...........................................................................................67
3.1.2.1
Predicted One-hour Maximum Concentrations from TPIA Sources Alone .................67
3.1.2.2 Predicted One-hour Maximum Concentrations From Off-site Sources Only ...............69
3.1.2.3 Predicted One-hour Maximum Concentrations From TPIA and Off-site
Sources Combined.........................................................................................................71
3.1.2.4 Predicted Maximum 8-Hour Concentrations ................................................................72
3.1.2.5
Predicted Annual Average Concentrations...................................................................73
3.1.3
Monitoring Results for CO and Comparison with AAQCs...............................................74
3.2
HHRA of Nitrogen Dioxide (NO2) ...........................................................................................75
3.2.1
Sources of NO2 ..................................................................................................................75
3.2.2
Predicted Concentrations of NO2 .....................................................................................77
3.2.2.1
TPIA Sources Alone .....................................................................................................77
3.2.2.2
Off-site Sources Alone..................................................................................................79
3.2.2.3
TPIA and Off-site Sources Combined ..........................................................................81
3.2.2.4 Monitoring Results for NO2 and NOx and Comparison with AAQCs..........................83
3.2.3
Concentration Ratios for NOx Converted to NO2 .............................................................84
3.3
HHRA for Sulphur Dioxide (SO2)............................................................................................86
3.3.1
Sources of SO2...................................................................................................................86
3.3.2
Predicted Concentrations of SO2 ......................................................................................87
3.3.2.1 TPIA Sources Alone ......................................................................................................87
3.3.2.2 Off-site Sources Alone...................................................................................................88
3.3.2.3 TPIA and Off-site Sources Combined ...........................................................................89
3.3.2.4
Predicted Maximum Annual Average SO2 Concentrations..........................................90
3.4
Particulate Matter (PM10)..........................................................................................................92
4.0
DISCUSSION OF RESULTS ....................................................................................................94
4.1
HHRA for VOCs, Carbonyl s and PAHs..................................................................................94
4.1.1
Exposure to Predicted TPIA Emissions Alone..................................................................94
4.1.2
Contribution to Overall Health Risks ...............................................................................95
4.1.3
Discussion of Key Assumptions in the HHRA for Long Term Exposures.........................96
4.1.3.1
Use of Environment Canada Data for Chemical Speciation.........................................96
4.1.3.2
Use of Recent Scientific and Regulatory Reviews of Formaldehyde...........................98
4.2
HHRA for CO, NO2 and SO2, ...................................................................................................98
4.2.1
Carbon Monoxide .............................................................................................................99
4.2.1.1
Exposure to Predicted TPIA Emissions Alone .............................................................99
4.2.1.2 Contribution to Overall Health Risks .........................................................................100
4.2.2.1
Exposure to Predicted TPIA Emissions Alone ...........................................................103
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4.2.2.2 Contribution to Overall Health Risks .........................................................................104
4.2.2.3 Discussion of Biomedical Evidence for Health Effects...............................................105
4.2.3
Sulphur Dioxide (SO2) ....................................................................................................109
4.2.3.1
Exposure to Predicted TPIA Emission Alone.............................................................109
4.2.3.2 Contribution to Overall Health Risks .........................................................................110
4.2.3.3 Discussion of Biomedical Evidence for Health Effects...............................................110
4.3
Particulate Matter (PM10)........................................................................................................112
4.4
Discussion of Uncertainties ....................................................................................................113
4.4.1
Uncertainties in Predicted Air Concentrations for Chemicals of Concern....................114
4.4.2
Uncertainties in Assessing Potential Health Risks .........................................................114
4.4.2.1
Uncertainty in the Toxicological Reference Values Used..........................................115
4.4.2.3 Historical NAPS data..................................................................................................117
4.4.2.4
Surrogacy of Mobile Emissions..................................................................................118
4.4.2.5
Dependence on Data from a Limited Number of Monitoring Sites............................119
4.4.2.6
Assignment of Chemicals of Concern ........................................................................119
4.4.2.7
Choice of Jet Exhaust Chemical Speciation ...............................................................120
4.4.2.8
Emissions for Particulate Matter.................................................................................120
4.4.2.9
Lack of Carbonyl Compound Data .............................................................................121
4.4.2.10 Characterization of PAHs ............................................................................................121
4.4.2.11 Calculation of Speciated Concentrations of VOCs Used in the HHRA ......................122
5.0
REFERENCES..........................................................................................................................123
APPENDIX A
TOXICITY ASSESSMENT
APPENDIX B
SPECIATION OF VOCs AND PAHs
APPENDIX C
CARBON MONOXIDE (CO)
APPENDIX D
NITROGEN DIOXIDE (NO2)
APPENDIX E
HEALTH EFFECTS FROM EXPOSURE TO PARTICULATE MATTER
APPENDIX F
JET AIRCRAFT EMISSIONS
APPENDIX G
EMISSIONS FROM THE COMBUSTION OF JET FUELS AND DIESEL
FUELS
APPENDIX H
FIGURES:
ANNUAL AVERAGE VOC FOR PHASES 1, 2 & 3
WET & DRY DEPOSTITION OF PARTICULATE MATTER
APPENDIX I
PEER REVIEW COMMENTS AND RESPONSES
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HUMAN HEALTH RISK ASSESSMENT OF PREDICTED EMISSIONS FROM
THE TORONTO PEARSON INTERNATIONAL AIRPORT (TPIA)
List of Tables
Table 1
Table 2
Table 3
Table 4
Table 5
Table 6
Table 7
Table 8
Table 9
Table 10
Table 11
Table 12
Table 13
Table 14
Table 15
Table 16
Table 17
Table 18
Table 19
Table 20
Table 21
Page
Predicted Total Annual VOC Concentrations (µg/m ) ......................................................... 18
Surrogate Compounds Assessed as Fuel Combustion Products ........................................... 20
Key Physical Parameters for Receptor Life Stages ............................................................. 22
Time-activity Patterns for Residential Receptors ................................................................. 26
Predicted Annual VOC Concentrations from TPIA Sources Alone and Both TPIA and Offsite Sources Combined (µg/m3) ........................................................................................... 36
Predicted Total Annual VOC and Speciated Chemical Concentrations from TPIA Sources
Alone.................................................................................................................................... 37
Predicted Total Annual VOC and Select Speciated Chemical Concentrations from TPIA
Sources Alone (Using the US EPA 1098 Fractionation Profile) ........................................ 38
Predicted Total Annual VOC and Speciated Chemical Concentrations from Off-site Sources
Alone.................................................................................................................................... 40
Predicted Total Annual VOC and Speciated Chemical Concentrations from Both TPIA and
Off-site Sources Combined.................................................................................................. 41
Bioavailability Values for Chemicals of Concern Evaluated in the Current Assessment .... 43
Summary of Exposure Limits for Human Receptors............................................................ 44
Cancer Risk Levels and Exposure Ratios for the Workplace Exposure Scenario (TPIA
Sources Alone)..................................................................................................................... 47
Risk Levels and Exposure Ratios for the Residential Exposure Scenario (TPIA Sources
Alone) .................................................................................................................................. 50
Cancer Risk Levels and Exposure Ratios for the Workplace Exposure Scenario (Off-site
Sources Alone)..................................................................................................................... 55
Cancer Risk Levels and Exposure Ratios for the Residential Exposure Scenario (Off-site
Sources Alone)..................................................................................................................... 56
Cancer Risk Levels and Exposure Ratios for the Workplace Exposure Scenario (Both TPIA
& Off-site Sources Combined) ............................................................................................ 59
Cancer Risk Levels and Exposure Ratios for the Residential Exposure Scenario (Both TPIA
& Off-site Sources Combined) ............................................................................................ 61
Maximum Predicted One-hour CO Concentrations From TPIA Sources Alone (µg/m3) ... 68
Concentration Ratios for Maximum Predicted One-hour CO Concentrations From TPIA
Alone.................................................................................................................................... 69
Maximum Predicted One-hour CO Concentrations From Off-site Sources Only................ 70
Concentration Ratios for Maximum Predicted One-hour CO Concentrations From Off-site
Sources Only........................................................................................................................ 70
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September 10, 2004
List of Tables
(Continued)
Page
Table 22
Table 23
Table 24
Table 25
Table 26
Table 27
Table 28
Table 29
Table 30
Table 31
Table 32
Table 33
Table 34
Table 35
Table 36
Table 37
Table 38
Table 39
Table 40
Table 41
Table 42
Table 43
Table 44
Table 45
Table 46
Predicted Maximum One-hour CO Concentrations From TPIA and Off-site Sources
Combined (µg/m3) ............................................................................................................... 71
Concentration Ratios for Maximum Predicted One-hour CO Concentrations From TPIA and
Off-site Sources Combined (µg/m3) .................................................................................... 72
Predicted 8-hour Concentrations and CR Values at Location of Maximum Off-site
Concentration....................................................................................................................... 73
Annual Average CO Concentrations ................................................................................... 73
Ambient Air Quality Criteria and Measured CO Levels of CO in 2000 .............................. 74
Predicted Maximum One-hour Concentrations of NOx From TPIA Alone (µg/m3) ............ 78
Predicted Maximum One-hour Concentration Ratios for NO2 From TPIA Sources Alone 78
Predicted Annual Average for NOx at Location of Maximum Concentrations - TPIA
Sources Alone ...................................................................................................................... 79
Predicted Maximum One-hour NOx Concentration From Off-site Sources Alone .............. 80
Predicted Maximum One-hour NO2 Concentration Ratios From Off-site Sources Alone... 80
Predicted Annual Average Concentration Ratios From Off-site Sources Alone.................. 80
Predicted Maximum One-hour NOx Concentrations From Both TPIA and Off-site Sources
Combined (µg/m3) ............................................................................................................... 81
Predicted Maximum One-hour NO2 Concentration Ratios From TPIA and Off-site Sources
Combined............................................................................................................................. 81
Predicted Annual Average Concentration Ratios for NOx/NO2 ) From TPIA and Off-site
Sources Combined ............................................................................................................... 82
Ambient Air Quality Criteria and Measured Levels of NO2 and NOx in 2000 .................... 83
Maximum Predicted One-hour SO2 Concentrations From TPIA Sources Alone (µg/m3).... 87
Concentration Ratios for Maximum Predicted One-hour SO2 Concentrations From TPIA
Sources Alone ...................................................................................................................... 88
Maximum Predicted One-hour SO2 Concentrations From Off-site Sources Alone.............. 89
Concentration Ratios for Maximum Predicted One-hour SO2 Concentrations From Off-site
Sources Alone ...................................................................................................................... 89
Predicted Maximum One-hour SO2 Concentrations From TPIA and Off-site Sources
Combined (µg/m3) ............................................................................................................... 90
Predicted Maximum One-hour SO2 Concentration Ratios From TPIA and Off-site Sources
Combined............................................................................................................................. 90
Maximum Annual Average SO2 Concentrations.................................................................. 91
Ambient Air Quality Criterion and Measured SO2 Levels in 2000 ...................................... 91
Summary Annual Concentration Ratios for SO2 .................................................................. 92
Ambient Air Quality Criteria for PM10 and PM2.5 ................................................................ 93
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ABBREVIATIONS
≈
µ
°C
AAQC
ADME
B[a]P
BC
bw
CAEP
CARB
CAS RN
CCME
CEI
CI
CO
CoC
COHb
COPD
CR
EC
CRL
DE
DNA
DPM
EPA
ER
ERMD
FAA
FDA
GC/MS
GIS
GM
GTA
GTAA
HAPs
HD
HHRA
approximate, approximately equal to
micro (prefix meaning 1/1,000,000)
degree Celsius
Ambient Air Quality Criterion
absorption / distribution / metabolism / excretion
benzo[a]pyrene
British Columbia
body weight
Committee on Aviation Environmental Protection
California Air Resources Board
Chemical Abstract Service registry number
Canadian Council of Ministers of the Environment
Cantox Environmental Inc.
chemiions
carbon monoxide
chemical of concern
carboxyhemoglobin
chronic obstructive pulmonary disease
concentration ratio
Environment Canada
Cancer Risk Level
diesel exhaust
deoxyribonucleic acid
diesel particulate matter
Environmental Protection Agency (U.S.)
exposure ratio
Emissions Research and Measurement Department
Federal Aviation Authority (U.S.)
Food and Drug Administration (U.S.)
gas chromatography-mass spectrometry
geographic information system
geometric mean
Greater Toronto Area
Greater Toronto Airport Authority
hazardous air pollutants
heavy-duty
human health risk assessment
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September 10, 2004
ABBREVIATIONS (CONTINUED)
HNO3
H2O
hr
H2SO4
IATA
ICAO
IHD
Jet A
Jet A-1
JP-5
JP-8
kN
LD
LTO
PAH
MA
MEK
MIBK
MOE
N2
NA
NAAQO
NAPS
NAQS
NH4+
NO2
NOx
N2O
NOAEL
NTP
OEHHA
off-site source
off-site location
PAH
PM2.5
nitric acid
water
hour
sulphuric acid
International Air Transport Association
International Civil Aviation Organization
ischemic heart disease
commercial aviation jet fuel (North American formulation)
commercial aviation jet fuel (United Kingdom formulation)
high performance jet fuel (U.S. Navy formulation)
high performance jet fuel (U.S. Air Force formulation)
kilo Newtons (1,000 Newtons, a unit of force)
light-duty
landing and takeoff
polycyclic aromatic hydrocarbons
Massachusetts
methyl ethyl ketone
methyl isobutyl ketone
Ministry of the Environment (Ontario)
nitrogen gas
not applicable
National Ambient Air Quality Objective (Canada)
National Air Pollution Surveillance
National Air Quality Standard
ammonium
nitrogen dioxide
nitrogen oxides
nitrous oxide
no observable adverse effect level
National Toxicology Program (U.S.)
Office of Environmental Health Hazard Assessment (California)
Refers to air emissions from sources outside the study area
Typically refers to a location off the property of the TPIA where
maximum concentrations of TPIA air emissions were predicted; this varies
from substance to substance and from year to year
polycyclic aromatic hydrocarbon
fine particulate matter (≤2.5 µm in aerodynamic diameter)
HHRA of Toronto Pearson International Airport
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ABBREVIATIONS (CONTINUED)
PM10
ppb
q1 *
RA
RfC
RfD
RWDI
SD
SO2
TCCR
TDI
TEQ
THC
TMB
TPIA
U.S.
VOC
WHO
particulate matter including fine and course fractions (≤10 µm in
aerodynamic diameter)
parts per billion
slope factor
risk assessment
reference concentration
reference dose
Rowan, William, Davies & Irwin Inc.
standard deviation
sulphur dioxide
Transparency, Clarity, Consistency and Reasonableness
tolerable daily intake
toxic equivalent quotient
total hydrocarbons
trimethybenzene
Toronto Pearson International Airport
United States
volatile organic compound
World Health Organization
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EXECUTIVE SUMMARY
Cantox Environmental Inc (CEI) was retained by Rowan Williams Davies & Irwin Inc. on behalf of the
Greater Toronto Airports Authority (GTAA) to conduct a Human Health Risk Assessment (HHRA) to
assess potential short-term and long-term adverse health effects from exposures to predicted atmospheric
chemical emissions associated with the current and future operations of the Toronto Pearson
International Airport (TPIA). This study is part of on-going work being conducted by the GTAA to
address environmental and human health issues associated with the TPIA, and to make information
available to concerned stakeholders, including the Federal Government, the Ontario Ministry of the
Environment and the public.1 The results of this study, and comments provided by stakeholders, will be
taken into consideration by the GTAA in its management of TPIA operations to minimize potential
health risks to the surrounding community.
In this HHRA, the following key questions were addressed:
1. What are the potential health risks associated with airport emissions only?
2. What difference do the incremental airport emissions make to the overall potential health risks to
the community)? 2
The HHRA undertaken by CEI investigated potential concerns related to the health of residents living
within a 7.5 km radius of the TPIA, using air dispersion modelling of the historical and predicted future
air emissions from TPIA operations for the years 2000, 2005, 2010 and 2015. Modelled emissions from
off-site sources was used for the year 2000, and assumed to remain unchanged until 2015. The air
dispersion modelling provided estimates of the ground level air concentrations of the chemicals of
concern. These estimates were used to predict exposures of people living and working in the area
surrounding the TPIA.
1
The mandate of the CEI study was to examine potential adverse human health effects only, and did not include potential
environmental effects.
2
It was not the purpose of the current study to perform a comprehensive human health risk assessment for people living in
the vicinity of the Airport. Not all sources of potential exposure to chemicals were examined, only potential exposure to
airborne chemicals of concern that may be associated with TPIA operations. Potential health risks of predicted exposure to
off-site sources of these chemicals were only addressed in order to place the potential risks of exposure to predicted
incremental Airport emissions in context (i.e., to assess the contribution of Airport emissions to potential cumulative health
effects).
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Figure 1.1 in Section 1, and the related discussion in that section, describes the study area and the
receptor locations considered (i.e., the locations in the study area where the possibility of human health
effects was examined). Risks were assessed using assumptions that represent typical exposures to
residents living in the study area as well as to people working in the study area (i.e., residential and
workplace exposures were both assessed)
This HHRA is part of a larger effort to assemble and analyze air emission data associated with current
and future TPIA operations. Specifically, this HHRA represents Phase 5 of a larger investigation.
Phases 1-3 involved air dispersion modelling exercises commissioned by the GTAA and performed by
RWDI3 to estimate airborne concentrations of chemical emissions from the TPIA alone (Phase 1), from
off-site sources only (Phase 2), and from TPIA and off-site emission sources combined (Phase 3).
Future scenarios took into account plans for expansion and reconfiguration of the TPIA as well as the
expected future operating conditions. The results of this modelling work provided predicted ground
level air concentrations of chemicals of concern at specific locations within the study area (RWDI,
2003a).
Phase 4, also conducted by RWDI for the GTAA, involved the collection of additional ambient
monitoring data at several monitoring sites around and on the TPIA property. These data were used by
RWDI for a simple comparison with the results from their predictive air dispersion models used in
Phases 1-3. They were also used by CEI in the HHRA to supplement historical monitoring data and to
provide additional guidance for the determination of chemical speciation for certain groups of
compounds (e.g., what relative amounts of specific VOCs are likely to be present as air pollutants from
aircraft emissions). Details of this additional monitoring activity are available in the Phase 4 report
(RWDI, 2003b).
Phase 5 therefore took as its starting point the modelled ground level air concentrations of chemicals and
the available data on chemical concentrations from monitoring activities, and examined the potential
human health effects of exposure to the chemicals of concern given their predicted concentrations in air.
More detailed discussion of the sources of data used in this HHRA is provided in Section 1 (discussion
of methodology) and throughout this report.
For this HHRA, chemical exposures via three pathways were considered:
3
•
air (i.e., breathing in air containing chemical contaminants);
•
surface soil and indoor dust (i.e., contact with soils or dusts contaminated with deposits of air
pollutants); and,
•
home garden produce (i.e., ingestion of produce from home gardens within the study area).
Rowan, Williams, Davies & Irwin Inc.: www.rwdi.com .
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Sources of atmospheric pollutants associated with the airport included:
•
aircraft movements (i.e., take-off, landing, taxiing and idling); and,
•
emissions generated by related or supporting operations (e.g., on-site vehicles such as trucks,
on-site electricity generation, evaporative emissions associated with fuels, and other airport
functions such as fire training exercises, etc.).
Off-site emission sources included all identifiable off-site mobile, area and fixed point sources that exist
around the perimeter of the TPIA property. Details of the emission inventories and air dispersion
modelling results are described elsewhere (RWDI, 2003a).
Summaries of the potential human health effects predicted by the HHRA results are presented in the
following Tables ES-2 and ES-3. These conclusions are discussed in greater detail in Section 4.
The risk assessment methodology applied in this HHRA employed a deterministic analysis based on
point estimate parameters (e.g., a single value for a person’s weight and a single value for the
concentration of the chemical being assessed). This is in contrast to the more complex and sophisticated
approach known as probabilistic analysis, which uses distributions of values rather than single point
values (e.g., a typical range of values for a person’s weight, or a range of chemical concentrations that
includes minimum, maximum and typical values). The deterministic approach establishes a “worstcase” estimate of potential risk by selecting either the most conservative single value or a reasonable
upper-bound value from the distribution of values for each of the relevant factors (e.g., maximum
ambient concentrations of the chemicals are selected as if these concentrations were present at all times
– a scenario that is unlikely to be realistic). The deterministic risk assessment approach is therefore
highly conservative in the sense that it would result in an overestimate of actual risks to the majority of
individuals.
The same principle applies to various other assumptions used in this risk assessment. It is common
practice to begin an investigation of potential health risks with conservative, worst-case assumptions,
primarily because a risk assessment based on more realistic assumptions requires the development of
detailed data, which entails significant time and resources. If a risk assessment based on conservative,
“worst-case” assumptions indicates no concerns for adverse health impacts, a strong argument can be
made that there are in fact no health risks.
The above considerations have important implications for the interpretation of the results of this HHRA.
Given the conservatism of the methodology, negative results (no predicted health effects) suggest that
real health risks are very unlikely. Positive results (i.e., exceedances of a given exposure or
concentration conservatively considered to be “safe”) do not necessarily suggest that there are actual
risks, but rather, they identify potential health effect issues that require further, more detailed
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investigation. This is particularly true where results indicate only marginal exceedances of limits
conservatively considered to be “safe”. In such cases, further professional interpretation of the available
data and consideration of the conservativeness of the various assumptions can lead to the conclusion that
adverse health effects are very unlikely, even if exposures or concentrations may exceed a highly
conservative limit. Overall, this risk assessment approach permits the efficient use of limited resources
to examine issues of concern, rather than expend resources on issues where even a cursory examination
can establish that adverse health effects are extremely unlikely.
The HHRA for the TPIA involved two different types of assessments of potential human health impacts
for different chemicals and chemical groups. A more detailed discussion of this key methodological
distinction is presented in Section 1 (Background and Methodology). The first group of chemicals can
be referred to as “systemic” chemicals, since they can produce adverse health effects at specific
locations within the body once they have entered the body through one of various possible pathways.
Generally, the effect of these chemicals is not dependent upon the pathway of exposure. For this
HHRA, these systemic chemicals include:
•
volatile organic compounds (VOCs, sometimes referred to as hazardous air pollutants [HAPs]4);
•
carbonyl compounds (e.g. formaldehyde, acetaldehyde)5 ; and,
•
polycyclic aromatic hydrocarbons (PAHs).
From the point of view of risk assessment methodology, there is no distinction between these three
groups: they are all assessed as systemic chemicals (in Section 2). However, different approaches were
required to identify and characterize the concentrations of each of these sub-groups of chemicals from
TPIA operations and from off-site sources.6 For this reason, the three different sub-groups have been
specified.
4
Since the focus of this study is on VOCs that have toxic potential, the VOCs examined fall into the category of HAPs.
It should be noted that the term HAPs refers to a class of pollutants that includes many VOCs but also non-VOCs.
5
Carbonyl compounds belong to the category of VOCs; however, a different methodology was required to estimate groundlevel concentrations for these compounds, so they were examined separately.
6
Off-site sources of carbonyls, in fact, could not be characterized individually based on available data.
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A different risk assessment methodology was applied to a second group of chemicals that can be
referred to as “point-of-contact” chemicals, since their ability to cause adverse health effects lies mainly
in their effect at the location of exposure, usually an irritant effect upon the lining of the lungs. For this
HHRA, these point-of-contact chemicals include:
•
carbon monoxide (CO);
•
nitrogen dioxide (NO2); and,
•
sulphur dioxide (SO2).
The outputs of the HHRA for the first group of (systemic) chemicals include Cancer Risk Levels (CRLs)
and Exposure Ratios (ERs). The outcome of the HHRA for the second group of (point-of-contact)
chemicals is a Concentration Ratio (CR) rather than an Exposure Ratio (ER). Section 1 provides more
detail regarding the different methodologies used for these distinct groups of chemicals.
The HHRA for the specific chemicals and chemical categories identified as systemic presented special
difficulties for two reasons. To assess health risks, the risks of exposure to individual chemicals (or to
surrogate chemicals that can represent larger groups of similarly acting chemicals) had to be considered.
The modelled emissions data available, however, generally included only percentage estimates of total
hydrocarbons (THC), not individual VOCs or other chemicals such as PAHs. It was therefore necessary
to use the overall concentrations of THC estimated by the air dispersion modelling to estimate
concentrations of individual VOCs, carbonyls and PAHs. This was accomplished through an analysis of
monitoring data from the following sources:
•
a comprehensive database of monitoring information supplied by the Ontario Ministry of the
Environment (MOE);
•
monitoring data from Environment Canada’s National Air Pollution Surveillance (NAPS)
programme; and,
•
information from a companion study which included an on-site and off-site monitoring
programme. (RWDI, 2003b)
A detailed presentation of the speciation of VOCs, carbonyls, PAHs, as well as the data sources used, is
presented in the appendices.
The second reason the HHRA of systemic chemicals presented difficulties was that there is no
established methodology for determining the human health risks of the specific mixture of chemicals
(especially VOCs) identified in the predicted air emissions from TPIA operations. Further discussion of
this issue is presented in Section 2.
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Two significant data gaps resulted in certain limitations regarding the HHRA for the TPIA.
a) the absence of some key data for PM10 emissions from the TPIA; and,
b) the absence of data for off-site sources of carbonyl compounds.
The most important of these was the absence of predicted emissions of PM10 for aircraft engine exhaust
and fugitive emissions from airport operations and construction activities. See Section 4.3 for further
discussion of this important air pollutant.
The other issue was the lack of information regarding off-site sources of carbonyl compounds in the
geographical area surrounding the TPIA. This meant that an analysis of the contribution of TPIA
emissions to overall health risks for this group of chemicals could not be performed. The conclusion
regarding potential adverse health effects from carbonyl compounds (including acrolein) was therefore
limited to predicted emissions of carbonyls from the TPIA alone.
The organization of the main body of the report is presented in Table ES-1. Various appendices are
attached to this report and provide detailed background information and further discussion regarding
specific issues related to this HHRA.
Table ES-1
Section 1
Section 2
Section 3
Section 4
Organization of Main Report
Description of the background and the methodologies used for this HHRA
HHRA for “systemic” chemicals: VOCs, carbonyls and PAHs
HHRA for “point-of-contact” chemicals: CO, NO2, SO2 ; Discussion of PM10 issues
Discussion of the results of Sections 2 and 3
Conclusions regarding potential adverse human health risks
Discussion of uncertainties
Tables ES-2 and ES-3 provide a brief summary of the conclusions of the risk assessments for each group
of chemicals. See Section 4 for a more detailed discussion.
Overall, the HHRA generated the following key results regarding predicted emissions from current and
future operations of the TPIA:
•
a marginal exceedance of reference concentrations for acrolein, although no health risks are
expected;
•
a marginal exceedance of reference concentrations for carbon monoxide (CO), although no
health risks are expected; and,
•
consistent exceedances of reference concentrations for NO2, with potential risks for short-term
health effects from exposure to NO2 from TPIA operations and a potential contribution to
overall health risks.
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There were no predicted health risks associated with any of the other chemicals examined. As noted
above, no conclusions regarding the potential health effects of exposure to PM10 could be established,
due to aircraft emission data limitations.
These conclusions are a summary of the results discussed in more detail in Section 4, which also
presents a detailed discussion of the degree of conservatism used in the HHRA, the degree of
uncertainty associated with the results, and a discussion of why marginal exceedances for acrolein and
CO were not thought to indicate potential health risks. The results also indicate that closer examination
of the potential for adverse human health effects from exposures to future emissions of NO2 is
warranted.
Notes to Tables ES-2 and ES-3:
7
•
Although no level of risk for carcinogens can be considered completely safe, a Cancer Risk
Level (CRL) of no more than one in a million is typically considered acceptable. (i.e., no more
than one additional cancer case for every one million persons exposed).
•
Exposure Ratio (ER) values greater than 0.2 indicate that further, more detailed assessment of
potential adverse health effects is warranted.7
•
Concentration Ratio (CR) values greater than 1 indicate that further, more detailed assessment of
potential adverse health effects is warranted.7
When a risk assessment includes all potential exposure pathways from all sources, an ER value greater than 1 would
indicate a need to examine the potential for adverse health effects in greater detail. Regulatory authorities often require
that the contribution to risk from any individual pathway should not exceed 20% of the acceptable limit (i.e., 0.2). In this
HHRA, most of the potential risk for systemic chemicals is attributed to one main exposure pathway (inhalation of indoor
and outdoor air). Therefore the more conservative value of 0.2 was used as a benchmark. This argument does not apply to
point-of-contact chemicals, where inhalation is essentially the only pathway of concern; the CR benchmark of 1 was
therefore used in these cases.
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Table ES-2
Health
Effect
Potential Health Effects from Predicted Exposure to Systemic Chemicals
Chemicals of
Concern
Contribution of TPIA Emissions to
Overall Health Risks
Risks from TPIA Emissions Alone
Cancer
VOCs
Acceptable (CRLs less than 1 in a million)8
No increase to overall health risks
predicted
Non-cancer
VOCs
No risks identified (ERs < 0.2)9
No increase to overall health risks
predicted
Cancer
Carbonyl
compounds
Non-cancer
Carbonyl
compounds
Acceptable (CRLs less than 1 in a million)
8
For acrolein, ERs up to 0.42 for worst case
scenario at three receptor locations.
However, no health risks are expected. See
discussion in Section 4.1.
For all other scenarios and locations, and for
all other carbonyls assessed, no risks were
identified (ERs < 0.2)9
Insufficient data to assess health risks
from TPIA and off-site sources
combined
Insufficient data to assess health risks
from TPIA and off-site sources
combined
Cancer
PAHs10
Acceptable (CRLs less than 1 in a million) 8
No increase to overall health risks
predicted
Non-cancer
PAHs
No risks identified (ERs < 0.2) 9
No increase to overall health risks
predicted
8
CRL values for all substances were 2 times lower to 7 orders of magnitude times lower than the 1 in a million level.
ER values for all substances (except acrolein, as discussed) were 1.4 times lower to 13 orders of magnitude times lower
than the 0.2 level.
10
Benzo[a]pyrene equivalents (surrogate for group of carcinogenic PAHs).
9
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Table ES-3 Potential Health Effects from Predicted Exposure to Point-of-Contact Chemicals
Chemicals
of
Concern
CO
NO2
SO2
11
12
13
Risks from TPIA Emissions Alone
All results except those predicted for year 2000
were below level considered safe (CR < 1).11
No health risks are expected. See discussion in
Section 4.1.
Potential health risks identified (CR > 1)12
Short-term exposures to TPIA emissions of NO2
could occasionally result in adverse health effects
for sensitive members of the population
No health risks identified (CR < 1)13
Contribution of TPIA Emissions to Overall
Health Risks
No increase to overall health risks predicted
There may be a contribution to overall health risks.
Predicted concentrations from TPIA and off-site
sources combined are marginally above the MOE 1-hr
AAQC. Contribution to these concentrations from
TPIA sources is relatively small (about 10%). As such,
there will be no increase to overall health risks. See
discussion in Section 4.2.
CR = 1.09 for “maximum off-site” location for 1-hr concentrations in the year 2000 only. CR < 1 for all 8-hr values (0.57
for 2000, about 0.4 for subsequent years). Long-term (chronic) exposures were not assessed for CO.
Maximum 1-hr concentration CRs for NO2 ranged from 3.6-5.5 for the “maximum off-site location”, from 1.3-2.8 for
locations assessed for commercial exposures, and from 0.1-1.9 for locations assessed for residential exposure (range
includes all years considered). CRs for maximum annual average concentrations were 0.56-.76 for NOx; 0.38-0.5 for
NO2.
CR ranges from 0.32 to 0.01 for all locations and years except for one value of 0.93 for “maximum off-site” location in
the year 2000. Annual average concentration CRs ranged from 0.04-0.09.
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1.0
BACKGROUND AND METHODOLOGY
1.1
Background
Cantox Environmental Inc (CEI) was retained by Rowan Williams Davies & Irwin Inc. (RWDI)14 on
behalf of the Greater Toronto Airports Authority (GTAA) to conduct a Human Health Risk Assessment
(HHRA) to assess potential short-term and long-term health impacts from exposure to predicted
atmospheric chemical emissions associated with the current and future operations of the Toronto
Pearson International Airport (TPIA). This study is part of on-going work being conducted by the
GTAA to address environmental and human health issues associated with the TPIA, and to make
information available to concerned stakeholders, including the Federal Government, the Ontario
Ministry of the Environment and the public.15 The results of this study, and comments provided by
stakeholders, will be taken into consideration by the GTAA in its management of TPIA operations to
minimize potential health risks to the surrounding community.
The following key questions were addressed in this HHRA:
1. What are the potential health risks associated with airport emissions only?
2. What difference do the incremental airport emissions make to the overall potential health risks to
the community)?16
The HHRA investigated potential concerns related to the health of residents living within a 7.5 km
radius of the TPIA, using modelled emissions of ground level chemical concentrations from normal
TPIA operations predicted for the years 2000, 2005, 2010 and 2015, and modelled emissions from offsite sources for the year 2000. The air dispersion modelling provided estimates of the ground level air
concentrations of the chemicals of concern, which were used to estimate exposures of people living and
working in the area surrounding the TPIA.
14
15
16
Rowan, Williams, Davies & Irwin Inc.: www.rwdi.com
The mandate of the CEI study was to examine potential adverse human health effects only, and did not include potential
environmental effects.
It was not the purpose of the current study to perform a comprehensive human health risk assessment for people living in
the vicinity of the Airport. Not all sources of potential exposure to chemicals were examined, only potential exposure to
airborne chemicals of concern that may be associated with TPIA operations. Potential health risks of predicted exposure
to off-site sources of these chemicals were only addressed in order to place the potential risks of exposure to predicted
incremental Airport emissions in context (i.e., to assess the contribution of Airport emissions to potential cumulative
health effects).
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Figure 1 shows the study area and the receptor locations assessed (i.e., the locations in the study area
where the possibility of human health effects were examined).
This HHRA is part of a larger effort to assemble and analyze air emission data associated with current
and future TPIA operations. Specifically, this HHRA represents Phase 5 of a larger investigation.
Phases 1-3 involved air dispersion modelling exercises commissioned by the GTAA and performed by
RWDI14 for the GTAA to estimate airborne concentrations of chemical emissions from the TPIA alone
(Phase 1), from off-site sources only (Phase 2), and from TPIA and off-site emission sources combined
(Phase 3). Future scenarios took into account plans for expansion and reconfiguration of the TPIA as
well as the expected future operating conditions. The results of this modelling work provided predicted
ground level air concentrations of chemicals of concern at specific locations within the study area.
(RDWI, 2003a).
Phase 4, also conducted by RWDI for the GTAA, involved the collection of additional ambient
monitoring data at several monitoring sites around and on the TPIA property. These data were used by
RWDI as a simple comparison with the results from their predictive air dispersion models used in
Phases 1-3. They were also used by CEI in the HHRA to supplement historical monitoring data and to
provide guidance for the determination of chemical speciation for certain groups of compounds (e.g.,
what relative amounts of specific VOCs are likely to be present as air pollutants from aircraft
emissions). Details of this additional monitoring activity are available in the Phase 4 report (RWDI,
2003b).
Phase 5 therefore took as its starting point the modelled ground level air concentrations of chemicals and
the available data on chemical concentrations from monitoring activities, and examined the potential
human health effects of exposure to the chemicals of concern given their predicted concentrations in air.
More detailed discussion of the sources of data used in this HHRA is provided in Section 1 (discussion
of methodology) and throughout this report.
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8
3
4
2
7
5
6
Receptor Location
Figure 1:
1
2
3
4
5
6
7
8
Receptor locations for this HHRA.
Squares correspond to locations in the table.
Maximum off site concentration (location not shown: varies depending on chemical)
Maximum at Hwy 427 and Dixon Road, Etobicoke
Maximum at Hotel Strip Dixon Road, Etobicoke
Longbourne Dr & Willowbridge Rd, Etobicoke
Centennial Park Rd (School), Etobicoke
Audubon Blvd, Mississauga
County Court Road, Brampton
Cattrick St., Malton
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For the systemic chemicals examined in this HHRA, chemical exposures via three pathways were
considered:
•
air (i.e., breathing air containing chemical contaminants);
•
surface soil and indoor dust (i.e., contact with soils or dusts contaminated with deposits of air
pollutants); and,
•
home garden produce (i.e., ingestion of produce from home gardens within the study area).
For the point-of-contact chemicals, only exposure via inhalation was considered.
Sources of atmospheric pollutants associated with the airport included aircraft movements (i.e., take-off,
landing, taxiing and idling), as well as emissions generated by related or supporting operations (e.g., onsite vehicles such as trucks, on-site electricity generation, evaporative emissions associated with fuels,
and other airport functions such as fire training exercises, etc.). Off-site emission sources included all
identifiable off-site mobile, area and fixed point sources that exist around the perimeter of the TPIA
property. Details of the emission inventories and modelling results are described elsewhere (RWDI,
2003a).
Recent reports and modelling programs relevant to assessing the human health impacts from airport
emissions were reviewed in designing this HHRA. An annotated bibliography of recent studies that
address airport operation and concerns for human health is available. (FAA, 2003)
The U.S. EPA has produced a series of materials useful for modelling aircraft emissions:
•
Evaluation of Air Pollution Emissions from Subsonic Commercial Jet Aircraft (U.S. EPA, 1999);
•
Aircraft Emissions Processing Program (AirportProc) (U.S. EPA, 2000b); and,
•
Example Application of Modelling Toxic Air Pollutants in Urban Areas (U.S. EPA, 2002a).
The assessment of air toxics and the health effects associated with aircraft operations and airports has
been the subject of a number of key studies with public and private support:
•
Study for Expanding the Great Lakes Emission Regional Inventory to Include Estimated
Emissions from Mobile Sources (Great Lakes Commission, 1998);
•
Addressing Community Health Concerns Around Sea Tac Airport (Washington State DOH and
U.S. EPA, March 2000);
•
Proposed Logan Airport Health Study (Massachusetts DOPH, 2002); and,
•
Select Resource Materials and Annotated Bibliography on the Topic of Hazardous Air Pollutants
(HAPs) Associated with Aircraft, Airports, and Aviation (FAA, 2003).
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In addition, emissions associated with the Chicago O’Hare Airport recently came under review with
regard to potential effects on the local communities, which requested an independent risk assessment of
and an evaluation of possible health impacts. Some of the conclusions of the studies have been made
available on the internet:
1.2
•
Preliminary risk evaluation of Mostardi-Platt Park Ridge Project data monitoring adjacent to
O’Hare Airport (City of Park Ridge, Illinois, 2000); and,
•
Preliminary study and analysis of toxic air pollutant emissions from O’Hare International
Airport and the resulting health risks created by these toxic emissions in surrounding residential
communities (City of Park Ridge, Illinois, 2000)
Methodology
The following sections provide an overview of risk assessment methodology in general, and as this
methodology was applied to the current assessment. More detailed discussion of the data sources and
approaches for estimating exposures and concentrations of individual chemical species that are members
of a chemical group (e.g., VOCs, carbonyls and PAHs) is presented in Section 2 and relevant
appendices.
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Figure 2:
1.2.1
Risk Assessment Framework
Risk Assessment Approaches for Systemic and Point-of-Contact Chemicals
A risk assessment is comprised of the four components presented in Figure 2. These components, as
they apply to this HHRA, are discussed in detail in the following sections.
