Air Toxics Risk Assessment
Reference Library
Volume 2
Facility-Specific Assessment
-------
U.S. Environmental Protection Agency
Office of Air Quality Planning and Standards
Research Triangle Park, NC
EPA-453-K-04-001B
www. epa. go v/ai r/oaq ps
April 2004
-------
EPA-453-K-04-001B
April 2004
Air Toxics Risk Assessment Reference Library
Volume 2
Facility-Specific Assessment
Prepared by:
ICF Consulting
Fairfax, Virginia
Prepared for:
Nona Smoke, Project Officer
Office of Policy Analysis and Review
Contract No. EP-D-04-005
Work Assignment No. 0-2
Rachael Schwartz, Project Officer
Clean Air Marketing Division
Contract No. 68-W-03-028
Work Assignment No. 11
Bruce Moore, Project Officer
Office of Air Quality Planning and Standards
Contract No. 68-DO1-052
Work Assignment No. 0-08
Work Assignment No. 0-09
U.S. Environmental Protection Agency
Office of Air Quality Planning and Standards
Emissions Standards Division
Research Triangle Park, NC
-------
Disclaimer
The information and procedures set forth here are intended as a technical resource to those
conducting air toxics risk assessments. This facility-specific assessment document does not
constitute rulemaking by the Agency, and cannot be relied on to create a substantive or
procedural right enforceable by any party in litigation with the United States. As indicated by
the use of non-mandatory language such as "may" and "should," it provides recommendations
and does not impose any legally binding requirements.
The statutory provisions and EPA regulations described in this document contain legally binding
requirements. This document is not a regulation itself, nor does not it change or substitute for
those provisions and regulations. While EPA has made every effort to ensure the accuracy of the
discussion in this guidance, the obligations of the regulated community are determined by
statutes, regulations, or other legally binding requirements. In the event of a conflict between the
discussion in this document and any statute or regulation, this document would not be
controlling.
The general description provided here may not apply to a particular situation based upon the
circumstances. Interested parties are free to raise questions and objections about the substance
of this guidance and the appropriateness of the application of this guidance to a particular
situation. EPA and other decision makers retain the discretion to adopt approaches on a case-by-
case basis that differ from those described in this guidance where appropriate. EPA may take
action that is at variance with the recommendations and procedures in this document and may
change them at any time without public notice. This is a living document and may be revised
periodically. EPA welcomes public input on this document at any time.
Reference herein to any specific commercial products, process, or service by trade name,
trademark, manufacturer, or otherwise, does not necessarily constitute or imply its endorsement,
recommendation, or favoring by the United States Government.
April 2004 Page i
-------
Acknowledgments
The U.S. Environmental Protection Agency's Air Toxics Risk Assessment reference library is a
product of the EPA's Office of Air Quality, Planning, and Standards (OAQPS) in conjunction
with EPA Regions 4 and 6 and the Office of Policy Analysis and Review. The interoffice
technical working group responsible for library development includes Dr. Kenneth L. Mitchell
(Region 4), Dr. Roy L. Smith (OAQPS), Dr. Deirdre Murphy (OAQPS), and Dr. Dave Guinnup
(OAQPS). In addition to formal peer review, an opportunity for review and comment on
Volumes 1 and 2 of the library was provided to various stakeholders, including internal EPA
reviewers, state and local air agencies, and the private sector. The working group would like to
thank these many internal and external stakeholders for their assistance and helpful comments on
various aspects of these two books. (Volume 3 of the library is currently under development and
is expected in late 2004.) The library is being prepared under contract to the U.S. EPA by ICF
Consulting, Robert Hegner, Ph.D., Project Manager.
April 2004 Page ii
-------
Authors, Contributors, and Reviewers
Authors
Roy L. Smith, Ph.D.
U.S.EPAOAQPS
Deirdre Murphy, Ph.D. Kenneth L. Mitchell, Ph.D.
U.S. EPA OAQPS U.S. EPA Region 4
External Peer Reviewers
Doug Crawford-Brown, Ph.D., University of North Carolina at Chapel Hill
Michael Dourson, Ph.D., D.A.B.T., Toxicology Excellence for Risk Assessment
Eric Hack, M.S., Toxicology Excellence for Risk Assessment
Bruce Hope, Ph.D., Oregon Department of Environmental Quality
Howard Feldman, M.S., American Petroleum Institute
Barbara Morin, Rhode Island Department of Environmental Management
Patricia Nance, M.A., M.Ed., Toxicology Excellence for Risk Assessment
Charles Pittinger, Ph.D., Toxicology Excellence for Risk Assessment, Exponent
Additional Contributors & Reviewers
John Ackermann, Ph.D., U.S. EPA Region 4
Carol Bellizzi, U.S. EPA Region 2
George Bollweg, U.S. EPA OAQPS
Pamela C. Campbell, ATSDR
Ruben Casso, U.S. EPA Region 6
Motria Caudill, U.S. EPA Region 5
Rich Cook, U.S. EPA, OTAQ
Paul Cort, U.S. EPA Region 9
David E. Cooper, Ph.D., U.S. EPA OSWER
Dave Crawford, U.S. EPA OSWER
Stan Durkee, U.S. EPA Office of Science Policy
Neal Fann, U.S. EPA OAQPS
Bob Fegley, U.S. EPA Office of Science Policy
Gina Ferreira, USEPA Region 2
Gerald Filbin, Ph.D., U.S. EPA OPEI
Danny France, U.S. EPA Region 4
Rick Gillam, U.S. EPA Region 4
Thomas Gillis, U.S. EPA OPEI
Barbara Glenn, Ph.D., U.S. EPA National
Center for Environmental Research
Dave Guinnup, Ph.D., U.S. EPA OAQPS
Bob Hetes, U.S. EPA National Health and
Environmental Effects Research Laboratory
James Hirtz, U.S. EPA Region 7
Ofia Hodoh, M.S., U.S. EPA Region 4
Ann Johnson, U.S. EPA OPEI
Brenda Johnson, U.S. EPA Region 4
Pauline Johnston, U.S. EPA ORIA
Stan Krivo, U.S. EPA Region 4
Deborah Luecken, U.S. EPA National Exposure
Research Laboratory
Thomas McCurdy, U.S. EPA National Exposure
Research Laboratory
Megan Mehaffey, Ph.D., U.S. EPA NERL
Latoya Miller, U.S. EPA Region 4
Erin Newman, U.S. EPA Region 5
David Lynch, U.S. EPA OPPTS
Ted Palma, M.S., U.S. EPA OAQPS
Michele Palmer, U.S. EPA Region 5
Solomon Pollard, Jr., Ph.D., U.S. EPA Region 4
Anne Pope, U.S. EPA OAQPS
Marybeth Smuts, Ph.D., U.S. EPA Region 1
Michel Stevens, U.S. EPA National Center for
Environmental Assessment
Allan Susten, Ph.D., D.A.B.T., ATSDR
Henry Topper, Ph.D., U.S. EPA OPPTS
Pam Tsai, Sc.D., D.A.B.T., U.S. EPA Region 9
Susan R. Wyatt, U.S. EPA (retired)
Jeff Yurk, M.S., U.S. EPA Region 6
April 2004
Page in
-------
(this page intentionally left blank)
April 2004 Page iv
-------
Table of Contents
Chapter I: Background 1
1.0 Introduction 1
1.1 Purpose of This Document I
1.2 Intended Audience 2
2.0 The Facility/Source Specific Risk Assessment Process 2
2.1 Facility/Source-Specific Human Health Risk Assessment 2
2.2 Facility/Source-Specific Ecological Assessment 4
2.3 Use of Site-Specific Risk Assessments in EPA's Air Toxics Program 5.
3.0 The Layout of This Resource Document 5.
Chapter II: Overview and Getting Started 9
1.0 Introduction 9
2.0 Overview of Risk Assessment and Risk Management 9
3.0 Concept of Tiered Assessment 12
4.0 Planning, Scoping, and Problem Formulation 1_5
4.1 Conceptual Model Development 16.
4.2 Determining Whether Multipathway Analyses are Appropriate lj$
5.0 One Method for Focusing the Assessment on the Most Important HAPs 20
Chapter III: Inhalation Pathway Risk Assessment 23_
1.0 Introduction 23_
2.0 Tiered Approach and Models Used 23_
3.0 Developing the Emissions Inventory for an Inhalation Analysis 2J$
3.1 Quantification of Emissions Rates 2ฃ
3.2 Quantification of Other Release Parameters 29
3.3 Dose-Response Values for "Ambiguous" Substances 29
3.4 Identification of Background Concentrations 30
4.0 Toxicity Assessment 30
5.0 Risk Characterization for Inhalation Exposure 3ฃ
5.1 Cancer Risk 38
5.2 Chronic Noncancer Hazard 40
5.3 Acute Noncancer Hazard 43_
5.4 Assessment and Presentation of Uncertainty 44
April 2004 Page v
-------
6.0 Tier 1 Inhalation Analysis 46
6.1 Introduction 46
6.2 Fate and Transport Modeling 47
6.2.1 Model Inputs 48
6.2.2 Model Runs 51.
6.3 Exposure Assessment 52
6.4 Risk Characterization 52
6.4.1 Reporting Results 52
6.4.2 Assessment and Presentation of Uncertainty 54
6.5 Focusing Tier 2 on the Most Important HAPs/Sources 54
7.0 Tier 2 Inhalation Analysis 54
7.1 Introduction 54
7.2 Fate and Transport Modeling 56
7.2.1 Model Inputs 56
7.2.2 Model Runs 59
7.3 Exposure Assessment 59
7.3.1 Chronic Exposures 59
7.3.2 Acute Exposures 60
7.3.3 HEM-3 Outputs 60
7.3.4 Monitoring Data 61
7.4 Risk Characterization 61
7.4.1 Reporting Results 65
7.4.2 Assessment and Presentation of Uncertainty 65
7.5 Focusing Tier 3 on the Most Important HAPs/Sources 65
8.0 Tier 3 Inhalation Analysis 66
8.1 Introduction 66
8.2 Fate and Transport Modeling 6ฃ
8.2.1 Model Inputs 69
8.2.2 Model Runs 71
8.3 Exposure Assessment 71
8.3.1 Characterization of the Study Area 72
8.3.2 Generation of Simulated Individuals 73_
8.3.3 Construction of A Sequence of Activity Events 74
8.3.4 Calculation of Concentrations in Microenvironments 74
8.3.5 Estimating Exposure 74
8.3.6 General Considerations 75
8.3.7 Monitoring Data 75
8.4 Risk Characterization 76
8.4.1 Reporting Results 76
8.4.2 Assessment and Presentation of Uncertainty 76
Chapter IV: Multipathway Risk Assessment 77
1.0 Introduction and Overview 77
2.0 Tiered Approach and Models Used 79
April 2004 Page vi
-------
3.0 Developing the Emissions Inventory for Multipathway Analyses 82
4.0 Multipathway Human Health Risk Assessment 82
4.1 Introduction and Overview 82
4.2 Pathways Evaluated 84
4.3 Estimating Dietary Intake 86
4.4 Ingestion Toxicity Assessment 87
4.5 Risk Characterization for Ingestion Analysis 8ฃ
4.5.1 Cancer Risk Estimates 89
4.5.1.1 Characterizing Individual Pollutant Risk 89
4.5.1.2 Characterizing Risk from Exposure to Multiple Pollutants 90
4.5.1.3 Combining Risk Estimates across Multiple Ingestion Pathways 91.
4.5.1.4 Evaluating Risk Estimates from Inhalation and Ingestion Exposures . ฃ1
4.5.2 Noncancer Hazard ฃ1
4.5.2.1 Characterizing Individual Pollutant Hazard 92
4.5.2.2 Multiple Pollutant Hazard 92
4.5.2.3 Evaluating Hazard Estimates From Inhalation and Ingestion Exposures
94
4.5.3 Consideration of Long-Range Transport and Background 94
4.5.4 Assessment and Presentation of Uncertainty 94
4.6 Tier 1 Multipathway Human Health Analysis 95
4.7 Tier 2 Multipathway Human Health Analysis 96
4.7.1 Introduction 96
4.7.2 Fate and Transport Modeling 96
4.7.2.1 Model Inputs 96
4.7.2.2 Model Runs 99
4.7.3 Exposure Assessment 100
4.7.3.1 Characterization of the Study Population 100
4.7.3.2 Defining the Point of Maximum Exposure 100
4.7.3.3 Defining the Exposure Scenario 101
4.7.3.4 Calculation of Exposure Concentration 101
4.7.3.5 Determining Exposure 102
4.7.3.6 Determining Intake 102
4.7.4 Risk Characterization 102
4.7.4.1 Reporting Results 102
4.7.4.2 Assessment and Presentation of Uncertainty 103
4.7.5 Potential Refinements of a Tier 2 Approach 103
4.8 Tier 3 Multipathway Human Health Analysis 104
4.8.1 Introduction 104
4.8.2 Fate and Transport Modeling 106
4.8.2.1 Model Inputs 106
4.8.2.2 Model Runs 106
4.8.3 Exposure Assessment 110
4.8.4 Risk Characterization Ill
4.8.4.1 Reporting Results 112
4.8.4.2 Assessment and Presentation of Uncertainty 112
5.0 Ecological Risk Assessment 113
5.1 Introduction and Overview 113
5.2 Ecological Risk Characterization 115
5.3 Tier 1 Ecological Analysis 117
April 2004 Page vii
-------
5.4 Tier 2 Ecological Analysis 117
5.4.1 Introduction 117
5.4.2 Fate and Transport Modeling 117
5.4.2.1 Model Inputs 117
5.4.2.2 Model Runs 117
5.4.3 Exposure Assessment 119
5.4.3.1 Characterization of Ecological Receptors 119
5.4.3.2 Defining the Point of Maximum Exposure 119
5.4.3.3 Calculation of Exposure Concentration 119
5.4.3.4 Determining Intake 120
5.4.4 Risk Characterization 120
5.4.4.1 Reporting Results 127
5.4.4.2 Assessment and Presentation of Uncertainty 127
5.5 Tier 3 Ecological Analysis 128
5.5.1 Introduction 128
5.5.2 Identification of Potentially Exposed Populations 131
5.5.3 Assessment Endpoints and Measures of Effect 132
5.5.4 Fate and Transport Modeling 134
5.5.5 Exposure Assessment 134
5.5.6 Risk Characterization 135
5.5.6.1 Reporting Results 136
5.5.6.2 Assessment and Presentation of Uncertainty 136
References 137
April 2004 Page viii
-------
List of Exhibits
Exhibit 1. The General Air Toxics Health Risk Assessment Process 3.
Exhibit 2. Overview of EPA's Air Toxics Risk Assessment Process K)
Exhibit 3. Generalized Representation of the Tiered Risk Assessment Concept .13.
Exhibit 4. Example Elements of Planning and Scoping for Facility/Source-Specific Risk Assessments
16
Exhibit 5. Example of a General Conceptual Model for a Facility/Source Specific Air Toxics Risk
Assessment JjS
Exhibit 6. FฃAPs of Concern for Persistence and Bioaccumulation 12
Exhibit 7. Example TWSA Calculation for Cancer Effects 2j_
Exhibit 8. Example TWSA Calculation for Noncancer Effects 22
Exhibit 9. Example Tiered Approach for Inhalation Pathway Risk Assessment 24
Exhibit 10. Specific Dose-Response Recommendations for Unspeciated FฃAP Data 3J_
Exhibit 11. Example Approach for A Tier 1 Assessment 47
Exhibit 12. Example Default Values for SCREEN3 Tier 1 Inputs 49
Exhibit 13. Example Presentation of Risk Characterization Results for Acute Exposure 53.
Exhibit 14. Example Approach for A Tier 2 Assessment 55.
Exhibit 15. Example of Interpolation to Calculate Concentrations at Census Block Internal Points . . . 58
Exhibit 16. Example Presentation of HEM-3 Individual Cancer Risk Estimates 62
Exhibit 17. Example Presentation of HEM-3 Individual Noncancer TOSHI Estimates 63.
Exhibit 18. Example Presentation of HEM-3 Population Cancer Risk Estimates 64
Exhibit 19. Example Presentation of HEM-3 Population Noncancer TOSHI Estimates 64
Exhibit 20. Example Approach for A Tier 3 Assessment 67
Exhibit 21. Volatile HAPs with Atmospheric Half-lives of Less than One Hour 70
Exhibit 22. Profile Variables in TRIM.ExpoInhalatlon 73
Exhibit 23. HAPs of Concern for Persistence and Bioaccumulation (PB-HAP Compounds) 7ฃ
Exhibit 24. Example Approach for a Multipathway Risk Assessment 80
Exhibit 25. Role of the TRIM Modeling System 83
Exhibit 26. Examples of Specific Pathways to be Analyzed for Each PB-HAP Compound 85.
Exhibit 27. Example Matrix for Estimating Excess Cancer Risks for Multiple Chemical Exposure
through Multiple Ingestion Pathways for a Particular Exposure Scenario 89
Exhibit 28. Example Matrix for Characterizing Hazard for Multiple Chemical Exposure through Multiple
Ingestion Pathways for a Particular Exposure Scenario 93.
Exhibit 29. Example Approach for a Tier 2 Multipathway Assessment 97
Exhibit 30. Example Approach for a Tier 3 Multipathway Assessment 105
Exhibit 31. Developing and Executing a TRIM.FaTE Simulation 107
Exhibit 32. Scenarios(a) Currently Supported by TRIM.ExpoIngestlon Ill
Exhibit 33. Commonly Used Point Estimates 114
Exhibit 34. Example Approach for a Tier 2 Ecological Assessment 118
Exhibit 35. Sources of Ecological Toxicity Reference Values (TRVs) or Benchmarks 121
Exhibit 36. Example Approach for a Tier 3 Ecological Assessment 129
Exhibit 37. TRIM Modules in the Context of EPA's Framework for Ecological Risk Assessment .. 130
Exhibit 38. Potential Ecological Receptors of Concern 131
Exhibit 39. Generic Ecological Assessment Endpoints 133
Exhibit 40. TRIM Metrics of Ecological Exposure and Metrics of Ecological Effects 135
April 2004
Page ix
-------
(this page intentionally left blank)
April 2004 Page x
-------
Chapter I: Background
1.0 Introduction
This technical resource document describes several methods for preparing a site-specific risk
assessment for a source (i.e., a single emission point within one facility), a group of sources (i.e.,
multiple emission points within one facility), or a group of similar facilities (e.g., within the
same source category) that emit(s) toxic air pollutants. Air toxics may be emitted from power
plants, factories, cars and trucks, and common household products. Sources that stay in one
place are referred to as stationary sources. Vehicles and other moving sources of air pollutants
are called mobile sources. This technical resource document is intended for assessing risks
associated with stationary sources of air toxics. While its primary focus is on Hazardous Air
Pollutants (HAPs), this resource document can be applied to all air pollutants (with the
exception of criteria air pollutants, which are assessed using different tools and methods).
1.1 Purpose of This Document
This technical resource document is the second of a three-volume set. Volume 1: Technical
Resource Manual discusses the overall air toxics risk assessment process and the basic
technical tools needed to perform these analyses. The manual addresses both human health and
ecological analyses. It also provides a basic overview of the process of managing and
communicating risk assessment results. Other evaluations (such as the public health assessment
process) are described to give assessors, risk managers, and other stakeholders a more holistic
understanding of the many issues that may come into play when evaluating the potential impact
of air toxics on human health and the environment. Readers with a limited understanding of
risk assessment are encouraged to consult Volume 1.
Volume 2: Facility-Specific Assessment (this volume) builds on the technical tools described in
Volume 1 by providing an example set of tools and procedures that can be used for
source-specific or facility-specific risk assessments. Information is also provided on tiered
approaches to source- or facility-specific risk analysis.
Volume 3: Community-Level Assessment builds on the information presented in Volume 1 to
describe to communities how they can evaluate and reduce air toxics risks at the local level. The
volume will include information on screening level and more detailed analytical approaches,
how to balance the need for assessment versus the need for action, and how to identify and
prioritize risk reduction options and measure success. Since community concerns and issues are
often not related solely to air toxics, the document will also present readily available information
on additional multimedia risk factors that may affect communities and strategies to reduce those
risks. The document will provide additional, focused information on stakeholder involvement,
communicating information in a community-based setting, and resources and methodologies that
may play a role in the overall process. Note that EPA's Office of Pollution Prevention and
Toxics has also developed a Community Air Screening How To Manual that will be available in
2004 and will be discussed in Volume 3 (Volume 3 will be available in late 2004).
April 2004 Page 1
-------
There are multiple ways to conduct a facility/source risk assessment, and the tools and methods
described in this document should not be viewed as prescriptive; nor is there a clear hierarchy of
tools and methods. The specific approach selected in a risk assessment often reflects a balance
between the complexity of the problem being evaluated, the uncertainty in the risk estimate that can
be tolerated, and available resources. A discussion of the planned approach during planning,
scoping, and problem formulation is strongly encouraged.
1.2 Intended Audience
Volume 2 is intended for three primary audiences:
Industries or facilities that choose to conduct site-specific risk assessments for air toxics.
EPA and state, local, and tribal (S/L/T) regulatory officials who may either conduct or
review site-specific risk assessments as part of implementing air toxics regulatory programs.
Members of affected communities who wish to participate in analytical procedures related to
facility-specific air toxics risk assessment.
2.0 The Facility/Source Specific Risk Assessment Process
Facility/source-specific air toxics risk assessment is the process by which the risks of adverse
health or environmental impacts associated with emissions of air toxics from a defined "site"
(e.g, a single facility or source) are estimated. In the context of this resource document (Volume
2) facility/source-specific risk assessment estimates are either:
The cumulative risk posed by the releases
of HAPs from source(s) within a single
source category located at a specific
facility; or
Cumulative risk refers to risk attributed to
simultaneous exposure to multiple chemicals via
a single or multiple pathways/routes
The cumulative risk posed by the releases of all HAPs from sources within all source
categories located at a specific facility.
2.1 Facility/Source-Specific Human
Health Risk Assessment
The human health risk assessment process is
divided into three main phases (see Exhibit
1). These phases are described in more detail
in Chapter II.
Planning, scoping, and problem
formulation is performed to articulate
clearly the assessment questions, state the
Risk assessment uses scientific principles and
methods to answer the following questions:
Who is exposed to air toxics?
What air toxics are they exposed to?
How are they exposed?
How much are they exposed to?
How dangerous are specific chemicals?
How likely is it that exposed people will
suffer illness because of the exposures?
How sure are we that our answers are correct?