The risk assessment methodology applied in this HHRA employed a deterministic analysis based on
point estimate parameters (e.g., a single value for a person’s weight and a single value for the
concentration of the chemical being assessed). This is in contrast to the more complex and sophisticated
approach known as probabilistic analysis, which uses distributions of values rather than single point
values (e.g., a typical range of values for a person’s weight, or a range of chemical concentrations that
includes minimum, maximum and typical values). The deterministic approach establishes a “worstcase” estimate of potential risk by selecting either the most conservative single value or a reasonable
upper-bound value from the distribution of values for each of the relevant factors (e.g., maximum
ambient concentrations of the chemicals are selected, as if these concentrations were present at all times
– a scenario that is unlikely to be realistic). The deterministic risk assessment approach is therefore
highly conservative in the sense that it is likely to result in an overestimate of actual risks to the majority
of individuals.
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The same principle applies to various other assumptions used in this risk assessment. It is common
practice to begin an investigation of potential health risks with conservative, worst-case assumptions,
primarily because a risk assessment based on more realistic assumptions requires the development of
detailed data, which entails significant time and resources. If a risk assessment based on conservative,
“worst-case” assumptions indicates no concerns for adverse health impacts, a strong argument can be
made that there are in fact no health risks.
The above considerations have important implications for the interpretation of the results of this HHRA.
Given the conservatism of the methodology, negative results (no predicted health effects) suggest that
real health risks are very unlikely. Positive results (i.e., exceedances of a given exposure or
concentration conservatively considered to be “safe”) do not necessarily suggest that there are actual
risks, but rather, they identify potential health effect issues that require further, more detailed
investigation. This is particularly true where results indicate only marginal exceedances of limits
conservatively considered to be “safe”. In such cases, further professional interpretation of the available
data and consideration of the conservativeness of the various assumptions can lead to the conclusion that
adverse health effects are very unlikely, even if exposures or concentrations may exceed a highly
conservative limit.
The HHRA for the TPIA involved two different types of assessments of potential human health impacts
for different chemicals and chemical groups. The first group of chemicals can be referred to as
“systemic” chemicals, since they can produce adverse health effects at specific locations within the body
once they have entered the body through one of various possible pathways. Generally, the effect of
these chemicals is not dependent upon the pathway of exposure. For this HHRA, these systemic
chemicals include:
17
18
•
volatile organic compounds (VOCs, sometimes referred to as hazardous air pollutants
[HAPs]17);
•
carbonyl compounds (e.g. formaldehyde, acetaldehyde)18 ; and,
•
polycyclic aromatic hydrocarbons (PAHs).
Since the focus of this study is on VOCs that have toxic potential, the VOCs examined fall into the category of HAPs.
It should be noted that the term HAPs refers to a class of pollutants that includes many VOCs but also non-VOCs.
Carbonyl compounds belong to the category of VOCs; however, a different methodology was required to estimate
ground-level concentrations for these compounds, so they were examined separately. See Section 2 (Emissions Data and
Exposure Concentrations).
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From the point of view of risk assessment methodology, there is no distinction between these three
groups: they are all assessed as systemic chemicals (in Section 2). However, different approaches were
required to identify and characterize the concentrations of each of these sub-groups of chemicals from
TPIA operations and from off-site sources.6 For this reason, the three different sub-groups have been
specified.
A different risk assessment methodology was applied to a second group of chemicals that can be
referred to as “point-of-contact” chemicals, since their ability to cause adverse health effects lies mainly
in their effect at the location of exposure, usually an irritant effect upon the lining of the lungs. For this
HHRA, these point-of-contact chemicals include:
•
carbon monoxide (CO);
•
nitrogen dioxide (NO2); and,
•
sulphur dioxide (SO2).
The outputs of the HHRA for the first group of (systemic) chemicals include Cancer Risk Levels (CRLs)
and Exposure Ratios (ERs). The outcome of the HHRA for the second group of (point-of-contact)
chemicals a Concentration Ratio (CR) rather than an Exposure Ratio (ER).
The HHRA for the specific chemicals and chemical categories identified as systemic chemicals
presented special difficulties in this HHRA for two reasons. To assess health risks, the risks of exposure
to individual chemicals (or to surrogate chemicals that can represent larger groups of similarly acting
chemicals) had to be considered. The emissions data available, however, generally included only
percentage estimates of total hydrocarbons (THC), not individual VOCs or other chemicals such as
PAHs. It was therefore necessary to use the overall concentrations of THC estimated by the air
dispersion modelling to estimate concentrations of individual VOCs, carbonyls and PAHs. This was
accomplished through an analysis of monitoring data from the following sources:
•
a comprehensive database of monitoring information supplied by the Ontario Ministry of the
Environment (MOE);
•
monitoring data from Environment Canada’s National Air Pollution Surveillance (NAPS)
programme; and,
•
information from a companion study which included an on-site and off-site monitoring
programme. (RWDI, 2003b)
A detailed presentation of the speciation of VOCs, carbonyls, PAHs, as well as the data sources used, is
presented in the appendices.
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The second reason the HHRA of systemic chemicals presented difficulties was that there is no
established methodology for determining the human health risks of the specific mixture of chemicals
(especially VOCs) identified in the predicted air emissions from TPIA operations. Further discussion of
this issue is presented in Section 2.
Two significant data gaps resulted in certain limitations regarding the HHRA for the TPIA:
a) the absence of data for PM10 emissions from aircraft using the TPIA; and,
b) the absence of data for off-site sources of carbonyl compounds.
The most important of these was the absence of predicted emissions of PM10 for aircraft engine exhaust
and fugitive emissions from airport operations and construction activities. See Section 4.3 for further
discussion of this important air pollutant.
The other issue was the lack of information regarding off-site sources of carbonyl compounds, which
meant that an analysis of the contribution of TPIA emissions to overall health risks for this group of
chemicals could not be performed. The conclusion regarding potential adverse health effects from
(including acrolein) was therefore limited to predicted emissions of carbonyls from the TPIA alone.
The organization of the main body of the report is presented in Table ES-1. Various detailed appendices
are attached to this report and provide detailed background information and further discussion regarding
specific issues related to this HHRA.
Potential health effects from short term exposures to systemic chemicals (the first group) are generally
not investigated in situations where typical operational air emissions from an industrial or commercial
facility are involved, since concentrations are usually well below levels associated with short term, acute
health effects.19 The portion of the HHRA that examined the potential for adverse health effects from
exposures to systemic chemicals was conducted in compliance with the risk assessment procedures
endorsed by regulatory agencies including Environment Canada, Health Canada, the Canadian Council
of Ministers of the Environment (CCME), and the United States Environmental Protection Agency (U.S.
EPA). The outputs of the HHRA for this group of chemicals included Cancer Risk Levels (CRLs) and
Exposure Ratios (ERs). See Section 1.2.5 (Risk Characterization).
A different risk assessment methodology – one typically applied to common air pollutants – was applied
to the following pollutants:
19
An exception would be in the case of an accidental spill or release, or in some occupational situations, where effects from
short term exposures (to VOCs, for example) could be considered.
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•
carbon monoxide (CO);
•
nitrogen dioxide (NO2); and,
•
sulphur dioxide (SO2).
This second group of chemicals was examined for potential adverse health effects using a different risk
assessment methodology because these chemicals are not known to cause systemic effects on the body,
but rather produce effects at point of contact (e.g., the respiratory system). The methodology used was
similar to the approach taken in previous studies throughout North America to assess the human health
risks of exposure to these common air pollutants. The outcome of this type of risk assessment is a
Concentration Ratio (CR) [rather than an Exposure Ratio (ER)], where an estimated ambient
concentration of the chemical is compared to an acceptable ambient concentration of the chemical in the
environment. See Section 1.2.5 (Risk Characterization).
The key differences between the risk assessment methodologies used to evaluate risks of exposure to
systemic and point-of-contact chemicals are:
a) how “exposures” to chemicals of concern are estimated; and,
b) how “safe levels of exposure” are determined for the chemicals of concern.
See Section 1.2.5 (Risk Characterization) for a discussion of how risks are estimated for different types
of chemicals.
1.2.2
Problem Formulation
In a risk assessment, problem formulation involves:
1. the identification of potential chemicals of concern;
2. the determination of relevant exposure scenarios and pathways; and,
3. the characterization of the site and the selection of types of receptors20 that may be exposed.
1.2.2.1
Chemicals of Concern
For this HHRA, chemicals of concern were selected based on a preliminary screening of estimated
ground level air concentrations for a variety of chemicals previously estimated or known to be
associated with aircraft emissions and airport ground operations. These chemicals include the major
pollutants that one would expect from any source of petroleum-based fuel combustion. The chemicals
and chemical groups of concern identified included:
20
In the case of an HHRA, receptors are people.
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•
volatile organic compounds (VOCs, sometimes referred to as hazardous air pollutants [HAPs]17);
•
carbonyl compounds [e.g. formaldehyde, acetaldehyde]21 ;
•
polycyclic aromatic hydrocarbons [PAHs].
•
carbon monoxide (CO);
•
nitrogen oxides (NOx) and in particular, nitrogen dioxide (NO2);
•
sulphur dioxide (SO2); and,
•
particulate matter (expressed as PM10).
1.2.2.2
Exposure Scenarios and Pathways
Exposure scenarios were prepared and impacts assessed with regard to the health of residents located at
selected points in the surrounding community where impacts might be anticipated. Potential exposures
were evaluated as either “residential” or “workplace” scenarios. The residential scenario assumed
exposures to individuals living in a residence at one of the assessed locations around the TPIA, while the
workplace scenarios evaluate exposures to adults working at one of the assessed locations directly
adjacent to the TPIA.
In the study area surrounding the TPIA, chemical exposures could occur through the following
pathways:
•
inhalation of outdoor and indoor air;
•
inhalation of airborne dusts (outdoors and indoors);
•
incidental ingestion of soils and dust;
•
dermal contact with soils and dusts; and,
•
ingestion of locally-grown foods (garden produce, beef and dairy products).
Estimated exposure concentrations of the chemicals of concern were therefore required for:
•
air;
•
surface soil and dusts; and
• home garden produce.
As one would expect from the source of the emissions and the classes of chemicals being evaluated, the
primary route of exposure proved to be indoor and outdoor air inhalation.
21
Carbonyl compounds are oxygenated species belonging to the category of VOCs, however a different methodology was
required to estimate ground-level concentrations for these compounds, so they were examined separately. See Section 2.
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1.2.2.3
Selection of Receptors and Receptor Locations
In human health risk assessment terminology, people in the study area who are potentially exposed to
the chemicals of concern are referred to as receptors. Receptors of concern in this case include people
who live and/or work near the TPIA. It is important that the criteria for selection of receptors included
in the risk assessment assure protection of not only the general population, but also individuals with a
greater likelihood of adverse health impacts as a result of higher levels of exposure or due to greater
individual susceptibility to the toxicity of the chemicals of concern. In general, the most sensitive
receptors should include:
•
female children living in nearby residences;
•
female workers;
•
individuals suffering from cardio-respiratory illnesses; and,
•
the elderly.
For the HHRA, surrogate receptors were selected throughout the communities most likely to be affected
by pollution based on dispersion modelling results. Worst-case scenarios were included, but reference
areas throughout the community provided a reasonable guide to the possibility of health impacts from
TPIA emissions.
1.2.3
Exposure Assessment
Exposure assessment involves the prediction of the rate at which receptors are exposed to chemicals of
concern; this is typically measured as milligrams of chemical per kilogram of receptor bodyweight per
day (mg/kg bw/day). Exposure is dependent on a number of factors, including:
•
environmental concentrations;
•
chemical-, site- and receptor-specific parameters which affect environmental fate and behaviour;
•
interaction between receptors and the contaminated media; and,
•
bioavailability.
Chemical exposures measured as a rate were estimated for the systemic chemicals group. For the pointof-contact chemicals the rate of exposure was not predicted; instead, predicted air concentrations of the
chemicals of concern were compared with ambient air criteria or guidelines.
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1.2.4
Hazard Assessment
The hazard assessment phase involves consideration of:
•
exposure limits and cancer potency factors recommended by regulatory agencies;
•
pharmacokinetics;
•
individual- and species-specific differences in sensitivity;
•
the identification of mechanism of action (toxicity);
•
dose-response relationships; and,
•
relevant toxic endpoints.
A detailed explanation of the exposure limits and toxicological information regarding chemicals of
concern addressed by this HHRA is provided in Appendix A. Summary reviews of accepted regulatory
toxicological exposure limits for CO (Appendix C), NO2 (Appendix D), and PM10 (Appendix E) are also
provided in the appendices. These reviews discuss the recent scientific, medical and epidemiological
literature with respect to health effects associated with urban air quality and exposure to ambient
concentrations of these common air pollutants in the urban environment.
1.2.5
Risk Characterization
For evaluating potential effects from exposures to chemicals in the “systemic” group, an Exposure Ratio
(ER) was calculated by dividing a predicted exposure by a toxicological criterion or reference
concentration. Exposures are measured as a rate, expressed in terms of the amount of the chemical the
receptor is in contact with (or ingests or inhales, depending on the media or source) per kilogram of
body weight per day (mg/kg bw/day). This rate is then compared to a reference dose (RfD) or reference
concentration (RfC), which is expressed in the same terms and represents a rate of exposure determined
to be “safe”. These reference values are determined through toxicological testing and the application of
appropriate safety factors. If the predicted exposure to the chemical of concern exceeds the reference
level, the possibility of adverse health effects cannot be eliminated, and further investigation is required
to determine whether the actual exposure falls within the safety margin built in by the use of safety
factors, or in fact represents a risk for adverse health effects.
For non-threshold-type chemicals assessed for potential cancer effects from long term exposures,
potential risks were expressed as Cancer Risk Levels (CRL). CRLs compare the estimated exposure
concentrations to a cancer potency value (determined during the hazard assessment phase).
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Assessing potential health risks for chemicals in the “point-of-contact” group involved a different
methodology that produces a Concentration Ratio (CR) as a measure of risk. The CR compares
predicted chemical concentrations in ambient media (air, soil, food) to accepted health-based regulatory
criteria for ambient chemical concentrations. “Exposure” is measured as the concentration of the
chemical of concern in the ambient air (or soil or food), and does not reflect the amount of chemical the
receptor actually comes into contact with, ingests or inhales. The regulatory criteria to which these
“exposure concentrations” are compared are also expressed as ambient chemical concentrations, and
represent levels thought to be “safe”. These safe levels are established based on chamber studies where
people are exposed to elevated concentrations of the individual air pollutants. Concentrations of the
chemicals of concern in ambient media are correlated with, but not the same as true exposures (i.e., it is
one step removed).
It is important to note that CRs are not comparable to ERs. CRs represent a comparison of the
conditions during a single time period (e.g. one-hour) against a criterion that has been developed as
protective of human health using margins of safety; however, such criteria do not specifically take into
account the actual exposure of an individual over time. Thus, the information necessary to evaluate
exposure, such as duration and frequency of pollution event(s), are not taken into account.
The concentration of common air pollutants in the ambient environment are subject to government
regulation by standards that are health-based, and that have been established to provide protection of
sensitive populations. These standards are reviewed from time to time to take into account new medical
findings. The effects of these pollutants – which include CO, NO2, SO2 – on human health can
measured by exposure to pure chemical concentrations in a clinical study. The effects of these specific
pollutants can also be inferred through their association with a combination of other common air
pollutants. This latter kind of information is available from epidemiological studies, although it is
typically difficult to attribute adverse health effects to individual air pollutants rather than to a mixture
of pollutants. In recent years, greater reliance has been put on the results of epidemiology studies to
draw conclusions regarding the associations between measures of health (e.g., hospital admission) and
ambient air quality. In this HHRA, relevant supplementary information including epidemiological
evidence has been considered in order to support the conclusions of the HHRA for CO, NO2, and SO2.
(See Appendices)
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2.0
HHRA OF VOCs, CARBONYLS AND PAHs
The objective of this Section to evaluate the potential impacts of emissions of volatile organic
compounds (VOCs), including aromatics (benzene, toluene, etc.), saturated and unsaturated
hydrocarbons (alkanes, naphthenes, alkynes, etc.), carbonyl compounds (e.g., acetaldehyde, acrolein,
formaldehyde, acetone, etc.) and polycyclic aromatic hydrocarbons (PAHs) that are expected to be
emitted during the future operations of the Toronto Pearson International Airport (TPIA). Only the
results of the HHRA for systemic chemicals are presented; a discussion of the implications of these
results for potential adverse health effects is presented in Section 4.
In this section, the term “VOC” is used in its broadest sense and includes all of the systemic chemicals
evaluated in this portion of the HHRA. Key data and results are presented during the discussion, while
numerous detailed data and results are presented in the collection of data tables placed at the end of this
section.
2.1
Predicted Emissions from TPIA and Off-site Sources
Predicted concentrations of VOC (expressed as total hydrocarbons, or THC) were estimated by RWDI
using complex emissions and air dispersion modelling. A description of the methods and results of the
procedure used to identify spatial distribution of VOC (expressed as THC) and determine expected
contributions of THC from operations at the TPIA has been presented by RWDI in their Phase 1-3
Report (RWDI, 2003a).
Conversion of THC concentrations into a profile of concentrations of individual chemical compounds –
a process called speciation – was performed by CEI using available models and data applicable to
aircraft and other operations found at airports. (See discussion below.)
Characterization of health risks associated with exposure to products of petroleum or other combustion
sources (after conversion of THC into specific chemical compounds) required three separate Phases.
Phase 1: The first step was to identify annual average ground level concentrations of chemical
emissions based on operations of the TPIA alone.
Predicted ground level chemical concentrations were modelled using EDMS software developed by the
Federal Aviation Authority (FAA) specifically for estimating impacts of pollutant emissions from
airports onto surrounding communities. This model is described in the Phase 1 to 3 Report by RWDI,
and accounts for mobile sources on the ground, evaporative emissions, various on-site activities such as
training in fire-fighting, energy generation, etc. around the TPIA facility. Dispersion of these
pollutants at the point of maximum off-site concentration, and into the surrounding community (offsite) was predicted using AERMOD (RWDI, 2003a).
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Although multiple sources were considered when modelling ground level concentrations of THC
associated with this and subsequent phases, a fundamental assumption of this health risk assessment
was to assign the primary source of emissions as aircraft. Therefore, THC concentrations expressed as
VOC in this study were directly related to aircraft operations, and more specifically to jet aircraft
turbine exhaust. Relevant aircraft operations for which emission rates of specified chemicals were
identified included:
•
parked idle;
•
taxi;
•
takeoff; and,
•
descent (landing).
Landing and take-off (LTO) cycles were prepared for many types of aircraft in use at the TPIA.
Separate emission rates for hydrocarbons (aromatics, saturated and unsaturated hydrocarbons) and
oxygenated hydrocarbons (carbonyl compounds) were assigned to all four stages of aircraft operations
that contributed to results of the EDMS model (see Appendix F for further details). The expected
changes in total aircraft exhaust emissions in future years was estimated using expected changes in
aircraft operations (frequency and volume data) as well as planned modifications in design of the TPIA
itself. For example, the establishment of new terminal facilities would not specifically change the
emissions, but it would alter the general location of sources, affecting the expected off-site
concentrations of pollutants. Emissions from the TPIA alone were modelled for the years 2000, 2005,
2010, and 2015.
Phase 2: This required the modelling and prediction of total area VOC emissions from all sources
excluding the TPIA. This was based on an emissions inventory of community sources and their
annual average distribution in a fifteen kilometre square around the TPIA facility. Estimated VOC
(expressed as THC) were modelled for a large number of stationary sources as well as very large
volumes of mobile emissions related to use of Highways 401, 427, 409, 407 and 410. This step
generated the modelled ground level concentrations of VOC within the identified area without the
contribution of emissions from the TPIA, and established the base case for all estimated emissions
using data resources for the year 2000 (RWDI, 2003a). The predicted THC levels were then speciated
by CEI to yield concentrations of individual chemicals of concern.
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Phase 3: In this phase, estimated annual ground level concentrations of combined off-site and TPIAspecific VOC in years 2000, 2005, 2010 and 2015 were prepared in order to predict the combined
impacts of emissions from both TPIA sources and off-site sources over time, using the results of the
modelling work performed in Phase 1 and Phase 2. The assumptions made and the inventories used to
characterize these emissions into the future are described in the RWDI report. (RWDI, 2003a) One
key assumption, made in conjunction with the MOE, was that the off-site emissions estimated for 2000
remained constant through 2015, although one would generally expect them to increase over time. The
relative comparison of emissions (and associated potential health effects) from the TPIA to emissions
(and potential health effects) from off-site sources, was therefore overestimated to some extent. Again,
THC levels were then speciated by CEI to yield concentrations of individual chemicals of concern.
Resources of information used to establish estimates of ground level concentrations of chemical
species at receptor locations are available in a number of appendices as described below:
•
Detailed graphical results of modelled annual average VOC concentrations for each of the three
phases are available from the figures presented in Appendix H. This appendix includes
modelling results for annual average wet and dry deposition of particulate matter for Phase 1.
•
A detailed rationale for the conversion of predicted THC for Phase 1 into VOC and PAH from
aircraft exhaust is given in Appendix F.
•
A detailed rationale for the conversion of annual average VOC concentrations described for
Phases 2 and 3 is given in Appendix B.
•
A description of the composition of jet fuels and their contribution to combustion or
evaporative emissions is discussed in Appendix G.
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Table 1
Year/Phase
2000/1a
2005/1
2010/1
2015/1
2000/2b
2000/3
2005/3
2010/3
2015/3
a
b
Predicted Total Annual VOC Concentrations (µg/m3)
Maximum
Off-site
36.12
38.3
44.88
52.55
147
150
155
160
169
#2
#3
#4
#5
#6
#7
#8
28.46
21.89
19.70
21.89
115
140
130
130
130
28.46
19.70
17.52
21.89
120
140
130
130
130
0.99
0.77
0.66
0.77
80
75
80
80
80
0.44
0.55
0.33
0.44
65
65
60
60
60
0.55
0.44
0.33
0.33
75
75
75
75
75
0.27
0.27
0.27
0.27
45
45
50
45
45
1.64
1.64
1.64
1.64
60
70
70
70
70
The total hydrocarbon (THC) concentrations predicted by RWDI for each location was converted to an equivalent total VOC concentration by applying
the US EPA-recommended conversion factor of 1.0947. Further discussion of the rationale behind this conversion can be found in Section F-2.1 of
Appendix F.
The total hydrocarbon (THC) concentrations predicted by RWDI for each location was converted to an equivalent total non-methane organic carbon
(NMOC) concentration by applying a correction factor (see Appendix B for a complete explanation of VOC speciation based on NAPS data from
Environment Canada).
For the purpose of the current assessment, it was assumed that all ambient VOC concentrations
evaluated in Phase 1 originated from jet aircraft exhaust. In 1997, the Emissions Research and
Measurement Division of Environment Canada reported on a study carried out at the MacdonaldCartier International Airport in Ottawa that detailed emissions profiles of turbine engines fuelled by
Jet A (Graham et al., 1997, Revised 2003). These emissions differ in volume and composition
according to the aircraft operation (LTO cycle). Based on operations described by GTAA staff, RWDI
prepared a composite emissions profile for emissions of chemicals from aircraft during LTO cycles
over the period of a year. This profile (accounting for 100% of the aircraft emissions) was used to
generate the approximately 12% of mass emission rate that corresponds to species of hydrocarbons
(thirty-six alkanes 2.5%, seventeen alkynes 3.9%, fifty HAPS 1.1%), and the sixteen compounds
(92.5% of mass emissions) that are constituted by oxygenated hydrocarbons or carbonyl compounds.
Similar emission profiles for jet aircraft described by U.S. EPA (e.g., Speciate 1098) apportion
approximately 32% for carbonyl and the remainder to hydrocarbon species, but these differ in some
respects from the Environment Canada profile for jet exhaust. A detailed discussion of these
differences is presented in an appendix to this document (see Appendix F).
No routine monitoring data were available for carbonyl compounds measured in the vicinity of the
TPIA (with the exception of a five-day monitoring period in August and September, 2002). For the
purposes of this assessment, all modelled estimated off-site concentrations of carbonyl compounds
were assumed to originate from the TPIA operations.
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Inspection of the annual VOC concentrations described for off-site sources (see Appendix H) clearly
shows the dominance of sources of mobile emissions as maximum concentrations are associated with
major vehicle routes (Highway 401, 427, 410, 407, 409). These concentrations were expressed as
isopleths of similar levels. Closely spaced isopleths characterize greater magnitude of predicted
concentrations that can be spatially associated.
As was the case for aircraft emissions, it was necessary to develop a method to convert total urban
VOC (expressed as total hydrocarbons) into specific compounds. A large data base of VOC chemical
speciation information was available from the Environment Canada National Air Pollution
Surveillance program. This data base provided annual average concentrations of a large number (155)
of chemicals actually monitored in the vicinity of the TPIA over the period 1993 to the present (except
during 1997) at Centennial Park in Etobicoke. A more recent data set of similar analyses is available
for another Environment Canada site located on Main Street in Brampton. Annual averages including
maximum and minimum concentrations of each VOC were determined over several years using this
database of ambient chemical information (described in Appendix B). Thus, this reference group of
VOC of known annual average concentration at the Centennial Park Road location could be used to
characterize (i.e., “fingerprint”) the modelled concentrations for other locations in the 15 kilometre
square area of interest.
The first step in this speciation process for VOCs from off-site sources was to convert a mass of
pollutant emissions defined as total hydrocarbons into a manageable number of compounds or
surrogate compound groups. As described in the rationale document (Appendix B), the initial number
of chemicals originally thought to be required for the health assessment could be reduced to a total of
twelve surrogates. The use of surrogate compounds is common practice in toxicology. Surrogate
substitution means that chemicals with similar physical and chemical properties also share
toxicological properties (a full explanation of toxicological properties of individual chemicals and
chemicals included in surrogate groups is provided in Appendix A).
Chemicals grouped under a surrogate class were arranged so their total mass contribution taken
together produced a single concentration value. This value was applied to approximate the
toxicological and human health impact of many compounds acting as one, assuming the toxicity of
each of the compounds within the surrogate group is additive in nature. The primary VOC of interest
for this assessment were those associated with fossil fuel combustion products. Only that fraction of
the VOC that would be reasonably associated with sources of fossil fuel combustion was considered
for this assessment, since these were among the key chemicals of interest as emissions from TPIA.
The twelve surrogate combustion HAPs are shown in Table 2.
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Table 2
Surrogate Compounds Assessed as Fuel Combustion Products
106-99-0
1,3-Butadiene
110-54-3
Hexane and related compounds
110-82-7
Cyclohexane and related compounds
100-42-5
Styrene
71-43-2
Benzene
108-88-3
Toluene
108-67-8
Trimethylbenzenes and related compounds
100-41-4
Ethylbenzene and related compounds
104-51-8
n-Butylbenzene and related compounds
95-47-6
Xylenes
91-20-3
Naphthalene
111-84-2
Alkane range from butane to dodecane, excluding hexane (nonane surrogate)
Annual average concentrations in micrograms per cubic meter (µg/m3) were determined for each
surrogate group at the Centennial Park Road monitoring location. These were used for purposes of
interpolation of chemical concentrations at other identified receptor locations. The stated objective of
the assessment was to determine the relative contribution of emissions from the TPIA operations to the
community, and to give the appropriate context for these emissions in comparison to other (mobile and
stationary) sources.
The speciation of VOC used for analysis of emissions from TPIA and off-site sources combined was
based on the NAPS profile (obtained from air monitoring stations in the region surrounding the TPIA),
rather than the aircraft turbine emissions. It is clear from the modelling results for the TPIA alone and
off-site sources alone that the majority of VOC emissions to which people in the surrounding
community may be exposed originate from off-site sources and not from the operations of the TPIA
itself. A precise characterization of emissions from TPIA operations from (generally similar) emissions
from mobile sources off-site was beyond the scope of this study. Since the comparative mass of
emissions from the TPIA is small, the sum of urban emissions was deemed to reflect the NAPS profile
most closely. Thus, the same mass fractions of VOC were assigned to isopleths of concentration
identified for TPIA and off-site emissions combined as had been used to calculate chemical
concentrations from off-site sources alone.
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2.2
Human Health Risk Assessment
As noted in Section 2, the four basic steps used to complete a typical human health risk assessment
include:
•
problem formulation;
•
exposure assessment;
•
toxicity assessment; and,
•
risk characterization.
2.2.1
Problem Formulation
2.2.1.1
Selection of Receptors
Potential health risks were determined for eight (8) specific locations in the area surrounding the TPIA
as shown in Figure 1. These locations included:
1.
2.
3.
4.
5.
6.
7.
8.
Maximum off-site Concentrations near TPIA
Maximum Concentrations at Highway 427 and Dixon Road in Etobicoke
Maximum Concentrations on Hotel Strip and Dixon Road in Etobicoke
Longbourne Drive and Willowbridge Road in Etobicoke
Centennial Park Road (School) in Etobicoke
Audubon Blvd. in Mississauga
County Court Road in Brampton
Cattrick Street in Malton
It should be noted that no specified location for receptor #1 is shown in Figure 1. This location refers to
a point of maximum concentration that could occur anywhere among the receptor locations shown in
Figure 1 that are off the TPIA property. The modelled receptors did not include any on-site locations
with the exception of the GTAA’s OPSIS monitoring station. Data for this location were reported
separately.
At each of these receptor locations, potential exposure scenarios were developed and potential health
impacts were evaluated for individuals working or living at the chosen locations based upon predicted
ground level airborne concentrations of the assessed chemicals.
It was not possible to consider exposures by all routes to every person (human receptor) within the area
around the TPIA who may be active at specific locations where there are predicted concentrations of
VOCs. On the other hand, it is important that the assessment is sufficiently comprehensive to ensure
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that overall risks have been adequately addressed. Accordingly, exposure scenarios were established
using a select group of receptors (i.e., representative individuals) that can be considered to be at greatest
potential risk for adverse health effects associated with VOCs. These scenarios were developed using
conservative assumptions, as discussed throughout this report. In this context, conservative is taken to
mean including the conditions of highest exposure that could be encountered by a person. The
assessment was prepared for the most adverse of conditions, and should exaggerate small effects.
For each exposure scenario, the most sensitive human receptors were considered. Characteristics of
human receptors were selected to reflect the most sensitive life stage class (sex and age group), and the
essential physical characteristics such as body weight, surface area, inhalation rate, and relative fitness.
The primary concern of this assessment was to address exposures to VOCs via inhalation. For the
current exposure scenarios, a female individual was selected for evaluation as females are typically more
sensitive to inhaled contaminants, such as VOCs, than their male counterparts. Table 3 provides an
overview of the key physical parameters used to represent each of the assessed life stages.
Table 3
Key Physical Parameters for Receptor Life Stages a
Receptor
b
Body weight (kilograms) b
Point Estimate
Mean ± SD
Point Estimate
Mean ± SD
Female Infant
(0 to 6 months of age)
2.1
2.1 ± 0.6
8.2
8.2 ± 2.9
Female Preschool Child
(>6 months to 5 years of age)
8.8
8.8 ± 2.4
16.4
16.4 ± 4.5
Female Child
(> 5 to 12 years of age)
14
14.0 ± 3.0
33.6
33.6 ± 9.3
Female Adolescent
(>12 years to 20 years of age)
14
14.0 ± 2.9
56.2
56.2 ± 10.2
14.4
14.4 ± 3.1
63.1
63.1 ± 11.8
Female Adult
(20 to 70 years of age)
a
Inhalation Rate (m3/day)b
O'Connor et al., 1997
Both inhalation and body weight have lognormal distributions in the Canadian population
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2.2.1.2
Selection of Chemicals of Concern
Chemicals of concern described in the current assessment were selected based upon the predicted
impacts of emissions from the TPIA. Particular attention has been given to the relevance of combustion
products and pollutant emissions from aircraft (emissions and operating conditions at the TPIA) and
ground operations. Currently available regulatory and acceptable aircraft-specific emission information
has been used to estimate pollutant loading at receptor locations. Table 2 lists chemicals carried forward
for evaluation as part of the human health risk assessment.
In addition to these core compounds, 6 additional groups of chemicals were added for analysis of TPIA
emissions alone based upon specific speciation of jet engine emissions. The additional chemical species
included in the assessment are listed below:
•
Acetaldehyde;
•
Acetone;
•
Acrolein (including methacrolein);
•
Benzo[a]pyrene (representing carcinogenic polyaromatic hydrocarbons);
•
Formaldehyde; and,
•
Methyl ethyl ketone.
At the request of the City of Toronto, the chemicals trichloroethylene, vinyl chloride, and
polychlorinated dioxins and furans group of compounds were added to the initial chemical list.
However, these chemicals were later removed from the final chemical list, as part of the screening
process. No emissions of these compounds were detected or predicted as a result of TPIA operations.
Detailed air dispersion modelling was conducted for overall THC levels to predict ground level airborne
vapour concentrations for VOCs predicted at distinct points surrounding the TPIA. The isopleths of
VOC concentration for all years assessed (i.e., 2000, 2005, 2010, and 2015) are included in Appendix H.
Ground level concentrations for each group of surrogate compounds were determined by interpolation of
modelled concentration isopleths of VOC using either of two methods as described in Appendix F.
Table 6, Table 8 and Table 9 provide an overview of the location- and chemical-specific data used in the
current assessment for analysis of TPIA emissions alone, off-site emissions, and both combined,
respectively. For comparison purposes, Table 7 provides an overview of the location- and chemicalspecific data for a subset of the chemicals in total VOCs (i.e., acetaldehyde, benzene, 1,3-butadiene, and
formaldehyde), based upon the US EPA 1098 fractionation profile. Only those chemicals that displayed
a significant difference in composition between the Environment Canada profile and the US EPA
fractionation profiles were selected for analysis in the current assessment.
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Meteorological data was also used by RWDI to predict wet and dry deposition of particulates at each of
these sites, which was then used to estimate potential soil and dust concentrations arising from
deposition contributions of each of the VOCs. Rainfall event frequency around the TPIA was also used
to evaluate potential wet deposition of vapour phase VOCs via rainfall vapour “scavenging” processes.
See Appendix H for a detailed discussion.
2.2.1.3
Selection of Exposure Scenarios
Exposure scenarios were selected so as to produce conservative estimates of conditions that would
demonstrate the highest incremental exposure arising from emissions from the TPIA. Each exposure
scenario evaluated seven different potential routes of exposure, based upon projected media-specific
concentrations of each of the chemicals of concern. These exposure pathways included:
•
Inhalation of Air: The release of atmospheric emissions from the TPIA will result in direct
exposure of the human population as these emissions falls to ground level. Humans will inhale
gaseous and particle-borne chemicals while indoors and out of doors.
•
Inhalation of Soils and Dusts: As air-borne chemicals, whether gaseous or particle-borne,
deposit onto soils and other surfaces, human exposure may occur through the inhalation of soils
and dusts, both indoors and outdoors. The rate of deposition depends upon local meteorological
conditions, such as wind speed and precipitation rates.
•
Ingestion of Soils and Dusts: Through typical indoor and outdoor activities which bring
receptors into contact with soil and dust, human receptors may accidentally ingest impacted soil
or dust particles. Children are typically more susceptible to this route of exposure, as they spend
more time in contact with the ground, and are more likely to put soiled articles, such as toys or
hands, into their mouths. This route of exposure may also include ingestion of soil through
inadequate washing of home-grown produce.
•
Dermal Exposure to Soils and Dusts: Through typical indoor and outdoor activities which
bring receptors into contact with soil and dust, the skin of human receptors may come in contact
impacted soil or dust particles.
•
Ingestion of Locally Grown Produce: Locally grown produce (such as vegetables and fruits
grown in backyard gardens, or wild berries growing in the vicinity) may itself pose a source of
exposure to chemicals emitted from the TPIA. As chemicals are deposited from air-borne
emissions, they may come in contact with leaves and fruit of crop plants, where they may remain
as a superficial contaminant, or actually be absorbed into the plant. Deposition of chemicals into
the soil may result in accumulation in plants through root uptake.
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As noted previously, soil (and ultimately home garden) concentrations of the VOCs were estimated
based upon wet and dry deposition. Indoor air and dust concentrations were also estimated based upon
outdoor concentrations. It is important to note that this is likely an overestimation of risk, as studies
have demonstrated that, with regard to indoor-outdoor relationships in homes, no correlation between
simultaneously measured indoor and outdoor concentrations were observed, and significantly higher
concentrations of VOCs were observed indoors versus those detected outdoors (Kim et al., 2001). As
such, emissions of VOCs from within a residence (i.e., from household supplies, carpets, furniture,
smoking, etc.) are typically considered a more significant influence on indoor VOC concentrations than
infiltration of outdoor air.
Each of the eight locations were evaluated as distinct scenarios for the current assessment. However,
based upon geography and receptor use patterns, differing sets of receptors were evaluated. These were
specified as follows:
Scenario 1
Workplace Scenario
Given the location and lack of residential housing, all exposures at the following sites were assumed to
be commercial/industrial in nature:
•
Maximum Off-Site Concentrations;
•
Maximum Concentrations at Highway 427 and Dixon Road near the TPIA; and,
•
Maximum Concentrations on Hotel Strip and Dixon Road near the TPIA.
The exposure assumptions for this scenario set are based on an expectation that a female adult worker
(considered the most sensitive of the adult receptors) works at the particular location, 8 hours per day, 5
days per week, for 50 weeks out of the year.
Scenario 2
Residential Scenario
The remaining locations were conservatively assumed to have emissions which fell onto residential
dwellings in the general area around the TPIA. To assess potential risks at these locations, exposures
were evaluated for the female preschool child for non-carcinogenic, threshold-based chemicals and a
female composite lifetime receptor for chemicals which may act through a carcinogenic mode of
toxicological action. Based upon their activity and behaviour patterns (e.g., larger inhalation rate to
bodyweight ratio, hand-to-mouth ingestion tendencies, outdoor versus indoors activity patterns, etc.), the
female preschool child is typically considered the most sensitive of all potential receptors, leading to the
highest degree of potential exposure to the VOCs under study.
Composite lifetime receptors, on the other hand, allow one to evaluate the potential impacts of long-term
exposure to specific cancer-causing compounds throughout the lifespan of an individual. To assess
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exposures to this particular type of hypothetical receptor, potential risks incurred in each of an
individual’s life stages, from birth to death (i.e., infant, preschool child, child, adolescent, and adult), are
summed to provide an overall estimation of potential cancer risk on a lifetime basis.
Table 4 provides a breakdown of the assumed time-activity patterns for each of the residential receptors,
for both summer and winter seasons, and indoor and outdoor exposure locations. Detailed data on
weekday versus weekend time-activity patterns for the child was used, where available.
Table 4
Time-activity Patterns for Residential Receptors
Receptor Activity Pattern (hours/day)
Summer/Spring/Fall
(8 months)*
Receptor
Winter
(4 months)*
References
Indoors
Outdoors
Indoors
Outdoors
Infant
(0 to 6 months)
23
1
24
0
Assumed
Toddler
(7 months to 4 years)
22
2
23.5
0.5
Assumed
Child
(5 to 11 years)
Week
ends
17
Week
days
19
Week
ends
7
Week
Days
5
Week
ends
17
Week
days
19
Week
ends
7
Week
Days
5
U.S. EPA, 1997a
Adolescent
(12 to 19 years)
21
1.5
21
1.5
U.S. EPA, 1997a
Adult
(20+ years)
21
1.5
21
1.5
U.S. EPA, 1997a
* Assumed 34 weeks of summer (243.3 days) and 17 weeks of winter (121.67 days)
Note:
The total number of hours will not add up to 24 hours/day, as the US EPA has assumed the remainder of the time is spent off-site (e.g., shopping,
errands, work, school, etc.).