April 2004
Page 2
-------
quantity and quality of data needed to answer those questions, provide an in-depth discussion
of how the analysis will be done, outline timing and resource considerations, identify product
and documentation needs, and identify who will participate in the overall process from start
to finish, along with their roles. In this example approach, planning, scoping, and problem
formulation are regarded as iterative processes that allow for the assessment's plan to be
adjusted as new information is obtained.
Exhibit 1. The General Air Toxics Health Risk Assessment Process
The ge
01
01
CO
Q.
To
c
-------
(descriptive) statements. Specifically, chemical-specific dose-response toxicity information
is mathematically combined with modeled or monitored exposure estimates and other
information about how exposure occurs to give numbers that represent the potential for the
exposure to cause an adverse health outcome.
Information about risk is extremely helpful to decision makers as they try to balance the
competing needs of protecting public health, sustaining economic development, evaluating
issues of fairness and equity, and other factors specific to the laws and regulations controlling
each risk management decision. The approach described in this document also can be used to
compare risks from different exposures (e.g., the risk from breathing contaminated air compared
to the risk from drinking contaminated water). Risk assessment is already used by EPA to
determine the safety of foods containing pesticides, clean contaminated land and water bodies,
regulate what chemicals can be imported into the United States, and set allowable limits on
chemicals in our drinking water. Volume 1 of this series, the Technical Resource Manual,
discusses the overall air toxics risk assessment process and the basic technical tools needed to
perform these analyses. The Manual addresses both human health and ecological analyses. It
also provides a basic overview of the process of managing and communicating risk assessment
results.
2.2 Facility/Source-Specific Ecological Assessment
When a specific set of air toxics that persist
and which also may bioaccumulate or
biomagnify (PB-HAP compounds) are
present in releases, the risk assessment
generally will need to include consideration
of exposure pathways that involve deposition
of air toxics onto soil, onto plants, and into
water; subsequent uptake by biota; and
potential exposures to ecological receptors
(e.g., birds, fish, plants) via direct exposure to
contaminated media and/or indirect exposure
through aquatic and terrestrial food chains.
Air toxics ecological risk assessment is the
process by which the risks of adverse impacts
to ecological receptors associated with
exposures to air toxics are estimated.
EPA is investigating whether it is possible to
develop a Tier 1 ecological risk assessment
methodology to allow sources/facilities that emit
small amounts of PB-HAP compounds to
demonstrate that risk targets are met using simple
look-up tables or graphs. EPA also is
investigating whether any HAPs pose ecological
problems in air at concentrations below the
human-health based Reference Concentration
(RfC). This resource document may be revised
to incorporate an example Tier 1 ecological risk
assessment methodology and/or an example
approach for performing ecological assessments
for direct exposure to air toxics in ambient air.
Congress has recognized the importance of protecting ecological receptors from adverse effects
resulting from exposure to air toxics. For example, Sections 112(f)(2) through (6) of the CAA
require EPA to promulgate standards beyond MACT when necessary to provide "an ample
margin of safety to protect public health" and to "prevent, considering costs, energy, safety, and
other relevant factors, an adverse environmental effect" (note that the requirements of other
authorities may vary). The major philosophical difference between ecological and health risk
management decision making is that health-based decisions intend to protect groups of
individuals (e.g., population subgroups), whereas ecologically-based decisions intend to protect
species and ecosystems.
April 2004
Page 4
-------
The ecological risk assessment process also has three main phases that broadly correspond to the
three basic phases of the human health risk assessment methodology.
Problem formulation, which
corresponds to the planning, scoping, and
problem formulation phase of the human
health risk assessment methodology;
Analysis, which corresponds to the
analysis phase of the human health risk
assessment methodology and includes the
exposure assessment and ecological
effects assessment steps; and
Risk characterization, which
corresponds to the risk characterization
phase of the human health risk assessment
methodology.
Ecological risk assessment uses scientific
principles and methods to answer the following
questions, which are analogous to those for
human health risk assessment:
What receptors are exposed to air toxics?
What air toxics are they are exposed to?
How are they exposed (including directly and
via food chains)?
How much are they exposed to?
How dangerous are the specific chemicals?
How likely is it that exposed receptors will
suffer adverse impacts because of the
exposures?
How sure are we that our answers are correct?
2.3 Use of Site-Specific Risk Assessments in EPA's Air Toxics Program
The results of any site-specific risk assessment can be used to support a number of activities,
including:
Development and implementation of source-specific standards and sector-based standards;
Development and implementation of area-wide risk assessments and strategies developed by
state or local air pollution control agencies to address air toxics in urban areas;
Implementation of national air toxics assessments (NATA) activities; and
Development of education and outreach tools.
3.0 The Layout of This Resource Document
The remainder of Volume 2 is divided into three chapters:
Chapter II: Overview and Getting Started provides an overview of risk assessment and
describes several important initial steps.
Section 1 provides an introduction to Chapter II.
Section 2 presents an overview of the risk assessment methodology, including the basic
phases and steps (planning, scoping, and problem formulation; exposure assessment; toxicity
assessment; and risk characterization).
April 2004
Page 5
-------
Section 3 introduces the concept of a tiered approach, starting with a relatively simple,
health-protective screening analysis and continuing with more complex and realistic analyses
as needed to answer specific assessment questions.
Section 4 describes the initial planning, scoping, and problem formulation steps that
generally are followed prior to conducting the risk assessment. Three key elements are
highlighted: developing a conceptual model, developing an analysis plan, and determining
whether multipathway analyses are needed.
Section 5 describes a toxicity-weighted screening analysis that can be used to focus the risk
analysis on a smaller subset of HAPs that contribute the most to risk.
Chapter III: Inhalation Pathway Risk Assessment describes one set of methods and
approaches that could be used to conduct human health risk assessments for inhalation
exposures.
Section 1 provides an introduction to Chapter III.
Section 2 provides an example of how to structure a tiered assessment approach (including
the use of different models at different tiers) for the inhalation analysis.
Section 3 provides an example of how to develop the emissions inventory for an inhalation
analysis.
Section 4 describes an example of how to perform an inhalation toxicity assessment for both
chronic and acute exposures.
Section 5 describes an example risk characterization for inhalation analyses.
Section 6 describes an example structure for a Tier 1 assessment highlighting a focus on a
protective estimate of the location of the maximum exposed individual.
Section 7 describes an example structure for a Tier 2 assessment highlighting a focus on a
more realistic estimate of the highest individual risk in areas that people are believed to
occupy.
Section 8 describes an example structure for a Tier 3 assessment, highlighting the use of
exposure modeling to assess variability and uncertainty in the activity patterns of the exposed
population.
Chapter IV: Multipathway Risk Assessment describes one set of methods and approaches for
conducting human health and ecological risk assessments for exposure pathways that involve
deposition of PB-HAP compounds to soils and surface waters and subsequent uptake and
ingestion exposures.
Section 1 provides an introduction to this Chapter IV.
April 2004 Page 6
-------
Section 2 provides an example of how to structure a tiered assessment approach (including
the use of different models at different tiers) for the inhalation analysis.
Section 3 provides an example of how to develop the emissions inventory for a multipathway
analysis.
Section 4 describes an example structure for a tiered multipathway human health risk
assessment for chronic exposures.
Section 5 describes an example structure for a tiered ecological risk assessment.
This document focuses on EPA risk assessment methods and resources. Note that many state
and local governments have air toxics programs. For example, California has an existing health
risk assessment methodology which has been scientifically peer reviewed and has gone through
extensive public comment http://www.oehha.ca.gov/air/hot spots/index.html. State and local
agencies may have existing methodologies that are acceptable for conducting facility/source-
specific health risk assessments.
April 2004 Page 7
-------
(this page intentionally left blank)
April 2004 Page,
-------
Chapter II: Overview and Getting Started
1.0 Introduction
This chapter provides an overview of the methodology EPA uses to quantitatively predict human
health risks from emissions of HAPs at a specific facility or source in a source category. It
introduces the tiered risk assessment process for facility-specific assessments. It also describes
important steps in getting started, including planning, scoping, problem formulation, and
conducting a toxicity-weighted emissions screening process to focus the analysis on the HAPs of
greatest potential human health concern. Basic risk assessment concepts, principles, and
methods are described in more detail in Volume 1 of this series. The remainder of this chapter is
divided into four sections:
Overview of Risk Assessment (Section 2);
Concept of Tiered Assessment (Section 3)
Planning, Scoping, and Problem Formulation (Section 4); and
Focusing on the Most Important HAPs (Section 5).
2.0 Overview of Risk Assessment and Risk Management
The site-specific risk assessment methodology follows the risk assessment frameworks
established for EPA's Framework for Cumulative Risk Assessment^ and Residual Risk Report to
Congress.(T> Volume 1 provides a more detailed discussion of these frameworks and their
relationship to the general risk assessment paradigm established by the National Academy of
Sciences (1983) and used throughout the federal government. The methodology includes the
following components (Exhibit 2):
Planning, scoping, and problem formulation;
Analysis (consisting of exposure assessment and toxicity assessment); and
Risk characterization (including qualitative or quantitative uncertainty analysis).
Any risk assessment begins with planning and scoping. Properly planning and scoping the risk
assessment at the beginning of the project is critical to the success of the overall effort. Planning
and scoping focuses on a communication step among managers, assessors, and other
stakeholders regarding the purpose, scope, participants, approaches, and resources available for
the risk assessment.
Problem formulation generally is conducted by both risk assessors and risk managers and
focuses on two key products. The conceptual model identifies sources of emissions, HAPs
emitted and emissions rates, the location of human and ecological receptors, potential exposure
pathways/routes, and any areas (land or water) that have the potential to be contaminated from
deposition of air toxics emitted from the facility/source. The conceptual model may be refined
as new information becomes available during the tiered assessment process. Risk assessors use
the study-specific conceptual model as a guide to help determine what types, amount, and quality
of data are needed for the study to answer the questions the risk assessment has set out to
evaluate. The analysis plan describes the specific requirements and methods to be used to
April 2004 Page 9
-------
obtain and analyze information on the source(s), pollutants, exposure pathways, exposed
population(s), and endpoints. It also may be refined during the assessment process. This phase
also may include a toxicity-emissions weighted screening analysis to identify which HAPs to
include in the Tier 1 assessment.
Exhibit 2. Overview of EPA's Air Toxics Risk Assessment Process
Planninc
and Scoping
Source: Modified from EPA 's Residual Risk Report to Congress^'
An exposure assessment is conducted to identify who is potentially exposed to toxic chemicals,
what chemicals they may be exposed to, and how they may be exposed to those chemicals. This
often includes three substeps: (1) further characterizing the emissions sources and emissions to
provide requisite model inputs; (2) performing fate and transport modeling and/or monitoring to
estimate ambient concentrations of HAPs in air, water, soil, and other abiotic and biotic media
(as applicable to the type of analysis); and (3) estimating inhalation exposure or oral intake
(where applicable). As noted in Volume 1, estimates of exposure concentrations may be based
on actual measurements (i.e. monitoring data) or and/or air quality modeling. Many studies may
April 2004
Page 10
-------
benefit by using some combination of modeling and monitoring, because the two approaches can
be complementary.
The toxicity assessment component of the risk assessment process considers: (1) the types of
adverse health effects associated with exposure to the chemicals in question, and (2) the
relationship between the amount of exposure and resulting response.
Hazard identification is the process of determining whether exposure to a chemical can
cause an increase in the incidence of an adverse health effect (e.g., cancer, birth defects), and
the nature and strength of the evidence for causation.
Dose-response assessment is the process of quantitatively characterizing the relationship
between the dose of the contaminant and the incidence of adverse health effects in the
exposed population. As information on dose at the site in the body where the response
occurs is rarely available, various surrogates (dose metrics) are employed, often with the
assistance of biologically-based pharmacokinetic or dosimetry models to predict the dose
metric from the inhalation exposure concentration or oral intake estimates. From this
quantitative dose-response relationship, dose-response values are derived for use in risk
characterization.(a) Most toxicity assessments are based on studies in which toxicologists
expose animals to chemicals in a laboratory and extrapolate the results to humans. For some
chemicals, information from actual human exposures is available (usually from studies of
workplace exposures).
The risk characterization phase integrates the exposure and toxicity assessments to estimate
risks. Cancer risk is expressed in numerical terms (e.g., 1 x 10"5 or 10 in a million) as the
incremental chance an individual will develop cancer in their lifetime as a result of the exposure,
and/or as the converse, the concentration corresponding to a particular level of risk. Noncancer
hazard is expressed as a Hazard Quotient (HQ), the ratio of the estimated exposure to the
noncancer dose-response value. For the assessment of exposures to mixtures of multiple
pollutants, a Hazard Index (HI, the sum of the HQs of each chemical in a mixture) may be
calculated. The individual HQs may be summed separately for chemicals that affect the same
target organ/organ system or act by similar toxicological processes (e.g., the sum of the HQs for
all HAPs that produce liver disease as a critical effect). Such a metric is called a Target Organ
Specific Hazard Index (TOSHI). Ecological risk is often expressed as an ecological HI derived
in a manner analogous to the human health HI.
Uncertainty and variability are inherent characteristics of risk assessments, and therefore the risk
characterization phase includes an analysis and presentation of uncertainty and variability. Air
toxics risk assessments make use of many different kinds of scientific concepts and data (e.g.,
exposure, toxicity, epidemiology, ecology), all of which are used to characterize the expected
risk in a particular environmental context. Informed use of reliable scientific information from
aDose-response values are numerical expressions of the relationship between a given level of exposure to an
air toxic and adverse health impacts. The two most common toxicity values for inhalation exposures are the upper-
bound inhalation unit risk estimates (ITJRs) for cancer effects and reference concentrations (RfCs) for noncancer
effects (which include uncertainty factors). Chapter III, Section 4 provides a more detailed discussion of toxicity
values.
April 2004 Page 11
-------
many different sources is a central feature of the risk assessment process. Reliable information
may or may not be available for many aspects of a risk assessment. Uncertainty and variability
are inherent in the risk assessment process, and risk managers almost always must make
decisions using assessments that are not as definitive in all important areas as would be
desirable. Risk assessments also incorporate a variety of professional and science policy
judgments (e.g., which models to use, where to locate monitors, which toxicity studies to use as
the basis of developing dose-response values). Risk managers need to understand the strengths
and the limitations of each assessment to communicate this information to all participants,
including the public.(3) Several techniques for assessing and describing uncertainty are described
more fully in Volume I (see this endnote for several key references).(4)
Risk management refers to the regulatory and other actions taken to limit or control exposures
to a chemical. Risk management considers the quantitative and qualitative expressions of risk
(along with attendant uncertainties) developed during the risk assessment, as well as a variety of
additional information (e.g., the cost of reducing emissions or exposures, the statutory authority
to take regulatory actions, and the acceptability of control options) to reach a final decision.
sx
This document focuses on the modeling approach to estimating exposure. Ambient concentrations
obtained by monitoring can be incorporated into facility/source-specific risk assessments, generally
after initial (Tier 1) assessments indicate a potential for risk. As noted in Volume 1:
The scope of monitoring is necessarily limited (i.e., spatially, temporally, and in number of
pollutants measured) by resources;
Monitoring cannot attribute exposures to sources;
Monitoring cannot estimate exposures below the detection limit;
Monitoring cannot predict the effects of various possible risk reduction options on future
exposures; and
Monitoring is therefore most effectively used to evaluate or further characterize modeled
concentrations and exposures.
Volume 1 and EPA's NATA web site (http://www.epa.gov/ttn/atw/nata/draft6 .html#secIV.B.D
.provide detailed discussions of how monitoring can complement modeling in the exposure assessment. ,
3.0 Concept of Tiered Assessment
The human health risk assessment methodology may be based on several tiers of analysis,
ranging from relatively simple, health-protective risk estimates based on limited information to
complex, more realistic estimates involving more intensive data collection and calculations (see
Exhibit 3).
April 2004 Page 12
-------
Exhibit 3. Generalized Representation of the Tiered Risk Assessment Concept
Tier 3: High Complexity
Complex exposure assessment
Detailed site-specific modeling
High cost
Decision-making cycle: Evaluating the
adequacy of the risk assessment and the
value of additional complexity/level of effort
Tier 2: Moderate Complexity
Exposure = residential air levels
More detailed modeling
Moderate cost
Decision-making cycle: Evaluating the
adequacy of the risk assessment and the
value of additional complexity/level of effort
Tier 1: Screening Level
Exposure = max offsite levels
Simple modeling
Low cost
This representation, adapted from Volume III of EPA's Risk Assessment Guidance for Superfitnd^
depicts three tiers of analysis. Each successive tier represents more complete characterization of
variability and/or uncertainty as well as a corresponding increase in complexity and resource
requirements.
Tier 1 is represented as a relatively simple, screening-level analysis using health-protective
exposure assumptions [e.g., receptors are located in the area with the highest estimated
concentrations] and relatively simple modeling (e.g., a model that requires few inputs, most of
which can be "generic," yet health-protective).
Tier 2 is represented as an intermediate-level analysis using more realistic exposure assumptions
(e.g., use of actual receptor locations) and more detailed modeling (e.g., a model that requires
additional facility/source-specific inputs).
Tier 3 is represented as an advanced analysis, capable of using probabilistic analysis for some
input variables (see Volume 1, Part VI for a discussion of these techniques) and more detailed
and/or intensive modeling.
This representation does not imply that there are clear distinctions between Tiers 1, 2, and 3. For
example, a series of refinements in a Tier 1 analysis might be indistinguishable from a Tier 2 analysis,
or a Tier 2 analysis could incorporate probabilistic techniques.
This representation also notes the decision-making cycle that occurs between each tier. In this cycle,
the existing risk assessment results are evaluated to determine whether they are sufficient for the risk
management decision, and if not, what refinements to the risk assessment are needed (including
moving up to the next tier).
April 2004
Page 13
-------
This document presents a three-tiered approach i\, TT . .~-~- >
A health-protective exposure estimate is an
estimate based on assumptions about exposure
(e.g., release, atmospheric dispersion, contact
with contaminated air) that would result in a
reasonable maximum level of exposure. It is
not necessarily the highest level of exposure
that theoretically could occur. The term
"conservative" is often used synonymously
with "health protective."
and describe the types of models and
assumptions that would be consistent with the
conservativeness of these tiers. This discussion
is modeled on EPA's general framework for
assessing residual risk pursuant to section
112(f) of the CAA. This resource document is
meant to provide an example and is not
intended to prescribe a specific approach that
must be used by EPA or others in a particular
risk assessment activity. In particular, various
modifications to this tiered approach may be both cost-effective and appropriate, such as
adding intermediate-level tiers that incorporate some features of the higher and lower tiers, or
conducting iterative, more refined analyses within a given tier.
/ \
The example Tiered approach presented in this document illustrates how an iterative risk
assessment process can be used to first screen out facilities/sources that represent a relatively low
risk and then focus the risk assessment on the sources andHAPs that may require emissions
reduction actions. Tier 1 and Tier 2 analyses generally are an appropriate basis for deciding not to
take any action or what to leave out of the next tier of analysis. Significant emissions reduction
actions are likely to need a Tier 3 analysis of the specific sources andHAPs that drive the exposure
. and risk. .
Facility-specific assessments by regulatory agencies are often designed to answer the question:
"Is the estimated risk from a facility or source category low enough to support a finding that it is
of negligible regulatory concern?" If a simple, health-protective Tier 1 assessment provides a
"yes" answer, there may be no need for regulatory action or further assessment. If the answer is
"no," the risk manager will need to decide whether to consider a regulatory response or to refine
the assessment at a higher tier. If a higher-tier assessment is performed, the decision process is
repeated.
For example, a Tier 1 analysis might consist of screening-level dispersion modeling using
SCREENS. The Tier 1 analysis would typically provide a single estimate of maximum ambient
air concentration that would be used to estimate inhalation risk based on an assumption that the
maximum exposed individual could reside at the offsite location of maximum concentration,
whether or not a person actually lived there. A Tier 2 analysis might then use the more refined
Human Exposure Model, version 3 (FIEM-3). FIEM-3 uses the Industrial Source Complex
Short-Term, version 3 (ISCST3) to provide spatially-resolved air concentrations. It combines
concentration data with U.S. Census Bureau population data (2000 census) to estimate risk and
hazard for the population in the most-exposed Census block. A Tier 3 analysis might couple
dispersion modeling using ISCST3 with exposure modeling using Trim.ExpoInhalation to estimate
risk and hazard for hypothetical individuals used to represent the exposed population based on
combinations of demographic characteristics and activity patterns. A Tier 3 approach might also
add a probabilistic exposure model to quantify the effects of variable human behavior on the
exposure and risk estimates. Because the lower tier analyses are generally designed to be more
April 2004 Page 14
-------
health-protective, a facility-specific assessment can be performed at the lowest tier that
demonstrates that applicable low-risk targets are met.
x ">
Determination of appropriate tiers may depend on the purpose of and regulatory context for the risk
assessment. For example, if the regulatory authority for a risk management decision does not
include consideration of population risk, a Tier 2 analysis might incorporate the use of a more
refined air quality model to more accurately estimate maximum impact. Choice of a particular
model to use within any Tier also may depend on facility/source-specific factors. For example, if
downwash is particularly important at a given facility, a model other than ISCST3 may be more
appropriate at Tier 2. If consideration of potential future land use is important, a model based on
current land use (e.g., HEM-3) may not be the appropriate tool. Finally, the assessment may need
to comply with specific S/L/T guidelines for how risk analyses should be conducted.
4.0 Planning, Scoping, and Problem Formulation
Volume I of this reference library discusses in detail the general planning, scoping, and problem
formulation process, including identifying the specific concerns; determining who will be
involved in the risk assessment process (including the risk managers, risk assessment technical
team, and stakeholders); communicating the purpose and scope of the risk assessment; and
determining what resources are available for the risk assessment. Volume I also provides a
detailed discussion of the problem formulation process, including developing a study-specific
conceptual model and developing the important plans that will guide the risk assessment,
including the analysis plan, and quality-related plans such as the Quality Assurance Project Plan
(QAPP).
This section does not repeat the general discussion provided in Volume 1. Instead, it focuses on
two aspects of planning, scoping, and problem formulation that are particularly important for
facility/source-specific air toxics risk assessments (Exhibit 4): developing the conceptual model
(Section 4.1); and determining whether multipathway analyses (human health ingestion and/or
ecological) are applicable (Section 4.2).
Note that planning, scoping, and problem formulation activities generally continue throughout
the risk assessment as new information is learned. The specific details of some activities also
will vary depending on which type of analysis (i.e., human health-inhalation, human health-
multipathway, ecological) and which tier of analysis is being performed.