Depending on the particular phase being evaluated, receptor exposures at each of these sites were
assessed for predicted chemical concentrations in the baseline year 2000, as well as 2005, 2010, and
2015. The following table provides an overview of the scenarios assessed for each phase.
Predictions of ambient background concentrations of the chemicals of concern, unrelated to emissions
from the TPIA, were only produced for the baseline year 2000. To allow a comparison between TPIA
exposure only and the combined TPIA and ambient exposures, ambient background exposures for the
year 2000 were used to represent ambient background concentrations of these chemicals in the years
2005, 2010, and 2015.
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2.2.2
Exposure Assessment
The assessment of potential occurrences of adverse effects from chemicals was based on the doseresponse concept that is fundamental to the responses of biological systems to chemicals (Filov et al.,
1979; Amdur et al., 1991). Since it is not usually practical to measure tissue or cellular concentrations
of chemicals at the actual site where the adverse response is likely to occur, these concentrations are
estimated based on either the dose of the chemical that actually enters a receptor or, more commonly, by
the concentrations in various environmental media that act as pathways for exposure. The degree of
exposure of receptors to chemicals in the environment therefore depends on the interactions of a number
of parameters, including:
•
the concentrations of chemicals in various environmental media, as determined by the magnitude
of point sources;
•
the characteristics of the chemicals of concern, which affect environmental fate and persistence
(e.g., physical-chemical properties);
•
the impact of site-specific characteristics, such as geology, geography and hydrogeology, on
chemical behaviour;
•
the physiological and behavioural characteristics of the receptors (e.g., respiration rate,
soils/dusts intake, time spent at various activities and in different environmental areas); and,
•
the various physical, chemical and biological factors that determine the bioavailability of
chemicals from various exposure pathways.
The primary objective of the exposure assessment is to predict the rate of exposure (in µg/kg body
weight/day), via a series of conservative assumptions, for each of the identified receptors to the
chemicals of concern via the various exposure scenarios and pathways identified in the problem
formulation.
2.2.3
Hazard Assessment
The toxic potency of a chemical, or the ability to produce any type of damage to the structure or function
of any part of the body, is dependent on the inherent toxicity of the chemical itself (i.e., its ability to
activate mechanisms resulting in toxicity), as well as the ability of the chemical to reach the site of
action (i.e., bioavailability). 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 person is
exposed to the chemical). For every chemical, there is a specific dose and duration of exposure
necessary to produce a toxic effect in humans (this is referred to as the "dose-response relationship" of a
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chemical). The dose-response principle is central to the risk assessment methodology. For a specific
chemical, toxicological effects are determined from experimental exposures. These include exposures
of organisms, either in the environment, from various point and non-point sources, or in the laboratory,
under controlled conditions (Doull et al., 1980; FDA, 1982). These data provide supporting evidence
for the choice of an exposure level at which no adverse effects would be expected to occur (i.e., the
toxicological criterion, expressed as µg chemical/kg body weight/day). Extrapolation factors are used to
account for interspecies and inter-individual variability of the dose-response relationship.
The development of toxicological criteria must incorporate consideration of factors which affect the
impact of a given chemical. These factors may be scenario-specific, such as variation in duration or
levels of exposure. Such adjustments insure that the toxicological criterion is derived from "realistic"
exposures representative of those occurring under practical conditions. For many chemicals, the toxic
endpoint is also dependent on the route of exposure, as exposure via different routes may impact tissues
only at the site of entry. In such a case, different toxicological criteria would be recommended for the
different routes of exposure. Toxic potency may be modified by organism-specific factors such as the
ability to resist, repair or adapt to the toxic impact, depending on the age, sex, etc., of the receptor. In
these situations, separate toxicological criteria might be used to ensure protection of sensitive subpopulations. In the final analysis, toxicological criteria for chemicals are based on a consensus opinion
and peer-reviewed by a number of experienced scientists with expertise in a wide range of scientific
disciplines.
One of the most important factors in determining exposure of target tissues to chemicals is
bioavailability, or the proportion of a chemical dose entering the blood stream following administration
via a particular route (i.e., oral, inhalation or dermal). It is inappropriate to convert exposure estimates
to absorbed doses if toxicity values (from recognized agencies) are based on administered doses. If an
exposure estimate was adjusted for bioavailability then it must be compared to an exposure limit which
is based on an absorbed dose; otherwise the estimation of potential health risk would be underestimated
since, within the scope of a health risk assessment, an absorbed dose is generally lower than an external
dose. Since most exposure limits are based on administered doses, it is not appropriate to consider
absolute bioavailability (fraction or percentage of an external dose which reaches the systemic
circulation) in the assessment of exposures in most instances. A better measure may be that of relative
bioavailability which can be determined by comparing of the extent of absorption among several routes
of exposure, forms of the same chemical, or vehicles of administration (such as food, soil, and water).
Systemic absorption of chemicals will differ according to whether the dose was received dermally,
orally or by inhalation. Also, the systemic absorption will differ whether the chemical is delivered in a
solvent vehicle, in water, in soil, in food, etc.
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It is also often necessary to consider route-to-route extrapolation when an exposure limit is not available
for the exposure route of concern and no other data (such as pharmacokinetic) is available. For
example, it is common to assess the risks posed by dermal absorption of a chemical based on the
exposure limit established for oral exposure. The systemic dose absorbed dermally is scaled to the
“equivalent” oral dose by correcting for the bioavailability of dermally-applied chemical relative to an
orally-administered dose.
For the purpose of the current assessment, the bioavailabilities described in Table 10 were employed.
Where study-specific bioavailabilities were unavailable, a bioavailability of 100% was assumed.
For each of the chemicals of concern, a toxicological assessment was conducted, involving identification
of mechanism of action and relevant toxic endpoints, and determination of receptor-specific
toxicological criteria. In many cases, such an assessment has been made by a regulatory agency, such as
Health Canada or the U.S. Environmental Protection Agency.
Two basic and quite different methods are commonly recognized by regulatory agencies for the
estimation of toxicological criteria for humans, and are applied depending on the mode of toxic action of
the compound (FDA, 1982; U.S. EPA, 1989). These are the threshold approach (or the no-observedadverse-effect levels [NOAELs] - extrapolation factor approach) and the non-threshold (or the
mathematical model-unit risk estimation approach).
The selection of the most appropriate to use in the establishment of an exposure limit depends on several
factors, including the characteristics of the relationship between level of exposure and adverse response
(i.e., the shape of the dose-response curve); and, scientific data available on the mechanism(s) by which
the chemical produces its adverse response (i.e., does the chemical cause damage to genetic material in
cells). In the case of the current assessment, all of the VOCs were evaluated as carcinogens
For chemicals with threshold-type dose-response relationships (i.e., for which NOAELs can be
determined), it is assumed, for practical purposes, that there is a threshold of exposure below which the
risk of adverse effects is essentially zero, and no adverse effects will occur. This threshold is commonly
referred to as a reference dose (RfD), a tolerable daily intake (TDI) or an allowable daily intake (ADI).
Conservative estimates of this threshold are based on an experimentally-determined NOAEL, with the
application of low-dose extrapolation factors. These factors are also called "safety factors" or
"uncertainty factors" (FDA, 1982; U.S. EPA, 1989; Health Canada, 1993), and their magnitude is
dependent on the level of confidence in the use of available data as a basis for extrapolation to the
exposure scenario of the risk assessment. This confidence is dependent on differences in species and
duration of exposure, safety of sensitive species and individuals, and the quality of available data (i.e.,
the weight of evidence of the supporting data).
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Where available, route-specific exposure limits are used to characterize the hazard of chemicals
(inhalation RfD and oral RfD). It should be noted that an inhalation RfD is analogous to an RfC, but is
reported on a µg/kg/day basis where:
RfC (µ g / m3 ) x Breathing Rate (m3 / day)
Inhalation RfD (µ g / kg / day) =
Body Weight (kg)
For the current assessment, a default breathing rate of 20µg/m3 and body weight of 70 kilograms were
assumed to allow for the conversion of an RfC to an RfD.
The mathematical model-unit risk estimation approach is based on the assumption that absolutely no risk
of the occurrence of adverse effects would only be observed when the rate of exposure or dose was zero.
This approach, generally applied to genotoxic carcinogens, yields an estimate of a cancer slope factor or
unit risk cancer potency estimate (q*). The q* may be used directly in risk characterization, to yield
predicted risks of cancer incidence in a population, or may be used to calculate a risk-specific dose
(RsD). Since, in theory, any exposure has the potential to cause damage and is accumulative over time,
the RsD specifies a dose or exposure level associated with a certain level of risk of the occurrence of an
adverse health effect; this limit is thus based on the consideration of an "acceptable" level of risk for a
given toxic endpoint. For example, the MOE has indicated that carcinogenic risk levels less than one-inone million (1 x 10-6) would be considered acceptable (MOEE, 1997a), that is, risks which are
associated with an increased risk of cancer in one person out of one million people. This is termed the
"acceptable incremental lifetime cancer risk level".
Individuals with compromised health or within sensitive life stages (e.g., pregnancy, newborn infants,
children, and the elderly) were considered in the assessment by ensuring that the selected exposure
limits for the VOC of concern were sufficiently stringent to protect such individuals under most
exposure conditions. Table 11 summarizes all the exposure limits used in the current assessment. Refer
to Appendix A for a more detailed discussion of the exposure limits used to characterize risk for the
current assessment.
Where a chemical has the potential to act under both a carcinogenic and non-carcinogenic (i.e.,
threshold) toxicological mode of action, both the cancer and non-cancer endpoints were evaluated
separately for that particular chemical of concern.
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2.2.4
Risk Characterization
The final step of the assessment is risk characterization, defined as the quantification and evaluation of
the potential health risks from exposure to chemicals present in air emissions. The risk characterization
involves the estimate, description, and evaluation of risk associated with exposure to chemicals of
concern (i.e., community exposure) by comparisons between the estimated exposure and the exposure
limit for the chemical.
Risk characterization consists of a comparison of the exposure limits (i.e., the rate of exposure that
would not produce adverse effects) against the total estimated exposure. This comparison is expressed
as an Exposure Ratio (ER) for non-carcinogenic chemicals and is calculated by dividing the predicted
exposure by the exposure limit, as indicated in the following equation:
Exposure Ratio =
Estimated Exposure (ug / kg / day)
Exposure Limit (ug / kg / day)
In the case of direct acting non-threshold carcinogenic chemicals, potential risks are expressed as a
cancer risk level (CRL), where:
CRL = Estimated Exposure (ug / kg / day) x q * (ug / kg / day) − 1
1
A CRL value represents the incremental risk of cancer over a lifetime to an individual member of the
population of a given size, and is expressed as a risk level. In order to evaluate this, the CRL must be
compared to a benchmark risk level that is considered acceptable. For presentation purposes, a risk level
of 1-in-1,000,000 (i.e., 1 x 10-6), the generally accepted acceptable level of carcinogenic risk in Ontario,
is used to indicate an acceptable level of risk.
ERs and CRLs are used to express the potential adverse health effects from exposures to the selected
chemicals for several reasons:
•
to allow comparisons of potential adverse effects on health between chemicals and different
exposure scenarios (e.g., typical Ontario versus site-specific conditions);
•
to estimate potential adverse effects on health from exposures to mixtures of chemicals that act
on similar biological systems (e.g., all chemicals that cause liver toxicity, or kidney toxicity, or
respiratory tract cancers); and,
•
to simplify the presentation of the assessment results so that the reader may have a clear
understanding of these results, and an appreciation of their significance.
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Using the deterministic approach, ERs and CRLs are given as point values. The evaluation of ERs and
CRLs can be applied with greatest confidence to situations where comparisons are made between the
ERs and CRLs of two or more independent exposure scenarios. From such comparisons, the
incremental difference in the potential for occurrence of adverse health effects between the two or more
different scenarios (e.g., site versus typical Ontario) can be assessed with reasonable confidence since
the same methodologies are used in addressing each situation. Most of the uncertainties in such
comparative health assessments are related to the accuracies in estimating the concentrations in various
environmental media that affect the different exposure pathways, and in the estimation of the
toxicological criterion based on the toxic potency of the chemical. Since the assumptions used in the
estimation of an exposure limit, in various exposure modifying factors and in different hypothetical
individual characteristics, are common across scenarios that are being compared, any uncertainties in
these parameters tend to cancel between the different scenarios.
For ERs, technically, if the total exposure to a chemical is equal to or less than the toxicological
criterion, then the ER would be 1.0 or less, and no adverse health effects would be expected. For human
exposure to non-carcinogens, the toxicological criteria represent the level of total exposure, derived
from multi source and multimedia exposures, which would not result in adverse health effect, regardless
of the source or route of exposure. In cases where total exposure has been estimated, that is, from
background sources as well as from the site, it would be valid to compare the estimated exposure to the
entire exposure limit, and an acceptable ER level would be 1.0. If the risk assessment addresses risks
associated with a single source and a limited number of environmental pathways, the selection of an ER
of 1.0 as a benchmark to indicate that exposure does not exceed the toxicological criterion is not valid.
In an attempt to address this problem, the MOE has apportioned 20% of the total exposure to any one
source or pathway (MOEE, 1996). This means that the total toxicological criterion must also be
apportioned for the single source (i.e., the contaminated site) under consideration. ER values for noncarcinogens which are less than 0.20 are considered to represent a situation in which site-related
exposures account for less than 20% of the toxicological criterion, and no adverse effects are expected to
be associated with the estimated level of exposure.
CRLs, as discussed above, represent the predicted incremental risk of cancer over a lifetime to an
individual member of a population of a given size, and are expressed as a risk level. Evaluation of
predicted cancer risks for a population must also consider predicted risks for a background or “typical”
concentration of these same chemicals in the ambient environment (i.e., chemical concentrations not
attributable to the TPIA). Background or “typical” concentrations are considered to be without
unacceptable cancer risks; therefore, predicted CRLs for receptors exposed to these concentrations can
provide a valid “acceptable level” of risk, given the commonality of methods in exposure and risk
assessment.
CR values less than 1.0 indicate that estimated chemical concentrations are less than reference
concentrations, and thus, adverse effects would not be predicted. As this is usually a simple comparison
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between predicted and regulatory concentrations, the resulting CR values are receptor-independent (i.e.,
the same value is calculated for all receptors).
In cases where the estimated exposures or risks are less than the acceptable level, it can be concluded
that no observable adverse health effects would be expected to occur, considering the most sensitive
members of the population or the majority of the exposure scenarios considered in the assessment.
Exposures that are substantially less than the acceptable level are not considered to require reevaluation.
If exposures or risks are predicted to be within the same magnitude as the acceptable level (e.g., ER
values in the range of 10-fold less than to somewhat greater than 1.0), this would indicate situations that
may require re-evaluation of model parameters (e.g., chemical concentration estimates, exposure
parameters, and toxicological criteria) before the potential risks to health can be characterized.
Consideration must be given to the possibility of adverse health effects, but such exceedances are not
necessarily indicative of potential risks, as they may reflect overestimation of risk due to the use of
overly conservative estimates (e.g., overestimating exposures through use of maximum soil ingestion
rates). It should also be noted that exposure limits have orders of magnitude of safety factors built in,
introducing additional conservatism in the risk estimates. This procedure is followed to ensure the
predicted potential impacts on human health were not under-estimated, but also to allow an
understanding of the potential magnitude of the conservatism built into the risk estimate. The data may
be interpreted as indicating that given the conservatism of the assessment, no adverse health effects
would be expected, or this evaluation may indicate that further action (i.e., progression to a more
complex risk analysis, qualitative or quantitative analysis of uncertainties, or recommendation for
remediation) is required.
When predicted exposures or risks are greater than the acceptable level, this may indicate the potential
for adverse effects in sensitive individuals or in some of the exposure scenarios considered. Reevaluation of such ERs or CRLs is extremely important since both the exposure estimation procedures
and the toxicological criteria are based on a series of conservative assumptions, particularly when
considering the maximum point estimate from deterministic analyses. A sensitivity analysis facilitates
the re-evaluation by focussing on the proportional contribution of various parameters to the final ER or
CRL value. Once the major contributing model parameters have been identified, they can be evaluated
to assess whether health risks have been either under-estimated or grossly over-estimated. A certain
amount of over-estimation of risk is inherently built into the risk assessment process. For example, in
cases where there is considerable uncertainty in the data such as the determination of toxicological
criteria for cancer causing chemicals (e.g., arsenic), a conservative dose-response extrapolation model is
used to derive the toxicological criterion to ensure the protection of human health. The outcome of this
analyses may include recommendations regarding progressing to a probabilistic analyses, or for the need
for remedial activities.
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Exposures to more than one chemical may result in interactions of the toxicological effects; this may
result in a combined toxicity which is equal to the sum of toxicities of the individual chemicals (an
additive interaction), greater than the sum (synergism or potentiation) or less than the sum (antagonism).
In general, toxicological interactions of chemicals are dependent on the chemicals present, their mode of
action and their concentrations. Most non-additive interactions can only be demonstrated at relatively
high exposures, where clear adverse effects are observed. Such interactions have not been observed or
quantified at the relatively low rates of exposure typical of those associated with most environmental
situations (NAS, 1983; Krewski and Thomas, 1992).
For the current assessment, groups of similarly acting chemicals were considered in an additive manner,
and were combined into surrogate groupings. However, it is important to note that it would not be
appropriate to sum the estimated risks for all assessed chemicals to provide an overall expression of
cumulative risk for the VOC mixture, because many of these chemicals act under completely different
toxicological mechanisms and on different target organs and systems. To provide an accurate reflection
of overall cumulative risk, it is only valid to sum those compounds which act under similar modes of
action, or have common toxicologically-active metabolites and endpoints.
2.3
Results of the HHRA
As part of the current assessment, health risks (in the form of ERs and CRLs) related to predicted
ambient concentrations were estimated for each of the assessed scenarios. The following sections
provide the results for each Phase under consideration (i.e., TPIA alone, off-site sources alone, and both
combined). Tables of the results can be found at the end of Section 2. In these tables, any CRL values
which exceeded the 1-in-a million (1 x 10-6) risk level and ER values which exceeded the risk threshold
of 0.2 were bolded for easier reviewer identification.
2.3.1
TPIA Emissions Only
The assessment of risks related to TPIA emissions only involved the evaluation of exposures related to
emissions from the TPIA only, without any contribution from ambient background sources. Table 12
provides the ER and CRL values for each chemical of concern for the years 2000, 2005, 2010, and 2015
for the female worker at the three non-residential locations, while Table 13 provides the ER and CRL
values for the female preschool child, female adult, and female lifetime composite receptor for each of
the residential site locations.
The interpretation of these results and their significance for predicting potential health effects from
predicted exposures to TPIA emissions is presented in Section 4.
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2.3.2
Off-site Sources Only
The assessment of risks related to off-site emission sources involved the evaluation of exposures related
to airborne concentrations arising from typical ambient background sources (e.g., automobiles, trucks,
nearby industry, etc.). The concentrations for this phase do not take into account any contribution from
the TPIA. As typical ambient background VOC concentrations were only predicted for the base year
2000, risk estimates were only produced for that particular year.
Table 14 provides the ER and CRL values for each chemical of concern for the years 2000, 2005, 2010,
and 2015 for the female worker at the three non-residential locations, while Table 15 provides the ER
and CRL values for the female preschool child, female adult and female lifetime composite receptor for
each of the residential site locations.
The interpretation of these results and their significance for predicting potential health effects from
predicted exposures to TPIA emissions is presented in Section 4.
2.3.3
TPIA and Off-site Sources Combined
The assessment of risks related to TPIA and off-site emission sources combined involved the evaluation
of combined exposures related to emissions from the TPIA, in addition to airborne concentrations
arising from typical ambient background sources (e.g., automobiles, trucks, nearby industry, etc.).
Table 16 provides the ER and CRL values for each chemical of concern for the years 2000, 2005, 2010,
and 2015 for the female worker at the three non-residential locations, while Table 17 provides the ER
and CRL values for the female preschool child, female adult, and female lifetime composite receptor for
each of the residential site locations.
The interpretation of these results and their significance for predicting potential health effects from
predicted exposures to TPIA emissions is presented in Section 4.
2.4
Data Tables
In this sub-section, a number of Tables are presented that provide the detailed results of the HHRA for
systemic chemicals. The Tables are arranged in sequence according to the modelled emissions and
assessment of risks for:
1. predicted emissions from the TPIA only (Phase 1);
2. predicted emissions from off-site sources only (Phase 2); and,
3. predicted emissions from TPIA and off-site sources combined (Phase 3).
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Table 5
Predicted Annual VOC Concentrations from TPIA Sources Alone and Both TPIA
and Off-site Sources Combined (µg/m3)
Year 2000
Assessed Location
Year 2005
Ratio
TPIA
TPIA:both
Year 2010
Both
Ratio
TPIA:both
52.5
169
31.1%
15.2%
21.9
130
16.8%
130
13.5%
21.9
130
16.8%
0.66
80
0.8%
0.77
80
1.0%
0.9%
0.33
60
0.6%
0.44
60
0.7%
0.6%
0.33
75
0.4%
0.33
75
0.4%
50
0.5%
0.27
45
0.6%
0.27
45
0.6%
70
2.3%
1.6
70
2.3%
1.6
70
2.3%
Both
Ratio
TPIA
TPIA:both
Year 2015
Both
Ratio
TPIA
TPIA:both
TPIA
Both
Max Off-Site
Concentration
36.1
150
24.1%
38.3
155
24.7%
44.9
160
28.1%
Hwy 427 and Dixon
Road
28.5
140
20.4%
21.9
130
16.8%
19.7
130
Hotel Strip Dixon
Road
28.5
140
20.4%
19.7
130
15.2%
17.5
Longbourne Drive and
Willowbridge Road
0.99
75
1.3%
0.77
80
1.0%
Centennial Park
0.44
65
0.7%
0.55
60
Audubon Blvd
0.55
75
0.7%
0.44
75
County Court Road
0.27
45
0.6%
0.27
Cattrick St.
1.6
70
2.3%
1.6
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Table 6
Predicted Total Annual VOC and Speciated Chemical Concentrations from TPIA Sources Alone
Predicted Concentrations (µg/m3)
Assessed Locations
Total VOC
AcetaldeAcetone Acrolein Benzene
hyde
Benzo[a]
pyrene
Butadiene (1,3-)
Butylbenzenes
Cyclohexanes
Ethylbenzenes
Formaldehyde
Hexanes
Methyl Ethyl Ketone
Naphthalene
Nonane
Toluene
Trimethylbenzenes and
substituted alkyl benzenes
Xylenes
Year 2000
Maximum Off-site
36.1
1.33
23.3
0.646
0.0907
1.56 x 10-6
0.0600
0.0202
0.0155
0.0191
5.98
0.00723
0.0936
0.015
0.683
0.0293
0.0798
0.0441
Hwy 427 and Dixon Road
28.5
1.047
18.327
0.509
0.071
1.23 x 10-6
0.0472
0.0159
0.0122
0.0151
4.71
0.00569
0.0737
0.012
0.539
0.0231
0.0629
0.0347
-6
Hotel Strip Dixon Road
28.5
1.047
18.327
0.509
0.071
1.23 x 10
0.0472
0.0159
0.0122
0.0151
4.71
0.00569
0.0737
0.012
0.539
0.0231
0.0629
0.0347
Longbourne Drive and Willowbridge Road
0.985
0.036
0.634
0.018
0.002
4.25 x 10-8
0.00164
5.52 x 10-4
4.24 x 10-4
5.22 x 10-4
0.163
1.97 x 10-4
0.00255
4.23 x 10-4
0.0186
7.98 x 10-4
0.00218
0.00120
Centennial Park
0.438
0.016
0.282
0.008
0.001
1.89 x 10-8
7.27 x 10-4
2.45 x 10-4
1.88 x 10-4
2.32 x 10-4
0.072
8.76 x 10-5
0.00113
1.88 x 10-4
0.00828
3.55 x 10-4
9.68 x 10-4
5.34 x 10-4
Audubon Blvd
0.547
0.020
0.352
0.010
0.001
2.36 x 10-8
9.09 x 10-4
3.07 x 10-4
2.35 x 10-4
2.90 x 10-4
0.091
1.09 x 10-4
0.00142
2.35 x 10-4
0.0104
4.43 x 10-4
0.00121
6.68 x 10-4
0.001
-8
-4
1.53 x 10
-4
1.18 x 10
-4
1.45 x 10
-4
0.045
5.47 x 10
-5
-4
7.06 x 10
-4
8.70 x 10
-4
3.28 x 10
-4
County Court Road
Cattrick St.
0.274
0.010
0.176
0.005
1.18 x 10
-8
4.54 x 10
0.272
7.09 x 10
-4
0.00425
1.17 x 10
-4
-4
0.00518
2.22 x 10
7.04 x 10
-4
0.0311
0.00133
6.05 x 10
-4
0.00363
3.34 x 10-4
1.64
0.060
1.057
0.029
0.004
7.09 x 10
0.00273
9.20 x 10
0.00200
Maximum Off-site
38.3
1.41
24.7
0.685
0.0962
1.65 x 10-6
0.0636
0.0215
0.0165
0.0203
6.34
0.00766
0.0992
0.0164
0.725
0.0310
0.0847
0.0467
Hwy 427 and Dixon Road
21.9
0.806
14.1
0.392
0.0550
9.45 x 10-7
0.0363
0.0123
0.00941
0.0116
3.62
0.00438
0.0567
0.00939
0.414
0.0177
0.0484
0.0267
Hotel Strip Dixon Road
19.7
0.725
12.7
0.353
0.0495
8.51 x 10-7
0.0327
0.0110
0.00847
0.0104
3.26
0.00394
0.0510
0.00845
0.373
0.0160
0.0435
0.0240
Longbourne Drive and Willowbridge Road
0.766
0.0282
0.493
0.0137
0.00192
3.31 x 10-8
0.00127
4.29 x 10-4
3.30 x 10-4
4.06 x 10-4
0.127
1.53 x 10-4
0.00198
3.29 x 10-4
0.0145
6.21 x 10-4
0.00169
9.35 x 10-4
Centennial Park
0.547
0.0201
0.352
0.0098
0.00137
2.36 x 10-8
9.09 x 10-4
3.07 x 10-4
2.35 x 10-4
2.90 x 10-4
0.0906
1.09 x 10-4
0.00142
2.35 x 10-4
0.0104
4.43 x 10-4
0.00121
6.68 x 10-4
0.00110
1.89 x 10
-8
7.27 x 10
-4
2.45 x 10
-4
1.88 x 10
-4
2.32 x 10
-4
0.0725
8.76 x 10
-5
0.00113
1.88 x 10
-4
1.18 x 10
-8
4.54 x 10
-4
1.53 x 10
-4
1.18 x 10
-4
1.45 x 10
-4
5.47 x 10
-5
1.17 x 10
-4
-4
7.06 x 10
-4
8.70 x 10
-4
0.272
3.28 x 10
-4
0.00425
7.04 x 10
-4
7.43
0.00898
0.116
0.0193
Year 2005
Audubon Blvd
County Court Road
0.438
0.274
Cattrick St.
0.0161
0.0101
0.282
0.176
0.00783
0.00490 6.87 x 10
-4
-8
1.6
0.0604
1.06
0.0294
0.00412
7.09 x 10
0.00273
9.20 x 10
44.9
1.65
28.9
0.803
0.113
1.94 x 10-6
0.0745
0.0251
0.0193
-7
0.0453
7.09 x 10
-4
3.55 x 10
-4
0.00518
2.22 x 10
-4
0.0311
0.00133
0.00363
0.00200
0.849
0.0364
0.0992
0.0548
0.0240
0.00828
9.68 x 10
-4
5.34 x 10-4
6.05 x 10
-4
3.34 x 10-4
2010
Maximum Off-site
0.0238
Hwy 427 and Dixon Road
19.7
0.725
12.7
0.353
0.0495
8.51 x 10
0.0327
0.0110
0.00847
0.0104
3.26
0.00394
0.0510
0.00845
0.373
0.0160
0.0435
Hotel Strip Dixon Road
17.5
0.645
11.3
0.313
0.0440
7.56 x 10-7
0.0291
0.00981
0.00753
0.00928
2.90
0.00350
0.0454
0.00751
0.331
0.0142
0.0387
0.0214
Longbourne Drive and Willowbridge Road
0.657
0.0242
0.423
0.0118
0.00165
2.84 x 10-8
0.00109
3.68 x 10-4
2.82 x 10-4
3.48 x 10-4
0.109
1.31 x 10-4
0.00170
2.82 x 10-4
0.0124
5.32 x 10-4
0.00145
8.01 x 10-4
Centennial Park
0.328
0.0121
0.211
0.00588 8.24 x 10-4
1.42 x 10-8
5.45 x 10-4
1.84 x 10-4
1.41 x 10-4
1.74 x 10-4
0.0544
6.57 x 10-5
8.51 x 10-4
1.41 x 10-4
0.00621
2.66 x 10-4
7.26 x 10-4
4.01 x 10-4
0.211
0.00588 8.24 x 10
-4
1.42 x 10
-8
5.45 x 10
-4
1.84 x 10
-4
1.41 x 10
-4
1.74 x 10
-4
0.0544
6.57 x 10
-5
8.51 x 10
-4
1.41 x 10
-4
0.00621
2.66 x 10
-4
7.26 x 10
-4
4.01 x 10-4
-4
1.18 x 10
-8
4.54 x 10
-4
1.53 x 10
-4
1.18 x 10
-4
1.45 x 10
-4
0.0453
5.47 x 10
-5
7.09 x 10
-4
1.17 x 10
-4
0.00518
2.22 x 10
-4
6.05 x 10
-4
3.34 x 10-4
Audubon Blvd
0.328
0.0121
County Court Road
0.274
0.0101
0.176
0.00490 6.87 x 10
Cattrick St.
1.64
0.0604
1.06
0.0294
0.00412
7.09 x 10-8
0.00273
9.20 x 10-4
7.06 x 10-4
8.70 x 10-4
0.272
3.28 x 10-4
0.00425
7.04 x 10-4
0.0311
0.00133
0.00363
0.00200
52.5
1.93
33.8
0.940
0.132
2.27 x 10-6
0.0872
0.0294
0.0226
0.0278
8.70
0.0105
0.136
0.0225
0.994
0.0426
0.116
0.0641
-7
0.0267
2015
Maximum Off-site
Hwy 427 and Dixon Road
21.9
0.806
14.1
0.392
0.0550
9.45 x 10
0.0363
0.0123
0.00941
0.0116
3.62
0.00438
0.0567
0.00939
0.414
0.0177
0.0484
Hotel Strip Dixon Road
21.9
0.806
14.1
0.392
0.0550
9.45 x 10-7
0.0363
0.0123
0.00941
0.0116
3.62
0.00438
0.0567
0.00939
0.414
0.0177
0.0484
0.0267
Longbourne Drive and Willowbridge Road
0.766
0.0282
0.493
0.0137
0.00192
3.31 x 10-8
0.00127
4.29 x 10-4
3.30 x 10-4
4.06 x 10-4
0.127
1.53 x 10-4
0.00198
3.29 x 10-4
0.0145
6.21 x 10-4
0.00169
9.35 x 10-4
Centennial Park
0.438
0.0161
0.282
0.00783
0.00110
1.89 x 10-8
7.27 x 10-4
2.45 x 10-4
1.88 x 10-4
2.32 x 10-4
0.0725
8.76 x 10-5
0.00113
1.88 x 10-4
0.00828
3.55 x 10-4
9.68 x 10-4
5.34 x 10-4
1.42 x 10
-8
5.45 x 10
-4
1.84 x 10
-4
1.41 x 10
-4
1.74 x 10
-4
0.0544
6.57 x 10
-5
8.51 x 10
-4
0.00621
2.66 x 10
-4
7.26 x 10
-4
4.01 x 10-4
1.18 x 10
-8
4.54 x 10
-4
1.53 x 10
-4
1.18 x 10
-4
1.45 x 10
-4
0.0453
5.47 x 10
-5
7.09 x 10
-4
0.00518
2.22 x 10
-4
6.05 x 10
-4
3.34 x 10-4
0.272
3.28 x 10-4
0.00425
0.0311
0.00133
Audubon Blvd
0.328
0.0121
0.211
0.00588 8.24 x 10
-4
-4
County Court Road
0.274
0.0101
0.176
0.00490 6.87 x 10
Cattrick St.
1.64
0.0604
1.06
0.0294
a
0.00412
0.00273
9.20 x 10-4
7.06 x 10-4
8.70 x 10-4
1.41 x 10
-4
1.17 x 10
-4
7.04 x 10-4
0.00363
0.00200
The total hydrocarbon (THC) concentrations predicted by RWDI for each location were converted to an equivalent total VOC concentration by applying the US EPA-recommended conversion factor of 1.0947. Further discussion of the rationale behind this conversion can be found in Section F-2.0 of Appendix F.
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc.
September 10, 2004
Page 37
Table 7
Predicted Total Annual VOC and Select Speciated Chemical Concentrations from
TPIA Sources Alone (Using the US EPA 1098 Fractionation Profile) a
Assessed Locations
Year 2000
Max Off-Site Concentration
Hwy 427 and Dixon Road
Hotel Strip Dixon Road
Longbourne Drive and Willowbridge
Road
Centennial Park
Audubon Blvd
County Court Road
Cattrick St.
Year 2005
Max Off-Site Concentration
Hwy 427 and Dixon Road
Hotel Strip Dixon Road
Longbourne Drive and Willowbridge
Road
Centennial Park
Audubon Blvd
County Court Road
Cattrick St.
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
Total VOC
Predicted Concentrations (µg/m3)
Acetaldehyde
Benzene
Butadiene (1,3-)
Formaldehyde
36.125
28.462
28.462
1.68
1.32
1.32
0.701
0.552
0.552
0.650
0.512
0.512
5.42
4.27
4.27
0.985
0.0458
0.0191
0.0177
0.148
0.438
0.547
0.274
1.642
0.0204
0.0255
0.0127
0.0764
0.00849
0.0106
0.00531
0.0319
0.00788
0.00985
0.00493
0.0296
0.0657
0.0822
0.0411
0.246
38.315
21.894
19.705
1.78
1.02
0.92
0.743
0.425
0.382
0.690
0.394
0.355
5.75
3.29
2.96
0.766
0.0356
0.0149
0.0138
0.115
0.547
0.438
0.274
1.642
0.0255
0.0204
0.0127
0.0764
0.0106
0.00849
0.00531
0.0319
0.00985
0.00788
0.00493
0.0296
0.0822
0.0657
0.0411
0.246
September 10, 2004
Page 38
Table 7
Predicted Total Annual VOC and Select Speciated Chemical Concentrations from
TPIA Sources Alone (Using the US EPA 1098 Fractionation Profile) a
Assessed Locations
Year 2010
Max Off-Site Concentration
Hwy 427 and Dixon Road
Hotel Strip Dixon Road
Longbourne Drive and Willowbridge
Road
Centennial Park
Audubon Blvd
County Court Road
Cattrick St.
Year 2015
Max Off-Site Concentration
Hwy 427 and Dixon Road
Hotel Strip Dixon Road
Longbourne Drive and Willowbridge
Road
Centennial Park
Audubon Blvd
County Court Road
Cattrick St.
a
Total VOC
Predicted Concentrations (µg/m3)
Acetaldehyde
Benzene
Butadiene (1,3-)
Formaldehyde
44.883
19.705
17.515
2.09
0.916
0.814
0.871
0.382
0.340
0.808
0.355
0.315
6.74
2.96
2.63
0.657
0.0305
0.0127
0.0118
0.0986
0.328
0.328
0.274
1.642
0.0153
0.0153
0.0127
0.0764
0.00637
0.00637
0.00531
0.0319
0.00591
0.00591
0.00493
0.0296
0.0493
0.0493
0.0411
0.246
52.546
21.894
21.894
2.44
1.02
1.02
1.02
0.425
0.425
0.946
0.394
0.394
7.89
3.29
3.29
0.766
0.0356
0.0149
0.0138
0.115
0.438
0.328
0.274
1.642
0.0204
0.0153
0.0127
0.0764
0.00849
0.00637
0.00531
0.0319
0.00788
0.00591
0.00493
0.0296
0.0657
0.0493
0.0411
0.246
Only those chemicals which displayed a significant difference in the two speciation profiles (i.e., Environment Canada versus US EPA) were assessed using
the US EPA 1098 fractionation profile.
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
September 10, 2004
Page 39
Table 8
Assessed
Location
Predicted Total Annual VOC and Speciated Chemical Concentrations from Off-site Sources Alone
Speciated/
Total
Total NMOC
VOC
Correction
Benzene
(µg/m3)
Factor
Predicted Concentrations (µg/m3)
Butadiene
(1,3-)
Butylbenzenes
Cyclohexane Ethylbenzene
Hexanes
Naphthalene
Nonane
Styrene
Toluene
Trimethylbenzenes
Xylenes
Year 2000
Max Off-Site
Concentration
147
80.92
4.39
0.558
0.445
2.26
3.72
7.55
1.85
23.7
1.53
17.0
6.95
11.3
Hwy 427 and
Dixon Road
115
63.31
3.44
0.437
0.348
1.77
2.91
5.91
1.44
18.5
1.20
13.3
5.44
8.86
Hotel Strip Dixon
Road
120
66.06
3.59
0.456
0.363
1.84
3.04
6.16
1.51
19.3
1.25
13.9
5.67
9.24
Longbourne
Drive and
Willowbridge
Road
80
44.04
2.39
0.304
0.242
1.23
2.03
4.11
1.00
12.9
0.832
9.26
3.78
6.16
Centennial Park
65
35.78
1.94
0.247
0.197
0.998
1.65
3.34
0.816
10.5
0.676
7.53
3.07
5.01
Audubon Blvd
75
41.29
2.24
0.285
0.227
1.15
1.90
3.85
0.941
12.1
0.780
8.68
3.55
5.78
County Court
Road
45
24.77
1.35
0.171
0.136
0.691
1.14
2.31
0.565
7.25
0.468
5.21
2.13
3.47
Cattrick St.
60
33.03
1.79
0.228
0.182
0.922
1.52
3.08
0.753
9.67
0.624
6.95
2.84
4.62
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
September 10, 2004
Page 40
Table 9
Predicted Total Annual VOC and Speciated Chemical Concentrations from Both TPIA and Off-site Sources
Combined
Site Name
Speciated/
Total
Total
VOC
NMOC
(µg/m3) Correction Benzene
Factor
Predicted Concentrations (µg/m3)
Butadiene
(1,3-)
Butyl- Cyclohexan Ethylbenzen Hexane Naphthalen
Nonane
benzenes
e
e
s
e
Styrene Toluene
Trimethylbenzenes
Xylenes
Year 2000
Max Off-Site
Concentration
150
82.58
4.48
0.570
0.454
2.30
3.80
7.70
1.88
24.2
1.56
17.4
7.09
11.6
Hwy 427 and Dixon
Road
140
77.07
4.18
0.532
0.424
2.15
3.55
7.19
1.76
22.6
1.46
16.2
6.62
10.8
Hotel Strip Dixon
Road
140
77.07
4.18
0.532
0.424
2.15
3.55
7.19
1.76
22.6
1.46
16.2
6.62
10.8
Longbourne Drive and
Willowbridge Road
75
41.29
2.24
0.285
0.227
1.15
1.90
3.85
0.941
12.1
0.780
8.68
3.55
5.78
Centennial Park
65
35.78
1.94
0.247
0.197
0.998
1.65
3.34
0.816
10.5
0.676
7.53
3.07
5.01
Audubon Blvd
75
41.29
2.24
0.285
0.227
1.15
1.90
3.85
0.941
12.1
0.780
8.68
3.55
5.78
County Court Road
45
24.77
1.35
0.171
0.136
0.691
1.14
2.31
0.565
7.25
0.468
5.21
2.13
3.47
Cattrick St.