April 2004 Page 15
-------
Exhibit 4. Example Elements of Planning and Scoping for Facility/Source-Specific Risk
Assessments
General Conceptual Model
for Air Toxics
Includes all pathways and receptors
discussed in Volume 2
Inhalation Pathway
Multipathway
Toxicity-emissions
Weighted Screening
Analysis
Include HAPs and sources
comprising a high proportion
of total toxicity-weighted
emissions mass (estimated
separately for cancer, chronic
noncancer, and acute
noncancer)
Include emissions of
all PB-HAP
compounds listed in
Exhibit 11-5
Tierl
Inhalation
T
Tierl
Multipathway
Modify general conceptual model to remove exposure pathways
and receptors not being assessed for the specific facility
4.1 Conceptual Model Development
The conceptual model describes the entire potential scope of the assessment, and then clarifies
which pieces will be addressed. In addition to the inhalation assessments that are more or less
automatic for emissions to air, the conceptual model in this example approach also considers two
important chemical properties of each HAP: its persistence (P) in the environment (i.e., as
determined by the HAP's half-life in air, water, soil, and sediment), and its potential to
bioaccumulate (B) in plant or animal tissues (i.e., as determined by the steady-state ratio between
environmental and tissue concentrations) and/or biomagnify in food chains. PB-HAP
compounds are HAPs that are deposited onto soils and surface water, accumulate in soils,
sediments, and/or biota, and normally pose a greater threat through non-inhalation pathways,
especially food consumption, than by inhalation (see Section 4.2 below). Exhibit 5 provides an
example of a conceptual model. The elements of a conceptual model are outlined below.
Sources. All sources (point and area) of pollutant emissions at the facility/source are
identified, and a determination is made about which - if not all - of those sources need to be
included in the risk assessment. In some cases, not all emission sources need to be included.
For example, if a facility/source releases pollutants from a large number of sources - both
April 2004
Page 16
-------
large and small - the toxicity-weighted screening analysis (TWSA) may be used to determine
which sources release negligible amounts of HAPs or low toxicity pollutants that might be
excluded from modeling (see Section 5 below). If data are readily available for emissions
from all sources, however, the risk assessor may choose to use those data in all tiers of
analyses.
Stressors. All HAPs released from the sources are identified. It also is helpful at this point
to characterize emissions from the sources and identify applicable dose-response values in
order to perform TWSA (described in Section 5). Additional information on characterizing
emissions and identifying dose-response values is provided in Section 5 below.
Exposure Pathways/Media/Routes. Potential exposure pathways/routes by which the
identified receptors can be exposed to the emitted HAPs are identified. The inhalation
pathway commonly is included for all facility-specific assessments. Additional exposure
pathways/routes, such as ingestion of animal and vegetable products raised on farms (human
health), or pathways of ecological exposure, may be performed if PB-HAP compounds are
present in emissions.
Receptors. Human and ecological
receptors that are potentially exposed to
the emitted HAPs are identified, located,
and characterized. This includes all areas
(land or water) that have the potential to
be contaminated from deposition of air
toxics emitted from the facility/source.
Special ecological receptors such as
endangered/threatened species or
wetlands are identified. The conceptual
model indicates areas where the
maximum exposures are expected.
While many facility/source-specific risk
assessments focus on current land use, it may be
helpful to assess risks associated with potential
future land use. Risk estimates based on current
conditions at the facility/source and current land
use could change if conditions at the
facility/source change (e.g., one process is
replaced by another) and/or land use changes
(e.g., a housing development is built on currently
undeveloped land).
Endpoints. The specific human health and ecological endpoints of concern for the emitted
HAPs are identified, along with specific target organs.
Metrics. The specific HAP-specific and cumulative metrics used to estimate risk/hazard
(e.g., cancer type, weight of evidence, target-organ-specific hazard index) are identified,
along with how they will be characterized for the exposed population (e.g., central tendency,
high-end, distributions).
Volume I (Chapter 6) of this reference library provides a more detailed discussion of how to
perform these important steps.
April 2004
Page 17
-------
Exhibit 5. Example of a General Conceptual Model for a Facility/Source Specific Air Toxics
Risk Assessment'3'
Sources
Stressors
Pathways/Media
Routes
ABC Facility
Point
Sources
Nonpoint
Sources
Volume
Sources
Other
Sources
Receptors
Endpoints
Metrics
Hispanic
African
American
White | | Other
Native
American
Asian
American
Elderly | | Other
Young
Children
Pregnant
Women
Cancers
Resp ra
ory Blood CMS Liver Kidney
Cardiovascular Other
L
Possible Carcinogens
mber of
specified
anges
Probable C
ircinogens
Known Carcinogens
Estimated
number of
cancer cases
-
!
|
Et .
CMS Hazard Inde
Blood Hazard Index
Respiratory System Hazard Index
Distribution
of estimated
HI values
Estimated number of
people within specified
ranges of HI values
X
Illustrative Example Only - not intended to be comprehensive. For example, endpoints and
measures for ecological receptors are not illustrated.
In this example approach, the conceptual model is developed prior to beginning any actual
estimation of exposure and risk and is iteratively modified during the planning and scoping
phase, as well as during the different phases and tiers of the risk assessment, to reflect new
and/or better information that is obtained. The activities that are described below are further
steps in the planning and scoping phase that involve information gathering and processing.
These activities will likely result in modifications to the conceptual model.
4.2 Determining Whether Multipathway Analyses are Appropriate
In this example approach, the human health inhalation pathway is evaluated in all site/source-
specific risk assessments. In addition, multipathway risk assessment may be needed when
specific HAPs are present in releases. In this example approach, multipathway modeling is
performed if any HAPs that persist and which also may bioconcentrate or biomagnify (i.e.,
PB-HAP compounds) are present in releases (see Exhibit 6). As noted in Volume 1 (Chapter
4), all of the PB-HAP compounds are identified on one or more other Agency lists of chemicals
of concern for persistence and bioaccumulation.
April 2004
Page 18
-------
Exhibit 6. HAPs of Concern for Persistence and Bioaccumulation (PB-HAPs)
PB-HAP Compound
Cadmium compounds
Chlordane
Chlorinated dibenzodioxins and furans
DDE
Heptachlor
Hexachlorobenzene
Hexachlorocyclohexane (all isomers)
Lead compounds
Mercury compounds
Methoxychlor
Polychlorinated biphenyls
Polycyclic organic matter
Toxaphene
Trifluralin
Pollution
Prevention
Priority PBTs
X
X(a)
X
X
X(0
X
X
X(d)
X
Great Waters
Pollutants of
Concern
X
X
X
X
X
X
X
X
X
X
X
TRI PBT
Chemicals
X
xoป
X
X
X
X
X
X
X(e)
X
X
(a) "Dioxins and furans" ("" denotes the phraseology of the source list)
^ "Dioxin and dioxin-like compounds"
(c) Alkyl lead
(d) Benzo[a]pyrene
(e) "Polycyclic aromatic compounds" andbenzo[g,h,i]perylene
It may be appropriate to consider multipathway analyses for other chemicals for which deposition
may impact other media, as identified in the conceptual model for the assessment. For example,
some inorganic compounds (e.g., chromium compounds, beryllium compounds) may be deposited
onto plants; some semivolatile compounds may persist in soils; and in some circumstances (e.g.,
lack of sunlight), certain volatile organic compounds may not break down in the atmosphere. Also,
some state and local agencies may have identified specific compounds or circumstances for which
multipathway analyses are required. Therefore, the list of PB-HAP compounds represents a
starting point for determining whether multipathway analyses are appropriate; risk assessments
may need to consider additional compounds.
April 2004
Page 19
-------
5.0 One Method for Focusing the Assessment on the Most Important HAPs
The initial conceptual model, which lays out the entire potential scope of the assessment,
generally identifies the chemicals of potential concern (COPC) for the risk assessment. The
results of the risk assessment often indicate that most of the risk is associated with a subset of the
COPC. At each tier of analysis, the risk assessor might choose to reduce the number of HAPs to
include in the assessment (i.e., reduce the number of COPC), with the objective (in the final tier
of analysis) of identifying the subset of HAPs that drives the risk management decisions. This
subset is referred to as chemicals of concern (COC). This step is optional. If the list of emitted
HAPs is not long and resources are adequate, it may be appropriate to include all HAPs in the
assessment.
For the Tier 1 inhalation assessment, the risk assessor might choose to reduce the number of
COPC by using a simple toxicity-emissions weighted screening approach. Note that in this
example approach, all PB-HAP compounds are included in the multipathway analysis The
toxicity-weighted screening analysis (TWSA) is one technique for narrowing the list of COPC
for the Tier 1 inhalation risk assessment. The TWSA, a relative risk evaluation, may be
calculated based on the emissions data for all HAPs released from the facility/source being
assessed. A TWSA is particularly useful if there are a large number of HAPs in the
facility/source emissions and there is a desire to focus the risk analysis on a smaller subset of
HAPs that contribute the most to risk. A TWSA can be performed as described below.
The TWSA is intended to be entirely f~., irc . rc-c
J 1ms example 1WSA approach uses a cutollol
99 percent of total toxicity-weighted emissions.
This is not intended as a suggested value, as
others (e.g., 90 or 95 percent) may be appropriate
for focusing a given risk assessment on the subset
of HAPs that are likely to drive the risk
management decision.
emissions- and toxicity-based, without
considering dispersion, fate, receptor
locations, and other exposure parameters. It
essentially normalizes the emissions rates of
each HAP to a hypothetical substance with an
inhalation unit risk value of
1 per |ig/m3 (for carcinogenic effects) and/or
a reference concentration (RfC) of 1 mg/m3
(for noncancer effects). It requires emissions information as well as the applicable
dose-response values (see Chapter III). This technique is especially helpful when the number of
HAPs and/or the number of emission points is large. The steps for emissions-based toxicity-
emissions weighted screening would include the following steps (see Exhibit 7 for an example
calculation):
1. Identify all the inhalation unit risks (lURs) and RfCs for the HAPs in the facility/source
emissions.
2. Determine the emission rate (e.g., tons/year) of each HAP.
3. Multiply the emission rate of each HAP by its IUR to obtain a toxicity-emissions product.
4. Rank-order the toxicity-emissions products and obtain the sum of all products.
5. Starting with the highest ranking product, proceed down the list until the cumulative sum of
the products reaches a large proportion (e.g., 99 percent) of the total of the products for all
the HAPs. Include in the assessment all the HAPs that contributed to this proportion of the
total.
April 2004 Page 20
-------
6. Repeat steps 3-5, but instead divide the emissions rate by the RfCs to obtain "noncancer
equivalent tons'Vyear.