70
38.54
2.09
0.266
0.212
1.08
1.77
3.60
0.879
11.3
0.728
8.10
3.31
5.39
Max Off-Site
Concentration
155
85.33
4.63
0.589
0.469
2.381
3.93
7.96
1.95
25.0
1.61
17.9
7.33
11.9
Hwy 427 and Dixon
Road
130
71.57
3.89
0.494
0.394
1.997
3.29
6.68
1.63
21.0
1.35
15.1
6.15
10.0
Hotel Strip Dixon
Road
130
71.57
3.89
0.494
0.394
1.997
3.29
6.68
1.63
21.0
1.35
15.1
6.15
10.0
Longbourne Drive and
Willowbridge Road
80
44.04
2.39
0.304
0.242
1.229
2.03
4.11
1.00
12.9
0.832
9.26
3.78
6.16
Centennial Park
60
33.03
1.79
0.228
0.182
0.922
1.52
3.08
0.753
9.67
0.624
6.95
2.84
4.62
Audubon Blvd
75
41.29
2.24
0.285
0.227
1.15
1.90
3.85
0.941
12.1
0.780
8.68
3.55
5.78
County Court Road
50
27.53
1.49
0.190
0.151
0.768
1.27
2.57
0.628
8.06
0.520
5.79
2.36
3.85
Cattrick St.
70
38.54
2.09
0.266
0.212
1.08
1.77
3.60
0.879
11.3
0.728
8.10
3.31
5.39
Year 2005
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
September 10, 2004
Page 41
Table 9
Predicted Total Annual VOC and Speciated Chemical Concentrations from Both TPIA and Off-site Sources
Combined
Site Name
Speciated/
Total
Total
VOC
NMOC
(µg/m3) Correction Benzene
Factor
Predicted Concentrations (µg/m3)
Butadiene
(1,3-)
Butyl- Cyclohexan Ethylbenzen Hexane Naphthalen
Nonane
benzenes
e
e
s
e
Styrene Toluene
Trimethylbenzenes
Xylenes
Year 2010
Max Off-Site
Concentration
160
88.08
4.78
0.608
0.484
2.46
4.05
8.22
2.01
25.8
1.66
18.5
7.57
12.3
Hwy 427 and Dixon
Road
130
71.57
3.89
0.494
0.394
2.00
3.29
6.68
1.63
21.0
1.35
15.1
6.15
10.0
Hotel Strip Dixon
Road
130
71.57
3.89
0.494
0.394
2.00
3.29
6.68
1.63
21.0
1.35
15.1
6.15
10.0
Longbourne Drive and
Willowbridge Road
80
44.04
2.39
0.304
0.242
1.23
2.03
4.11
1.00
12.9
0.832
9.26
3.78
6.16
Centennial Park
60
33.03
1.79
0.228
0.182
0.922
1.52
3.08
0.753
9.67
0.624
6.95
2.84
4.62
Audubon Blvd
75
41.29
2.24
0.285
0.227
1.15
1.90
3.85
0.941
12.1
0.780
8.68
3.55
5.78
County Court Road
45
24.77
1.35
0.171
0.136
0.691
1.14
2.31
0.565
7.25
0.468
5.21
2.13
3.47
Cattrick St.
70
38.54
2.09
0.266
0.212
1.08
1.77
3.60
0.879
11.3
0.728
8.10
3.31
5.39
Max Off-Site
Concentration
169
93.03
5.05
0.642
0.512
2.60
4.28
8.68
2.12
27.2
1.76
19.6
7.99
13.0
Hwy 427 and Dixon
Road
130
71.57
3.89
0.494
0.394
2.00
3.29
6.68
1.63
21.0
1.35
15.1
6.15
10.0
Hotel Strip Dixon
Road
130
71.57
3.89
0.494
0.394
2.00
3.29
6.68
1.63
21.0
1.35
15.1
6.15
10.0
Longbourne Drive and
Willowbridge Road
80
44.04
2.39
0.304
0.242
1.23
2.03
4.11
1.00
12.9
0.832
9.26
3.78
6.16
Year 2015
Centennial Park
60
33.03
1.79
0.228
0.182
0.922
1.52
3.08
0.753
9.67
0.624
6.95
2.84
4.62
Audubon Blvd
75
41.29
2.24
0.285
0.227
1.15
1.90
3.85
0.941
12.1
0.780
8.68
3.55
5.78
County Court Road
45
24.77
1.35
0.171
0.136
0.691
1.14
2.31
0.565
7.25
0.468
5.21
2.13
3.47
Cattrick St.
70
38.54
2.09
0.266
0.212
1.08
1.77
3.60
0.879
11.3
0.728
8.10
3.31
5.39
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
September 10, 2004
Page 42
Table 10
Bioavailability Values for Chemicals of Concern Evaluated in the Current Assessment
BIOAVAILABILITIES (%)
COMPOUND
Oral
Reference
Inhalation
Reference
Dermal
Reference
Acetaldehyde
80
U.S. EPA, 1995a
45 - 70
Egle, 1970
1
U.S. EPA, 1995a
Acetone
100
Kalant, 1985
77
Kagan, 1924
0
Assumed
Acrolein
80
U.S. EPA, 1995a
80
Assumed
1
U.S. EPA, 1995a
Benzene
100
Park and Williams, 1953; Nomiyama and
Nomiyama, 1974a, b; Dementi, 1978;
Sabourin et al., 1987
20 - 60
Srbova et al., 1950; Nomiyama
and Nomiyama, 1974a, b;
ATSDR, 1993
1-3
Cooper and Snyder, 1988;
IARC, 1982; ATSDR, 1993
Benzo(a)pyrene group
10
Foth et al., 1988
16
Assumed
0.3 – 1.4
Van Rooij et al., 1993
Butylbenzene
100
Assumed
100
Assumed
100
Assumed
Cyclohexane
50
U.S. EPA, 1995a
61
Cavender, 1994
1
U.S. EPA, 1995a
Ethylbenzene
72 - 100
El Masry et al., 1956
50 – 80
Assumed
3
Assumed
Formaldehyde
95
Galli et al., 1983
95 – 100
Egle, 1972
1
Jeffcoat et al., 1983
Hexane
80
U.S. EPA, 1995b
50 – 80
Assumed
1
U.S. EPA, 1995a
Methyl ethyl ketone
80
ATSDR, 1992
80
Assumed
1
U.A. EPA, 1995a
60 – 75
Rahman et al., 1986; Van Rooij et al.,
1993
50 - 80
Rahman et al., 1986; Van Rooij
et al., 1993
0.3 – 1.4
Van Rooij et al., 1993
Nonane
100
Assumed
50 – 80
Assumed
3
Assumed
Styrene
95
Saueroff et al., 1976
89
Fernandez & Caperos, 1977
5
Wieczorek, 1985
Toluene
80
ATSDR, 1989
50
Antti-Poika et al., 1987
1
U.S. EPA, 1995a
3
Assumed
1
U.S. EPA, 1995a
Naphthalene
Trimethylbenzene
(1,2,4-)
Xylenes
72 - 100
El Masry et al., 1956; Climie et al., 1983
49 - 64
Bardodej and Bardodejova,
1970
80
U.S. EPA, 1995a
50 – 79
Brain and Mosier, 1980
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
September 10, 2004
Page 43
Table 11
Chemical
Summary of Exposure Limits for Human Receptors
Route
Exposure Limit
Type
Valuea
Endpoint
Study
Regulatory Agency
VOLATILE ORGANIC COMPOUNDS
Acetaldehyde
Acetone
Acrolein
Benzene
q1*
7.70 x 10-6
RfD
2.57
Inhalation
RfD
100
Oral
RfD
100
Inhalation
RfD
0.114
Oral
RfD
0.5
Inhalation
q1*
2.73 x 10-5
RfD
8.57
q1*
5.50 x 10-5
RfD
4.00
Inhalation
Oral
Nasal squamous cell carcinoma and
Woutersen and Appleman, 1984
U.S. EPA, 2003
adenocarcinoma in rats
Degeneration of olfactory epithelium Appleman et al., 1982; 1986
U.S. EPA, 2003
in rats
Not specified
Route extrapolation by U.S. EPA U.S. EPA Region 9,
Region 9
2002
Increased liver and kidney weights
American Biogenics
U.S. EPA, 1993
and nephrotoxicity
Corporation, 1986
Increase in non-neoplastic lesions in
Cassee et al., 1996
EC/HC, 2000
the nasal respiratory epithelium of
rats
Decreased survival, chronic gavage
Parent et al., 1992
U.S. EPA, 2003
rat study
Leukemia in humans
Decreased lymphocyte count in
humans
Leukemia in humans
Benzo(a) pyrene
(TEF)
Inhalation
Oral
q1*
q1*
0.0062
1.80 x 10-5
Decreased lymphocyte count in
humans
Tumours in humans and rodents
Not specified
1,3-Butadiene
Inhalation
q1*
1.05 x 10-4
Leukemia in humans
Oral
RfD
RfD
0.571
0.571
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
Ovarian atrophy in mice
Not available
Rinsky et al., 1981, 1987;
Paustenbach et al., 1993; Crump
and Allen, 1984; Crump, 1994;
U.S. EPA, 1998
Rothman et al., 1996
U.S. EPA, 2000d
Route extrapolated from
inhalation slope factor
Route extrapolated from
inhalation benchmark dose
Numerous studies
Route extrapolation in
accordance with MOE
Delzell et al., 1995; Health
Canada, 1998
NTP, 1993
Calculated from Inhalation RfC
U.S. EPA, 2000d
U.S. EPA, 2003
U.S. EPA, 2003
MOEE, 1997
MOEE, 1997; MOEE,
2000b, Pers. Comm.
U.S. EPA, 2002b
U.S. EPA, 2002b
U.S. EPA, 2002b
September 10, 2004
Page 44
Table 11
Summary of Exposure Limits for Human Receptors
Exposure Limit
Chemical
Route
Butylbenzene
(-n)
Inhalation
RfD
10
Not specified
Oral
RfD
10
Not specified
Route extrapolation by U.S.
EPA Region 6
NCEA value
Inhalation
RfD
5700
Not specified
NCEA value
Oral
RfD
5700
Not specified
Inhalation
RfD
286
Oral
Inhalation
Oral
Inhalation
RfD
q1*
RfD
RfD
100
6.65 x 10-10
200
57.1
Oral
RfD
60
Inhalation
RfD
286
Developmental toxicity in rats and
rabbits
Liver and kidney toxicity in rats
Upper respiratory tract cancer
Reduced weight gain in rats
Epithelial lesions in nasal cavities in
mice; neurotoxicity in humans
Neuropathy and atrophy in rats;
neurotoxicity in humans
Decreased fetal birth weight in mice
Oral
Inhalation
RfD
RfD
600
0.857
Route extrapolation by U.S. EPA
Region 9
Andrew et al., 1981; Hardin et
al., 1981
Wolf et al., 1956
CIIT, 1999
Til et al., 1989
Dunnick et al., 1989; Sanagi et
al., 1980
Krasavage et al., 1980; Sanagi et
al., 1980
Schwetz et al., 1991; Mast et al.,
1989
Cox et al., 1975
NTP, 1992
Oral
RfD
20
Inhalation
RfD
57.1
Oral
RfD
100
Cyclohexane
Ethylbenzene
Formaldehyde
Hexane
Methyl ethyl
ketone
Naphthalene
Nonane (alkanes
surrogate)
Type
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
Endpoint
Valuea
Decreased fetal birth weight in rats
Hyperplasia and metaplasia in
respiratory and olfactory epithelium
in mice
Decreased mean terminal body
weight in rats
Irreversible effects to nervous system
in rats
Increased liver and kidney weights in
rats
Study
Regulatory Agency
U.S. EPA Region 6,
2002
U.S. EPA Region 6,
2002
U.S. EPA Region 9,
2002
U.S. EPA Region 9,
2002
U.S. EPA, 2003
U.S. EPA, 2003
CEPA, 1999
U.S. EPA, 1990
U.S. EPA, 1993
U.S. EPA Region 9,
2002
U.S. EPA, 2003
U.S. EPA, 1993
U.S. EPA, 1998
BCL, 1980
U.S. EPA, 1998
Lund et al., 1995
MADEP, 2002
Anon, 1991; TPHCWG, 1997
MADEP, 2002
September 10, 2004
Page 45
Table 11
Chemical
Styrene
Toluene
1,2,4-Trimethylbenzene
Xylenes
a
b
Summary of Exposure Limits for Human Receptors
Route
Exposure Limit
Type
Endpoint
Valuea
Inhalation
RfD
286
Oral
RfD
200
Inhalation
RfD
114
Oral
RfD
200
Inhalation
RfD
1.70
Oral
RfD
50
Inhalation
Oral
RfD
RfD
28.6
200
Central nervous system effects in
humans
Red blood cell and liver effects in
dogs
Neurological effects in humans;
degeneration of nasal epithelium in
rats
Changes in liver and kidney weights
in rats
Not specified
Study
Regulatory Agency
Mutti et al., 1984
U.S. EPA, 1993
Quast et al., 1979
U.S. EPA, 1990
Foo et al., 1990; NTP, 1990
U.S. EPA, 2003
NTP, 1989
U.S. EPA, 1994
NCEA provisional value
U.S. EPA Region 9,
2002
U.S. EPA Region 9,
2002
U.S. EPA, 2003
U.S. EPA, 2003
Not specified
NCEA provisional value
Impaired motor coordination in rats
Decreased body weight and
increased mortality in rats
Korsak et al., 1994
NTP, 1986
The exposure limits are in units of µg/kg body weight per day for RfD values, (µg/kg body weight/day)-1 for q1* values and µg/m3 for RfC values.
Benzo[a]pyrene (and related compounds) which includes the carcinogenic PAHs was assessed using two approaches - the whole mixture method and the toxic equivalency
factor method. These methods are discussed in greater detail below. Benzo[a]pyrene (and related compounds) includes benzo(a)anthracene, benzo(b&k)fluoranthene,
benzo(g,h,i)perylene, dibenzo(a,h)chrysene, chrysene, benzo(b)chrysene, indeno(1,2,3-cd)pyrene, 2-methyl-cholanthrene, phenanthrene and benzo(a)pyrene
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
September 10, 2004
Page 46
Table 12
Cancer Risk Levels and Exposure Ratios for the Workplace Exposure Scenario (TPIA Sources Alone)
Assessed Chemicals
Predicted CRL/ER Values for a Female Worker
YEAR 2000
YEAR 2005
YEAR 2010
YEAR 2015
1,3-Butadiene
3.28 x 10-7
3.48 x 10-7
4.08 x 10-7
4.77 x 10-7
Acetaldehyde
3.74 x 10
-7
-7
-7
5.42 x 10-7
Benzene
8.93 x 10-8
9.47 x 10-8
1.11 x 10-7
1.30 x 10-7
Benzo(a)pyrene Group
3.53 x 10-10
3.74 x 10-10
4.38 x 10-10
5.13 x 10-10
-10
-10
-10
2.13 x 10-10
Site 1 – Maximum Off-site Concentrations
Cancer Risk Levels (unitless)
Formaldehyde
1.47 x 10
3.96 x 10
1.55 x 10
4.63 x 10
1.82 x 10
Exposure Ratios (unitless)
1,3-Butadiene
0.00536
0.00568
0.00666
0.00779
Acetaldehyde
0.0264
0.0280
0.0328
0.0383
Acetone
0.0119
0.0126
0.0148
0.0173
Acrolein
0.289
0.307
-4
0.360
-4
0.421
-4
7.86 x 10-4
Benzene
5.40 x 10
Cyclohexane
1.39 x 10-7
1.48 x 10-7
1.73 x 10-7
2.02 x 10-7
Ethylbenzene
3.41 x 10-6
3.62 x 10-6
4.25 x 10-6
4.96 x 10-6
-15
-15
-15
7.27 x 10-15
5.73 x 10
6.73 x 10
Formaldehyde
5.00 x 10
Hexane
6.48 x 10-6
6.86 x 10-6
8.04 x 10-6
9.41 x 10-6
Methyl Ethyl Ketone
1.67 x 10-5
1.77 x 10-5
2.07 x 10-5
2.43 x 10-5
Naphthalene
9.24 x 10-4
9.77 x 10-4
0.00115
0.00134
n-Butylbenzene
1.03 x 10
-4
1.10 x 10-4
1.28 x 10-4
1.50 x 10-4
Nonane
6.10 x 10-4
6.48 x 10-4
7.59 x 10-4
8.88 x 10-4
Toluene
1.31 x 10-5
1.39 x 10-5
1.63 x 10-5
1.90 x 10-5
0.00238
0.00253
0.00296
0.00346
Trimethylbenzene-1,2,4
Xylenes
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
7.88 x 10
-5
5.30 x 10
8.35 x 10
-5
6.21 x 10
9.79 x 10
-5
1.15 x 10-4
September 10, 2004
Page 47
Table 12
Cancer Risk Levels and Exposure Ratios for the Workplace Exposure Scenario (TPIA Sources Alone)
Assessed Chemicals
Predicted CRL/ER Values for a Female Worker
YEAR 2000
YEAR 2005
YEAR 2010
YEAR 2015
1,3-Butadiene
2.58 x 10-7
1.99 x 10-7
1.79 x 10-7
1.99 x 10-7
Acetaldehyde
2.95 x 10-7
2.26 x 10-7
2.04 x 10-7
2.26 x 10-7
-8
-8
-8
5.42 x 10-8
Site 2 – Maximum Concentrations at Highway 427 and Dixon Road
Cancer Risk Levels (unitless)
Benzene
7.03 x 10
Benzo(a)pyrene Group
2.78 x 10-10
2.14 x 10-10
1.92 x 10-10
2.14 x 10-10
Formaldehyde
1.16 x 10-10
8.89 x 10-11
7.98 x 10-11
8.89 x 10-11
1,3-Butadiene
0.00422
0.00324
0.00292
0.00324
Acetaldehyde
0.0209
0.0160
0.0144
0.0160
Acetone
0.00934
0.00720
0.00648
0.00720
Acrolein
0.228
0.176
0.158
0.176
5.42 x 10
4.87 x 10
Exposure Ratios (unitless)
-4
-4
-4
3.28 x 10-4
Benzene
4.25 x 10
Cyclohexane
1.09 x 10-7
8.43 x 10-8
7.59 x 10-8
8.43 x 10-8
-6
-6
-6
2.07 x 10-6
3.28 x 10
2.95 x 10
Ethylbenzene
2.70 x 10
Formaldehyde
3.94 x 10-15
3.03 x 10-15
2.73 x 10-15
3.03 x 10-15
Hexane
5.10 x 10-6
3.92 x 10-6
3.53 x 10-6
3.92 x 10-6
Methyl Ethyl Ketone
1.32 x 10-5
1.01 x 10-5
9.11 x 10-6
1.01 x 10-5
-4
-4
-4
5.59 x 10-4
2.07 x 10
1.86 x 10
Naphthalene
7.27 x 10
n-Butylbenzene
8.12 x 10-5
6.28 x 10-5
5.62 x 10-5
6.28 x 10-5
Nonane
4.82 x 10-4
3.70 x 10-4
3.33 x 10-4
3.70 x 10-4
Toluene
-5
-6
-6
7.91 x 10-6
Trimethylbenzene-1,2,4
Xylenes
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
1.03 x 10
0.00188
6.20 x 10
-5
5.59 x 10
7.91 x 10
0.00145
4.77 x 10
-5
5.03 x 10
7.15 x 10
0.00130
4.29 x 10
-5
0.00145
4.77 x 10-5
September 10, 2004
Page 48
Table 12
Cancer Risk Levels and Exposure Ratios for the Workplace Exposure Scenario (TPIA Sources Alone)
Assessed Chemicals
Predicted CRL/ER Values for a Female Worker
YEAR 2000
YEAR 2005
YEAR 2010
YEAR 2015
1,3-Butadiene
2.58 x 10-7
1.79 x 10-7
1.59 x 10-7
1.99 x 10-7
Acetaldehyde
2.95 x 10-7
2.04 x 10-7
1.81 x 10-7
2.26 x 10-7
-8
-8
-8
5.42 x 10-8
Site 3 – Maximum Concentrations on Hotel Strip and Dixon Road
Cancer Risk Levels (unitless)
Benzene
7.03 x 10
Benzo(a)pyrene Group
2.78 x 10-10
1.92 x 10-10
1.71 x 10-10
2.14 x 10-10
Formaldehyde
1.16 x 10-10
7.98 x 10-11
7.10 x 10-11
8.89 x 10-11
0.00422
0.00292
0.00260
0.00324
4.87 x 10
4.33 x 10
Exposure Ratios (unitless)
1,3-Butadiene
Acetaldehyde
0.0209
0.0144
0.0128
0.0160
Acetone
0.00934
0.00648
0.00577
0.00720
Acrolein
0.228
0.158
0.140
0.176
-4
-4
-4
3.28 x 10-4
Benzene
4.25 x 10
Cyclohexane
1.09 x 10-7
7.59 x 10-8
6.75 x 10-8
8.43 x 10-8
-6
-6
-6
2.07 x 10-6
2.95 x 10
2.62 x 10
Ethylbenzene
2.70 x 10
Formaldehyde
3.94 x 10-15
2.73 x 10-15
2.42 x 10-15
3.03 x 10-15
Hexane
5.10 x 10-6
3.53 x 10-6
3.14 x 10-6
3.92 x 10-6
-5
-6
-6
1.01 x 10-5
1.86 x 10
1.66 x 10
Methyl Ethyl Ketone
1.32 x 10
Naphthalene
7.27 x 10-4
5.03 x 10-4
4.47 x 10-4
5.59 x 10-4
n-Butylbenzene
8.12 x 10-5
5.62 x 10-5
5.01 x 10-5
6.28 x 10-5
Nonane
4.82 x 10-4
3.33 x 10-4
2.96 x 10-4
3.70 x 10-4
Toluene
-5
-6
-6
7.91 x 10-6
Trimethylbenzene-1,2,4
Xylenes
1.03 x 10
0.00188
6.20 x 10
-5
9.11 x 10
7.15 x 10
0.00130
4.29 x 10
-5
8.11 x 10
6.34 x 10
0.00116
3.82 x 10
-5
0.00145
4.77 x 10-5
Note: Those CRL or ER values which exceed their relevant regulatory benchmark (i.e., 1 x 10-6 and 0.2, respectively) are highlighted in bold format for ease of identification.
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
September 10, 2004
Page 49
Table 13
Risk Levels and Exposure Ratios for the Residential Exposure Scenario (TPIA Sources Alone)
YEAR 2000
Assessed Chemicals
Female
Preschool
Child
YEAR 2005
Female
Female
Female
Preschool
Adult Composite a
Child
Female
Adult
YEAR 2010
Female
Composite Preschool
Child
Female
Adult
YEAR 2015
Female
Composite Preschool
Child
Female
Adult
Female
Composite
Site 4 - Longbourne Drive and Willowbridge Road
Cancer Risk Levels (unitless)
1,3-Butadiene
Acetaldehyde
Benzene
Benzo(a)pyrene Group
Formaldehyde
8.48 x 10-9 3.76 x 10-8 6.31 x 10-8 6.57 x 10-9 2.91 x 10-8 4.89 x 10-8 5.64 x 10-9 2.50 x 10-8 4.20 x 10-8 6.57 x 10-9 2.91 x 10-8 4.89 x 10-8
9.64 x 10-9 4.27 x 10-8 7.17 x 10-8 7.49 x 10-9 3.32 x 10-8 5.57 x 10-8 6.43 x 10-9 2.85 x 10-8 4.78 x 10-8 7.49 x 10-9 3.32 x 10-8 5.57 x 10-8
2.30 x 10-9 1.02 x 10-8 1.71 x 10-8 1.79 x 10-9 7.92 x 10-9 1.33 x 10-8 1.54 x 10-9 6.81 x 10-9 1.14 x 10-8 1.79 x 10-9 7.92 x 10-9 1.33 x 10-8
9.19 x 10-12 4.08 x 10-11 6.85 x 10-11 7.08 x 10-12 3.14 x 10-11 5.26 x 10-11 6.07 x 10-12 2.69 x 10-11 4.51 x 10-11 7.16 x 10-12 3.18 x 10-11 5.33 x 10-11
3.78 x 10-12 1.67 x 10-11 2.81 x 10-11 2.94 x 10-12 1.31 x 10-11 1.49 x 10-11 2.53 x 10-12 1.12 x 10-11 1.88 x 10-11 2.94 x 10-12 1.31 x 10-11 2.19 x 10-11
Exposure Ratios (unitless)
1,3-Butadiene
Acetaldehyde
Acetone
Acrolein
Benzene
Cyclohexane
Ethylbenzene
Formaldehyde
Hexane
Methyl Ethyl Ketone
Naphthalene
n-Butylbenzene
Nonane
Toluene
Trimethylbenzene-1,2,4
Xylenes
0.00154
6.14 x 10-4
0.00758
0.00302
0.00340
0.00136
0.0828
0.0330
1.55 x 10-4 6.17 x 10-5
3.99 x 10-8 1.59 x 10-8
9.80 x 10-7 3.91 x 10-7
6.20 x 10-12 3.07 x 10-12
1.85 x 10-6 7.40 x 10-7
4.79 x 10-6 1.91 x 10-6
2.65 x 10-4 1.06 x 10-4
2.96 x 10-5 1.18 x 10-5
1.75 x 10-4 6.97 x 10-5
3.75 x 10-6 1.49 x 10-6
6.84 x 10-4 2.73 x 10-4
2.25 x 10-5 8.99 x 10-6
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
-
0.00119
4.75 x 10-4
0.00589
0.00235
0.00265
0.00105
0.0645
0.0257
1.20 x 10-4 4.79 x 10-5
3.11 x 10-8 1.24 x 10-8
7.62 x 10-7 3.04 x 10-7
4.83 x 10-12 2.39 x 10-12
1.44 x 10-6 5.75 x 10-7
3.72 x 10-6 1.48 x 10-6
2.06 x 10-4 8.21 x 10-5
2.30 x 10-5 9.18 x 10-6
1.36 x 10-4 5.43 x 10-5
2.91 x 10-6 1.16 x 10-6
5.30 x 10-4 2.11 x 10-4
1.76 x 10-5 7.00 x 10-6
-
0.00102
4.08 x 10-4
0.00505
0.00201
0.00227
9.05 x 10-4
0.0555
0.0221
1.03 x 10-4 4.12 x 10-5
2.66 x 10-8 1.06 x 10-8
6.53 x 10-7 2.60 x 10-7
4.15 x 10-12 2.05 x 10-12
1.24 x 10-6 4.93 x 10-7
3.19 x 10-6 1.27 x 10-6
1.76 x 10-4 7.03 x 10-5
1.97 x 10-5 7.87 x 10-6
1.16 x 10-4 4.64 x 10-5
2.50 x 10-6 9.96 x 10-7
4.55 x 10-4 1.81 x 10-4
1.50 x 10-5 6.00 x 10-6
-
0.00119
4.75 x 10-4
0.00589
0.00235
0.00265
0.00105
0.0645
0.0257
1.20 x 10-4 4.79 x 10-5
3.11 x 10-8 1.24 x 10-8
7.62 x 10-7 3.04 x 10-7
4.83 x 10-12 2.39 x 10-12
1.44 x 10-6 5.74 x 10-7
3.72 x 10-6 1.48 x 10-6
2.06 x 10-4 8.21 x 10-5
2.30 x 10-5 9.18 x 10-6
1.36 x 10-4 5.43 x 10-5
2.92 x 10-6 1.16 x 10-6
5.30 x 10-4 2.11 x 10-4
1.76 x 10-5 7.00 x 10-6
-
September 10, 2004
Page 50
Table 13
Risk Levels and Exposure Ratios for the Residential Exposure Scenario (TPIA Sources Alone)
YEAR 2000
Assessed Chemicals
Female
Preschool
Child
YEAR 2005
Female
Female
Female
Preschool
Adult Composite a
Child
Female
Adult
YEAR 2010
Female
Composite Preschool
Child
Female
Adult
YEAR 2015
Female
Composite Preschool
Child
Female
Adult
Female
Composite
Site 5 - Centennial Park Road (School)
Cancer Risk Levels (unitless)
1,3-Butadiene
Acetaldehyde
Benzene
Benzo(a)pyrene Group
Formaldehyde
3.76 x 10-9 1.67 x 10-8 2.80 x 10-8 4.70 x 10-9 2.08 x 10-8 3.50 x 10-8 2.82 x 10-9 1.25 x 10-8 2.10 x 10-8 3.76 x 10-9 1.67 x 10-8 2.80 x 10-8
4.28 x 10-9 1.89 x 10-8 3.18 x 10-8 5.34 x 10-9 2.36 x 10-8 3.97 x 10-8 3.21 x 10-9 1.42 x 10-8 2.39 x 10-8 4.28 x 10-9 1.89 x 10-8 3.18 x 10-8
1.02 x 10-9 4.54 x 10-9 7.62 x 10-9 1.28 x 10-9 5.65 x 10-9 9.49 x 10-9 7.68 x 10-10 3.40 x 10-9 5.71 x 10-9 1.02 x 10-9 4.54 x 10-9 7.62 x 10-9
4.16 x 10-12 1.85 x 10-11 3.11 x 10-11 5.05 x 10-12 2.24 x 10-11 3.76 x 10-11 3.03 x 10-12 1.34 x 10-11 2.26 x 10-11 4.15 x 10-12 1.85 x 10-11 3.11 x 10-11
1.68 x 10-12 7.46 x 10-12 1.25 x 10-11 2.10 x 10-12 9.31 x 10-12 1.56 x 10-11 1.26 x 10-12 5.60 x 10-12 9.38 x 10-12 1.68 x 10-12 7.46 x 10-12 1.24 x 10-11
Exposure Ratios (unitless)
1,3-Butadiene
Acetaldehyde
Acetone
Acrolein
Benzene
Cyclohexane
Ethylbenzene
Formaldehyde
Hexane
Methyl Ethyl Ketone
Naphthalene
n-Butylbenzene
Nonane
Toluene
Trimethylbenzene-1,2,4
Xylenes
6.83 x 10-4 2.72 x 10-4
0.00336
0.00134
0.00151
6.03 x 10-4
0.0369
0.0147
6.89 x 10-5 2.75 x 10-5
1.77 x 10-8 7.07 x 10-9
4.35 x 10-7 1.74 x 10-7
2.76 x 10-12 1.37 x 10-12
8.24 x 10-7 3.29 x 10-7
2.12 x 10-6 8.46 x 10-7
1.18 x 10-4 4.69 x 10-5
1.32 x 10-5 5.25 x 10-6
7.78 x 10-5 3.10 x 10-5
1.67 x 10-6 6.64 x 10-7
3.04 x 10-4 1.21 x 10-4
1.00 x 10-5 4.00 x 10-6
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
-
8.53 x 10-4 3.40 x 10-4
0.00420
0.00167
0.00189
7.53 x 10-4
0.0461
0.0184
8.58 x 10-5 3.42 x 10-5
2.22 x 10-8 8.83 x 10-9
5.44 x 10-7 2.17 x 10-7
3.45 x 10-12 1.71 x 10-12
1.03 x 10-6 4.11 x 10-7
2.67 x 10-6 1.06 x 10-6
1.47 x 10-4 5.86 x 10-5
1.64 x 10-5 6.56 x 10-6
9.77 x 10-5 3.89 x 10-5
2.08 x 10-6 8.30 x 10-7
3.80 x 10-4 1.51 x 10-4
1.25 x 10-5 5.00 x 10-6
-
5.12 x 10-4 2.04 x 10-4
0.00253
0.00101
0.00113
4.51 x 10-4
0.0277
0.0110
5.16 x 10-5 2.06 x 10-5
1.33 x 10-8 5.30 x 10-9
3.27 x 10-7 1.30 x 10-7
2.07 x 10-12 1.03 x 10-12
6.18 x 10-7 2.47 x 10-7
1.60 x 10-6 6.37 x 10-7
8.82 x 10-5 3.52 x 10-5
9.87 x 10-6 3.93 x 10-6
5.83 x 10-5 2.33 x 10-5
1.25 x 10-6 4.98 x 10-7
2.28 x 10-4 9.08 x 10-5
7.52 x 10-6 3.00 x 10-6
-
6.83 x 10-4 2.72 x 10-4
0.00336
0.00134
0.00151
6.03 x 10-4
0.0369
0.0147
6.89 x 10-5 2.75 x 10-5
1.77 x 10-8 7.06 x 10-9
4.35 x 10-7 1.74 x 10-7
2.76 x 10-12 1.37 x 10-12
8.25 x 10-7 3.29 x 10-7
2.12 x 10-6 8.46 x 10-7
1.18 x 10-4 4.69 x 10-5
1.31 x 10-5 5.24 x 10-6
7.78 x 10-5 3.10 x 10-5
1.67 x 10-6 6.65 x 10-7
3.04 x 10-4 1.21 x 10-4
1.00 x 10-5 4.00 x 10-6
-
September 10, 2004
Page 51
Table 13
Risk Levels and Exposure Ratios for the Residential Exposure Scenario (TPIA Sources Alone)
YEAR 2000
Assessed Chemicals
Female
Preschool
Child
YEAR 2005
Female
Female
Female
Preschool
Adult Composite a
Child
Female
Adult
YEAR 2010
Female
Composite Preschool
Child
Female
Adult
YEAR 2015
Female
Composite Preschool
Child
Female
Adult
Female
Composite
Site 6 - Audubon Blvd. in Mississauga
Cancer Risk Levels (unitless)
1,3-Butadiene
Acetaldehyde
Benzene
Benzo(a)pyrene Group
Formaldehyde
4.70 x 10-9 2.08 x 10-8 3.50 x 10-8 3.76 x 10-9 1.67 x 10-8 2.80 x 10-8 2.82 x 10-9 1.25 x 10-8 2.10 x 10-8 2.82 x 10-9 1.25 x 10-8 2.10 x 10-8
5.34 x 10-9 2.36 x 10-8 3.97 x 10-8 4.28 x 10-9 1.89 x 10-8 3.18 x 10-8 3.21 x 10-9 1.42 x 10-8 2.39 x 10-8 3.21 x 10-9 1.42 x 10-8 2.39 x 10-8
1.28 x 10-9 5.65 x 10-9 9.49 x 10-9 1.02 x 10-9 4.54 x 10-9 7.62 x 10-9 7.68 x 10-10 3.40 x 10-9 5.71 x 10-9 7.67 x 10-10 3.40 x 10-9 5.71 x 10-9
5.12 x 10-12 2.27 x 10-11 3.81 x 10-11 4.04 x 10-12 1.79 x 10-11 3.01 x 10-11 3.03 x 10-12 1.34 x 10-11 2.26 x 10-11 3.10 x 10-12 1.38 x 10-11 2.31 x 10-11
2.10 x 10-12 9.31 x 10-12 1.56 x 10-11 1.68 x 10-12 7.46 x 10-12 1.25 x 10-11 1.26 x 10-12 9.38 x 10-12 9.38 x 10-12 1.26 x 10-12 5.60 x 10-12 9.38 x 10-12
Exposure Ratios (unitless)
1,3-Butadiene
Acetaldehyde
Acetone
Acrolein
Benzene
Cyclohexane
Ethylbenzene
Formaldehyde
Hexane
Methyl Ethyl Ketone
Naphthalene
n-Butylbenzene
Nonane
Toluene
Trimethylbenzene-1,2,4
Xylenes
8.53 x 10-4 3.40 x 10-4
0.00420
0.00167
0.00189
7.53 x 10-4
0.0461
0.0184
8.58 x 10-5 3.42 x 10-5
2.22 x 10-8 8.83 x 10-9
5.44 x 10-7 2.17 x 10-7
3.45 x 10-12 1.71 x 10-12
1.03 x 10-6 4.11 x 10-7
2.67 x 10-6 1.06 x 10-6
1.47 x 10-4 5.86 x 10-5
1.64 x 10-5 6.56 x 10-6
9.77 x 10-5 3.89 x 10-5
2.08 x 10-6 8.30 x 10-7
3.80 x 10-4 1.51 x 10-4
1.25 x 10-5 5.00 x 10-6
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
-
6.83 x 10-4 2.72 x 10-4
0.00336
0.00134
0.00151
6.03 x 10-4
0.0369
0.0147
6.89 x 10-5 2.75 x 10-5
1.77 x 10-8 7.07 x 10-9
4.35 x 10-7 1.74 x 10-7
2.76 x 10-12 1.37 x 10-12
8.24 x 10-7 3.29 x 10-7
2.12 x 10-6 8.46 x 10-7
1.18 x 10-4 4.69 x 10-5
1.32 x 10-5 5.25 x 10-6
7.78 x 10-5 3.10 x 10-5
1.67 x 10-6 6.64 x 10-7
3.04 x 10-4 1.21 x 10-4
1.00 x 10-5 4.00 x 10-6
-
5.12 x 10-4 2.04 x 10-4
0.00253
0.00101
0.00113
4.51 x 10-4
0.0277
0.0110
5.16 x 10-5 2.06 x 10-5
1.33 x 10-8 5.30 x 10-9
3.27 x 10-7 1.30 x 10-7
2.07 x 10-12 1.03 x 10-12
6.18 x 10-7 2.47 x 10-7
1.60 x 10-6 6.37 x 10-7
8.82 x 10-5 3.52 x 10-5
9.87 x 10-6 3.93 x 10-6
5.83 x 10-5 2.33 x 10-5
1.25 x 10-6 4.98 x 10-7
2.28 x 10-4 9.08 x 10-5
7.52 x 10-6 3.00 x 10-6
-
5.12 x 10-4 2.04 x 10-4
0.00253
0.00101
0.00113
4.51 x 10-4
0.0277
0.0110
5.16 x 10-5 2.06 x 10-5
1.33 x 10-8 5.29 x 10-9
3.26 x 10-7 1.30 x 10-7
2.07 x 10-12 1.03 x 10-12
6.18 x 10-7 2.47 x 10-7
1.60 x 10-6 6.37 x 10-7
8.83 x 10-5 3.52 x 10-5
9.87 x 10-6 3.94 x 10-6
5.83 x 10-5 2.33 x 10-5
1.25 x 10-6 4.98 x 10-7
2.28 x 10-4 9.08 x 10-5
7.52 x 10-6 3.00 x 10-6
-
September 10, 2004
Page 52
Site 7 - County Court Road in Brampton
Cancer Risk Levels (unitless)
1,3-Butadiene
Acetaldehyde
Benzene
Benzo(a)pyrene Group
Formaldehyde
2.35 x 10-9 1.04 x 10-8 1.75 x 10-8 2.35 x 10-9 1.04 x 10-8 1.75 x 10-8 2.35 x 10-9 1.04 x 10-8 1.75 x 10-8 2.35 x 10-9 1.04 x 10-8 1.75 x 10-8
2.68 x 10-9 1.19 x 10-8 2.00 x 10-8 2.68 x 10-9 1.19 x 10-8 2.00 x 10-8 2.68 x 10-9 1.19 x 10-8 2.00 x 10-8 2.68 x 10-9 1.19 x 10-8 2.00 x 10-8
6.40 x 10-10 2.83 x 10-9 4.76 x 10-9 6.40 x 10-10 2.83 x 10-9 4.76 x 10-9 6.40 x 10-10 2.83 x 10-9 4.76 x 10-9 6.40 x 10-10 2.83 x 10-9 4.76 x 10-9
2.63 x 10-12 1.17 x 10-11 1.97 x 10-11 2.53 x 10-12 1.12 x 10-11 1.88 x 10-11 2.52 x 10-12 1.12 x 10-11 1.88 x 10-11 2.59 x 10-12 1.16 x 10-11 1.94 x 10-11
1.05 x 10-12 4.66 x 10-13 7.80 x 10-12 1.05 x 10-12 4.66 x 10-12 7.80 x 10-12 1.05 x 10-12 4.66 x 10-12 7.80 x 10-12 1.05 x 10-12 4.66 x 10-12 7.80 x 10-12
Exposure Ratios (unitless)
1,3-Butadiene
Acetaldehyde
Acetone
Acrolein
Benzene
Cyclohexane
Ethylbenzene
Formaldehyde
Hexane
Methyl Ethyl Ketone
Naphthalene
n-Butylbenzene
Nonane
Toluene
Trimethylbenzene-1,2,4
Xylenes
4.27 x 10-4 1.70 x 10-4
0.00211
8.41 x 10-4
-4
9.44 x 10
3.77 x 10-4
0.0231
0.00920
4.30 x 10-5 1.71 x 10-5
1.11 x 10-8 4.42 x 10-9
2.72 x 10-7 1.08 x 10-7
1.72 x 10-12 8.54 x 10-13
5.15 x 10-7 2.05 x 10-7
1.33 x 10-6 5.31 x 10-7
7.35 x 10-5 2.93 x 10-5
8.22 x 10-6 3.28 x 10-6
4.86 x 10-5 1.94 x 10-5
1.04 x 10-6 4.15 x 10-7
1.90 x 10-4 7.57 x 10-5
6.27 x 10-6 2.50 x 10-6
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
-
4.27 x 10-4 1.70 x 10-4
0.00211
8.41 x 10-4
-4
9.44 x 10
3.77 x 10-4
0.0231
0.00920
4.30 x 10-5 1.71 x 10-5
1.11 x 10-8 4.42 x 10-9
2.72 x 10-7 1.08 x 10-7
1.72 x 10-12 8.54 x 10-13
5.15 x 10-7 2.05 x 10-7
1.33 x 10-6 5.31 x 10-7
7.35 x 10-5 2.93 x 10-5
8.22 x 10-6 3.28 x 10-6
4.86 x 10-5 1.94 x 10-5
1.04 x 10-6 4.15 x 10-7
1.90 x 10-4 7.57 x 10-5
6.27 x 10-6 2.50 x 10-6
-
4.26 x 10-4 1.70 x 10-4
0.00211
8.41 x 10-4
-4
9.44 x 10
3.77 x 10-4
0.0231
0.00920
4.30 x 10-5 1.71 x 10-5
1.11 x 10-8 4.43 x 10-9
2.72 x 10-7 1.08 x 10-7
1.72 x 10-12 8.54 x 10-13
5.15 x 10-7 2.05 x 10-7
1.33 x 10-6 5.31 x 10-7
7.32 x 10-5 2.92 x 10-5
8.21 x 10-6 3.27 x 10-6
4.86 x 10-5 1.94 x 10-5
1.04 x 10-6 4.16 x 10-7
1.90 x 10-4 7.57 x 10-5
6.27 x 10-6 2.50 x 10-6
-
4.26 x 10-4 1.70 x 10-4
0.00211
8.41 x 10-4
-4
9.44 x 10
3.77 x 10-4
0.0231
0.00920
4.30 x 10-5 1.71 x 10-5
1.11 x 10-8 4.43 x 10-9
2.72 x 10-7 1.08 x 10-7
1.72 x 10-12 8.54 x 10-13
5.15 x 10-7 2.05 x 10-7
1.33 x 10-6 5.31 x 10-7
7.32 x 10-5 2.92 x 10-5
8.21 x 10-6 3.27 x 10-6
4.86 x 10-5 1.94 x 10-5
1.04 x 10-6 4.16 x 10-7
1.90 x 10-4 7.57 x 10-5
6.27 x 10-6 2.50 x 10-6
-
September 10, 2004
Page 53
Site 8 - Cattrick Street in Malton
Cancer Risk Levels (unitless)
1,3-Butadiene
Acetaldehyde
Benzene
Benzo(a)pyrene Group
Formaldehyde
1.41 x 10-8 6.26 x 10-8 1.05 x 10-7 1.41 x 10-8 6.26 x 10-8 1.05 x 10-7 1.41 x 10-8 6.26 x 10-8 1.05 x 10-7 1.41 x 10-8 6.26 x 10-8 1.05 x 10-7
1.60 x 10-8 7.11 x 10-8 1.19 x 10-7 1.60 x 10-8 7.11 x 10-8 1.19 x 10-7 1.60 x 10-8 7.11 x 10-8 1.19 x 10-7 1.60 x 10-8 7.11 x 10-8 1.19 x 10-7
3.84 x 10-9 1.70 x 10-8 2.85 x 10-8 3.84 x 10-9 1.70 x 10-8 2.85 x 10-8 3.84 x 10-9 1.70 x 10-8 2.85 x 10-8 3.84 x 10-9 1.70 x 10-8 2.85 x 10-8
1.52 x 10-11 6.74 x 10-11 1.13 x 10-10 1.52 x 10-11 6.72 x 10-11 1.13 x 10-10 1.52 x 10-11 6.72 x 10-11 1.13 x 10-10 1.52 x 10-11 6.74 x 10-11 1.13 x 10-10
6.30 x 10-12 2.79 x 10-11 4.69 x 10-11 6.30 x 10-12 2.79 x 10-11 4.69 x 10-11 6.30 x 10-12 2.79 x 10-11 4.69 x 10-11 6.30 x 10-12 2.79 x 10-11 4.69 x 10-11
Exposure Ratios (unitless)
1,3-Butadiene
Acetaldehyde
Acetone
Acrolein
Benzene
Cyclohexane
Ethylbenzene
Formaldehyde
Hexane
Methyl Ethyl Ketone
Naphthalene
n-Butylbenzene
Nonane
Toluene
Trimethylbenzene-1,2,4
Xylenes
0.00256
0.00102
0.0126
0.00503
0.00569
0.00227
0.138
0.0552
2.58 x 10-4 1.03 x 10-4
6.65 x 10-8 2.65 x 10-8
1.63 x 10-6 6.51 x 10-7
1.03 x 10-11 5.13 x 10-12
3.09 x 10-6 1.23 x 10-6
7.98 x 10-6 3.18 x 10-6
4.41 x 10-4 1.76 x 10-4
4.94 x 10-5 1.97 x 10-5
2.92 x 10-4 1.16 x 10-4
6.24 x 10-6 2.49 x 10-6
0.00114
4.54 x 10-4
-5
3.76 x 10
1.50 x 10-5
a
-
0.00256
0.00102
0.0126
0.00503
0.00569
0.00227
0.138
0.0552
2.58 x 10-4 1.03 x 10-4
6.65 x 10-8 2.65 x 10-8
1.63 x 10-6 6.51 x 10-7
1.03 x 10-11 5.13 x 10-12
3.09 x 10-6 1.23 x 10-6
7.98 x 10-6 3.18 x 10-6
4.41 x 10-4 1.76 x 10-4
4.94 x 10-5 1.97 x 10-5
2.92 x 10-4 1.16 x 10-4
6.24 x 10-6 2.49 x 10-6
0.00114
4.54 x 10-4
-5
3.76 x 10
1.50 x 10-5
-
0.00256
0.00102
0.0126
0.00503
0.00569
0.00227
0.138
0.0552
2.58 x 10-4 1.03 x 10-4
6.65 x 10-8 2.65 x 10-8
1.63 x 10-6 6.51 x 10-7
1.03 x 10-11 5.13 x 10-12
3.09 x 10-6 1.23 x 10-6
7.98 x 10-6 3.18 x 10-6
4.41 x 10-4 1.76 x 10-4
4.94 x 10-5 1.97 x 10-5
2.92 x 10-4 1.16 x 10-4
6.24 x 10-6 2.49 x 10-6
0.00114
4.54 x 10-4
-5
3.76 x 10
1.50 x 10-5
-
0.00256
0.00102
0.0126
0.00503
0.00569
0.00227
0.138
0.0551
2.58 x 10-4 1.03 x 10-4
6.65 x 10-8 2.65 x 10-8
1.63 x 10-6 6.51 x 10-7
1.03 x 10-11 5.13 x 10-12
3.09 x 10-6 1.23 x 10-6
7.98 x 10-6 3.18 x 10-6
4.41 x 10-4 1.76 x 10-4
4.94 x 10-5 1.97 x 10-5
2.92 x 10-4 1.16 x 10-4
6.24 x 10-6 2.49 x 10-6
0.00114
4.54 x 10-4
-5
3.76 x 10
1.50 x 10-5
-
Female lifetime composite receptors are used to evaluate lifetime exposures to carcinogenic chemicals, and are not appropriate for chemicals which act through a threshold toxicological mode of action (i.e., noncarcinogens).