Exhibit 7. Example TWSA Calculation for Cancer Effects
Air Toxic
1,3 butadiene
carbon tetrachloride
beryllium compounds
arsenic compounds
2,3,7,8-TCDD
chromium (VI) compounds
polycyclic organic matter(a)
cadmium compounds
formaldehyde
1 , 3 -dichloropropene
allyl chloride
methylene chloride
benzene
Emissions
(tons/year)
8.2 x 101
1.5 x 102
8.6 x ID'1
4.2 x ID'1
2.0 x ID'5
3.7 x ID'2
4.3
1.0 x 1Q-1
8.9
5.2
2.8
1.9 x 101
9.3 x IQ-2
IUR
3.0 x IQ-5
1.5 x 1Q-5
2.4 x IQ-3
4.3 x IQ-3
3.3 x 1Q1
1.2 x IQ-2
2.1 x 1Q-1
1.8 x IQ-3
1.3 x IQ-5
4.0 x IQ-6
6.0 x IQ-6
4.7 x IQ-7
7.8 x IQ-6
Total
Cancer
Equivalent
Tons/year
2.5 x IQ-3
2.2 x IQ-3
2.1 x IQ-3
1.8 x IQ-3
6.6 x IQ-4
4.4 x IQ-4
3.7 x IQ-4
1.8 x IQ-4
1.2 x IQ-4
2.1 x 1Q-5
1.7 x IQ-5
8.7 x IQ-6
7.3 x IQ-7
1.0 x IQ-2
Percent
of Total
23.8%
21.3%
19.8%
17.5%
6.4%
4.3%
3.6%
1.8%
1.1%
0.2%
0.2%
0.1%
0.0%
100.0%
Cumulative
Percent
23.8%
45.1%
64.9%
82.4%
88.8%
93.1%
96.7%
98.4%
99.5%
99.7%
99.9%
100.0%
100.0%
Heavy line denotes 99% cutoff. In this example, 1,3 -dichloropropene, allyl chloride, methylene
chloride, and benzene could be dropped from the cancer analysis.
(a) Cancer equivalent tons/year and IUR are based on the assumption that benzo(a)pyrene represents 5%
of emissions.
Note that in subsequent tiers of analysis, a risk-based analysis can be used to further focus the
assessment on the significant HAPs of concern. This approach would be similar to the TWSA,
except that the risk assessor would use the Tier 1 estimates of individual cancer risk and
noncancer hazard instead of toxi city-weighted emissions. The risk-based approach would
include the following steps (see an example calculation in Exhibit 8):
1. Using applicable input data, run a simple dispersion and/or exposure model (with
conservative assumptions) and calculate cancer risk at a selected point (e.g., maximum
exposed individual location).
April 2004
Page 21
-------
2. Rank-order the individual risk estimates for each emitted HAP and obtain the sum of the
cancer risk.
3. Starting with the highest ranking cancer risk, proceed down the list until the individual HAPs
contributing a large proportion (e.g., 99 percent) of the total risk estimate are included.
Include those HAPs in subsequent tiers of analysis.
4. Repeat steps 1-3 for noncancer hazard.
Exhibit 8. Example TWSA Calculation for Noncancer Effects
Air Toxic
beryllium compounds
1,3 butadiene
arsenic compounds
cadmium compounds
carbon tetrachloride
allyl chloride
formaldehyde
2,3,7,8-TCDD
chromium (VI) compounds
toluene
1 , 3 -dichloropropene
methylene chloride
benzene
Emissions
(tons/year)
8.6 x ID'1
8.2 x 101
4.2 x ID'1
1.0 x ID'1
1.5 x 102
2.8
8.9
2.0 x IQ-5
3.7 x 10-2
1.3 x IQ2
5.2
1.9 x 101
9.3 x IQ-2
RfC
2.0 x IQ-5
2.0 x IQ-3
3.0 x IQ-5
2.0 x IQ-5
4.0 x IQ-2
1.0 x IQ-3
9.8 x IQ-3
4.0 x IQ-8
1.0 x IQ-4
4.0 x 1Q-1
2.0 x IQ-2
1
6.0 x IQ-2
Total
Noncancer
Equivalent
Tons/year
4.3 x IQ4
4.1 x IQ4
1.4 x 104
5.1 x IQ3
3.7 x 103
2.8 x IQ3
9.1 x IQ2
5.0 x 102
3.7 x 102
3.2 x 102
2.6 x 102
1.9 x 101
1.6
1.1 x 105
Percent
of Total
38.3%
36.7%
12.6%
4.6%
3.3%
2.5%
0.8%
0.4%
0.3%
0.3%
0.2%
0.0%
0.0%
100.0%
Cumulative
Percent
38.3%
75.0%
87.6%
92.1%
95.4%
97.9%
98.7%
99.1%
99.5%
99.8%
100.0%
100.0%
100.0%
Heavy line denotes 99% cutoff. In this example, chromium (VI) compounds, toluene, 1,3-
dichloropropene, methylene chloride, and benzene could be dropped from the noncancer analysis.
April 2004
Page 22
-------
Chapter III: Inhalation Pathway Risk Assessment
1.0 Introduction
This chapter describes an example three- /I, ., ~ ~ ., , . ... ,. \
^ ^ The three-tier approach described in this chapter
tiered approach to conducting site-specific
is only one of a number of potential paradigms
human health-inhalation risk assessments for i that may be appropnate wd considered.
air toxics. The tiers range from a relatively > S
simple, health-protective screening analysis
(Tier 1) to a complex probabilistic assessment (Tier 3). A risk assessor may decide to complete
only the lowest-tier analysis that fits the purpose of the assessment (e.g., to determine that a
facility's cumulative risk is lower than a risk manager's level of concern). Conversely, an
assessor may choose not to complete a lower-tier analysis before completing a higher-tier
analysis (e.g., the risk assessor could go directly to Tier 3).
The discussion in this chapter is divided into the following sections:
Tiered Approach and Models Used (Section 2);
Developing the Emissions Inventory for an Inhalation Analysis (Section 3);
Toxicity Assessment (Section 4);
Risk Characterization for Inhalation Exposures (Section 5);
Tier 1 Inhalation Analysis (Section 6);
Tier 2 Inhalation Analysis (Section 7); and
Tier 3 Inhalation Analysis (Section 8).
2.0 Tiered Approach and Models Used
This example inhalation risk assessment methodology includes three tiers of analysis, each with
example models for dispersion, exposure, and risk (see Exhibit 9).
Tier 1 would use a model like SCREENS, which is a screening-level Gaussian dispersion
model that estimates an hourly maximum ambient concentration based on hourly emission
rates. A relatively large degree of conservatism is incorporated in the SCREEN modeling
procedure to provide reasonable assurance that maximum concentrations will not be
underestimated.(6) Example default SCREENS inputs are identified for use in the absence of
facility/source-specific data and are based on health-protective assumptions. The key output
is an estimate of the highest modeled offsite concentration per model run, which is used as a
surrogate for exposure. This point may be referred to as the point of maximum exposed
individual (MEI). This concentration is combined with inhalation dose-response values
(either for individual HAPs, or for HAPs combined by toxicity weighting) to calculate an
estimate of the cumulative cancer risk and noncancer hazard to the most exposed individual.
Note that SCREENS predicts 1-hour concentrations and requires a conversion factor in order
to do the risk assessment for chronic effects (see Section 6.2.1 below).
April 2004 Page 23
-------
Exhibit 9. Example Tiered Approach for Inhalation Pathway Risk Assessment
Conservative Default
Release Parameters
Ves
Site-specific
Release Parameters
yes
Ier
"E" ~t ,H'ghest
Residential Cones.
Often only those
HAPs/sources
comprising a high
proportion of the total
risk estimate are taken
to next tier
Monitoring to evaluate
modeled concentrations
and exposures
Tier3
ISCST3 -+ TRIM.EXPOlnhalatlon -* TRIM.RiskHH
^ Activity-Based Exposures
yes
Risk Targets Met
Risk Targets Not Met
April 2004
Page 24
-------
Tier 2 would use a model like the Human
Exposure Model (HEM-3) (7) HEM-3
incorporates the Industrial Source
Complex-Short Term (ISCST3) model,
which is a more advanced Gaussian
dispersion model that provides hourly
estimates of ambient concentrations by
modeling hourly emissions and
meteorology. The focus in Tier 2 is on
the maximum concentration to which an
individual is exposed (i.e., a person who
resides at the point of maximum
exposure). This point may be referred to
as the point of the maximum individual
risk (MIR). This is done within HEM-3
using the internal point of the Census
block with the highest modeled exposure
or risk. It may be appropriate to consider
available ambient air measurement data or
conduct monitoring at Tier 2 to evaluate
or further characterize modeled
concentrations at specific receptor
locations.
Key Locations for Estimating Chronic EC
Point of maximum modeled concentration.
The location where the maximum modeled
ambient concentration occurs, regardless of
whether there is a person there or not. This
would provide a health-protective estimate of
exposure unless someone actually lives there.
This point may be referred to as the point of
the maximum exposed individual (MEI).
Point of maximum modeled concentration
at an actual receptor location. The
populated location with the highest modeled
ambient concentration. This location may be
an actual residence, a location within a Census
block, or some other populated area. In some
cases the risk assessor may decide to consider
future residential use. The concentration may
be interpolated between unpopulated values.
This point may be referred to as the point of
the maximum individual risk (MIR).
Tier 3 would use a model like the ISCST3 model for ambient concentration estimates, but
would also incorporate an exposure model like TRIM.ExpOjnj^.,,^ to provide a more realistic
estimate of individual exposures. Tier 3 would also use a model like TRIM.RiskjQj for risk
calculations. ISCST3 uses facility/source-specific source and meteorology data and provides
spatially-resolved air concentrations at receptor locations. These concentrations (and/or
monitoring data) are used as inputs to TRIM.ExpoInhalation, which are used to calculate
exposure to a set of hypothetical individuals, taking into account human activity patterns.
TRIM.Riskjjjj combines the exposure estimates with dose-response values to calculate more
refined estimates of inhalation cancer risk and noncancer hazards that account for individual
differences in daily activities, including where people live and work within the assessment
area. As with Tier 2, monitoring data may be helpful for evaluating the estimated ambient
air concentrations (e.g., from ISCST3). Additional measurements (e.g., indoor and outdoor
concentrations in specific locations where people live and work), as available, may be useful
in evaluating the exposure modeling component.
As noted earlier, other models may be appropriate for these tiers (e.g., AERMOD could be
used at Tier 2).
April 2004
Page 25
-------
Overview of Models Cited in This Example Approach
Air Quality Models
SCREENS. SCREENS is a screening-level Gaussian dispersion model that estimates an hourly
maximum ambient concentration based on hourly emission rates. Short-term concentration results are
used to estimate maximum annual averages via conversion factors that account for meteorological
variation and the type of process that produces the emissions. Results are not direction-specific (i.e.,
wind direction is not taken into account). SCREENS calculates ambient concentrations assuming no
deposition or atmospheric reactions, "worst-case" generic meteorological conditions, and flat terrain.
Data requirements are relatively low. For example, SCREENS uses facility/source-specific data (e.g.,
stack height, diameter, flow rate, downwash) but does not use facility/source-specific meteorology
data. Data processing requirements are low; it is easy to use for quick assessment of a single facility or
source. SCREENS does not estimate deposition rates. SCREEN 3 is available at
(http://www.epa. gov/ttn/scram/).(8)
Industrial Source Complex - Short Term (ISCST3). ISCST3 is a more advanced Gaussian
dispersion model that provides hourly estimates of ambient concentrations by modeling hourly
emissions and meteorology. The model includes removal effects for wet and dry deposition flux for
any locations specified by the user. Data requirements are higher than for SCREENS. For example,
ISCST3 requires hourly, site-specific, processed meteorological data; and physical characteristics of
emissions. Terrain information is optional. ISCST3 can accommodate variable emission rates. More
expertise (e.g., specific technical and computer skills) is required to use ISCST3. Unlike SCREENS,
ISCST3 estimates annual concentrations by integrating the hourly concentrations (i.e., no multiplier is
used). The ISC model is available at (http://www.epa.gov/ttn/scram/).(9)
Exposure and Risk Models
Human Exposure Model (HEM-3). HEM-3 is designed to screen major stationary sources of air
pollutant emissions efficiently, ranking the sources according to the potential cancer risks and
noncancer hazard associated with long-term (annual) average exposure concentrations. The current
version is implemented on a Windows platform for ease of use. HEM-3 contains the Gaussian
atmospheric dispersion model ISCST3 (with included meteorological data), and U.S. Census Bureau
population data (2000) at the Census block level. A limited amount of source data are required as
model inputs (e.g., pollutant emission rates, facility/source location, height of the emission release,
stack gas exit velocity, stack diameter, temperature of the off-gases, pollutant properties and source
location). HEM-3 estimates the magnitude and distribution of ambient air concentrations of pollutant
in the vicinity of each source. The model usually estimates these concentrations within a radial
distance of 50 kilometers (30.8 miles) from the source. Exposure concentrations for the residents of
each Census block are assumed to be the outdoor concentration at the Census block "internal point."
This actually represents a surrogate for exposure, as important exposure variables (e.g., indoor-outdoor
concentration differences, human mobility patterns, residential occupancy period, breathing rates) are
not explicitly addressed. Multiple facilities, including clusters of facilities, each having multiple
emission points can be addressed by HEM-3. Variability and uncertainty in input data and parameters
are not considered. The current version of HEM is available at http ://www.epa. gov/ttn/fera/.(7)
April 2004 Page 26
-------
Overview of Models Cited in This Example Approach (continued)
Exposure and Risk Models (continued)
TRIM.ExpoInhalation. TRIM.ExpoInhalatlon (also known as APEX3) uses a personal profile approach
rather than a cohort simulation approach. That is, individuals are selected for simulation by selecting
combinations of demographic characteristics and matching activity patterns, rather than directly
selecting an activity pattern. If the selection probabilities for the demographic characteristics are the
same as within the population to be simulated, this approach will provide a representative sample of
population activity patterns without the need for post-simulation weighting of results. The current
version (APEX3) includes a number of useful features, including automatic site selection from large
(e.g., national) databases, a series of new output tables providing summary statistics, and a thoroughly
reorganized method of describing microenvironments and their parameters. The model has the
capability to estimate microenvironment concentration from the mass-balance method, but also
provides the option of using the factors method. Most of the spatial and temporal constraints were
removed or relaxed in APEX3. The model's spatial resolution is flexible enough to allow for the use
of finely resolved modeled air quality values, as well as sparser measured values. Averaging times for
exposure concentrations are equally flexible. The current version of TRIM.ExpoInhalatlon is available at
http://www.epa.gov/ttn/fera/.(10)
TRIM.Riskjjjj. In TRIM.RiskHH estimates of human exposures are characterized with regard to
potential risk using the corresponding exposure- or dose-response relationships. The output from
TRIM.Riskjjjj includes documentation of the input data, assumptions in the analysis, and the results of
risk calculations and exposure analysis. The current version of TRIM.Riskjjjj is available at
http://www.epa.gov/ttn/fera/.
Detailed Documentation
EPA's Technology Transfer Network provides detailed information regarding individual models,
including software/code for each model, user's manuals, and other support documentation.
Documentation for dispersion models may be found on EPA's Support Center for Regulatory Air
Models (SCRAM) web page (http://www.epa.gov/scramOOI/).
Documentation for exposure and risk models may be found on EPA's Fate, Exposure, and Risk
Analysis (FERA) web page (http://www.epa.gov/ttn/fera/).
April 2004 Page 27
-------
3.0 Developing the Emissions Inventory for an Inhalation Analysis
Developing the emissions inventory includes (1) quantifying emissions/release rates; (2)
quantifying other emissions parameters important for the exposure assessment (e.g., temperature,
stack height); (3) identifying the chemical species of the emitted HAPs (where applicable); and
(4) identifying background concentrations of the HAPs being released (in some instances). Each
of these is discussed in a separate subsection below.
3.1 Quantification of Emissions Rates
The risk assessor is encouraged to use the highest quality, most detailed emissions data, even in
Tier 1 assessments. Depending on the objective of the risk assessment, acceptable data may
include (1) actual measured emissions from a recent high-activity, high-emission year, (2)
measured emissions extrapolated to a high-activity, high-emission year, (3) facility/source-
specific engineering estimates of a high-activity, high emission year (with documentation); and
(4) permitted emissions, (e.g., the maximum allowed under MACT, or under a permit) with
documentation that the permitted limits are not exceeded.
In this example approach, Tier 1 analyses use
high-end estimates of emissions in order to
ensure the assessment will produce health-
protective results; in subsequent tiers of
analysis, more realistic emissions data (e.g.,
Tier 2 analyses uses average emissions for
assessing cancer risks, and Tier 3 analyses
may consider other factors such as spatial and
temporal characteristics of releases in greater
detail). The inventories commonly include
the following release parameters for each
HAP released from each source: volume,
schedule, emission factors, and applicable
time periods. Emissions commonly represent
conditions typical of a high-activity, high-
emission year.
In this example approach, the risk
assessments consider emissions controls in
y^
use at the facility/source. The default
assumption is that the facility's sources are in
compliance with the appropriate standards and permit requirements, although it may be
reasonable to modify this assumption if additional emissions controls are in place. The
documentation for the assessment includes the specific emissions inventories that are used.
Highest Quality vs. High-End Emissions Data
Emissions data generally are a critical starting
point for air toxics risk assessments (e.g., as input
data for air quality models). Use of the highest
quality emissions data reduces the overall
uncertainty in the resulting risk and hazard
estimates.
Because Tier 1 analyses are intended to be
health-protective, they often are based on
reasonable high-end emissions. For example,
suppose five years of emissions data from a
facility/source indicate that emissions vary from
year-to-year. The Tier 1 analysis might be based
on the single year with the highest emissions. If
the resulting analysis indicates a potential for
risk, subsequent Tiers of analysis could
incorporate the more detailed information on
emissions patterns.
April 2004
Page 28
-------
3.2 Quantification of Other Release Parameters
Other release parameters will be needed as inputs for the various dispersion models used in the
analysis. Depending on the tier of analysis, these may include parameters such as stack height,
distance from the release point to the receptor, land use types, and terrain features. In general,
models used in higher tiers will need greater detail and accuracy of input parameters. Where
facility-specific information is not available, health-protective defaults generally are used. Some
examples are provided in this reference manual (e.g., see Exhibit 12).
3.3 Dose-Response Values for "Ambiguous" Substances
This section clarifies how some specific dose-response ambiguities can be addressed in
screening and tier 1 calculations (i.e., those designed to prioritize substances and sources with
health-protective estimates). For the purposes of this technical resource document, an
"ambiguous" substance is a HAP for which more than one dose-response assessment value could
apply. Note that there may be many other uncertainties in dose-response values for a single
chemical; these uncertainties are not addressed here.
Dose-response ambiguities often arise from unspeciated emissions data. That is, where: (1)
substances can exist in more than one chemical form, (2) the different forms have different toxic
potencies, and (3) emissions data do not identify the forms that are emitted. Examples of HAPs
with different chemical forms and toxic potencies include chromium and polycyclic organic
matter (POM). A second type of dose-response ambiguity can occur when there are multiple
dose-response values for the same chemical form (e.g., different values for whole-life and adult
exposures, for different interpretations of the dose-response data, or for food and drinking water
ingestion). HAPs with this kind of ambiguity
include vinyl chloride, benzene, and ^ v
manganese, respectively. A single
assessment (e.g., the assessment of vinyl
chloride in EPA's Integrated Risk
Information System [IRIS]) may provide
more than one value, and therefore risk
assessors have to choose which value to use.
EPA has developed a table of recommended
screening-level, chronic dose-response values
(available with supporting materials on-line
at
http ://www. epa. gov/ttn/atw/toxsource/summa
ry.html) that resolves ambiguities of the
second type (dose-response assessments that
provide more than one value for the same
chemical form) by listing only the values
appropriate for screening. Recommendations
to resolve ambiguities of the first type
(unspeciated emissions data) are presented
below.
This section discusses an approach for evaluating
HAPs that have presented ambiguity issues in
past assessments of chronic exposure, but it may
not be comprehensive. For air toxics not
addressed here, and for all acute exposure
scenarios, a commonly used default in lieu of
sufficient information supporting an alternative is
always the most protective chronic dose-response
value(s):
The smallest reference concentration (RfC)
and reference dose (RfD);
The largest inhalation unit risk estimate (IUR)
and cancer potency factor (CPF).
This is consistent with the general philosophy
behind screening-level risk assessments, in which
data gaps are routinely covered by protective
assumptions. This effectively minimizes the
chance of a false negative (i.e., overlooking an
important risk driver in the more refined
assessment that follows).
April 2004
Page 29
-------
The CAA lists some HAPs as groups (e.g., POM, glycol ethers, various metal compounds) that
include multiple individual compounds. Toxic potency may vary widely among compounds
within each of these groups. For example, many POM compounds having between 4 and 6
aromatic rings are potent mutagens and carcinogens, whereas most other POM compounds
having more or fewer rings are thought to pose relatively less noncancer hazard. Hexavalent
chromium (Cr+6) is a carcinogen and poses risks of other effects, whereas trivalent chromium
(Cr+3) is not thought to be carcinogenic, is far less toxic, and is essential in the diet. However,
the Toxics Release Inventory (TRI) and the National Emissions Inventory (NEI) report much of
the total emitted mass of these and other ambiguous HAPs only as "total POM," "chromium
compounds," or similar total values.
Exhibit 10 provides specific dose-response recommendations for screening-level risk
assessments that use unspeciated HAP data. These dose-response values cover chronic
exposures by ingestion (appropriate for PB-HAPs) and inhalation, and include both cancer and
noncancer effects. They are based on either (1) the most toxic chemical compound or valence
within the HAP group, or (2) a high-end estimate of the toxicity of mixtures emitted from
different source categories. In this example approach, these recommendations are considered
general-purpose screening-level defaults, to be used unless speciation information (e.g.,
source-specific monitoring data, EPA-approved emission factors) is available for the sources in
the assessment.
3.4 Identification of Background Concentrations
For the assessment of direct source impacts, background concentrations of the released HAPs
generally are not explicitly considered. However, analysis of site-specific background
concentrations may be included as part of higher-tier risk assessments to place source-related
risks in context with similar risks from other sources (or if total exposure is of concern). Note
that consideration of background may or may not be appropriate pursuant to the specific legal
and regulatory authorities under which the risk assessment is being conducted.
4.0 Toxicity Assessment
As noted in Volume 1 of this reference library (Chapter 12), toxicity assessment is accomplished
in two steps: hazard identification and dose-response assessment. Although air toxics risk
assessors need to understand the underlying scientific basis and uncertainties associated with
dose-response values, they will usually rely on those values already developed and available in
the literature.