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
September 10, 2004
Page 54
Table 14
Cancer Risk Levels and Exposure Ratios for the Workplace Exposure Scenario
(Off-site Sources Alone)
Predicted CRL/ER Values for a Female Worker
Assessed Chemicals
Maximum Off-site
Concentration
Maximum Concentrations at
Highway 427 and Dixon
Road
Maximum
Concentrations at Hotel
Strip and Dixon Road
3.05 x 10-6
4.32 x 10-6
2.39 x 10-6
3.39 x 10-6
2.49 x 10-6
3.54 x 10-6
0.0499
0.0262
2.02 x 10-5
6.64 x 10-4
0.00676
0.110
0.00227
0.0212
2.73 x 10-4
0.00760
0.0391
0.0205
1.59 x 10-5
5.20 x 10-4
0.00529
0.0858
0.00178
0.0165
2.14 x 10-4
0.00594
0.162
0.0158
0.0407
0.0214
1.65 x 10-5
5.43 x 10-4
0.00552
0.0900
0.00185
0.0173
2.23 x 10-4
0.00621
0.169
0.0165
Cancer Risk Levels (unitless)
1,3-Butadiene
Benzene
Exposure Ratios (unitless)
1,3-Butadiene
Benzene
Cyclohexane
Ethylbenzene
Hexane
Naphthalene
n-Butylbenzene
Nonane
Styrene
Toluene
Trimethylbenzene-1,2,4
Xylenes
0.208
0.0202
Note: Those CRL or ER values which exceed their relevant regulatory benchmark (i.e., 1 x 10-6 and 0.2, respectively) are highlighted in bold
format for ease of identification.
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
September 10, 2004
Page 55
Table 15
Cancer Risk Levels and Exposure Ratios for the Residential Exposure Scenario
(Off-site Sources Alone)
YEAR 2000
Assessed Chemicals
Female Preschool
Child
Female Adult
Female Composite a
1.57 x 10-6
2.23 x 10-6
6.97 x 10-6
9.86 x 10-6
1.17 x 10-5
1.66 x 10-5
0.285
0.150
1.16 x 10-4
0.00381
0.0387
0.114
0.0597
4.62 x 10-5
0.00152
0.0154
0.626
0.0130
0.121
0.00156
0.0435
0.250
0.00518
0.0483
6.22 x 10-4
0.0173
1.19
0.116
0.473
0.0461
-
1.28 x 10-6
1.81 x 10-6
5.66 x 10-6
8.00 x 10-6
9.51 x 10-6
1.34 x 10-5
0.232
0.121
9.39 x 10-5
0.00310
0.0314
0.0925
0.0484
3.75 x 10-5
0.00123
0.0125
0.511
0.0106
0.0987
0.00127
0.0354
0.204
0.00421
0.0394
5.06 x 10-4
0.0141
0.963
0.0941
0.384
0.0375
-
Site 4 - Longbourne Drive and Willowbridge Road in Etobicoke
Cancer Risk Levels (unitless)
1,3-Butadiene
Benzene
Exposure Ratios (unitless)
1,3-Butadiene
Benzene
Cyclohexane
Ethylbenzene
Hexane
Naphthalene
n-Butylbenzene
Nonane
Styrene
Toluene
Trimethylbenzene-1,2,4
Xylenes
Site 5 - Centennial Park Road (School) in Etobicoke
Cancer Risk Levels (unitless)
1,3-Butadiene
Benzene
Exposure Ratios (unitless)
1,3-Butadiene
Benzene
Cyclohexane
Ethylbenzene
Hexane
Naphthalene
n-Butylbenzene
Nonane
Styrene
Toluene
Trimethylbenzene-1,2,4
Xylenes
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
September 10, 2004
Page 56
Site 6 - Audubon Blvd. in Mississauga
Cancer Risk Levels (unitless)
1,3-Butadiene
Benzene
Exposure Ratios (unitless)
1,3-Butadiene
Benzene
Cyclohexane
Ethylbenzene
Hexane
Naphthalene
n-Butylbenzene
Nonane
Styrene
Toluene
Trimethylbenzene-1,2,4
Xylenes
1.47 x 10-6
2.09 x 10-6
6.53 x 10-6
9.24 x 10-6
1.10 x 10-5
1.55 x 10-5
0.268
0.140
1.08 x 10-4
0.00356
0.0362
0.107
0.0559
4.32 x 10-5
0.00142
0.0144
0.589
0.0122
0.114
0.00146
0.0407
0.235
0.00486
0.0453
5.83 x 10-4
0.0162
1.11
0.109
0.444
0.0433
-
8.85 x 10-7
1.26 x 10-6
3.92 x 10-6
5.57 x 10-6
6.58 x 10-6
9.35 x 10-6
0.161
0.0845
6.50 x 10-5
0.00214
0.0217
0.354
0.00730
0.0681
8.78 x 10-4
0.0245
0.064
0.0337
2.59 x 10-5
8.53 x 10-4
0.00867
0.141
0.00291
0.0272
3.50 x 10-4
0.0098
0.668
0.0652
0.266
0.0260
-
Site 7 - County Court Road in Brampton
Cancer Risk Levels (unitless)
1,3-Butadiene
Benzene
Exposure Ratios (unitless)
1,3-Butadiene
Benzene
Cyclohexane
Ethylbenzene
Hexane
Naphthalene
n-Butylbenzene
Nonane
Styrene
Toluene
Trimethylbenzene-1,2,4
Xylenes
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
September 10, 2004
Page 57
Site 8 - Cattrick Street in Malton
Cancer Risk Levels (unitless)
1,3-Butadiene
Benzene
Exposure Ratios (unitless)
1,3-Butadiene
Benzene
Cyclohexane
Ethylbenzene
Hexane
Naphthalene
n-Butylbenzene
Nonane
Styrene
Toluene
Trimethylbenzene-1,2,4
Xylenes
a
1.18 x 10-6
1.67 x 10-6
5.23 x 10-6
7.39 x 10-6
8.77 x 10-6
1.24 x 10-5
0.214
0.112
8.68 x 10-5
0.00285
0.0290
0.471
0.00976
0.0909
0.00117
0.0326
0.0854
0.0447
3.46 x 10-5
0.00114
0.0116
0.188
0.00389
0.0362
4.67 x 10-4
0.0130
0.891
0.0868
0.355
0.0346
-
Female lifetime composite receptors are used to evaluate lifetime exposures to carcinogenic chemicals, and are not appropriate for chemicals which act
through a threshold toxicological mode of action (i.e., non-carcinogens).
Note: Those CRL or ER values which exceed their relevant regulatory benchmark (i.e., 1 x 10-6 and 0.2, respectively) are highlighted in bold format for
ease of identification.
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
September 10, 2004
Page 58
Table 16
Cancer Risk Levels and Exposure Ratios for the Workplace Exposure Scenario
(Both TPIA & Off-site Sources Combined)
Assessed Chemicals
Predicted CRL/ER Values for a Female Worker
YEAR 2000
YEAR 2005
YEAR 2010
YEAR 2015
Site 1 – Maximum Off-site Concentrations
Cancer Risk Levels (unitless)
1,3-Butadiene
Benzene
Exposure Ratios (unitless)
1,3-Butadiene
Benzene
Cyclohexane
Ethylbenzene
Hexane
Naphthalene
n-Butylbenzene
Nonane
Styrene
Toluene
Trimethylbenzene-1,2,4
Xylenes
3.12 x 10-6
4.41 x 10-6
3.22 x 10-6
4.56 x 10-6
3.33 x 10-6
4.71 x 10-6
3.51 x 10-6
4.97 x 10-6
0.0510
0.0267
2.06 x 10-5
6.78 x 10-4
0.00690
0.112
0.00232
0.0216
2.79 x 10-4
0.00777
0.0527
0.0276
2.13 x 10-5
7.02 x 10-4
0.00713
0.116
0.00239
0.0223
2.87 x 10-4
0.00800
0.0544
0.0285
2.20 x 10-5
7.23 x 10-4
0.00736
0.120
0.00247
0.0231
2.96 x 10-4
0.00827
0.0574
0.0301
2.33 x 10-5
7.64 x 10-4
0.00778
0.126
0.00261
0.0243
3.14 x 10-4
0.00876
0.212
0.0207
0.219
0.0213
0.226
0.0220
0.239
0.0232
Site 2 – Maximum Concentrations at Highway 427 and Dixon Road
Cancer Risk Levels (unitless)
1,3-Butadiene
Benzene
2.91 x 10-6
4.12 x 10-6
2.70 x 10-6
3.83 x 10-6
2.70 x 10-6
3.83 x 10-6
2.70 x 10-6
3.83 x 10-6
Exposure Ratios (unitless)
1,3-Butadiene
Benzene
Cyclohexane
Ethylbenzene
Hexane
Naphthalene
n-Butylbenzene
Nonane
Styrene
Toluene
Trimethylbenzene-1,2,4
Xylenes
0.0476
0.0249
1.93 x 10-5
6.34 x 10-4
0.00644
0.105
0.00217
0.0202
2.61 x 10-4
0.00724
0.198
0.0193
0.0442
0.0232
1.79 x 10-5
5.87 x 10-4
0.00598
0.0971
0.00201
0.0188
2.41 x 10-4
0.00675
0.184
0.0179
0.0442
0.0232
1.79 x 10-5
5.87 x 10-4
0.00598
0.0971
0.00201
0.0188
2.41 x 10-4
0.00675
0.184
0.0179
0.0442
0.0232
1.79 x 10-5
5.87 x 10-4
0.00598
0.0971
0.00201
0.0188
2.41 x 10-4
0.00675
0.184
0.0179
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
September 10, 2004
Page 59
Site 3 – Maximum Concentrations on Hotel Strip and Dixon Road
Cancer Risk Levels (unitless)
1,3-Butadiene
Benzene
2.91 x 10-6
4.12 x 10-6
2.70 x 10-6
3.83 x 10-6
2.70 x 10-6
3.83 x 10-6
2.70 x 10-6
3.83 x 10-6
Exposure Ratios (unitless)
1,3-Butadiene
Benzene
Cyclohexane
Ethylbenzene
Hexane
Naphthalene
n-Butylbenzene
Nonane
Styrene
Toluene
Trimethylbenzene-1,2,4
Xylenes
0.0476
0.0249
1.93 x 10-5
6.34 x 10-4
0.00644
0.105
0.00217
0.0202
2.61 x 10-4
0.00724
0.198
0.0193
0.0442
0.0232
1.79 x 10-5
5.87 x 10-4
0.00598
0.0971
0.00201
0.0188
2.41 x 10-4
0.00675
0.184
0.0179
0.0442
0.0232
1.79 x 10-5
5.87 x 10-4
0.00598
0.0971
0.00201
0.0188
2.41 x 10-4
0.00675
0.184
0.0179
0.0442
0.0232
1.79 x 10-5
5.87 x 10-4
0.00598
0.0971
0.00201
0.0188
2.41 x 10-4
0.00675
0.184
0.0179
Note: Those CRL or ER values which exceed their relevant regulatory benchmark (i.e., 1 x 10-6 and 0.2, respectively) are highlighted in bold format for
ease of identification.
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
September 10, 2004
Page 60
Table 17
Cancer Risk Levels and Exposure Ratios for the Residential Exposure Scenario (Both TPIA & Off-site Sources
Combined)
YEAR 2000
Assessed Chemicals
Female
Preschool
Child
YEAR 2005
Female
Female
Female
Preschool
Adult Composite a
Child
Female
Adult
YEAR 2010
Female
Female
Preschool
Composite
Child
Female
Adult
YEAR 2015
Female
Female
Preschool
Composite
Child
Female
Adult
Female
Composite
Site 4 - Longbourne Drive and Willowbridge Road
Cancer Risk Levels (unitless)
1,3-Butadiene
1.47 x 10-6
Benzene
2.09 x 10-6
Exposure Ratios (unitless)
1,3-Butadiene
0.268
Benzene
0.140
Cyclohexane
1.08 x 10-4
Ethylbenzene
0.00356
Hexane
0.0362
Naphthalene
0.589
n-Butylbenzene
0.0122
Nonane
0.114
Styrene
0.00146
Toluene
0.0407
Trimethylbenzene-1,2,4
1.11
Xylenes
0.109
6.53 x 10-6
9.24 x 10-6
1.10 x 10-5
1.55 x 10-5
1.57 x 10-6 6.97 x 10-6
2.23 x 10-6 9.86 x 10-6
1.17 x 10-5
1.66 x 10-5
1.57 x 10-6
2.23 x 10-6
6.97 x 10-6
9.86 x 10-6
1.17 x 10-5
1.66 x 10-5
1.57 x 10-6
2.23 x 10-6
6.97 x 10-6
9.86 x 10-6
1.17 x 10-5
1.66 x 10-5
0.107
0.0559
4.32 x 10-5
0.00142
0.0144
-
0.114
0.286
0.150
0.0597
1.16 x 10-4 4.62 x 10-5
0.00381
0.00152
0.0387
0.0154
-
0.286
0.150
1.16 x 10-4
0.00381
0.0387
0.114
0.0597
4.62 x 10-5
0.00152
0.0154
0.286
0.150
1.16 x 10-4
0.00381
0.0387
0.114
0.0597
4.62 x 10-5
0.00152
0.0154
0.626
0.0130
0.121
0.00156
0.0435
0.250
0.00518
0.0483
6.22 x 10-4
0.0173
0.626
0.0130
0.121
0.00156
0.0435
0.250
0.00518
0.048
6.22 x 10-4
0.0173
1.19
0.116
0.473
0.0461
-
1.19
0.116
0.473
0.0461
-
0.235
0.00486
0.0453
5.83 x 10-4
0.0162
0.444
0.0433
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
0.626
0.0130
0.121
0.00156
0.0435
0.250
0.00518
0.0483
6.22 x 10-4
0.0173
1.19
0.116
0.473
0.0461
September 10, 2004
Page 61
Table 17
Cancer Risk Levels and Exposure Ratios for the Residential Exposure Scenario (Both TPIA & Off-site Sources
Combined)
YEAR 2000
Assessed Chemicals
Female
Preschool
Child
YEAR 2005
Female
Female
Female
Preschool
Adult Composite a
Child
Female
Adult
YEAR 2010
Female
Female
Preschool
Composite
Child
Female
Adult
YEAR 2015
Female
Female
Preschool
Composite
Child
Female
Adult
Female
Composite
5.23 x 10-6
7.39 x 10-6
8.77 x 10-6
1.24 x 10-5
Site 5 - Centennial Park Road (School)
Cancer Risk Levels (unitless)
1,3-Butadiene
1.28 x 10-6
Benzene
1.81 x 10-6
Exposure Ratios (unitless)
1,3-Butadiene
0.232
Benzene
0.121
Cyclohexane
9.39 x 10-5
Ethylbenzene
0.00310
Hexane
0.0314
Naphthalene
0.511
n-Butylbenzene
0.0106
Nonane
0.0986
Styrene
0.00127
Toluene
0.0354
Trimethylbenzene-1,2,4
0.963
Xylenes
0.0941
5.66 x 10-6
8.00 x 10-6
9.51 x 10-6
1.34 x 10-5
1.18 x 10-6 5.23 x 10-6
1.67 x 10-6 7.39 x 10-6
8.77 x 10-6
1.24 x 10-5
1.18 x 10-6
1.67 x 10-6
5.23 x 10-6
7.39 x 10-6
8.77 x 10-6
1.24 x 10-5
0.0925
0.0484
3.75 x 10-5
0.00123
0.0125
-
0.0854
0.214
0.112
0.0447
8.68 x 10-5 3.46 x 10-5
0.00285
0.00114
0.0290
0.0116
0.188
0.471
0.00976
0.00389
0.0908
0.0362
0.00117
4.67 x 10-4
0.0326
0.0130
-
0.214
0.112
8.68 x 10-5
0.00285
0.0290
0.471
0.00976
0.0908
0.00117
0.0326
0.0854
0.0447
3.46 x 10-5
0.00114
0.0116
0.188
0.00389
0.0362
4.67 x 10-4
0.0130
0.891
0.0868
0.355
0.0346
-
0.204
0.00421
0.0393
5.06 x 10-4
0.0141
0.384
0.0375
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
0.891
0.0868
0.355
0.0346
1.18 x 10-6
1.67 x 10-6
0.0854
0.214
0.112
0.0447
8.68 x 10-5 3.46 x 10-5
0.00285
0.00114
0.0290
0.0116
0.188
0.471
0.00976
0.00389
0.0908
0.0362
0.00117 4.67 x 10-4
0.0326
0.0130
0.891
0.0868
0.355
0.0346
-
September 10, 2004
Page 62
Site 6 - Audubon Blvd. in Mississauga
Cancer Risk Levels (unitless)
1,3-Butadiene
1.47 x 10-6
Benzene
2.09 x 10-6
Exposure Ratios (unitless)
1,3-Butadiene
0.268
Benzene
0.140
Cyclohexane
1.08 x 10-4
Ethylbenzene
0.00356
Hexane
0.0362
Naphthalene
0.589
n-Butylbenzene
0.0122
Nonane
0.114
Styrene
0.00146
Toluene
0.0407
Trimethylbenzene-1,2,4
1.11
Xylenes
0.109
6.53 x 10-6
9.24 x 10-6
1.10 x 10-5
1.55 x 10-5
1.47 x 10-6 6.53 x 10-6
2.09 x 10-6 9.24 x 10-6
1.10 x 10-5
1.55 x 10-5
1.47 x 10-6
2.09 x 10-6
6.53 x 10-6
9.24 x 10-6
1.10 x 10-5
1.55 x 10-5
1.47 x 10-6 6.53 x 10-6
2.09 x 10-6 9.24 x 10-6
1.10 x 10-5
1.55 x 10-5
0.107
0.0559
4.32 x 10-5
0.00142
0.0144
-
0.107
0.268
0.140
0.0559
1.08 x 10-4 4.32 x 10-5
0.00356
0.00142
0.0362
0.0144
-
0.268
0.140
1.08 x 10-4
0.00356
0.0362
0.107
0.0559
4.32 x 10-5
0.00142
0.0144
0.107
0.268
0.140
0.0559
1.08 x 10-4 4.32 x 10-5
0.00356
0.00142
0.0362
0.0144
0.589
0.0122
0.114
0.00146
0.0407
0.235
0.00486
0.0453
5.83 x 10-4
0.0162
1.11
0.109
0.444
0.0433
-
-
0.235
0.00486
0.0453
5.83 x 10-4
0.0162
0.444
0.0433
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
0.589
0.0122
0.114
0.00146
0.0407
0.235
0.00486
0.0453
5.83 x 10-4
0.0162
1.11
0.109
0.444
0.0433
0.589
0.0122
0.114
0.00146
0.0407
0.235
0.00486
0.0453
5.83 x 10-4
0.0162
1.11
0.109
0.444
0.0433
September 10, 2004
Page 63
Site 7 - County Court Road in Brampton
Cancer Risk Levels (unitless)
1,3-Butadiene
8.85 x 10-7
Benzene
1.26 x 10-6
Exposure Ratios (unitless)
1,3-Butadiene
0.161
Benzene
0.0845
Cyclohexane
6.50 x 10-5
Ethylbenzene
0.00214
Hexane
0.0217
Naphthalene
0.354
n-Butylbenzene
0.00730
Nonane
0.0681
Styrene
8.78 x 10-4
Toluene
0.0245
Trimethylbenzene-1,2,4
0.668
Xylenes
0.0652
3.92 x 10-6
5.57 x 10-6
6.58 x 10-6
9.35 x 10-6
9.83 x 10-7 4.35 x 10-6
1.39 x 10-6 6.15 x 10-6
7.31 x 10-6
1.03 x 10-5
8.85 x 10-7
0.0641
0.0337
2.59 x 10-5
8.53 x 10-4
0.00867
0.141
0.00291
0.0272
3.50 x 10-4
0.00975
-
0.179
0.0712
0.0933
0.0372
7.23 x 10-5 2.88 x 10-5
0.00238
9.50 x 10-4
0.0242
0.00965
0.157
0.393
0.00810
0.00323
0.0757
0.0302
9.76 x 10-4 3.89 x 10-4
0.0272
0.0108
-
0.161
0.0845
6.50 x 10-5
0.00214
0.0217
0.266
0.0260
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
0.740
0.0723
0.295
0.0288
3.92 x 10-6
5.57 x 10-6
6.58 x 10-6
9.35 x 10-6
8.85 x 10-7 3.92 x 10-6
1.26 x 10-6 5.57 x 10-6
6.58 x 10-6
9.35 x 10-6
0.354
0.00730
0.0681
8.78 x 10-4
0.0245
0.0641
0.0337
2.59 x 10-5
8.53 x 10-4
0.00867
0.141
0.00291
0.0272
3.50 x 10-4
0.00975
0.161
0.0641
0.0845
0.0337
6.50 x 10-5 2.59 x 10-5
0.00214 8.53 x 10-4
0.0217
0.00867
0.141
0.354
0.00730
0.00291
0.0681
0.0272
8.78 x 10-4 3.50 x 10-4
0.0245
0.00975
0.668
0.0652
0.266
0.0260
-
-
1.26 x 10
-6
0.668
0.0652
0.266
0.0260
September 10, 2004
Page 64
Site 8 - Cattrick Street in Malton
Cancer Risk Levels (unitless)
1,3-Butadiene
1.38 x 10-6
Benzene
1.95 x 10-6
Exposure Ratios (unitless)
1,3-Butadiene
0.250
Benzene
0.131
Cyclohexane
1.02 x 10-4
Ethylbenzene
0.00332
Hexane
0.0339
Naphthalene
0.550
n-Butylbenzene
0.0114
Nonane
0.106
Styrene
0.00137
Toluene
0.0380
Trimethylbenzene-1,2,4
1.04
Xylenes
0.101
6.10 x 10-6
8.62 x 10-6
1.02 x 10-5
1.45 x 10-5
1.38 x 10-6 6.10 x 10-6
1.95 x 10-6 8.62 x 10-6
1.02 x 10-5
1.45 x 10-5
1.38 x 10-6
1.95 x 10-6
6.10 x 10-6
8.62 x 10-6
1.02 x 10-5
1.45 x 10-5
1.38 x 10-6 6.10 x 10-6
1.95 x 10-6 8.62 x 10-6
1.02 x 10-5
1.45 x 10-5
0.100
0.0522
4.05 x 10-5
0.00132
0.0135
-
0.100
0.250
0.131
0.0522
1.02 x 10-4 4.05 x 10-5
0.00332
0.00132
0.0339
0.0135
-
0.250
0.131
1.02 x 10-4
0.00332
0.0339
0.100
0.0522
4.05 x 10-5
0.00132
0.0135
0.100
0.250
0.131
0.0522
1.02 x 10-4 4.05 x 10-5
0.00332
0.00132
0.0339
0.0135
0.550
0.0114
0.106
0.00137
0.0380
0.219
0.00454
0.0423
5.45 x 10-4
0.0152
1.04
0.101
0.414
0.0404
-
-
0.219
0.00454
0.0423
5.45 x 10-4
0.0152
0.414
0.0404
0.550
0.0114
0.106
0.00137
0.0380
0.219
0.00454
0.0423
5.45 x 10-4
0.0152
1.04
0.101
0.414
0.0404
0.550
0.0114
0.106
0.00137
0.0380
0.219
0.00454
0.0423
5.45 x 10-4
0.0152
1.04
0.101
0.414
0.0404
a
Female lifetime composite receptors are used to evaluate lifetime exposures to carcinogenic chemicals, and are not appropriate for chemicals which act through a threshold toxicological mode of action (i.e.,
non-carcinogens).
Note: Those CRL or ER values which exceed their relevant regulatory benchmark (i.e., 1 x 10-6 and 0.2, respectively) are highlighted in bold format for ease of identification.
HHRA of Toronto Pearson International Airport
Cantox Environmental Inc
September 10, 2004
Page 65
3.0
HHRA FOR CO, NO2 AND SO2
This Section presents the results of the HHRA for point-of-contact chemicals. A discussion of the
implications of these results for potential adverse health effects is presented in Section 4. Although an
HHRA was not performed for PM10 (due to the lack of key emission data), a review of relevant
background information that could be used in an HHRA is presented in Section 3. More detailed
information regarding the health effects of PM10 is provided in Appendix E.
3.1
HHRA for Carbon Monoxide
3.1.1
Sources of CO
There are a number of sources that contribute to the ambient air concentrations of CO. Therefore,
exposures related to vehicular traffic have to be evaluated with cognizance of total exposures from all
sources.
These include sources related to:
•
Various human activities (i.e., anthropogenic sources),
•
Natural activities that are independent of human activities (biogenic sources)
Carbon monoxide is produced when organic materials such as gasoline, coal, wood or garbage are
incompletely burned. In Ontario, provincial CO emissions showed a small decline (4.1 per cent)
between 1991 and 2000 due to the fleet change to newer vehicles with more stringent emission
standards. The transportation sector accounts for 65 per cent of the provincial total CO emissions
(MOE, 2000). In urban areas, mobile sources such as the automobile are responsible for a greater part
of the CO detected in routine monitoring. At the TPIA, the majority of CO emissions identified in the
model are associated with ground operations, not aircraft. The conjunction of several major highways
around the TPIA (401, 421, 409, 407 and 410) tends to significantly increase the potential for mobile
emissions and especially CO because of the high vehicle density on these major transport routes. Major
point sources include the fossil fuel-fired (coal or gas) electricity generation and incinerators. The
largest source of personal exposure to CO is tobacco smoke. Biogenic emissions of CO are minor in
comparison to anthropogenic combustion sources.
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3.1.2
Predicted CO Concentrations
Table 18, Table 19 and Table 20 present the following information on ambient air concentrations of CO:
1. The predicted maximum one-hour concentration of CO at various selected receptor sites that
arise from the uses of the TPIA. Sites chosen by the GTAA Air Quality Environment SubCommittee are shown in Figure 1.
2. Concentration Ratios for CO comparing expected concentrations at these locations to the AAQC
for TPIA Operations alone, for Off-site sources alone based on the Year 2000, and the combined
modelled maximum one-hour concentrations from both TPIA and off-site sources;
3. The predicted annual average air concentrations of CO at the location of maximum off-site
concentration in the study area of the TPIA.
Concentration Ratio (CR) values were calculated for these ambient air concentrations according to:
CR =
Ambient Air Concentration
Ambient Air Quality Criterion
A CR value less than one would mean that the ambient air concentration of concern was less than the
MOE’s Ambient Air Quality Criterion (AAQC) value.
The CR values (see Table 19, Table 21 and Table 23) using the Ontario AAQC (see Table 26) were
generally less than a value of one, indicating predicted ambient air concentrations of CO from the TPIA
were less than the Ontario ambient air quality criteria for the maximum value, and for the highest value
at the chosen receptor locations. One exception for the year 2000 is discussed in this report (Section 4)
and in the Phase 1-3 Report (RWDI, 2003).
3.1.2.1
Predicted One-hour Maximum Concentrations from TPIA Sources Alone
Modelled ground concentrations of CO resulting from air traffic and ground operations scenarios for the
TPIA alone are shown in Table 18. The results of modelled impacts of the TPIA operations alone are
presented for each of the years 2000, 2005, 2010 and 2015. The scenarios used by RWDI to generate
predicted maximum one-hour ground level concentrations have taken into account the anticipated
construction and operational changes for ground-based activity as well as expected growth in aircraft
operations during those years. The maximum one-hour concentration at a chosen receptor was for the
theoretical maximum impact (off-site). Concentrations at other receptor locations were estimated based
on concentration isopleths for the maximum one-hour concentration of CO as described by modelling
results. The health-based regulatory criterion for a 1-hour concentration of CO established by the MOE
is 30 ppm (36,200 µg/m3) (RWDI, 2003).
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With the exception of the location of predicted maximum off-site concentration from TPIA sources for
the year 2000, incremental maximum one-hour CO levels were predicted to be less than the one-hour
AAQC. The CR expresses the ratio between the actual or anticipated level of exposure and the
regulatory limit. The concentration ratio (CR) for maximum one-hour concentrations of CO for all other
years at off-site locations was less than one. CRs in the community were substantially less than one.
The AAQC for CO set by the MOE is based on human health and contains safety factors to ensure
conservatism. A discussion of the health effects associated with exposure to ambient concentrations of
CO in the urban environment is presented in Appendix C. Modelled values for maximum
concentrations of CO from off-site sources alone (Table 20) closely parallel historical levels of CO
reported at monitoring sites maintained by the MOE.
Table 18
Maximum Predicted One-hour CO Concentrations From TPIA Sources Alone
(µg/m3)
Receptor Location
2000
2005
2010
2015
Maximum Off-Site
Maximum at Hwy 427 and Dixon Road
Maximum at Hotel Strip Dixon Road
Longbourne Dr & Willowbridge Rd, Toronto
Centennial Pk Rd (School), Toronto
Audubon Blvd, Mississauga
County Court Road, Brampton
Cattrick St., Malton
39,537
18,000
20,000
8,500
1,750
2,000
1,250
3,000
25,648
20,000
12,000
7,000
1,750
1,750
1,250
4,000
23,742
20,000
16,000
6,000
2,000
1,750
1,250
4,000
29,533
20,000
16,000
8,000
2,000
2,000
1,250
6,000
Table 19 shows that compared to maximum one-hour air quality criteria, those impacts of CO
attributable to operations at the TPIA were well within the criteria for one-hour maximum concentration
CO from the facility. Since the AAQC for CO is health-based, emissions of this pollutant at the location
of predicted maximum off-site concentration could be a concern to the community. Predicted maximum
one-hour CO concentrations at selected receptor locations (at permanent residential locations) were
considerably lower than the maximum location of predicted maximum off-site concentration. There is
no annual air quality criterion for carbon monoxide set by the MOE.
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Table 19
Concentration Ratios for Maximum Predicted One-hour CO
Concentrations From TPIA Alone
Receptor Location
2000
2005
2010
2015
Maximum Off-Site
Maximum at Hwy 427 and Dixon Road
Maximum at Hotel Strip Dixon Road
Longbourne Dr & Willowbridge Rd, Toronto
Centennial Pk Rd (School), Toronto
Audubon Blvd, Mississauga
County Court Road, Brampton
Cattrick St., Malton
1.09
0.50
0.55
0.23
0.05
0.06
0.03
0.08
0.71
0.55
0.33
0.19
0.05
0.05
0.03
0.11
0.66
0.55
0.44
0.17
0.06
0.05
0.03
0.11
0.82
0.55
0.44
0.22
0.06
0.06
0.03
0.17
3.1.2.2
Predicted One-hour Maximum Concentrations From Off-site Sources Only
Table 20 presents the modelled maximum one-hour CO concentrations expected from off-site sources
for the base year 2000. The calculations did not include any TPIA sources, and are based on historical
emission inventories from industrial point sources, area sources and mobile sources. The off-sitesources case is designed to demonstrate the projected impacts of the various mobile and fixed sources of
emission to the area surrounding the TPIA, but without the activities of the TPIA being specifically
taken into consideration. The location of the maximum off-site concentration near the TPIA boundary
was along Highway 401 rather than nearer to the Dixon Road and Highway 427. The maximum
predicted one-hour concentration at the location of predicted maximum off-site concentration was 9.6
ppm, much less than the 30 ppm AAQC. It is also less than the more stringent California inhalation
reference exposure level of 20 ppm (Table 21).
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Table 20
Maximum Predicted One-hour CO Concentrations From Off-site Sources Only
Receptor Location
Maximum Off-Site
Maximum at Hwy 427 and Dixon Road
Maximum at Hotel Strip Dixon Road
Longbourne Dr & Willowbridge Rd, Toronto
Centennial Pk Rd (School), Toronto
Audubon Blvd, Mississauga
County Court Road, Brampton
Cattrick St., Malton
CO from Off-site Sources (µg/m3)
11,583
7,250
8,500
9,250
10,750
8,250
6,250
3,700
Table 21 shows CRs for CO from off-site sources only. Compared to maximum one-hour air quality
criteria, those impacts of CO attributable to off-site sources (mobile, stationary and area sources other
than TPIA) were well within the criteria for the one-hour maximum concentration. For off-site sources,
the maximum CR of 0.32 suggests short-term concentrations of CO should not exceed the criterion.
Predicted maximum one-hour CO concentrations at off-site receptor locations (at permanent residential
locations) were considerably lower than the highest off-site receptor location.
Table 21
Concentration Ratios for Maximum Predicted One-hour CO Concentrations From
Off-site Sources Only
Receptor Location
Maximum Off-Site
Maximum at Hwy 427 and Dixon Road
Maximum at Hotel Strip Dixon Road
Longbourne Dr & Willowbridge Rd, Toronto
Centennial Pk Rd (School), Toronto
Audubon Blvd, Mississauga
County Court Road, Brampton
Cattrick St., Malton
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CR for Off-site Sources
0.32
0.20
0.23
0.26
0.30
0.23
0.17
0.10
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3.1.2.3
Predicted One-hour Maximum Concentrations From TPIA and Off-site Sources
Combined
Table 22 presents the modelled CO concentrations expected within the community from combined
sources (TPIA and off-site) for the years 2000, 2005, 2010 and 2015. This case is designed to
demonstrate the combined projected maximum one-hour impacts (expressed as predicted ground level
concentrations) of the various mobile and fixed sources of emission to the area surrounding the TPIA,
and includes emissions from TPIA operations. In the year 2000, the predicted maximum one-hour
concentration of CO at the location of predicted maximum off-site concentration exceeded the AAQC.
For all other years, and at all other locations, combined emissions produced ground level concentrations
that were below the criterion of 36,200 µg/m3.
Table 22
Predicted Maximum One-hour CO Concentrations From TPIA and Off-site Sources
Combined (µg/m3)
Receptor Location
2000
2005
2010
2015
Maximum Off-Site
Maximum at Hwy 427 and Dixon Road
Maximum at Hotel Strip Dixon Road
Longbourne Dr & Willowbridge Rd, Toronto
Centennial Pk Rd (School), Toronto
Audubon Blvd, Mississauga
County Court Road, Brampton
Cattrick St., Malton
45,355
24,000
17,000
15,000
10,000
9,000
6,000
5,000
29,196
22,000
15,000
14,000
10,000
8,000
6,000
6,000
28,667
24,000
16,000
13,000
10,000
9,000
6,000
7,000
32,780
28,000
20,000
15,000
10,000
9,000
6,000
8,000
Table 23 shows the summary data for concentration ratios for predicted one-hour maximum carbon
monoxide at the location of maximum off-site concentration based on combined sources.
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Table 23
Concentration Ratios for Maximum Predicted One-hour CO Concentrations From
TPIA and Off-site Sources Combined (µg/m3)
Receptor Location
2000
2005
2010
2015
Maximum Off-Site
Maximum at Hwy 427 and Dixon Road
Maximum at Hotel Strip Dixon Road
Longbourne Dr & Willowbridge Rd, Toronto
Centennial Pk Rd (School), Toronto
Audubon Blvd, Mississauga
County Court Road, Brampton
Cattrick St., Malton
1.25
0.66
0.47
0.41
0.28
0.25
0.17
0.14
0.81
0.61
0.41
0.38
0.28
0.22
0.17
0.17
0.79
0.66
0.44
0.39
0.28
0.25
0.17
0.19
0.90
0.77
0.55
0.41
0.28
0.25
0.17
0.22
3.1.2.4
Predicted Maximum 8-Hour Concentrations
Sub-chronic exposures (eight hours) to elevated ambient levels of CO have been directly associated with
health impacts. Table 24 shows predicted maximum 8-hour average concentrations for CO at the
location of maximum off-site concentration for all years and all phases. The longer period of
monitoring relates to the potential increase in carboxyhemoglobin concentration in blood that is
indicative of exposure to elevated concentrations of CO. Adverse health responses of the cardiovascular
system (especially among susceptible individuals with existing cardiac problems) have been associated
with accumulation of carboxyhemoglobin. The 8-hour AAQC (Table 26) is the relevant standard by
which potential for health impacts should be assessed. Acute increases in CO are of less concern than
exposures over intermediate periods that lead to increased carboxyhemoglobin concentrations (see
Appendix C).
The data presented in Table 24 demonstrate the predicted concentrations and CR values for maximum
off-site concentrations of CO. These are not necessarily indicative of concentrations that might be
experienced at residential receptors (#4 to #8). Possible health effects associated with 8-hour average
CO concentrations are discussed in Section 4.
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Table 24
Predicted 8-hour Concentrations and CR Values at Location of Maximum Off-site
Concentration
Year 2000
Sources
TPIA Alone
Off-site Sources Alone
Both TPIA & Off-site
Sources Combined
a
Year 2005
3
µg/m
8,941
2,807
a
CR
0.57
0.18
3
µg/m
6,175
-
9,454
0.60
6,688
Year 2010
Year 2015
CR
0.39
-
3
µg/m
5,633
-
CR
0.36
-
µg/m3
6,322
-
CR
0.40
-
0.46
6,627
0.42
6,812
0.43
AAQC = 15,700 µg/m3
3.1.2.5
Predicted Annual Average Concentrations
Chronic exposure to low ambient levels of CO have not been directly associated with health impacts.
Table 25 shows predicted annual average concentrations for CO at the location of maximum off-site
concentration. In general more informative health indicators for CO are associated with exposures of
approximately 8-hour duration. This is why there is an 8-hour AAQC (Table 26). Acute increases in
CO are of less concern than exposures over intermediate periods that lead to increased
carboxyhemoglobin concentrations (see Appendix C)
Table 25
Annual Average CO Concentrations a
Sources
Year 2000
Year 2005
Year 2010
Year 2015
TPIA Alone
Off-site Sources Alone
Both TPIA & Off-site
Sources Combined
425 µg/m3
240 µg/m3
338 µg/m3
394 µg/m3
462 µg/m3
589 µg/m3
489 µg/m3
544 µg/m3
618 µg/m3
a
Based on maximum modelled off-site concentration.
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3.1.3
Monitoring Results for CO and Comparison with AAQCs
Table 26 contains comparative data for the year 2000 showing maximum and mean concentrations of
carbon monoxide monitored during the year 2000 at MOE continuous monitoring sites surrounding the
TPIA.
In addition to MOE monitoring locations, maximum one-hour measured concentrations were available
for the OPSIS site located on TPIA property adjacent to Runway 24R. For the years 1999 to 2001,
maximum one-hour CO measurements were 8,923, 5,667 and 10,008 µg/m3.
In the year 2000, the maximum one-hour CO concentration at Centennial Park MOE station was 9,309
µg/m3, while the model predicted a maximum one-hour concentration at that site of 9,950 µg/m3. This
suggests that the model is slightly conservative and is probably an accurate reflection of CO
concentrations in the surrounding urban area. These predictions included TPIA and off-site sources for
the year 2000.
Table 26
Ambient Air Quality Criteria and Measured CO Levels of CO in 2000
JURISDICTION
Ontario
Annual Mean
No AAQC
CARB (OEHHA)
1 Hour AAQC
30 ppm
(36,200 µg/m3)
20 ppm
(24,130 µg/m3)
8 hour AAQC
13 ppm (15,700 µg/m3)
LOCATION
Annual Mean
1 h max COa
8 h max CO
Toronto West Centennial
Park
1.77 ppm
(2,134 µg/m3)
7.72 ppm
(9,309 µg/m3)
6.6 ppm
(7,964 µg/m3)
5.22 ppm
(6,305 µg/m3)
3.71ppm
(4,477 µg/m3)
Brampton, Main St N
a
b
(insufficient data)
Maximum observed (MOE year 2000 data)
Conversion used for CO in ppm into µg/m3 assumed the factor was (1,150 µg/m3 /ppm) (OEHHA, 1999).
As shown in Table 26, the Ontario AAQC for CO has been set at 30 ppm. A somewhat more stringent
inhalation reference concentration has been established by the California Office of Environmental
Health Hazard Assessment (OEHHA, 1999). The California Air Resources Board (CARB) has
estimated that 70% of the CO present in California urban atmospheres was due to emissions from
mobile sources. California has significantly less energy use per capita for heating when compared with
Canada and the Greater Toronto Area (GTA). The proportion of CO from all sources, including
stationary (residential and industrial) and mobile sources in the GTA may be higher than estimated by
CARB for urban sites in California. When these contributions from off-site sources were considered in
isolation, the largest impact of criteria pollutant concentration showed clearly the effects of two major
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highway systems close to the southern edge of the TPIA property. The Ontario AAQC value has been
based on a conservative and careful analysis of possible adverse effects associated with acute exposure
to elevated concentrations of CO. Additional discussion of the health effects associated with ambient
levels of CO in urban areas is addressed in Appendix C.
See Section 4 for a discussion of the implications of the results of the HHRA for CO for potential
adverse health effects.
3.2
HHRA of Nitrogen Dioxide (NO2)
Oxides of nitrogen (NOx) consist of a mixture of nitric oxide (NO) and nitrogen dioxide (NO2). NO2 is
spontaneously formed in the atmosphere by a reaction between NOx and O3 and depends on the
concentration of NO. The health effects of NOx have been largely attributed to NO2 effects in the lung
(Persinger et al., 2002). NO2 is formed by the combustion of fossil fuels and is a primary pollutant
found in both indoor and outdoor air. Although ambient NOx levels generally remain below 95 µg/m3
(0.05 ppm), in urban areas with high levels of automobile traffic, the level of NOx in outdoor air can
reach measured values of 4,000 µg/m3 (2 ppm) or greater during heavy traffic (Persinger et al., 2002).
3.2.1
Sources of NO2
There are a number of sources that contribute to the ambient air concentrations of NO2, so it is necessary
to consider exposures related to vehicular traffic with cognisance of total exposures from all sources.
Sources of exposure to NO2 are not limited to the outdoor environment.
These include sources related to:
•
Various human activities (i.e., anthropogenic sources); and,
•
Natural activities independent of and largely unrelated to human activities (biogenic sources).
In addition, NO2 present in the ambient environment can undergo a variety of reactions that create
secondary products that have the potential to cause indirect impacts of NO2 on the environment. These
are fully discussed in Appendix D to this report.
Emissions of NO2 are produced primarily by combustion processes during which oxygen reacts with
nitrogen at temperatures above about 2,200 degrees Celsius (oC). Such combustion occurs principally
when burning fossil fuels and when burning petroleum products in internal combustion engines. At
common vehicle combustion temperatures, the NOx in the product gas is almost completely composed
of NO. As this gas leaves the combustion zone, it cools and some NO is oxidized to NO2. After
entering the atmosphere, both NO and NO2 participate in a series of chemical reactions to form other
compounds such as ozone and particulate nitrate (CalEPA, 1997).
Natural events that produce NOx include lightning, soils, wildfires, stratospheric intrusion, and the
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oceans. Of these, lightning and soils are the major contributors. Lightning produces high enough
temperatures to allow N2 and O2 in the atmosphere to be converted to NO. NO is the principal NOx
species emitted from soils, with emission rates depending mainly on fertilization amounts and soil
temperature; highest emissions occur in the summer.
Soil emissions of NO result from two major microbial processes: nitrification and denitrification.
Nitrification is the process by which microbes in the soil fix nitrogen by oxidizing ammonium ions
(NH4+) to produce nitrites and nitrates. During the intermediate stages of this process, NO is formed and
subsequently diffuses through the soil into the atmosphere. During the decay of biological material such
as leaf litter, an anaerobic process (denitrification) converts nitrate to N2 and N2O; but once again, NO is
formed in an intermediate stage and diffuses to the atmosphere.
In the atmosphere, NO2 reacts with common hydrocarbons to form a wide variety of secondary products
that have the potential to cause adverse environmental impacts. Some of these secondary reaction
products have the potential to react with DNA and produce mutagenic and/or genotoxic changes.
Examples of such products include the nitrate radical, peroxyacetyl nitrate, nitroarenes, and nitrosamines
(CARB, 1986). Toxicological data on many of these compounds are limited, making it difficult to
discuss effects of specific reaction products. In addition, NO2 reacts with various anthropogenic and
biogenic volatile organic chemicals which, in the presence of ultra violet light from the sun results in the
production of ground level ozone (See Section D-2.3.4 of Appendix D). Ground level ozone is known to
be associated with a range of adverse effects on human health and the environment.
Further details on these secondary products from reactions with NOx are outlined in Section D-2.3 of
Appendix D. The potential for production of secondary reaction products from oxides of nitrogen
provides additional reasons for the minimization of the emissions of NOx to ensure the protection of
human health and the general environment. The evaluation of the relevance of these secondary products
to the emissions of NO2 from the proposed TPIA has been based on comparisons with ambient air
quality criteria for NO2, and with its possible impacts on human health as documented in the biomedical
literature.
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3.2.2
Predicted Concentrations of NO2
3.2.2.1
TPIA Sources Alone
Results for modelled air traffic and ground operations scenarios for the TPIA are shown in Table 27.
The results of modelled impacts of the TPIA operations alone are presented for each of the years 2000,
2005, 2010 and 2015. The scenarios used by RWDI to generate predicted emissions have taken into
account the anticipated construction and operational changes for ground-based activity as well as
expected growth in aircraft operations during those years. The highest concentration at a chosen
receptor was at the approximate intersection of Hwy 427 and Dixon Road that is the main public access
to the TPIA. Concentrations at other receptor locations have been estimated based on concentration
isopleths for the maximum one-hour concentration of NOx as described by modelling results.
The health-based regulatory criterion for a 1-hour concentration of NO2 established by the MOE is 200
ppb (400 µg/m3). It may sometimes be assumed that NOx and NO2 are interchangeable; however, this is
a very conservative assumption. For purposes of this assessment, correction factors have been applied
to more accurately represent the concentration of NO2 in total oxides of nitrogen (NOx). A factor of
0.34 (RWDI, 2003a) was applied to the predicted NOx concentrations to estimate the actual
concentration of NO2, which is considered the component of NOx with toxicological potential. Based on
the increase in NO2 expected to occur under worst case conditions, the concentration ratio (CR) is
greater than one. The CR expresses the ratio between the actual or anticipated level of exposure and the
regulatory limit. This suggests that using the health criteria accepted by the MOE, adverse effects could
result from acute exposure to emissions containing NO, NOx, and NO2 from the operation of the TPIA.
Table 27, Table 28, and Table 29 present the following information on ambient air concentrations of
NO2 and NOx:
1. The predicted maximum off-site 1-hour ambient concentration of NO2 as well as at the seven
selected receptor locations around the TPIA as selected by the GTAA Air Quality
Environment Sub-Committee around the TPIA;
2. Concentration Ratios for NOx and NO2 at these locations; and,
3. The predicted annual average air concentrations of NO2 at the maximum off-site location.
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Table 27
Predicted Maximum One-hour Concentrations of NOx From TPIA Alone (µg/m3)
Receptor Location
2000
2005
2010
2015
Maximum Off-Site Location
Maximum at Hwy 427 and Dixon Road
Maximum at Hotel Strip Dixon Road
Longbourne Dr & Willowbridge Rd, Toronto
Centennial Pk Rd (School), Toronto
Audubon Blvd, Mississauga
County Court Road, Brampton
Cattrick St., Malton
6,521
3,250
2,000
1,325
375
375
250
400
4,882
3,000
1,500
750
375
250
100
500
4,238
2,750
1,750
1,000
375
375
250
500
4,755
3,250
3,250
2,250
450
350
250
500
Concentration Ratio (CR) values were calculated for these ambient air concentrations according to:
CR =
Ambient Air Concentration
Ambient Air Quality Criterion
A CR value less than one would mean that the ambient air concentration of concern was less than the
Ambient Air Quality Criterion (AAQC) value.
Table 28
Predicted Maximum One-hour Concentration Ratios for NO2 From TPIA
Sources Alone a
Receptor Location
Maximum Off-Site Location
Maximum at Hwy 427 and Dixon Road
Maximum at Hotel Strip Dixon Road
Longbourne Dr & Willowbridge Rd, Toronto
Centennial Pk Rd (School), Toronto
Audubon Blvd, Mississauga
County Court Road, Brampton
Cattrick St., Malton
a
2000
2005
2010
2015
5.5
2.8
1.7
1.1
0.3
0.3
0.2
0.3
4.1
2.6
1.3
0.6
0.3
0.2
0.1
0.4
3.6
2.3
1.5
0.8
0.3
0.3
0.2
0.4
4.0
2.8
2.8
1.9
0.4
0.3
0.2
0.4
CR (NO2) = [NOx] x 0.34 ÷ 400 µg/m3
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The CR values (see Table 28) comparing the Ontario AAQC for maximum one-hour concentration (see
Table 36) were in excess of one. As such, predicted one-hour ambient air concentrations of NO2
contributed by operations at the TPIA alone would exceed the Ontario ambient air quality criteria.
Results of modelling for maximum annual predicted ground level concentrations of oxides of nitrogen
(NOx) for TPIA sources alone are described below. These maxima are for off-site modelled values.
There is no AAQC for the annual average concentration of NOx, so there is no guidance with respect to
whether these expected concentrations are outside norms for the region. In the GTA, there was no
monitored location that recorded an annual average for NOx greater than 126 µg/m3 or 63.1 ppb.
Table 29
a
b
c
Predicted Annual Average for NOx at Location of Maximum Concentrations - TPIA
Sources Alone
YEAR
Predicted Maximum a
µg/m3
Concentration Ratio b
NOx
Concentration Ratio b, c
NO2
2000
2005
2010
2015
74
65
56
66
0.74
0.65
0.56
0.66
0.50
0.44
0.38
0.45
Modelled values reported by RWDI
CR is the ratio of predicted annual concentration to the NAAQO (objective) of 100 µg/m3 and is based on maximum off-site modelled annual
concentration. NO2 = NOx
Annual conversion factor for CRs of NOx into NO2 of 0.68 was used based on experience in Ontario (RWDI, 2003a)
3.2.2.2
Off-site Sources Alone
Table 30 presents the modelled NOx concentrations expected for the community for the base year 2000.
This case is designed to demonstrate the projected impacts of the various mobile and fixed sources of
emission to the area surrounding the TPIA, but without the activities of the TPIA being specifically
taken into consideration.
Modelled maximum one-hour concentrations of NO2 at receptor locations in the community (Table 30)
for the year 2000 generally exceeded the AAQC.
Modelled values for maximum concentrations of NOx for off-site sources alone overestimate historical
levels of oxides of nitrogen reported at monitoring sites maintained by the MOE. During the year 2000,
the maximum one-hour NOx concentration recorded at Centennial Park was 549 ppb (~1,088 µg/m3 ),
but the maximum predicted one-hour concentration from off-site sources alone at that location was
2,250 µg/m3.
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Table 30
Predicted Maximum One-hour NOx Concentration From Off-site Sources Alone
NOx from Off-site Sources Alone
(µg/m3)
Receptor Location
Maximum Off-Site Location
Maximum at Hwy 427 and Dixon Road
Maximum at Hotel Strip Dixon Road
Longbourne Dr & Willowbridge Rd, Toronto
Centennial Pk Rd (School), Toronto
Audubon Blvd, Mississauga
County Court Road, Brampton
Cattrick St., Malton
Table 31
2,511
2,125
2,250
2,250
2,250
2,125
1,500
1,000
Predicted Maximum One-hour NO2 Concentration Ratios From Off-site Sources
Alone a
Receptor Location
Concentration Ratio
Maximum Off-Site Location
Maximum at Hwy 427 and Dixon Road
Maximum at Hotel Strip Dixon Road
Longbourne Dr & Willowbridge Rd, Toronto
Centennial Pk Rd (School), Toronto
Audubon Blvd, Mississauga
County Court Road, Brampton
Cattrick St., Malton
a
2.1
1.8
1.9
1.9
1.9
1.8
1.3
0.8
CR (NO2) = [NOx] x 0.34 ÷ 400 µg/m3
Results of modelling for predicted annual average ground level concentrations of oxides of nitrogen
(NOx) from off-site sources alone are described in Table 32. These maxima are for off-site modelled
values.
Table 32
a
b
c
Predicted Annual Average Concentration Ratios From Off-site Sources Alone
YEAR
Predicted Maximum a
µg/m3
Concentration Ratio b
NOx
Concentration Ratio b, c
NO2
2000
55
0.55
0.37
Modelled values reported by RWDI
CR is the ratio of predicted annual concentration to the NAAQO (objective) of 100 µg/m3 and is based on maximum off-site modelled annual
concentration. NO2 = NOx
Annual conversion factor for CRs of NOx into NO2 of 0.68 was used based on experience in Ontario (RWDI, 2003a)
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3.2.2.3
TPIA and Off-site Sources Combined
Table 33 presents the modelled NOx concentrations expected for the community for the base year 2000.
This case combines the projected impacts of the various mobile and fixed sources of off-site emissions
in combination with the activities and operations of the TPIA.
CRs for one-hour maximum NOx for the combined TPIA and off-site sources for the years 2000 to 2015
all showed predicted exceedances of the one-hour maximum AAQC (Table 34).
Table 33
Predicted Maximum One-hour NOx Concentrations From Both TPIA and Off-site
Sources Combined (µg/m3)
Receptor Location
2000
2005
2010
2015
Maximum Off-Site Location
Maximum at Hwy 427 and Dixon Road
Maximum at Hotel Strip Dixon Road
Longbourne Dr & Willowbridge Rd, Toronto
Centennial Pk Rd (School), Toronto
Audubon Blvd, Mississauga
County Court Road, Brampton
Cattrick St., Malton
6,954
4,250
3,250
3,250
2,125
2,250
1,500
1,325
5,260
4,250
3,500
3,000
2,125
2,250
1,500
1,250
5,484
4,250
3,500
3,000
2,125
2,250
1,500
1,500
6,167
4,500
4,000
3,250
2,250
2,250
1,500
1,750
Table 34
Predicted Maximum One-hour NO2 Concentration Ratios From TPIA and Off-site
Sources Combined a
Receptor Location
Maximum Off-Site Location
Maximum at Hwy 427 and Dixon Road
Maximum at Hotel Strip Dixon Road
Longbourne Dr & Willowbridge Rd, Toronto
Centennial Pk Rd (School), Toronto
Audubon Blvd, Mississauga
County Court Road, Brampton
Cattrick St., Malton
a
2000
2005
2010
2015
5.9
3.6
2.8
2.8
1.8
1.9
1.3
1.1
4.5
3.6
3.0
2.6
1.8
1.9
1.3
1.1
4.7
3.6
3.0
2.6
1.8
1.9
1.3
1.3
5.2
3.8
3.4
2.8
1.9
1.9
1.3
1.5
CR (NO2) = [NOx] x 0.34 ÷ 400 µg/m3
Results of modelling for maximum annual predicted ground level concentrations of oxides of nitrogen
(NOx) from both TPIA and off-site sources combined are described in Table 35. These maxima are for
modelled off-site values expected. Emissions of NOx attributable to TPIA were predicted to increase in
the years 2000 through 2015; however, modelled impacts indicate that there will be no significant
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increase in maximum concentrations.
Table 35
a
b
c
Predicted Annual Average Concentration Ratios for NOx/NO2 ) From TPIA and
Off-site Sources Combined
YEAR
Predicted Maximum a
µg/m3
Concentration Ratio b
NOx
Concentration Ratio b, c
NO2
2000
2005
2010
2015
117
106
104
115
1.17
1.06
1.04
1.15
0.8
0.7
0.7
0.8
Modelled values reported by RWDI
CR is the ratio of predicted annual concentration to the NAAQO (objective) of 100 µg/m3 and is based on maximum off-site modelled annual
concentration. NO2 = NOx
Annual conversion factor for CRs of NOx into NO2 of 0.68 was used based on experience in Ontario (RWDI, 2003)
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3.2.2.4
Monitoring Results for NO2 and NOx and Comparison with AAQCs
Table 36 contains the relevant criterion information as well as comparative ambient measurements for
the year 2000 including maximum and mean concentrations of oxides of nitrogen at a number of
selected sites surrounding the TPIA.
Table 36
Ambient Air Quality Criteria and Measured Levels of NO2 and NOx in 2000
JURISDICTION
Ontario
24 hour AAQC
No AAQC
200 ppb (400µg/m3)
100 ppb (200 µg/m3)
Annual Mean NO2
1 h max NO2a
24 h max NO2
23.2 ppb (46 µg/m3)
84 ppb (166 µg/m3)
50.1 ppb (99.3 µg/m3)
(insufficient data)
72 ppb (143 µg/m3)
42.2 ppb (83.6 µg/m3)
Annual Mean NOx
1 h max NOxb
24 h max NOx
42.3 ppb (84 µg/m3)
549 ppb (1088 µg/m3)
207.8 ppb (412 µg/m3)
(insufficient data)
439 ppb (870 µg/m3)
142.3 ppb (282 µg/m3)
50 ppb (100 µg/m3)
United States (EPA)
AQS
< 50 ppb (100 µg/m3)
Toronto West
Centennial Park
Brampton, Main St N
LOCATION
Toronto West
Centennial Park
Brampton, Main St N
b
1 HOUR AAQC
Environment Canada
NAAQO
LOCATION
a
Annual Mean NO2
Maximum observed (MOE year 2000 data)
Conversion used for NOx in ppb into µg/m3 assumed the factor was corrected to 10 oC (200µg/m3 /100.9 ppb) as for NO2
When assessing the potential health impacts from exposure to oxides of nitrogen, it is sometimes
considered reasonable practice to assume all of the oxides as having equal toxicity, although the major
form of the mixture of gases in the ambient environment is for NO2. Recent health studies
(epidemiology) of the effects of air pollution on selected groups from among large populations have
included annual average concentrations of NO2 as well as other pollutant concentrations as a metric for
assessing health impacts. These have been reviewed in Appendix D. A brief review of the health
effects of NO2, including a review of recent studies on children and adults receiving NO2 exposures
from traffic-related sources is presented in Section 4. These exposures involve the simultaneous
exposure to other pollutants, so it is difficult to know when a response observed is to the gas directly or
to the gas acting as a surrogate compound for complex emissions from fossil fuel combustion. We
address this by incorporating studies that examine the health impact of indoor as well as outdoor sources
of NO2.
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3.2.3
Concentration Ratios for NOx Converted to NO2
Comparison of predicted off-site annual concentrations of NO2 to the Environment Canada NAAQO of
100 µg/m3 suggests that concentrations contributed from TPIA activities alone will not exceed the
criterion over the next fifteen years (Table 29).
A conservative assumption for the purposes of health impact assessment would be to consider NOx and
NO2 as equal. Since this is not the case, a more reasonable assumption is to apply a correction factor
that gives a truer representation of the NO2 (potentially more toxic) concentration. The adjustment
factor of 0.68 is based on an analysis of spatially distributed annual monitoring reports for the Province
of Ontario. As shown in Table 35, application of this factor shows that the predicted concentration of
NO2 off-site would be less than the NAAQO (CR = 0.7 to 0.8 depending on the year and configuration
of the TPIA examined) after estimating the concentration of NO2 from NOx.
On-site monitoring of NOx using the OPSIS system showed maximum annual concentrations of 80, 81
and 74 µg/m3 for the years 1999, 2000 and 2001 respectively. These values are already under the
NAAQO, but correction for actual content of NO2 using the factor of 0.68 suggests the actual annual
off-site NO2 concentrations ranged between 50 and 55µg/m3. The calculated concentration ratios based
on the 100 µg/m3 NAAQO would then be 0.5 to 0.55.
Table 28, Table 29, Table 31, Table 32, Table 34 and Table 35 show the summary data for concentration
ratios (adjusted from NOx) for predicted maximum one-hour, and predicted annual average
concentrations of NO2 at the location of maximum concentration as identified in the modelled
conditions. The tables show that compared to the air quality criteria, predicted impacts of NO2 at the
location of maximum off-site concentration, and thus attributable to operations at the TPIA are well in
excess of the one-hour criteria (AAQC).
Predicted emissions from the TPIA alone in the base year 2000, and in each of the years 2005, 2010 and
2015, the maximum one-hour concentration of NO2 at the boundary will exceed the criterion by at least
four fold, and by as much as 5.5 fold (Table 28). Annual maximum one-hour NOx concentrations
monitored on-site at the OPSIS site (located near the theoretical maximum on-site concentration) were
697, 966 and 552 µg/m3 respectively for 1999 to 2001. Actual measured maximum one-hour
concentrations for NO2 at this location were 204, 211 and 160 µg/m3, respectively, for the same years.
These latter values should be compared to the maximum-one hour criterion for NO2 of 400 µg/m3. The
actual historical concentration ratios for NO2 were CRactual = 0.51 (1999); 0.53 (2000); and 0.4 (2001).
The predicted maximum one-hour ground level concentrations for NO2 from the TPIA generated by
assumptions used in the EDMS model were far greater than what was actually experienced in 2000
(Table 28 and Table 31). Table 30 also shows a predicted maximum one-hour concentration of NOx at
Centennial Park of 2,250 µg/m3. The monitored maximum one-hour for NOx at this site in the year
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2000 was 1,088 µg/m3. Thus, the actual maximum NOx concentration recorded off-site suggests that the
modelled concentrations were greater than actual values by a factor of about two. This suggests that the
model behaves in a conservative manner, and thus could predict higher maximum one-hour
concentrations that might ordinarily be anticipated both when using on-site and off-site sourced
emission inventories.
Predicted maximum one-hour concentrations for each year represent a unique event generated by
conditions selected by the model. Unfortunately, concentration ranges at a specified location necessary
to calculate the 90th percentile, for example, were not available to better characterize events with high
NOx over a period of a year. However, the fact that predicted annual concentrations of NO2 were within
the accepted objective (see below) suggests that the conditions that lead to very high concentrations
produced in the worst case may not be frequent.
The analysis of TPIA emissions alone predicted worst case maximum one-hour concentrations of NO2
(expressed as a fraction of NOx) at off site permanent residential receptor locations that were
considerably lower than the maximum off-site concentration. The range of CRs for off-site locations
based on the sole contribution from TPIA operations was highest at the Etobicoke location near
Longbourne Drive and Willowbridge Road where CRs exceeded 1.0 in 2000 and 2015. All other offsite residential locations would not exceed the criterion based only on TPIA operations.
Maximum one-hour concentrations of NO2 (expressed as a fraction of NOx) from off-site sources only
exceeded the criterion at most off site permanent residential receptor locations, as well as both
commercial areas of the Hotel Strip along Dixon Road and in the vicinity of the entrance of the TPIA
(CRs ranged from 2.1 to 0.8). It is important to recall that an actual exceedance of the criterion has not
been recorded in the area, demonstrating the conservatism of the predicted modelled values for ground
level concentrations of NO2.
Since the maximum one-hour concentration of NO2 predicted for existing ambient conditions already
exceeded the criterion at all but one receptor location, the combination of off-site and on-site sources
resulted in the prediction of substantial exceedances of the one-hour criterion of 400 µg/m3 for NO2.
Greater predicted exceedances were expected to occur at locations near the TPIA itself and in the areas
of commercial activity. Predicted one-hour maximum concentrations of NO2 in Etobicoke at
Longbourne Dr. and Willowbridge Rd. were greater than 2.5 times the criterion. Every receptor
identified in the study experienced a prediction for an exceedance of NO2 for ground level
concentrations from both TPIA and off-site sources combined.
Ground level concentrations of NO2 predicted through modelling either at the TPIA or at off-site
locations consistently overestimated the historical concentration levels actually experienced through
monitoring. This fact may be considered acceptable, since it is preferred that the assumptions associated
with risk of adverse effects be conservative, and therefore predict greater potential for health impacts
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than actual experience would suggest or support.
No gauge was available to determine the relative severity of exposure conditions at any receptor site.
Modelled results produced a one-time occurrence for an event. Important additional information would
include possible health risk associated with increased frequency of exposure or with conditions of
prolonged duration of exposure. Thus it would be impossible to predict effects beyond irritation in
response to a one-hour exposure.
Although there is no MOE annual AAQC for NO2 the Canadian Federal government through
Environment Canada has stipulated an annual ambient air quality objective (NAAQO) of 50 ppb or 100
µg/m3. Based on this annual objective, chronic exposures to NO2 from the facility would be acceptable
(all values less than 50% of the objective). Predicted annual average ground level concentrations for
NO2 (expressed as a fraction of NOx) for all phases were below the objective of 100 µg/m3 at all
receptor locations in this study (Table 29, Table 32 and Table 35).
Since exposures to oxides of nitrogen in the ambient environment are never observed in isolation, and
they are always found in conjunction with emissions from other sources (black smoke, elemental carbon,
diesel emissions and biogenic materials such as allergens), chronic exposure to predicted concentrations
of NO2 would result in some noticeable impacts on susceptible individuals. A precise prediction of the
health impacts specifically attributed to NO2 from both TPIA and off-site sources combined, but they
would likely be small for the large majority of the population in the study area.
3.3
HHRA for Sulphur Dioxide (SO2)
3.3.1
Sources of SO2
On a global scale, most SO2 is produced by volcanoes and by the oxidation of sulphur gases produced
by the decomposition of plants. The main anthropogenic source of SO2 is coal combustion. Large point
sources include non-ferrous smelting and electric utilities supplied by coal combustion. Sulphur occurs
as a few percent in crude oil, but is reduced to the parts per million level during refining into gasoline,
diesel and other fuels. In Canada, limits to the content of sulphur in fuels have been set and are very
stringent, and these are expected to be achieved in the near future.
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3.3.2
Predicted Concentrations of SO2
3.3.2.1
TPIA Sources Alone
Results for modelled ground level concentrations of SO2 at selected receptor locations based on air
traffic and ground operations scenarios for the TPIA are shown in Table 37. The results of modelled
impacts of the TPIA operations alone are presented for each of the years 2000, 2005, 2010 and 2015.
The scenarios used by RWDI to generate predicted concentrations have taken into account the
anticipated construction and operational changes for ground-based activity as well as expected growth in
aircraft operations during those years. The highest concentration at a chosen receptor was the maximum
off-site location. Lower concentrations were predicted at the approximate intersection of Hwy 427 and
Dixon Road that is the main public access to the TPIA. Concentrations at other receptor locations have
been estimated based on concentration isopleths for the maximum one-hour concentration of SO2 as
described in the RWDI Phase 1 to 3 Report (2003a).
Additional modelled concentrations were prepared by RWDI for predicted concentrations of SO2 at the
location of the OPSIS monitoring station located adjacent to the Runway 24L (see the Phase 1 to 3
Report, RWDI, 2003a). Maximum predicted one-hour concentrations for SO2 at this location were 643,
217, 191 and 213 µg/m3 for the years 2000, 2005, 2010 and 2015 respectively. The expected ground
level concentrations at this location were somewhat lower than at the point of maximum impact found
by the model.
Table 37
Maximum Predicted One-hour SO2 Concentrations From TPIA Sources
Alone (µg/m3)
Receptor Location
Maximum Off-Site
Maximum at Hwy 427 and Dixon Road
Maximum at Hotel Strip Dixon Road
Longbourne Dr & Willowbridge Rd, Toronto
Centennial Pk Rd (School), Toronto
Audubon Blvd, Mississauga
County Court Road, Brampton
Cattrick St., Malton
2000
2005
2010
2015
643
150
100
50
20
20
15
20
216
140
80
50
25
20
10
25
191
150
90
55
25
20
15
30
218
200
160
65
25
20
15
30
The health-based regulatory criterion for a 1-hour concentration of SO2 established by the MOE is 250
ppb (690 µg/m3). For purposes of this assessment, and to be conservative, it has been assumed that SOx
and SO2 are interchangeable. Based on the incremental increase in SO2 expected to occur under worst
case conditions for the TPIA alone, the concentration ratio (CR) was less than one for each year assessed
as shown in Table 38. All values in Table 37 were less than the criterion of 690 µg/m3. The CR
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expresses the ratio between the actual or anticipated level of exposure and the regulatory limit. This
suggests that using the health criteria accepted by the MOE, no adverse effects could result from acute
exposure to emissions containing SO2 from the operation of the TPIA.
The CR values for predicted ground level concentrations for TPIA operations (see Table 38) using the
Ontario AAQC (see Table 44) were all less than a value of one, indicating predicted ambient air
concentrations of SO2 from the TPIA were less than the Ontario ambient air quality criteria for the
maximum one-hour value.
Table 38
Concentration Ratios for Maximum Predicted One-hour SO2 Concentrations From
TPIA Sources Alone
Receptor Location
2000
2005
2010
2015
Maximum Off-Site
Maximum at Hwy 427 and Dixon Road
Maximum at Hotel Strip Dixon Road
Longbourne Dr & Willowbridge Rd, Toronto
Centennial Pk Rd (School), Toronto
Audubon Blvd, Mississauga
County Court Road, Brampton
Cattrick St., Malton
0.93
0.22
0.14
0.07
0.03
0.03
0.02
0.02
0.31
0.20
0.11
0.07
0.04
0.03
0.01
0.04
0.28
0.22
0.13
0.15
0.04
0.03
0.02
0.04
0.32
0.29
0.23
0.09
0.04
0.03
0.02
0.04
3.3.2.2
Off-site Sources Alone
Table 39 presents the modelled SO2 concentrations expected for the community for the base year 2000.
This case is designed to demonstrate the projected impacts of the various mobile and fixed sources of
emission to the area surrounding the TPIA, specifically excluding the activities of the TPIA. Off-site
sources were based on emission inventories for the area, traffic patterns, etc.
Based on contributions from off-site sources (existing background) recorded for the year 2000, predicted
maximum one-hour concentrations for SO2 would exceed the criterion of 690 µg/m3 (772 µg/m3). It is
important to recognize that the modelled maximum one-hour values are single maxima for a specified
location. The results show that ground level concentrations of SO2 due to off-site sources could on
occasion approach the one-hour AAQC. Another AAQC for SO2 was available based on 24-hr average.
Twenty-four-hour averages provide better bases for evaluating expected health impacts because they
indicate potential duration of exposure to elevated concentrations of pollutant gases. Predicted ground
level annual average concentrations at the chosen risk assessment receptor locations were not available.
Predicted concentrations from off-site sources in the community could exceed the one-hour maximum
concentration criterion, but not the annual AAQC.
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Table 39
Maximum Predicted One-hour SO2 Concentrations From Off-site Sources Alone
Receptor Location
Maximum Off-Site
Maximum at Hwy 427 and Dixon Road
Maximum at Hotel Strip Dixon Road
Longbourne Dr & Willowbridge Rd, Toronto
Centennial Pk Rd (School), Toronto
Audubon Blvd, Mississauga
County Court Road, Brampton
Cattrick St., Malton
Table 40
772
600
650
650
500
650
400
350
Concentration Ratios for Maximum Predicted One-hour SO2 Concentrations From
Off-site Sources Alone
Receptor Location
Maximum Off-Site
Maximum at Hwy 427 and Dixon Road
Maximum at Hotel Strip Dixon Road
Longbourne Dr & Willowbridge Rd, Toronto
Centennial Pk Rd (School), Toronto
Audubon Blvd, Mississauga
County Court Road, Brampton
Cattrick St., Malton
3.3.2.3
SO2 from Off-site Sources (µg/m3)
CRs for SO2 from Off-site Sources
Alone
1.12
0.87
0.94
0.94
0.72
0.94
0.58
0.51
TPIA and Off-site Sources Combined
Table 41 presents the modelled SO2 concentrations expected from the combination of off-site sources
and sources including the TPIA for the base year 2000, 2005, 2010 and 2015. This case combines the
projected impacts of the various mobile and fixed sources of off-site emissions in combination with the
activities and operations of the TPIA. The maximum off-site predicted one-hour concentration of SO2
and predicted concentrations in the vicinity of the commercial hotel strip and main entrance to the TPIA
all exceeded the criterion in all years modelled for this case. All values for one-hour maxima at
residential receptors were less than the one-hour AAQC of 690 µg/m3.
Results presented in Table 41 suggest that over the period of the year for which predictions of ground
level concentration were made, there would be occasions when the AAQC would be exceeded.
Although the predicted contribution from the TPIA itself was relatively small, when combined with
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existing off-site sources, some exceedance of the AAQC could be expected. Actual monitoring data
both on the TPIA property and at Centennial Park suggest that the model is somewhat conservative, and
that the predicted one-hour events could be rare. This is discussed in more detail below.
Table 41
Predicted Maximum One-hour SO2 Concentrations From TPIA and Off-site
Sources Combined (µg/m3)
Receptor Location
Maximum Off-Site
Maximum at Hwy 427 and Dixon Road
Maximum at Hotel Strip Dixon Road
Longbourne Dr & Willowbridge Rd, Toronto
Centennial Pk Rd (School), Toronto
Audubon Blvd, Mississauga
County Court Road, Brampton
Cattrick St., Malton
Table 42
2005
2010
2015
884
700
700
675
500
650
400
400
774
700
700
650
500
675
400
400
812
750
750
650
500
650
400
400
845
750
750
650
500
650
400
400
Predicted Maximum One-hour SO2 Concentration Ratios From TPIA and Off-site
Sources Combined
Receptor Location
Maximum Off-Site
Maximum at Hwy 427 and Dixon Road
Maximum at Hotel Strip Dixon Road
Longbourne Dr & Willowbridge Rd, Toronto
Centennial Pk Rd (School), Toronto
Audubon Blvd, Mississauga
County Court Road, Brampton
Cattrick St., Malton
3.3.2.4
2000
2000
2005
2010
2015
1.3
1.0
1.0
1.0
0.7
0.9
0.6
0.6
1.1
1.0
1.0
0.9
0.7
1.0
0.6
0.6
1.2
1.1
1.1
0.9
0.7
0.9
0.6
0.6
1.2
1.1
1.1
0.9
0.7
0.9
0.6
0.6
Predicted Maximum Annual Average SO2 Concentrations
Results of modelling for annual average concentration of oxides of sulphur are described in Table 43.
These maxima are for modelled values expected at a specific location near the TPIA. The annual
average measured at the point of maximum off-site concentration from off-site sources alone of 18
µg/m3 (6.5 ppb) for the base year 2000 was approximately 33 % of the annual AAQC for oxides of
sulphur (20 ppb). The predicted annual average SO2 concentration expected at the Centennial Park
location from both TPIA and off-site sources combined was 9 µg/m3 (3.3 ppb) (RWDI, 2003a). The
annual average concentration actually monitored at Centennial Park in 2000 of 3.6 ppb was very close to
the maximum level predicted by the model.
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Table 43
a
Maximum Annual Average SO2 Concentrations (µg/m3)
YEAR
TPIA Sources Alone a
Off-site Sources Alone
Both
2000
2005
2010
2015
5 (1.8 ppb)
2.4 (0.9 ppb)
2.8 (1.0 ppb)
3.4 (1.2 ppb)
18 (6.5 ppb)
-
18 (6.5 ppb)
18 (6.5 ppb)
18 (6.5 ppb)
18 (6.5 ppb)
Modelled values reported by RWDI
Values for combined maximum expected concentrations of SO2 from both TPIA and off-site sources
combined (Table 43) for the years 2000 through 2015 will remain below the annual AAQC, but show
that local impacts for oxides of sulphur are unlikely to change into the future.
Table 44
Ambient Air Quality Criterion and Measured SO2 Levels in 2000
Annual AAQC Mean
SO2
1 Hour AAQC
24 hour AAQC
20 ppb (55 µg/m3)
250 ppb (690 µg/m3)
100 ppb (275 µg/m3)
Annual Mean
1 h max SO2a
24 h max SO2
Toronto West Centennial
Park
3.6 ppb (10 µg/m3)
165 ppb (455 µg/m3)
24.8 ppb (68 µg/m3)
Brampton, Main St N
–(insufficient data)-
50 ppb (138 µg/m3)
11.1 ppb (30.6 µg/m3)
JURISDICTION
Ontario
LOCATION
a
b
Maximum observed (MOE year 2000 data)
Conversion used for SO2 in ppb into µg/m3 assumed the factor was (276 µg/m3 /100ppb)
The AAQC for the annual average concentration of SO2 is 20 ppb (Table 44). In the vicinity of the
TPIA, the annual average for SO2 is predicted to be 33% of the AAQC. In the GTA, there was no
monitored location that recorded an annual average for SO2 greater than 5.2 ppb (14.3 µg/m3) during
2000, and at Centennial Park, the annual mean was 3.6 ppb (~10 µg/m3). Thus, it is likely that the
model predictions for annual average SO2 are not overly conservative.
Predictions of ground level concentrations that would permit comparison to the 24-hour AAQC set by
the MOE were not available. Although such information could provide a more reliable basis for
assessment of acute health responses to SO2, monitoring data for the study area recorded at MOE
stations (see Table 44) do not show that one-hour maximum SO2 concentrations were exceeded in the
year 2000 at Centennial Park, or Main St in Brampton. Recorded maximum one-hour SO2 at the OPSIS
monitoring location on the TPIA property was 380 µg/m3 in the year 2000. The maximum modelled
one-hour concentration for this location in 2000 was 643 µg/m3, suggesting that the modeled values may
be conservative (predicts higher levels than actually experienced). At Centennial Park, there was a
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smaller difference between modelled and actual maximum one-hour SO2 concentrations (500 µg/m3
modelled versus 455 µg/m3 monitored for the year 2000). Therefore, it should be accepted that the
predicted concentrations from modelling were not overly conservative.
The primary concern of this assessment is the contribution of the TPIA to potential for health impacts to
be experienced off-site. The CRs for modelled predicted annual average concentrations at the point of
maximum off-site concentration from the TPIA operations (Table 45) were quite low (CR = 0.04 to 0.1).
The fact that they are so low indicates that the exceedance of the one-hour criterion may be very
infrequent.
By comparison, CRs for annual average SO2 from off-site sources that are important contributors to
predicted concentrations were much higher (CR = 0.33). The annual average AAQC for SO2 is healthbased. The off-site sources provide by far the greater contribution to the daily exposure to SO2 in urban
community that surrounds the TPIA.
Table 45
Summary Annual Concentration Ratios for SO2 a
Year
2000
2005
2010
2015
TPIA Alone
Off-site Sources Alone
TPIA and Off-site Sources
Combined
0.09
0.33
0.04
0.05
0.06
0.33
0.33
0.33
0.33
a
AAQC Annual SO2 = 20 ppb or 55 µg/m. CR is based on maximum modelled concentration at the location of maximum off-site concentration.
3.4
Particulate Matter (PM10)
As discussed in Section 4.3, an HHRA could not be performed for PM10 due to the absence of complete
predictive data for TPIA aircraft and construction-related fugitive emissions. Background information
on PM10 that may be helpful in developing an HHRA for PM10 in future has been assembled in this
Section.
Particulate matter (PM10) is the generic term for a broad class of chemically and physically diverse
substances that exist as discrete particles (either liquid droplets or solids) over a wide range of sizes.
PM10 originates from a variety of anthropogenic stationary and mobile sources as well as from natural
sources. PM10 may either be emitted directly or formed in the atmosphere by the transformations of
gaseous emissions of compounds including NOx, VOCs, and sulphur oxides (SOx). The chemical and
physical properties of PM10 vary greatly with time, region, meteorology, and source category, thus
complicating the assessment of health and welfare effects.
Some examples of Air Quality Standards, regulatory criteria, objectives and guidelines are reproduced in
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Table 46.
Table 46
Ambient Air Quality Criteria for PM10 and PM2.5
Regulatory Authority/Agency
Ambient Air Quality Criteria
MOE Interim Guideline
50 µg/m3 for PM10
CCME
30 µg/m3 for PM2.5 by 2010 24-H average 98th percentile over three
consecutive years
BC Environment
50 µg/m3 (a 24-h period guideline)
Health Canada
California
U.S. EPA
World Health Organization
Reference Concentration: PM10 = 25 µg/m3 (24-H avg)
PM2.5 = 15 µg/m3 (24-H avg)
50 µg/m3 (a 24-h standard)
30 µg/m3 (an annual standard)
50 µg/m3 (annual), 150 µg/m3 (a 24-H maximum)
15 µg/m3 PM2.5 (annual), 65 µg/m3 PM2.5 (24-H)
70 µg/m3 (guideline)
PM10 refers to particles with an aerodynamic diameter less than or equal to a nominal 10 micrometers.
A detailed discussion of the physical composition and potential health impacts of particulate matter have
been described in the United States EPA Third Draft Criteria Document for Particulate Matter (U.S.
EPA, 2002b). PM10 is a measure of both fine particles (less than 2.5 microns (µm)) and the coarse
particle fraction (particles between 2.5 and 10 µm). In addition to the evidence found for health effects
associated with fine particles, some research has suggested that exposure to coarse fraction particles is
associated with aggravation of asthma and increased respiratory illness. There may be chronic health
effects associated with long-term exposure to high concentrations of coarse particles, especially in
occupational settings (See Appendix E and Section F-4.0 of Appendix F).
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4.0
DISCUSSION OF RESULTS
4.1
HHRA for VOCs, Carbonyl s and PAHs
A detailed discussion of the HHRA for VOCs, carbonyl compounds and PAHs, and the results of the
risk assessment, can be found in Section 2. This section discusses the potential for adverse health
effects from predicted exposures to VOCs, carbonyl compounds and PAHs from the TPIA, based on the
HHRA results. These chemicals are known to cause systemic effects on the body as a result of longterm exposures. As discussed in Section 2, the methodology for assessing risks of exposure to these
chemicals is based on a comparison of predicted exposure rates with exposure rates considered to be
safe.
4.1.1
Exposure to Predicted TPIA Emissions Alone
Lifetime cancer risks from exposure to modelled concentrations of VOC, carbonyl compounds and
PAHs from current and future TPIA operations were calculated for the most sensitive receptor groups
for both recreational and commercial exposure scenarios (preschool child and adult female worker,
respectively). In all cases, risks associated with these predicted chronic exposures were below than the
acceptable level of risk of one in a million (1x10-6) for the years 2000, 2005, 2010 and 2015. Cancer
Risk Level (CRL) values for the commercial sites were approximately 2 to 5,000 times lower than the
acceptable risk level of 1-in-1-million. CRL values for the residential sites were approximately 9.5 to
7,500,000-fold lower than the 1-in-1-million acceptable risk level. These results, which are already
based on conservative assumptions, suggest that the chemicals assessed are estimated to be present in
concentrations that are much lower than levels that may be associated with cancer risks.
The human health risk assessment (HHRA) for potential non-cancer health effects from long-term
exposures indicate that, with the exception of acrolein, none of the chemical exposures predicted from
current or future TPIA operations exceeded the relevant exposure limit for any of the locations assessed.
In other words, all of the Exposure Ratios were below 0.2, except for a few of the modelled
concentrations for acrolein. Exposure Ratio (ER) values for the commercial sites, excluding acrolein,
ranged from 5 times lower to 13 orders of magnitude lower than the acceptable risk level of 0.2. ER
values for the residential sites ranged from 1.4 times lower to 12 orders of magnitude lower than the 0.2
acceptable risk level. These results, which are already based on conservative assumptions, suggest that
the chemicals assessed are estimated to be present in concentrations that are much lower than levels that
may be associated with non-cancer health risks from long term exposures.
Results of the assessment of the potential health impacts for exposures to ambient concentrations of
acrolein arising from TPIA emissions indicate that health risks at the commercial locations (i.e.,
locations directly adjacent to the TPIA) show minor exceedances of the established 0.2 risk benchmark.
For example, ERs for acrolein at the location of maximum off-site concentrations were estimated to
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range from 0.289 to 0.421, depending on which scenario year is evaluated. While these predicted ERs
do exceed the established risk benchmark of 0.2, given the small degree of exceedance (i.e., the highest
single value is just over 2 times above the risk benchmark) and the considerable degree of conservatism
inherent within the assumptions used in this assessment (see discussion of uncertainties in Section 5.3),
it is our opinion that the predicted airborne concentrations of acrolein emitted from the TPIA would not
result in any increase in health impacts to those working in the area surrounding the TPIA.
It is also important to note that the predicted health risks related to the location of maximum off-site
concentrations are related to exposures to the maximum airborne concentrations predicted for each of
chemicals. The conservative assumption is that the commercial adult worker was employed at this
location and was exposed to this maximum concentration each day, for the entire year being assessed.
Beyond the inherent conservatism in assuming maximal exposures, unlike the other modeled locations
(i.e., locations 2 through 8), the location of maximum off-site concentrations is not fixed but shifts
position around the site daily, depending a variety of site-specific conditions such as wind direction,
taxiing patterns, weather conditions, etc. Therefore, assuming an adult worker is present at this shifting
location and is exposed to the projected maximal air concentration is a very conservative assumption.
In summary, long term exposure to ambient concentrations of VOCs, carbonyls and PAHs from
predicted current and future emissions from the TPIA alone would not be expected to result in any
detectable health impacts to individuals living or working in the area surrounding the TPIA.
4.1.2
Contribution to Overall Health Risks
Although an assessment of potential risks from exposure to a given chemical from TPIA emissions
alone may indicate that no health risks would be anticipated, this does not preclude the possibility that
exposure from TPIA emissions could contribute to overall health risks in the context of all sources of
exposure, including off-site sources, where such health risks may exist. If predicted exposures to offsite sources and TPIA emissions combined is associated with potential adverse health effects, and if
TPIA emissions – although relatively small taken alone – represent a significant portion of the overall
chemical concentrations, then TPIA emissions would be considered to be making a contribution to
overall risk. The purpose of modelling emissions from off-site sources only (Phase 2) and from TPIA
off-site sources combined (Phase 3) was to provide a context for evaluating the contribution of TPIA
emissions to overall health risks, where potential risks from exposure to emissions from all sources may
exist.
The assessment of health risks from exposure to off-site sources was based on estimated exposures for
the year 2000 only. Results of the risk assessment indicate exceedances of the ER values for most offsite exposure locations for the following chemicals:
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•
1,3-butadiene;
•
benzene;
•
naphthalene; and,
•
1,2,4-trimethylbenzene.
These exceedances were only moderately above their respective toxicological reference points (i.e.,
within a factor of 10 above the reference level) and are typical for urban areas (refer to discussion in
Appendix B).
The assessment of health risks from exposure to predicted TPIA emissions and off-site sources
combined produced results very similar to those observed in the assessment of risk from exposure to offsite sources alone, with only marginally higher levels of risk.
As such, results of the assessment indicate that, though potential risks of adverse health effects may exist
from exposure (in the vicinity of the TPIA) to emissions of the above four chemicals from all sources,
the incremental contribution to this potential risk from TPIA sources alone is likely to be very small.
This conclusion is consistent with the fact that the estimated emissions from the TPIA represent about
2% of total hydrocarbons estimated to be emitted from all sources including automobiles and nearby
industrial activity.
4.1.3
Discussion of Key Assumptions in the HHRA for Long Term Exposures
4.1.3.1
Use of Environment Canada Data for Chemical Speciation
One of the key assumptions in developing this HHRA involved the development of a “fingerprint”
profile used to predict the concentration of individual chemicals based on the predicted concentrations of
total hydrocarbons (THC) at each of the assessed locations around the TPIA.
The development of concentrations for each of the chemicals of concern evaluated in the current
assessment was based upon a speciation profile developed by researchers at Environment Canada
(Graham and Ainslie, 1997). These data provide an up-to-date speciation profile for airports similar to
the Toronto Pearson International Airport, based upon current fleet specifications and fuel mixtures.
Based upon a review of three available speciation profiles, these data were considered to be the most
representative of conditions at the TPIA, and selected for primary use in the current assessment.
It is important to note that the U.S. EPA has published recommended speciation profiles which do not
completely agree with those specified by the Environment Canada research. For comparison purposes,
an assessment of the risks related to exposures to a subset of the chemicals of concern which were
already close to the respective risk threshold using the Environment Canada profile (i.e., acetaldehyde,
benzene, 1,3-butadiene, and formaldehyde), was also conducted for predicted TPIA emissions alone,
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using the US EPA 1098 fractionation profile. If the US EPA 1098 fractionation profile were used to
predict ambient concentrations for these chemicals, the risks predicted for acetaldehyde, benzene, and
1,3-butadiene for TPIA emissions only would increase 1.3-fold, 7.8-fold, and 10.8-fold, respectively,
while the risks predicted for formaldehyde would remain about the same (1.1-fold less). A complete
overview of the differences between the two profiles can be obtained by comparing the ambient air
concentrations predicted using each of the profiles in Tables 6 and 7.
The source of the U.S. EPA HAPs emission factors and chemical species profiles for commercial
aircraft outlined in the US EPA 1098 document, are based largely on the work by Spicer (1984). This
work was conducted in the mid-1980s and reported in scientific literature during the mid-1990s. The
data were derived from the testing of two smaller aircraft engines: one commercial and one military, for
a variety of PAHs (FAA, 2003).
These data have been subsequently evaluated by the Federal Aviation Authority (FAA) in the United
States and, while they acknowledged that the work by Spicer was thorough and considered high quality
(including the testing of engine emissions under varying power settings), the data was recognized as
being appreciably limited as only two aircraft engines were tested (FAA, 2003). Testing was not
conducted on the larger commercial engines currently making up the bulk of the aircraft fleet at the
TPIA (i.e., Boeing 737 class), but on smaller military and executive class jets. As a practical matter, the
FAA has indicated that the EPA 1098 speciation profile is intended to be used for preparation of
estimates in support of macro-scale analyses of aviation-related emissions, and that they were not
intended to provide exact estimates of emissions from any particular aircraft or airport facility. U.S.
EPA indicates that due to unconfirmed assumptions, many uncertainties, and lack of data, these
emission factors are imprecise and deficient (FAA 2003). In particular, engine specifications and fuel
compositions have changed considerably in the past two decades, as technologies and methodologies
have improved (as discussed in Appendix G).
Based upon these and other analyses, the Environment Canada data was believed to provide a more
accurate and representative reflection of speciated emission patterns for the TPIA (e.g., fleet engine and
fuel specifications), and that the use of the US EPA profile would likely overestimate risks. More
detailed discussion of these profiles and their relative advantages and disadvantages can be found in
Appendix F.
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4.1.3.2
Use of Recent Scientific and Regulatory Reviews of Formaldehyde
Given the potentially elevated concentrations of formaldehyde and related carbonyls emitted by jet
engines from the TPIA, it is important to evaluate the toxicology of this compound carefully. The U.S.
EPA (1991) provides a cancer slope factor based upon the incidence of squamous cell carcinoma in rats.
However, recent research (CIIT, 1999) has provided a more detailed biologically-based model for doseextrapolation of upper respiratory tract cancers by which the cancer slope factor can be calculated for
humans. This research has been reviewed and adopted by a number of regulatory agencies (GC/EC/HC,
2000b; WHO, 2002; Liteplo and Meek, 2003), and was selected for use in the current assessment as it
represents the most up-to-date analysis of the toxicological mechanism of formaldehyde. The difference
between the older EPA slope factor and the updated CIIT slope factor is quite significant: using the
older data would result in predicted cancer risks related to exposures to formaldehyde that are
approximately 68,500-fold higher than cancer risks predicted using the more current data.
4.2
HHRA for CO, NO2 and SO2,
A detailed discussion of the HHRA for CO, NO2, SO2 and the results of these risk assessments can be
found in Section 3. The current section discusses the potential for adverse health effects from predicted
exposures to these substances, based on the HHRA results.
This section discusses the potential for adverse health effects resulting from predicted exposures to CO,
NO2 and SO2, and also presents a discussion of issues and information regarding PM10 issues. These
chemicals are not known to cause systemic effects on the body, but rather produce effects at the point of
contact (i.e., the respiratory system). As discussed in Section 2, the methodology for assessing risks of
exposure to these chemicals is based on a comparison of predicted ambient air concentrations with air
quality limits established by regulatory agencies. These limits are designed to be protective of human
health, and are based on clinical and epidemiological evidence for adverse health effects from exposure
to these chemicals. For each chemical assessed, a discussion of relevant clinical and epidemiological
evidence used to interpret the results of this HHRA is provided, as well as a discussion of relevant
methodological considerations.
As discussed in general in Section 2, and for each chemical in Section 3, the HHRA for these chemicals
was constrained in some cases due to the type of predicted and measured ambient air concentration data
available. Potential health effects from short-term (acute) exposures were considered for all four
chemicals. Data for predicted long-term (chronic) exposure to NO2 and SO2 were limited to annual
average concentrations at the location of maximum off-site ground level concentration, with no
reference to predicted annual concentrations at other receptor locations. In the case of carbon monoxide,
chronic exposures (e.g., annual 24-hr average concentrations) were not considered relevant for the
purposes of estimation of health effects. An assessment of potential health risks for exposure to PM10
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could not be performed, since predicted emissions and exposures that include the operations of aircraft
could not be generated.
For each of these chemicals or chemical groups, predicted short-term concentrations of pollutants were
limited to maximum one-hour values for the year in question (2000, 2005, 2010 or 2015). In the event
that predicted concentrations exceeded the established one-hour criterion, no reference was available to
suggest how frequently such an event might occur. Frequency information is a critical component of
exposure assessment, as well as for the estimation of responses to acute exposure to predicted pollutant
concentrations.
The evaluation of potential health impacts from the current and future predicted maximum one-hour
concentrations of these chemicals within the TPIA study area years was based on three types of
comparisons:
•
•
•
comparisons to various ambient air quality criteria adopted by regulatory agencies;
comparison of various sources that contribute to ambient air concentrations; and,
consideration of health impacts associated with various sources of these substances as
documented in the published biomedical literature.
4.2.1
Carbon Monoxide
4.2.1.1
Exposure to Predicted TPIA Emissions Alone
Predicted maximum one-hour concentrations from TPIA operations alone resulted in one exceedance of
the AAQC for CO: in the year 2000 only, and only at the location of maximum off-site concentration.
The exceedance in this single case was very minor: CR = 1.09. Predicted concentrations in the TPIA
entrance and the commercial areas were half, or less than half of the AAQC (i.e., CRs ≤ 0.5). For all
residential receptor locations identified in this study, in 2000 and in subsequent years (2005-2015),
contributions of CO from TPIA operations to maximum one-hour concentrations of CO were small (CRs
ranged from 0.03 to 0.23). Predicted CO concentrations at or near the entrance to the TPIA and along
the hotel strip would not exceed health-based exposure limits (CRs <1.0) based on modelled maximum
one-hour concentrations from the TPIA operations alone (Table 19).
Health impacts that have been characterized for exposure of sensitive persons to elevated concentrations
of CO are generally based on increased concentrations over an eight-hour period. Incremental increases
in ambient levels of CO in comparison to prolonged average exposure to CO have been linked to
increased hospitalization in large populations. The one-time maximum modelled one-hour
concentration of CO from combined sources predicted for the ambient environment was less than the
concentrations of 42 to 102 ppm required to produce 2% COHb, and less than the 117 ppm required to
modify cardiovascular function in sensitive people (Allred, 1991). Therefore, direct adverse health
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impacts would not be expected based on the single 1-hr maximum exceedance indicated by the analysis
of the air concentration modelling results. See also the discussion of uncertainties, which suggests that
there is some degree conservatism in the modelling, which further supports the interpretation of no
expected adverse health effects.
For the purpose of health assessment, the most appropriate guidance regarding potential effects of CO is
predicted concentration over a period of eight hours. Sub-chronic exposures (eight hours) to elevated
ambient levels of CO have been directly associated with health impacts. Predicted maximum 8-hour
average concentrations for CO at the location of maximum off-site concentration were predicted for all
years and all phases, and all were well below the AAQC of 15,700 µg/m3. CR values were 0.57 for the
year 2000 (the year of the exceedance of the CR based on 1-hr maximum values at this location), and
about 0.4 for subsequent years.
Overall, the interpretation of the results leads to the conclusion that no adverse health effects from
exposure to predicted levels of CO from the TPIA alone are expected.
4.2.1.2
Contribution to Overall Health Risks
Maximum one-hour concentrations of CO due to off-site sources that excluded TPIA operations at the
various receptor locations in the community were all well under the AAQC (CR range 0.1 to 0.32).
Concentration ratios that describe potential impacts from combined TPIA and off-site sources are shown
in Table 23. The maximum one-hour predicted concentrations of CO that could be experienced by
people residing, working or partaking in recreational activities in the 7.5 km radius of the TPIA would
be less than the one-hour criterion (CR range 0.17 to 0.90) at all locations for all years, with the
exception of the location of maximum off-site concentration in the year 2000 (CR = 1.25). Modelled
maximum 1-hour CO concentrations for subsequent years were not predicted to exceed the AAQC based
on current expectations for growth and its effects on urban air quality in Toronto (CR values below 0.8
for commercial locations, and 0.4 or less for residential locations). As discussed above, despite the
(minor) exceedance for one predicted modelling result in 2000 at the maximum off-site location, no
impact on human health from CO emissions predicted from the TPIA and off-site sources combined is
expected. Predicted CO emissions would therefore not be expected to contribute to overall adverse
health effects.
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4.2.1.3
Discussion of Biomedical Evidence for Health Effects
Incremental changes in health due to effects of CO are generally assessed on the basis of a specified
incremental deviation from a mean 8-hour, rather than on a single maximum 8-hour ground level
concentration. It is apparent that ambient levels of CO well within the accepted regulatory limits may
produce adverse responses in susceptible persons aged 40 > 60 years (Mann et al., 2002). Impacts were
clearly greater among individuals already diagnosed with either arrhythmia, congestive heart failure or
both. In a study in Southern California, first-time patients with no prior history of heart disease were
much less likely to require hospital care.
Where the mean 8-hour concentration of CO reached 2,510 µg/m3 (SD ± 1,480 µg/m3) an increase of
1,150 µg/m3 CO could have adverse health impact on individuals already diagnosed with congestive
heart failure or arrhythmia. The 8-hour maximum CO concentration experienced in cities of the GTA
(4,255 to 5,750 µg/m3) is just above the 8-hour mean for Southern California. The range of 8-hour CO
concentrations experienced in the California study area was nearly twice those annually experienced in
Brampton, Mississauga or Etobicoke (Mann et al., 2002). Modelled estimates of maximum 8-hour
ground level concentration (Table 24) for CO in the communities around the TPIA were for the worst
case, maximum off-site concentration experienced during a year. A more comprehensive study would
be necessary to estimate the frequency of events leading to conditions when CO concentrations might
result in increased cardiovascular morbidity.
Urban air pollution is recognized as a public health concern by a large number of regulatory authorities
(e.g. Health Canada; the Ontario Medical Association, U.S. EPA, WHO). Groups of sensitive
individuals with pre-disposing diseases have been identified as those most likely to show adverse health
effects from exposures to elevated ambient air pollution. These sensitive sub-population groups are
broadly categorized as the very young and members of the community greater than sixty years of age.
Among the latter, those suffering from a group of related cardiovascular diseases including congestive
heart failure, ischemic heart disease and chronic obstructive pulmonary disease show greater risks for
adverse health outcomes associated with elevated levels of air pollution.
Some studies have shown that CO was associated with primary hospital admissions for congestive heart
failure, ischemic heart disease and arrhythmia (Burnett et al., 1997). Recent studies have re-examined
this potential relationship between ambient CO concentrations and hospital admissions for ischemic
heart disease (IHD) among individuals already diagnosed with arrhythmia and congestive heart failure
(a sensitive sub-group) and ambient air pollutants (Mann et al., 2002, see Appendix C for details). The
study reported that high ambient concentrations of CO (1 ppm, 8 hour average or 1,200 µg/m3) resulted
in a 3.6% increase in daily hospital admissions for congestive heart failure and a 3% increase in
admissions for cardiac arrhythmia for people with pre-diagnosed cardiovascular conditions (Mann et al.,
2002). Smaller associations were observed in people not pre-diagnosed with cardiovascular conditions.
However, PM10 concentrations (24-hr) were also elevated (>50 µg/m3) more than half the time in the
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study area. Thus, this study could not isolate CO as the single causative factor for the increase in
hospital admissions.
Controlled exposure studies conducted on individuals with pre-disposed cardiovascular diseases have
shown associations between exposures to CO and various cardiovascular biomedical end points. For
example, studies conducted in isolation chambers where individuals with ischemic heart disease (IHD)
were exposed to controlled and monitored concentrations of carbon monoxide demonstrate that
sufficient concentrations of carbon monoxide (117 ppm or ~140,400 µg/m3) will cause adverse effects
on their heart function, including symptoms of angina during exercise (Allred et al. 1991; see Appendix
C for details).
No overt human health effects have been association with CO unless blood carboxyhemoglobin (COHb)
concentrations were 2% or greater (see Appendix C). To achieve a COHb concentration of 2% in the
blood human, volunteers had to be exposure to air concentrations of CO between 42 and 102 ppm for up
to an hour (Allred et al., 1991).
Evidence that there may be an association between elevated ambient levels of CO as a portion of the air
pollution mixture, and cardiovascular disease (including ischemic heart disease and congestive heart
failure) has been obtained from a variety of epidemiological studies (Appendix C). Experts in this field
conclude that products of emissions from automobiles and trucks are the primary source of this
association (Mann et al., 2002), but that CO does not appear to be a primary causative agent. Rather,
CO is an indicator, and the appropriate interpretation of the susceptibility of persons with cardiovascular
diseases to ambient levels of CO lies with the co-pollutants generated by the combustion of gasoline and
diesel, and other fuels (A full discussion of the effects of exposure to CO at ambient levels present in
urban air is given in Appendix C).
The available literature demonstrates the strongest association between increased mortality in sensitive
populations and elevations in the concentrations of ambient particulate matter. Multi-pollutant models
report weak associations between increased mortality and other air pollutants, such as oxides of
nitrogen, and carbon monoxide. Generally, such associations have not been found to be significant in
rigorously analyzed epidemiological studies (Samet et al., 2000).
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4.2.2
Nitrogen Dioxide (NO2)
Oxides of nitrogen (NOx) consist of a mixture of nitric oxide (NO) and nitrogen dioxide (NO2). The
health effects of NOx have been largely attributed to NO2 effects in the lung (Persinger et al., 2002). Air
Quality Objectives (AQOs) established by regulatory agencies typically identify NO2 rather than NOx.
The HHRA therefore focusses largely on potential health effects of NO2.
Modelled annual average concentrations of NO2 for the TPIA alone, for off-site sources and for both
combined were available for the point of maximum off-site concentrations only. For off-site sources, an
annual average concentration of NOx was predicted for the Centennial Park MOE monitoring station.
No annual average concentrations for NO2 or NOx were predicted for other sites in the surrounding
community. Comparison between actual and modelled values for annual average concentrations of NO2
show that the model was conservative, and over-predicted the expected concentration of NO2 by
approximately two-fold.
The monitored annual average NO2 concentration in the recent past for both on-site and off-site
locations was substantially below the National Ambient Air Quality Objective (NAAQO) established by
Environment Canada.
4.2.2.1
Exposure to Predicted TPIA Emissions Alone
Based on predicted ground level concentrations of NOx, exceedances of the health-based criterion
maximum one-hour concentration of NO2 were predicted for each year modelled. These exceedances
were limited mainly to receptor locations near the TPIA boundary, but also were predicted to occur for
each year modelled at selected points within the community. Three of eight sites examined included
non-residential and commercial areas near the TPIA entrance and along Dixon Road where many hotels
are located. Additional modelled exceedances (CR > 1.0) were predicted at one site in Etobicoke (#4).
Predicted annual average NO2 concentrations contributed by the TPIA alone at the maximum off-site
receptor location, and at the Centennial Park MOE Station, were well below the NAAQO. The range of
Concentration Ratios (CRs) for the years 2000 –2015 was 0.38 to 0.50.
Health implications of a single event over a year of modelled values are difficult to predict. It is known
that the predicted maximum one-hour concentration of NO2 at off-site receptors would be sufficient to
exacerbate asthma for those already diagnosed with asthma, or for persons with recognized pre-existing
cardiovascular or respiratory conditions such as chronic obstructive pulmonary disease (COPD).
Predicted maximum one-hour concentrations of NO2 were well below concentrations considered
immediately dangerous to health, or sufficient to cause temporary or permanent physiological damage to
respiratory structures of the lung in exposed individuals. The health-based one-hour criterion has
substantial margins of safety built-in, and predicted concentrations from the model were conservative
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when compared to actual monitored levels on- and off-site. Historically, there has never been a recorded
exceedance of the NO2 criterion (AAQC) at MOE’s Centennial Park location, despite the fact that the
model predicted concentrations for the year 2000 that exceed the AAQC limit.
As a conservative conclusion, it is possible that exposure to future emissions of NO2 from the TPIA
alone may occasionally contribute to adverse health effects for some sensitive individuals, such as those
with asthma or other pre-existing cardiovascular or respiratory conditions. However, there is evidence
that the predicted concentrations are overestimates of the actual exposures that would take place.
4.2.2.2
Contribution to Overall Health Risks
Based on the modelled results for air emissions from off-site sources alone, maximum one-hour NO2
concentrations were predicted to exceed the criterion at least once in the year 2000 at every receptor
location examined in this study with one exception of (site #8: Malton). CR values ranged from 0.8 to
2.1. As stated above, there has never been a recorded exceedance of NO2 at either on- or off-site
monitoring locations in the vicinity of the TPIA. The model therefore appears to have overestimated
predicted concentrations by a factor of about 2 to 4. Using the historical monitoring data for the year
2000, CR values would have been below the criterion (0.4 to 0.53).
Modelled results of combined TPIA and off-site sources of NO2 for all years resulted in exceedances of
the one-hour maximum criterion at all of the eight receptor sites. CR values ranged from 1.1 to 2.8 for
residential locations, 2.8 to 3.8 for commercial locations, and 4.7 to 5.9 at the maximum off-site
location.
The predicted annual average concentrations for NO2 from off-site sources alone at the location of
maximum off-site concentration were within the annual NAAQO (CR = 0.37). Predicted annual
average concentrations for NO2 for TPIA and off-site sources combined, for all years, were also within
the annual objective (NAAQO) (CR range 0.7 to 0.8).
Exposure to the predicted maximum one-hour concentrations for NO2 from TPIA and off-site sources
combined at the location of maximum off-site impact would most likely result in adverse health effects
for persons receiving exposures in excess of one hour in duration. The predicted maximum off-site
concentration in the areas around the commercial and hotel areas near the TPIA would be both irritating
to normal healthy individuals (bronchial constriction) and likely to cause sufficient health distress in
asthmatics to lead some to seek medical attention.
At other receptor sites located away from the immediate TPIA boundary near Highway 427 and Dixon
Road, predicted maximum one-hour levels of NO2 from TPIA and off-site sources combined were
approximately twice as high as from off-site sources alone. While it is difficult to predict health impacts
for isolated events (i.e., no frequency data are available for these exceedances), the predicted future
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emissions NO2 from TPIA and off-site sources combined could result in temporary ground level
concentrations that could result in adverse health responses.
As pointed out above, the health-based one-hour criterion has substantial margins of safety built-in, and
predicted concentrations from the model were overestimated when compared to actual monitored levels
on- and off-site. Historically, there has never been a recorded exceedance of the NO2 criterion (AAQC)
at MOE’s Centennial Park location. It is also worth noting that predicted concentrations of NO2 for
residential locations from TPIA and off-site sources combined were substantially lower than values for
the location of maximum off-site concentration, and comparable to levels predicted from off-site sources
alone.
Overall, it can be concluded that the risk of adverse health effects from exposure to NO2 could be
increased by the contribution of predicted future emissions of NO2 attributed to the operations of the
TPIA.
4.2.2.3
Discussion of Biomedical Evidence for Health Effects
Oxides of nitrogen including NO2 are clearly toxic to the respiratory system in circumstances where
exposure concentrations are sufficiently high. The review of the recent biomedical literature
(documented in Appendix D) on the possible health impacts of acute exposure of humans to NO2
confirmed that both the 24-hr and one-hour Ontario AAQC of 200 µg/m3 (100 ppb) and 400 µg/m3 (200
ppb) (MOE, 2001) respectively, would be protective of human health for the purposes of assessing the
risks from exposure to NO2 alone. The review included a paper on an allergenic challenge to sensitive,
mildly asthmatic/allergic individuals.
Recent studies that have addressed the impact of traffic-related pollution on children and adults suggests
that there is a dose-response effect governing measurable impacts of air pollution that is associated with
the average annual level of some pollutants including particulate matter (PM2.5) and NO2 or acidic
vapour (Gauderman et al., 2002). Annual averages for NO2 and particulate matter experienced in
Etobicoke (Toronto), Brampton and Mississauga are generally above that recorded for the least polluted
community described in this study, and well below the communities studied at the upper end of the
pollution scale. Unlike studies that have made inter-city comparisons of the effect of pollutants on
mortality, there is insufficient basis for establishing a dose-response relationship between health impacts
associated with concentrations of NO2 in one community and frequency of such impacts in Etobicoke.
The only conclusion that can be drawn is that many urban areas where respiratory impacts have been
recorded have annual mean concentrations for NO2 which are considerably in excess of means observed
in Etobicoke, Mississauga and Brampton (Krämer et al., 2000).
Studies that estimate the effect of air pollution on the growth of lung function among children in
California suggest the pollutant(s) most clearly “responsible” for the reduction in growth are acid
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vapour, elemental carbon and fine particulate matter. These are pollutants that are most frequently
observed with diesel emissions. In terms of comparisons between Etobicoke, Mississauga and
Brampton and the pollutant profiles for communities in California described by Gauderman et al.
(2002), these communities would fall between the California communities of Lake Elsinore and
Riverside. However, great caution should be taken in making such comparisons, since it is generally
believed that the pollution mix observed in communities in North East of the US and Eastern Canada
share little in common with cities located in California (U.S. EPA, 2002b).
Therefore, since the predicted concentrations of NO2 were in excess of the AAQC values, there is a
possible risk of adverse health effects from NO2 arising from the commercial air transport activity of the
TPIA. A major uncertainty inherent in this provisional conclusion exists with respect to the
conservatism of the model used by RWDI to estimate emissions. These estimates apply directly to both
the interpretation of the expected operations at the TPIA and to the emission inventories used to evaluate
contributions from the community. In both instances, the dispersion models overestimated pollutant
concentrations when compared to actual monitoring data for the community. The predicted NO2
concentrations from the uses of the TPIA were the maximum hourly values. Average annual levels
(annual means) should be substantially less than those maximum one-hour levels. It remains unclear
whether model predictions would have sufficient accuracy and robustness to determine whether annual
means for these pollutants would undergo appreciable change from the years 2000 to 2015. The results
of dispersion modelling are not intended to be used as absolute indicators of magnitude. They function
as a predictive tool to assess the incremental changes in concentration.
High exposures to NO2 have been associated with adverse impacts on human health, and a broad range
of detrimental effects to the environment. The available epidemiological evidence shows that the
association between adverse health impacts and ambient concentrations of nitrogen dioxide is much
weaker than for associations with ambient concentrations of ozone and particulate matter. A fraction of
the oxides of nitrogen in ambient air are unequivocally identified as NO2. Adverse heath effects from
exposure to NO2 are considered more serious than exposures to similar concentrations of NOx.
In outdoor air, nitrogen dioxide is often highly correlated with other combustion products, notably fine
particulate matter. In most circumstances, nitrogen dioxide serves as a surrogate for all traffic-related
combustion products (Brunekreef and Holgate, 2002).
Recent research has shown associations between increased risk of respiratory symptoms and exposures
to NO2, proximity of homes to traffic arteries and traffic densities, especially truck traffic, although
these associations are less clear in the very young (see Section D-3.5.1 Appendix D). Most of these
studies have not been able to separate the associations between specified health effects and specific air
contaminants.
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A major deficiency in most studies is the lack of specific data to enable reliable estimations of
exposures, particularly to NO2 (see Sections D-3, Appendix D). Proximity to road traffic, census data
on car traffic and/or truck traffic, and self-reported traffic intensities were used in many studies as
proxies for exposure to traffic exhaust. Exposure modelling has been used to estimate exposures in some
studies. The separation of indoor from outdoor exposures has proved difficult, but critical to the
interpretation of causal associations give the high concentrations of NO2 that can arise from the many
indoor sources. Indoor sources of NO2 include primary and second-hand tobacco smoke, fuel oil and
natural gas heating furnaces, kerosene heaters, gas cooking stoves, and gas powered ice scrapers used in
hockey rinks. Increased relative risk for respiratory infections and illness in children has been
associated with high exposure to NO2 from gas-cooking stoves and gas-fired heating appliances.
Clinical evidence from controlled human exposure studies shows that the inhalation of high
concentrations of NO2 causes functional changes in the lung, in addition to biochemical and
morphological changes in the trachea, bronchi, bronchioles, alveolar ducts, and the proximal airways
(see Section D-3.4 of Appendix D). Decrements in lung function, particularly increased airway
resistance in resting healthy subjects has been observed after 2-hour exposures to NO2 at concentrations
of 4700 µg/m3 (~2500 ppb). The World Health Organization (IPCS, 1997) concluded that the available
data are insufficient to determine the nature of the concentration-response relationship to enable
predictions of effects at lower air concentrations.
No responses were observed in asthmatics exposed under controlled conditions for short time periods to
NO2 at concentrations of 500 µg/m3 (~250 ppb, or comparable to concentrations in poor air quality
urban environments); however, these patients showed greater responses to allergens administered
following a prior controlled exposure to NO2. These results provided evidence that allergic responses
among sensitive members of the population may be increased in response to ambient NO2 through the
enhancement of allergic reactions in the lung.
There have been frequent references to asthmatics being more sensitive to the effects of NO2 than nonasthmatic children. This is not supported by the epidemiology studies, and it is more likely that other
components of combustion emissions such as elemental carbon from diesel emissions are responsible for
the increased sensitivity of asthmatic children to traffic. Traffic-related air pollution is an established
source of irritability and is associated with increased frequency of access to medical services by
asthmatics.
Motor vehicle traffic is a major source of air pollutants such as nitrogen dioxide (NO2) and suspended
particulate matter. Recent research has focused on the impact of traffic-related air pollution on
morbidity and mortality (Brunekreef and Holgate, 2002). Whereas most epidemiological studies deal
with short-term effects, only a few studies have characterized effects of long-term exposure on
morbidity and mortality (Abbey et al., 1999; Zemp et al., 1999; Pope et al., 1995; Dockery et al., 1993).
Recently additional epidemiology studies have linked reductions in lung function and respiratory
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development to air pollution exposure among preschool and school age children (Gauderman et al.,
2002; Horak et al., 2002).
A number of epidemiology and exposure studies in children and adults have examined the direct health
impacts and associations between asthma, allergy and other endpoints associated with exposure to NO2
levels present in the ambient urban environment. Several studies have indicated that exposure to NO2,
and the proximity of homes to roadsides (Oosterlee et al., 1996) and motorways (Alm et al., 1999) as
well as exposure to high rates of road traffic (English et al., 1999) and in particular to truck traffic (van
Vliet et al., 1997; Duhme et al., 1998; Ciccone et al., 1998; Wilkinson et al., 1999; Venn et al., 2001;
Krämer et al., 2000; Brauer et al., 2002) increases the risk of respiratory symptoms.
A major deficiency in many of these studies involves the estimation of exposure. Proximity to road
traffic, census data on car traffic and/or truck traffic, and self-reported traffic intensities were used as
proxies for exposure to traffic exhaust. One study used modelled NO2 concentrations (Oozsterlee et al.,
1996). Only a few studies relied on exposure measurements. Since it is not feasible to measure personal
exposure for large study populations, exposure modelling based on either pollution dispersion models or
measurement data seems to be a useful approach. A regression-based approach for mapping long-term
exposure to NO2 and SO2 using geographic information systems (GIS), has been successfully applied to
spatial distribution of these pollutant gases, the interpolation from outdoor to personal exposures
remained difficult to interpret, or to associate with specific reported health impacts (Briggs et al., 2000).
The details of these studies are summarized in Section D-2.5.4 of Appendix D.
The associations between traffic-related air pollution and asthma and lung function among the very
young are less clear (Gehring et al., 2002; Kunzli et al., 2000). A positive association between hospital
admission for asthma and traffic density among children was reported by one case-control study
(English et al., 1999), whereas another case-control study failed to show such an association (Magnus et
al., 1998). In two studies lung function was found to be decreased with increasing traffic density (van
Vliet et al., 1997), whereas no associations with pulmonary function measures were found in others.
Several studies have investigated the association between traffic-related air pollution and respiratory
disease and symptoms in children. A number of these have encountered problems with key components
of population studies including self assessment, reliance on traffic density and monitoring at different
locations. The majority of the studies reported for children show associations between traffic and
exposure-related wheezing, although some are negative (see Section D-2.5 of Appendix D). As with
general epidemiological studies, there was difficulty separating the adverse health outcomes reported
with NO2 compared to other pollutants, including outdoor particulate matter and SO2 plus indoor factors
such as tobacco smoke, moulds, pets, and familial allergies (see Section D-2.5.1 of Appendix D).
Recent studies have shown associations between retarded lung development in young children (fourth
graders) and living near high traffic areas. Several pollutants were monitored in these studies, including
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NO2, PM10, PM2.5, Ozone and inorganic acid vapours. The strongest associations were with acid
vapours, although the differences were not sufficiently significant to draw firm conclusions (see Section
D-2.5.2 of Appendix D).
Increased sensitization to outdoor, but not indoor, allergens has been associated with traffic density on
streets near residences, and this association was strongest with truck traffic. There is evidence to show
that this sensitization may be related to the atmospheric entrainment of various pollens that are ground
into fine particles by vehicle tires. These associations have not been related to ambient NO2
concentrations, but were associated with ambient concentrations of fine particulate matter. However, at
higher ambient concentrations of NO2 observed in Western Europe, 50 µg/m3 changes in NOx to have
been associated increased hospital admissions for the treatment of asthma symptoms (see Section D2.5.3 of Appendix D).
4.2.3
Sulphur Dioxide (SO2)
Although sulphur oxides (SOx) include other oxides besides SO2, the major form of the mixture of gases
in the ambient environment is SO2. Air quality criteria are generally based on SO2, and it is SO2 that is
routinely monitored in air monitoring surveys.
Current and anticipated reductions of sulphur in petroleum products including aircraft jet fuels suggest
that there will be no significant increases in contributions of SO2 emissions from TPIA operations in the
future (to year 2015). At the location of maximum off-site concentration, predicted SO2 concentrations
in year 2015 were one-third of those modelled for year 2000.
4.2.3.1
Exposure to Predicted TPIA Emission Alone
Predicted maximum off-site one-hour concentrations of SO2 from TIPA sources alone were within the
Ambient Air Quality Criterion (AAQC) of 250 ppb at all receptor locations. CR values ranged from
0.01 to 0.15 for residential locations, from 0.11 to 0.29 for commercial locations, and from 0.28 (in
2020) to 0.93 (in 2000) at the maximum off-site location.
Annual average concentrations of SO2 predicted to occur at the maximum point of off-site concentration
were small (less than 0.1 of the annual average AAQC of 20 ppb). These would be much lower at
selected receptor locations off site.
On the basis of modelled results for SO2 emissions from the TPIA alone, no adverse health effects
would be expected.
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4.2.3.2
Contribution to Overall Health Risks
Predicted maximum one-hour concentrations of SO2 from off-site sources in the vicinity of the TPIA
approached or exceeded the one-hour AAQC in the modelled results for the year 2000 (CR = 1.12 at the
maximum off-site location; CRs ranged at other locations ranged from 0.51 to 0.94).
Concentration Ratio values (CRs) for predicted one-hour maximum SO2 concentrations at receptor
locations for TPIA and off-site sources combined were slightly higher than those from off-site sources
alone. (CR = 1.3 for maximum off-site location in 2000; all other locations and years ranges from 0.6 to
1.2) This suggests that the contribution of TPIA sources to overall concentrations that receptors could
be exposed to would be minor (i.e., of the order of 10%). However, this small contribution from the
TPIA is not necessarily insignificant, since ambient 1-hr maximum concentrations are in many cases
very near the AAQC level, and the additional contribution from the TPIA resulted in a prediction of an
air concentration in excess of the air quality criterion.
Predicted maximum annual average SO2 concentrations for TPIA and off-site sources combined were
well below (about one third of) the relevant AAQC. The contribution of TPIA sources to these annual
average concentrations was small in comparison with the contribution of off-site sources (typically less
than 20%).
It is important to realize that marginal exceedances of an AAQC – and particularly a 1-hr maximum
AAQC as opposed to a longer-term measure – are unlikely to result in adverse health effects. The
conservativeness of the approach taken in this assessment suggests that predicted SO2 emissions from
the TPIA would not contribute to adverse health effects overall.
4.2.3.3
Discussion of Biomedical Evidence for Health Effects
Below is a brief review of the health effects of SO2 including a review of recent studies on children and
adults receiving SO2 exposures from traffic-related sources. These exposures involve the simultaneous
exposure to other pollutants, so it is difficult to know when a response observed is to the gas directly or
to the gas acting as a surrogate compound for complex emissions from fossil fuel combustion. This is
addressed by incorporating studies that examine the health impact of indoor as well as outdoor sources
of SO2.
Sulphur dioxide is a colourless gas with a pungent odour that dissolves readily in water. There are
multiple emission sources for sulphur dioxide, but most are related to the combustion of fossil fuels.
Major industrial sources include coal-fired electricity generating stations, primary steel production,
copper and nickel smelting, and pulp and paper mills. Sulphur in fuels (diesel fuel and gasoline) are the
major sources of SO2 from mobile sources. As a result of actions being implemented by the automotive
and petroleum sub-sectors, SO2 emissions from mobile sources are projected to decrease substantially in
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the future with the implementation of low-emission vehicles and cleaner fuels (MOE, 2002). Only a
small proportion of oxides of sulphur in the urban ambient environment are emissions from natural
sources.
In Ontario, industrial operations continue to be major sources of acidic vapours and SO2 emissions.
Through the Countdown Acid Rain Program between 1990 and 1999, industrial sources achieved a
reduction of approximately 500 kilotonnes of SO2. Despite this effort, in 1999 industry (excluding
electricity) remained a significant contributor, at about 68 per cent of provincial SO2 emissions. The
electricity sector, which accounts for about 27 per cent of SO2 emissions, has recently been required to
reduce emissions under the Emissions Reduction Trading Regulation. However, most other industrial
point sources remain without such annual emissions limits. Projections indicate that some industry subsectors will increase production levels and emissions of SO2 (MOE, 2002).
Once released as a product of fossil fuel combustion, sulphur dioxide can be converted to sulphuric acid,
sulphur trioxide, and sulphates. Sulphur dioxide dissolves in water to form sulphurous acid.
Sulphur dioxide can irritate the respiratory system. Exposure to elevated concentrations >250 ppb (the
maximum one-hour AAQC in Ontario) can cause constriction of the bronchi and increase mucous
production. These physiological responses result in breathing difficulties in exposed individuals.
Children, the elderly and those with chronic lung disease, as well as asthmatics are especially
susceptible to the effects of inhalation of sulphur dioxide. Activity such as physical exertion and
exercising increases breathing by mouth leading to more pronounced responses to acidic airborne
pollution. Exercising asthmatics are sensitive to the respiratory effects of low concentrations (25 ppb)
of sulphur dioxide (ATSDR, 1998). Therefore, on days or in conditions when the maximum one-hour
concentration approaches or exceeds the criterion, sensitive members of the population may experience
adverse effects. The frequency with which such events might occur can not be predicted from a single
one-hour predicted ground level concentration that might occur at any time over the period of a year.
At higher levels of exposure (600 ppb) SO2 effects include immediate lung and throat irritation. Longer
periods of exposure at this level (600 ppb) can impair the respiratory system’s defences against foreign
particles and bacteria. Coincidental exposure to both SO2 and ozone can be responsible for increased
airway constriction (resistance to breathing) among susceptible individuals. Responses to exposure to
SO2 can be also be exacerbated in the urban environment where other acidic pollutants (e.g. from oxides
of sulphur), particulate matter or aerosols are present.
Short-term exposures to high levels of sulphur dioxide can be life-threatening. Exposure to 100 ppm of
SO2 is considered immediately dangerous to life and health. Long-term exposure to persistent levels of
sulphur dioxide can produce permanent changes in respiratory tissues that result in health effects. Lung
function changes have been observed in some workers who received occupational exposures of 400 to
3000 ppb sulphur dioxide over periods of 20 years or more. Such long-term exposures are often mixed
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with a great many other pollutants as well as effects introduced by lifestyle (smoking and alcohol), and
this creates difficulties for the exact attribution of health effects to sulphur dioxide exposure alone.
Nevertheless, the response to chronic conditions of exposure to SO2 is more informative in terms of
predicting adverse effects than using a single one-hour maximum value.
Most of the effects of sulphur dioxide exposure that occur in adults (i.e., difficulty breathing, changes in
the ability to breathe as deeply or take in as much air per breath, and burning of the nose and throat) are
also of potential concern in children. Children may be exposed to more sulphur dioxide than adults
because they breathe more air for their body weight than adults do. Children also exercise more
frequently than adults, and exercise increases breathing rate. This increase results in both a greater
amount of sulphur dioxide in the lungs and enhanced effects on the lungs. One study suggested that a
person's respiratory health, and not his or her age, determines vulnerability to the effects of breathing
sulphur dioxide. This study implies that healthy adolescents (ages 12-17) are no more vulnerable to the
effects of breathing sulphur dioxide than healthy senior citizens (ATSDR, 1998).
Indirect effects from SO2 can occur through exposure a combination of sulphates from SO2 emissions
with particulate matter (PM10). These have been associated with morbidity and mortality in a large
number of studies over very large population bases (Samet et al., 2000).
Long-term studies surveying large numbers of children have indicated possible associations between
sulphur dioxide pollution and respiratory symptoms or reduced breathing ability. Children with
respiratory exposure to sulphur dioxide pollution may develop more breathing problems as they get
older, may make more emergency room visits for treatment of wheeze, and may get more respiratory
illnesses than is typical for children (Brunekreef and Holgate, 2002).
Sulphur dioxide is a pollutant that participates in formation of acidic particulate matter (sulphates) and
the formation aerosols (sulphurous acid). These secondary pollutants have been well characterized with
respect to the production of health impacts at elevated concentrations, and they have been identified as
having associations with increased morbidity and mortality in urban areas of reduced or poor air quality.
The planned future reduction of sulphur in gasoline, diesel fuels and aircraft fuels will have significant
effects on the level of primary sources of SO2 to the ambient environment.
4.3
Particulate Matter (PM10)
For PM10, there are no models currently available for predicting the profile of aircraft emissions or
fugitive emissions from other airport operations. No predictions for ground level concentrations of
PM10 were available from the concentrations predicted by the FAA (EDMS) model. There was
therefore insufficient information available to develop a human health risk assessment for current or
future emissions of PM10 from TPIA operations. Future modelling capabilities may permit development
of a means to estimate emission rates of particulate matter PM10 from aircraft. Background information
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on PM10 that may be helpful in developing an HHRA for PM10 in future has been assembled in Section
3.4.
The absence of sufficient information on potential PM10 emissions and associated health effects is an
important data gap in the assessment of potential risks from TPIA operations, for the following reasons:
1. It is reasonable to assume that TPIA operations would contribute to overall PM10 emissions from
aircraft and other airport operations (e.g., from products of the incomplete combustion associated
with take-off and landing).
2. The density of vehicle traffic in this urban area is likely associated with significant
concentrations of PM10, and with adverse health effects, as is typical for such urban locations.
3. Epidemiological studies have typically encountered difficulty in isolating the effects of
components of ambient pollutants such as CO, NO2, SO2 and PM10, as well as others (e.g.,
ozone). There is some evidence to suggest that, of these components of ambient air pollutants, it
is in fact exposure to PM10 that is mainly responsible for adverse health effects, and that the
association of adverse health effects with the other components of air pollution are in fact a result
of confounding with the effects of PM10.
Studies that compare chronic exposure to particulate matter for large urban populations have
demonstrated that those populations that live in cities that differ from other urban areas in annual 24-hr
average concentration of PM10 by 10 µg/m3 experience up to a 4% increase in annual mortality from
respiratory and cardiovascular causes. These studies have examined a wide variety of urban settings. A
more complete discussion of the health effects associated with human exposure to mobile source
emissions is given in Appendix E.
Specific components of ambient air pollution related to traffic exhaust, especially diesel combustion
products have been identified as likely important contributors to health impacts associated with exposure
to poor urban air quality. Analyses have suggested that particulate matter effects are larger in areas with
high nitrogen dioxide (i.e., traffic density) or in areas with high emissions of particulate matter from
highway vehicles (Brunekreef and Holgate, 2002). A number of epidemiologic investigations (timeseries) have demonstrated that individuals who live near major roads have higher relative risks of death
and respiratory ailments than people who live away from main roads (discussed in the attached PM10
appendix E).
4.4
Discussion of Uncertainties
Many areas of uncertainty can be identified in such a complex study, including, in the broadest sense:
1. uncertainties and assumptions with respect to the model that generated the predicted ambient air
concentrations for the chemicals of concern; and,
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2. uncertainties and assumptions with respect to the assessment of human health risks associated
with exposure to the predicted concentrations of chemicals of concern.
4.4.1
Uncertainties in Predicted Air Concentrations for Chemicals of Concern
There are a number of uncertainties in the estimation of ambient air concentrations of the chemicals
examined in this study. These predicted (modelled) concentrations were the basis of the Human Health
Risk Assessment (HHRA). Areas of uncertainty in the prediction of air concentrations for the chemicals
of concern are identified in the following list. (RWDI, 2003a)
•
Emission factors within EDMS and how well they reflect sources at TPIA.
•
This project commenced prior to September 11, 2001 and uses the accepted aviation growth
factors available at that time.
•
Model physics and the model’s ability to provide reliable estimates of ambient concentrations.
•
Meteorological parameters applied in the modelling and how well they reflect the stochastic
nature of the atmosphere.
•
Predicted PM10 concentrations do not include aircraft exhaust or fugitive sources, such as
construction activities at TPIA.
•
Environment Canada database for off-site emissions is based on 1995 levels. Emissions for
future years were assumed to be unchanged relative to 1995.
•
There is a 30 to 40% variance in emissions of CO between current and previous releases of
Environment Canada’s inventory.
•
The study did not account for long-range transport of contaminants into the study region.
•
Speciation profiles applied to VOC concentrations and how well they reflect the sources in the
study area.
•
Off-site emissions were averaged over 2.5 by 2.5 km grid cells.
It is difficult to explicitly quantify the effect of these uncertainties on the predicted impacts
presented in the Phase 1 to 3 Report (RWDI, 2003a). The comparison of modelled and measured
results near the TPIA and at Centennial Park, however, indicates that in general, the model
performed reasonably well for most contaminants and averaging periods.
4.4.2
Uncertainties in Assessing Potential Health Risks
When assumptions need to be made during the risk assessment process because of data gaps,
environmental fate complexities or during the selection of representative behavioural receptor
characteristics, etc., each assumption inherently results in some degree of uncertainty in the overall
conclusions of the assessment. In order to ensure that the risk assessment does not underestimate the
potential for occurrence of adverse effects, it is necessary to make assumptions which are conservative.
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In other words, assumptions should be made that tend to overestimate exposure and toxicity, the two key
factors that make up risk.
The following discussion describes areas of uncertainty in the current risk assessment, and evaluates the
potential impact of these uncertainties on the conclusions drawn from the assessment. Given the
tendency for the assumptions described below to overestimate both exposure and toxicity, it is
considered extremely unlikely that the overall risk characterization resulted in underestimated potential
health risks.
For a screening level analysis, a high degree of uncertainty is often acceptable, provided that
conservative assumptions are used to bias potential error toward protecting human health. Regional or
area studies are also less certain than site-specific health assessments in which exposures and hazards
can be more precisely defined and more accurately characterized.
A number of areas of uncertainty have been identified with the interpretation of data that act as the basis
for this health assessment. These are identified below and then addressed in detail.
1. Uncertainty in the toxicological reference values used
2. Results from simultaneous monitoring at four active sites, five days out of a year
3. Historical NAPS data
4. Surrogacy of mobile emissions introduces uncertainty (VOC of interest)
5. Uncertainty related to dependence on data from a limited number of monitoring sites
6. Uncertainty related to assignment of chemicals of concern in TPIA emissions
7. Uncertainty related to the choice of jet exhaust chemical speciation
8. Uncertainty relating to emissions for particulate matter from the TPIA
9. Lack of carbonyl compound data in NAPS database for Centennial Park
10. Uncertain characterization of PAHs from aircraft sources
11. Uncertainties in VOC speciation
4.4.2.1
Uncertainty in the Toxicological Reference Values Used
The reference concentration (RfC), or dose identified during toxicological assessment and data review,
is defined as an “estimate (with uncertainty spanning perhaps an order of magnitude) of a daily exposure
to the human population (including sensitive subgroups) that is likely to be without appreciable risk of
deleterious effects during a lifetime”. An RfC is not an estimate of the threshold dose for non-cancer
effects in humans. An RfC describes that dose considered to have no significant risk of adverse noncancer effects given a lifetime exposure at the concentration identified as the reference concentration.
An RfC is derived from a combination of experimental results, review of scientific literature and expert
judgment. There is always substantial uncertainty associated with extrapolations from effects
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characterized in animals to effects in humans. Additional extrapolations must be made to accommodate:
•
extrapolations from effects observed at high doses in animals to the low doses expected in the
ambient environment;
•
from short- to long-term exposures;
•
from effect- to no-effect-levels; and,
•
from average to sensitive individuals.
Accepted regulatory practice assumes that doses equal to or below the RfC are likely safe from noncancer effects, it does not automatically follow that doses above this level are not safe.
It is important to note a number of other conservative assumptions which are inherent in the
development of toxicological criteria for the chemicals of concern. These include:
•
For genotoxic carcinogens, it was assumed that no repair of genetic lesions occurs, and that,
therefore, no threshold can exist for chemicals that produce self-replicating lesions. However,
the existence of enzymes that routinely repair damage to DNA are well documented in the
scientific literature, and the potential adverse effects arising from damage to DNA would only be
observed if the ability of these repair enzymes to "fix" the damage was exceeded.
•
Large safety factors (i.e., 100-fold or greater) were used in the estimation of the RfC/RfD values
for threshold-type chemicals. These safety factors were applied to exposure levels from studies
where no adverse effects are observed (i.e., to the NOAEL), by regulatory agencies who have
established these reference levels. Thus, exceeding the toxicological criterion does not mean that
adverse effects would occur, rather it means that the safety factor beyond the no-effect exposure
is somewhat reduced.
•
Humans were assumed to be the most sensitive species with respect to toxic effects of chemical.
However, for obvious reasons, toxicity assays are not generally conducted on humans, so
toxicological data from the most sensitive laboratory species were used in the estimation of
toxicological criteria for humans.
•
The most sensitive toxicological endpoint (for example decreased growth, body weight loss/gain,
reproductive effects) was selected for each chemical from the available scientific literature to
represent the exposure limit.
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4.4.2.2
Results from Simultaneous Monitoring
Data for all pollutant species of interest collected during the Phase 4 (Ambient Air Monitoring)
represented only five days at the on-site and off-site (i.e., Albion Road) locations, whereas routine
monitoring for at least some of the chemicals of interest had been routinely collected over a period of
years. Not all pollutants were monitored at all sites on all occasions. Although the general conclusion
was that there appeared to be few if any differences that clearly indicated an impact of the TPIA on
monitoring results, the number of samples actually collected were insufficient to exclude the possibility
that exposure to hazardous air pollutants might result from operations at the TPIA.
Differences in PAHs detected off-site did not appear to correlate with emissions from aircraft
operations. The sources of these compounds may have been other mobile emissions such as those
associated with motor vehicle traffic (e.g., automobiles and diesel trucks) in the vicinity.
4.4.2.3
Historical NAPS data
The historical data from the NAPS programme was a key element that facilitated the interpolation of
total VOC predicted by the modelling generated by RWDI (as isopleths of concentration) into
concentrations of specific component chemicals. The rationale for this approach to “reconstructing” the
pollutant constituents has been described in detail in Appendix B of this document.
The information associated with chemical concentrations of VOC in the areas of Centennial Park in
Etobicoke and in Brampton can be considered very reliable. These data were produced by a very
experienced laboratory programme (ERMD), as part of a long-standing routine monitoring programme
at the Centennial Park site. This team recently initiated a monitoring programme in Brampton. The
annual averages that were used in this assessment are considered conservative. During the data
reduction process, no values were assigned for chemical concentrations recorded as below the detection
limit (reported as 0). All zero values were removed from the database. It is usual to insert a value of
one-half of the detection limit when analytical chemical results fail to demonstrate a clear signature
(e.g., retention time) for a chemical. By not attributing lower values to the non-detects, the
mathematical mean concentration conservatively rose, since only assured positive values were included
to determine an annual average. This step may have slightly over estimated the mass in µg/m3 for
chemical species of interest. The ability to access multiple years of data for VOC at Centennial Park
(from 1993 to 2002 except 1997) assured that the annual averages were stable, and because they were
based on a large number of samples (>50 per year), it is likely that values were truly representative of
long-term exposure concentrations. This is critical for evaluating risks associated with chronic exposure
to HAPs.
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All VOC concentrations recorded in the NAPS database were in the same units (µg/m3) that were
generated by the models used by RWDI. This allowed a transparent means for the conversion of a
predicted concentration of total VOC into constituent chemical species at a specific receptor location.
An additional source of uncertainty could be the failure to accurately determine the portion of “total
VOC” generated by the model were is actually included among the chemicals determined in the suite of
158 compounds identified by NAPS. An element of uncertainty was introduced into the calculation
used in the interpolation of VOC into specific chemical groups. It was assumed that the “total VOC”
described by the model was equivalent to the total crude mass of chemical constituents identified in the
NAPS data. According to historical NAPS data, approximately 40 to 45% of the mass of material
collected during a 24-hour monitoring period can not be identified by EPA Method TO-14A. This
means that the 158 or so chemicals that are reported for each NAPS monitoring result constitute
approximately 55 to 60% of the mass of material collected. The method routinely used at Centennial
Park for analysis of VOC organics does not detect oxygenated organics (carbonyl compounds) or
compounds of high molecular weight. This ratio (40:60) was the approximate ratio between oxygenated
hydrocarbons and pure hydrocarbons detected in jet turbine exhaust.
Thus, when undertaking the conversion of isopleths of total VOC into chemical constituents at a
location, knowledge of the size of this mass fraction was required. As this data could not be provided
for Toronto (Centennial Park), data from different urban communities was relied on to calculate the
fraction of total mass, determined (identified as specific compounds) as a percent of the total VOC
collected over a 24-hour period. This does not appear to vary greatly from one urban area in Eastern
Canada to another, but it could introduce some additional uncertainty into assigning a total weight to the
average sample, and might produce small changes in the distribution of masses for the constituent
chemicals of interest.
4.4.2.4
Surrogacy of Mobile Emissions
The focus of the current assessment was to consider the impact of petroleum fuel-related combustion
emission products generated at the TPIA on the community. These were primarily so-called “mobile”
emissions. Therefore, the chemicals in the NAPS database were examined to consider those that could
be included in such combustion products. This resulted in a list of approximately 47 compounds (VOCs
of Interest) out of the 158 determined by NAPS. It was considered that these would be generated during
operations at the TPIA, and since they were not unique to TPIA operations, additional sources would
occur within the community at large. The mass fraction of the total “VOCs of interest” was given the
sum of all the annual averages of the 47 compounds identified as likely to be mobile emissions.
This was considered too great a number to assess individually. Therefore, groups of chemicals were
prepared that we could characterize as acting in a similar manner (refer to Appendices A and B). Some
chemicals were treated separately because they are clearly identified with health effects by themselves
(e.g., benzene, xylenes, toluene, 1,3-butadiene). For each group of chemicals, one chemical was chosen
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as the surrogate, and it was given the sum of all the masses of the chemicals in that surrogate group.
This procedure would naturally lead to some uncertainty, both because some chemicals were not
included, but also because one reference concentration (RfC) was assigned to multiple chemicals. This
approach would be considered as conservative, as it would tend overestimate the concentration of the
chemicals of highest potential toxicity.
4.4.2.5
Dependence on Data from a Limited Number of Monitoring Sites
Results from the modelling predicted local differences in the concentration of chemicals of concern.
The ratio of TPIA and Urban contributions varied within the model predictions, but the output
concentration as described by an isopleth of concentration did treat total VOC as the same, regardless of
source. In reality, emissions from a point source such as an aircraft engine would be different from the
mixture experienced in the wider urban environment. To some degree this was considered through the
use of different chemical speciation profiles for modelling concentrations from TPIA sources or from
off-site sources. However, there was no clear method for readily segregating the chemicals emitted
from operations of the TPIA from those contributed from the rest of the community when they were
analysed together in Phase 3. This was outside the scope of the current study. The proportion of total
emissions from the TPIA operations was very small in comparison to the mass of VOC associated with
mobile and other fossil fuel combustion emissions contributed by the urban community. Therefore one
method for attributing chemical concentration to “Total VOC” isopleths in Phase 3 was used in this
assessment.
4.4.2.6
Assignment of Chemicals of Concern
The EDMS model considers emissions from a great many sources other than aircraft exhaust. Some of
these are evaporative fuel emissions, mobile emissions from transportation and ground equipment,
supplementary power supplies, electricity generation and fire fighting. The concentration of total
hydrocarbons generated by the model was not subdivided by source so the fraction contributed by any of
the sources at a specified on-site or off-site location was not available. This was outside the scope of the
current study. Since virtually all of the mobile sources from ground-related operations would be
identical to the emissions experienced in the general community, it was decided to treat the modelled
total hydrocarbon concentrations as if they were jet aircraft exhaust.
This decision was taken because it was considered conservative, included a proportion of carbonyl
compounds, and addressed the clearest difference between activities that characterize an TPIA as
distinct from the greater urban community. Concerns expressed by members of the public on the TPIA
environmental sub-committee with regard to health and environmental impact have been directed at
aircraft operations and the potential hazards to health that such operations present. Concern for health
impacts associated with increased ground traffic into and out of the TPIA was also a concern of the Subcommittee. A basic assumption of this assessment was the evaluation of the health impact associated
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with those activities (aircraft) that distinguish the TPIA from the adjacent community.
Thus, the assumption that all emissions of THC modelled by the EDMS software should be speciated
according to aircraft speciation profiles adds some uncertainty to the risk assessment.
4.4.2.7
Choice of Jet Exhaust Chemical Speciation
The selection of emission factors and chemical profiles for aircraft emissions has been addressed in
Appendix F. Criteria for this selection focused on two aspects of the emission profile. The first was the
history for the profile in question (when was it generated and where). It was concluded that the most
recent profile prepared by Environment Canada (ERMD) was most appropriate. Earlier profiles (EPA
#1098 and Atlanta #2572) were considered less adequate because of the number of compounds
evaluated in jet turbine exhaust. The use of earlier profiles was considered a questionable basis on
which to model future engine performance and exhaust composition. The ERMD profile used to
characterize fuel combustion exhaust in this health assessment was recent (1997), more comprehensive,
and had been prepared by the same laboratory that routinely evaluated ambient monitoring data for
NAPS.
The second criterion for selection of emissions profile examined existing monitoring data both on- and
off-site in order to inform the choice of aircraft exhaust chemical speciation profile. CEI was asked to
examine the data from the on-site OPSIS system and to compare it to data produced by the NAPS
programme. The intent of this comparison was to assist in the choice of the most suitable emission
profile for aircraft from the three available to be chosen. The expansion of on-site monitoring
information afforded by inclusion of the OPSIS data was attractive. This was viewed as a means to
reduce the uncertainty surrounding emissions generated onsite. Off-site emissions were already
sufficiently characterized by NAPS data. Unfortunately there was insufficient basis for comparison of
results produced by the two systems (NAPS and OPSIS). Despite limiting OPSIS and NAPS inputs to
the same 24-hour periods over several years of monitoring, no reasonable algorithm could be developed
the relate the two monitoring processes. Thus, it was not possible to use the OPSIS data to assist in the
choice of jet exhaust speciation profile.
4.4.2.8
Emissions for Particulate Matter
The EDMS model developed by the FAA and used to estimate environmental impacts of TPIA
operations does not account for all emissions of particulate matter (PM2.5 and PM10). Aircraft engine
exhaust and fugitive dust emissions are not accounted for. This led to estimates of small to insignificant
off-site inputs of particulate matter to the adjacent environment. Precursors to PM10 have been
discussed in the risk assessment, but the fractional contribution of such emissions to the total loading
experienced by the community could not be discerned from the EDMS model. Clearly the portion of
exhaust gases released during take-off and taxiing contributing to the accumulated PM10 loadings for the
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community are a concern of members of the Environmental sub-committee. As there is no currently
available means to convert exhaust gases (that are primarily in accumulation mode) into PM10, it is not
possible to estimate effects attributable to TPIA operations. The modelled estimates for PM10 seem low,
but perhaps they are reasonable. Quantifiable differences for PM2.5 monitored at Centennial Park in
comparison to other sites in Toronto are not great. Any contribution to the already abundant emissions
from those contributed from the mobile sources on the major Highways 401, 427, 409, 410 and 407
would undoubtedly be small. Nevertheless, additional monitoring of PM2.5 on the TPIA site should be
considered.
4.4.2.9
Lack of Carbonyl Compound Data
Carbonyl compounds were assessed for emissions from TPIA alone, but there was no reasonable means
to attribute a carbonyl component to the annual total VOC isopleths identified for emissions from offsite sources alone or for emissions from both sources. Thus, the relative contribution of the TPIA
operations in comparison to background could not be clearly delineated. However, data describing
historical concentrations of carbonyl compounds and annual averaged at a commercial site in Toronto
and at a rural agricultural site (Simcoe) were useful to show the relative background for such
compounds. Examination of the routine monitoring data suggest that despite the difference in
abundance of mobile sources that characterize urban environments, there is really little difference in the
carbonyl compound composition between urban and rural sites. This suggests that regional
concentrations are the prime concern with respect to health impacts, and that local area sources such as
the TPIA do not greatly affect changes in concentration of carbonyl compounds.
Results of on- and off-site simultaneous monitoring of carbonyl compounds also suggest that the TPIA
is not a significant source of such compounds to the surrounding community. Modelling results and the
selection of exhaust speciation profile suggested that acrolein would be in excess of the exposure limit
and pose a potential risk in the vicinity of the TPIA. In fact, the predicted concentrations were much
lower than those routinely experienced in Southern Ontario at rural and urban sites. This suggests that
other sources regularly contribute acrolein to the environment (refer to discussion in Appendix B).
The ambient level of acrolein in the environment produces a moderate risk to health, but the relative
contribution attributable to the TPIA operations may be considered as only a portion of what is already
present in the ambient environment from other sources. This is a problem that should be addressed by
the entire community, and not the TPIA alone.
4.4.2.10
Characterization of PAHs
PAHs were estimated for aircraft emissions based on a proportion of total VOC using a ratio provided
by the U.S. EPA. Emissions of carcinogenic PAH from aircraft are limited by the nature of the fuel
composition. This was reflected in the results of on- and off-site simultaneous monitoring data that
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failed to differentiate between the TPIA and the surrounding community. This suggests the component
of carcinogenic PAH attributable to aircraft operations is such a small fraction of the total PAH present
in the urban environment generated from other sources that it is not measurable at this time. There is
some uncertainty associated with the estimates of PAH, since the modelled emissions did not explicitly
include estimates of PAH at isopleth locations. Generally, PAH emissions from fuels are controllable
through the reduction of aromatic content of fuels, and through reduction of naphthalene content.
Although the contribution of PAH in aircraft emissions is uncertain, their consideration in this
assessment has been adequately addressed.
4.4.2.11
Calculation of Speciated Concentrations of VOCs Used in the HHRA
Appendix B (Rationale for quantitative estimation of VOC) provides a complete description of the
rationale and calculation of specific hydrocarbon species from interpolated values. Annual average
concentrations (expressed as total VOC in µg/m3) were specified for receptor site locations (predicted by
RWDI as isopleths of concentration). The annual average concentration of VOC at a receptor location
was converted into a number of constituent compounds (described in Appendix B)
A sensitivity analysis compared actual monitored values (NAPS) to predicted concentrations. This
analysis showed that interpolated concentrations of benzene overestimated actual monitored values
recorded at Centennial Park. The monitored annual average concentration for benzene at Centennial
Park (NAPS) in 2000 was 1.34 µg/m3 but the value used in the exposure estimation to determine longterm risk was 1.94 µg/m3 for the base year 2000. The use of this value (145% of the monitored
concentration) adds considerable conservatism to the risk assessment.
Likewise, concentrations predicted for other VOC using the conversion method for urban VOC
described in Appendix B would be somewhat in excess of the modelled concentration for that chemical
at Centennial Park. The conservative assumptions incorporated into the predicted concentrations of
VOC offer added assurance for health protection.
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5.0
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