April 2004 Page 30
-------
Exhibit 10. Specific Dose-Response Recommendations for Unspeciated HAP Data
HAP
Issue
Default Assumption for Screening-
Level Risk Assessment Where
Speciated Data are Lacking(a)
Chromium compounds
Hexavalent chromium (Cr+6) is
carcinogenic when inhaled, and
has much higher
noncarcinogenic potency than
trivalent chromium (Cr+3)
All chromium compounds are 100%
Cr+6 for inhalation
Cyanide (CN) compounds
RfDs vary among compounds;
only hydrogen cyanide (HCN)
has an RfC
All cyanide compounds are HCN for
inhalation
Glycol ethers
Both RfDs and RfCs vary among
compounds
All compounds are ethylene glycol
methyl ether for inhalation
Hexachlorocyclohexane
(HCH) (lindane and
isomers)
lURs, CPFs, and RfCs vary
among compounds; only lindane
has an RfD
All HCH isomers are cc-HCH for
cancer risk (inhalation and ingestion)
and lindane for noncancer hazard
(inhalation and ingestion)
Mercury (Hg) compounds
RfC exists only for elemental
mercury; RfDs vary between
methyl mercury and mercuric
chloride
All Hg is elemental for inhalation; for
ingestion assume methylmercury for
fish and HgCl2 for other food items
Nickel (Ni) compounds
lURs exist only for nickel
subsulfide and refinery dust;
RfCs vary between nickel oxide
and other nickel compounds
All Ni compounds are Ni3S2 for
cancer risk (inhalation) and NiO for
noncancer hazard (inhalation)
Polycyclic organic matter
(POM)
lURs, CPFs, and RfDs vary
widely among compounds
For cancer risk, emissions reported as
total POM, total PAH, or 16-PAH are
equivalent to 5% benzo[a]pyrene
(BaP), and emissions reported as 7-
PAH are equivalent to 18% BAP(b)
(inhalation and ingestion); for
noncancer hazard, all POM are
pyrene
(a) Assumptions for ingestion exposure are not included for substances that are not identified as PB-HAPs
^ High-end potency estimates for POM mixtures developed for the EPA National-Scale Air Toxics Assessment;
available online as Appendix H to the Science Advisory Board review draft of the assessment at
http://www.epa.gov/ttn/atw/sab/appendix-h.pdf
A major determination made during the hazard identification step concerns the potential of a
chemical to cause cancer in humans. This determination, which involves considering (or
April 2004
Page 31
-------
weighing) all the available evidence, is called the weight of evidence (WOE) determination.
This determination is complicated by possible inadequacies of the published studies as well as
differences in body processes between people and laboratory animals. EPA's Guidelines for
Carcinogen Risk Assessment^ guide scientists in interpreting available studies to assess the
potential human carcinogenicity of environmental pollutants. When compared with EPA's
original 1986 guidelines, the 1999 interim Guidelines recommend a more comprehensive
evaluation of the evidence with regard to a chemical's potential mode of action, and a more
complete description of the context of a chemical's carcinogenic potential (e.g., "likely
carcinogenic by inhalation and not likely carcinogenic by oral exposure"). The WOE
determination now includes one of five descriptors and is accompanied by additional text that
more completely summarizes EPA's interpretation of the evidence. The narrative statements
consider the quality and adequacy of data and the consistency of responses induced by the agent
in question (see Volume 1, Chapter 12).
Dose-response values (e.g., lURs, RfCs) are used in risk assessment to estimate the potential for
adverse impacts resulting from exposure to a given concentration of a HAP. Identifying critical
human health endpoints (cancer vs. non-cancer) and target organs is crucial for structuring the
risk assessment, including determining what exposure pathways and routes are of potential
concern, and how to sum the risks from exposure to multiple HAPs. Volume 1 of this series
provides more details of this process. For each HAP included in a risk assessment, the risk
assessor identifies the critical human health endpoints and target organs to ensure that cumulative
risk across all HAPs is estimated in a manner consistent with risk assessment principles during
the risk characterization step. The discussion of health effects criteria used by EPA in the NAT A
1996 National-Scale Assessment02' provides one example of how to identify dose-response
values for a specific assessment when data from a variety of sources are available.
As noted in Volume 1 (Chapter 12), the derivation of dose-response values includes uncertainty
factors and confidence levels, which vary widely among chemicals. This information should be
included in the risk assessment and discussed in the risk characterization.
Chronic effects. EPA/OAQPS has developed a set of recommended chronic human health
dose-response values for many HAPs. This information includes the type of hazard (e.g.,
cancer, non-cancer) and the applicable dose-response values for each HAP (e.g., RfCs,
lURs). It is presented in Appendix C of Volume 1. The most up-to-date list of default
screening level dose-response values recommended by EPA for the 188 HAPs is provided at
http://www.epa.gov/ttn/atw/toxsource/summary.html. This dose-response information is
generally appropriate to use in any tier of a risk assessment. However, OAQPS recognizes
that other independently-reviewed dose-response values may also be appropriate to use in tier
2 and 3 assessments. These values should be consistent with EPA risk assessment guidelines
and agreed upon in advance with the appropriate regulatory authority for assessments that
have regulatory implications. Descriptive information on the type of health hazards
associated with each HAP (e.g., cancer, noncancer) maybe found at
http://www.epa.gov/ttn/atw/hapindex.html.
- The Inhalation Unit Risk (IUR) is used to estimate inhalation cancer risk. The IUR is
defined as the upper-bound excess lifetime cancer risk estimated to result from
continuous exposure to an agent via inhalation per 1 ug/m3 over a lifetime. The
April 2004 Page 32
-------
interpretation of unit risk would be as follows: if the IUR = 1.5 x 10~6 per ug/m3, then not
more thanl.5 excess tumors may be expected to develop per 1,000,000 people if exposed
continuously for a lifetime to 1 ug of the chemical per cubic meter of air inhaled. The
number of expected tumors may be less; it may even be none.
- The Reference Concentration (RfC) is used to estimate the potential for adverse effects
due to chronic inhalation exposures. The RfC is defined as an estimate (with uncertainty
spanning perhaps an order of magnitude) of a continuous inhalation exposure to the
human population (including sensitive subpopulations) that is likely to be without an
appreciable risk of deleterious effects during a lifetime. RfCs are normally expressed as
milligrams per cubic meter (mg/m3). This is generally used in EPA's health effects
assessments for effects other than cancer.
Acute effects. Volume 1 of this reference library (Chapter 12) identifies and describes a
variety of short term, acute exposure values that may be used to assess the potential for
adverse impacts due to acute inhalation exposures. As noted in Volume 1, acute criteria are
developed to match specific time scales of exposure (available sources use different exposure
times) and desired effect levels (e.g., no-effect or mild reversible effects). One-hour acute
exposure times are commonly used for facility/source-specific risk assessments. EPA
suggests comparing estimated 1-hour exposures to a range of acute dose-response values
from the sources noted below. Note that these values have been developed for different
purposes (e.g., some may represent mild effect levels, and some may consider economics or
technical feasibility) and should be used with caution.
- Acute Reference Exposure (ARE) values. The ARE is an informed estimate of the
highest inhalation exposure (concentration and duration) that is not likely to cause
adverse effects in a human population, including sensitive subgroups, exposed to that
scenario, even on an intermittent basis.(13) For these purposes, acute exposures are single
continuous exposures lasting 24 hours or less; AREs may be derived for any duration of
interest within that period. "Intermittent" implies sufficient time between exposures such
that one exposure has no effect on the health outcome produced by the next exposure.
EPA is in the process of finalizing the methodology for development of AREs.
- 1-hour Acute Exposure Guideline Levels (AEGL-1 values). The AEGL-1 is the
airborne concentration, parts per million (ppm) or mg/m3 of a substance above which it is
predicted that the general population, including "susceptible" but excluding
"hypersusceptible" individuals, could experience notable discomfort, irritation, or certain
asymptomatic non-sensory effects. However, the effects are not disabling and are
transient and reversible upon cessation of exposure. These values are not intended for
evaluating the acute effects associated with frequent exposures; however, the use here is
in comparison to the highest 1-hour exposure concentration. AEGL-1 values and
supplementary information are developed by a National Advisory Committee, for use by
federal, state, and local agencies and organizations in the private sector concerned with
emergency planning, prevention, and response.
- Acute Reference Exposure Levels (REL values). The REL is a chemical-specific acute
exposure level estimate for noncancer effects (with an uncertainty spanning an order of
April 2004 Page 33
-------
magnitude) that is not likely to cause adverse effects in a human population after acute
exposure to inhaled chemicals other than criteria air pollutants. Note that some acute
RELs have different averaging periods other than one hour (e.g., 4, 5, and 6 hours). RELs
are developed by the California Office of Environmental Health Hazard Assessment
(OEHHA), and are available with supporting information at
http://www.oehha.ca.gov/air/acute_rels/index.html.
Emergency Response Planning Guidelines (ERPG-1 values). The ERPG-1 is the
maximum concentration in air below which it is believed that nearly all individuals could
be exposed for up to one hour without experiencing other than mild transient adverse
health effects or perceiving a clearly defined objectionable odor. These values are not
intended for evaluating the acute effects associated with frequent exposures; however, the
use here is in comparison to the highest 1-hour exposure concentration. ERPG-1 values
are developed by the American Industrial Hygiene Association (AIHA) and are available
on-line via the US Department of Energy at http://www.bnl.gov/scapa/scapawl.htm.
Acute Minimum Risk Levels (MRL values). The MRL is an estimate of human
exposure to a substance that is likely to be without an appreciable risk of adverse effects
(other than cancer) over a specified duration of exposure, and can be derived for acute
exposures by the inhalation and oral routes. Unlike the one-hour focus of most of the
other values listed here, acute MRLs are derived for exposures of 1 to 14 days duration.
Acute MRLs are developed by the US Agency for Toxic Substances and Disease Registry
(ATSDR), and are available at http://www.atsdr.cdc.gov/mrls.html.
1/10 Levels Imminently Dangerous to Life and Health (IDLH/10 Values). IDLH
values are exactly as described, and are intended to trigger immediate evacuation of work
areas. However, levels one-tenth of the IDLH tend to be generally similar to mild effect
levels such as AEGL-ls or ERG-ls, and are included with EPA/OAQPS's acute values
table on this basis. The IDLH/10 has been used commonly as the level of concern
(superceded by ERPG and AEGL values, as available) in the Agency's emergency
planning programs pursuant to the Emergency Planning and Community Right-to-Know
Act (EPCRA) and Section 112(r) of the Clean Air Act. Although the use of IDLH/10
values is not ideal, in many cases these values represent the only readily-available acute
dose-response value. IDLHs are developed by the National Institute for Occupational
Safety and Health (NIOSH) as part of its mission to study and protect worker health, and
are available at http ://www. cdc. gov/niosh/idlh/idlh-1 .html.
April 2004 Page 34
-------
Derivation of Dose-Response Values
To understand the potential toxicity of a specific chemical, risk assessors must know both the type of
effect it produces (the hazard) and the level of exposure required to produce that effect (the dose-
response relationship). Both hazard and dose-response information are derived from available
human epidemiologic data, experimental animal studies, and supporting information such as in vitro
laboratory tests. This information can provide a quantitative estimate of the relationship between dose,
the level of exposure, and response, the increased likelihood and/or severity of adverse effects.
Dose-response assessment is the process of quantitatively evaluating toxicity information,
characterizing the relationship between the dose of the contaminant administered and the incidence of
adverse health effects in the exposed subjects (which may be animal or human) and then, as
appropriate, extrapolating these results to human populations. Depending on the type of effect and the
chemical, there are two types of dose-response values that traditionally may be derived: predictive
cancer risk estimates, such as the inhalation unit risk estimate (IUR), and the reference value, such
as the reference concentration (RfC). Both types of dose-response value may be developed for the
same chemical, as appropriate.
An important aspect of dose-response relationships is whether the available evidence suggests the
existence of a threshold. For many types of toxic responses, there is a threshold dose below which
there are thought to be no adverse effects from exposure to the chemical. The human body has
defenses against many toxic agents. Cells in human organs, especially in the liver and kidneys, break
down many chemicals into less toxic substances that can be eliminated from the body. In this way, the
human body can withstand some toxic insult (at doses below the threshold) and still remain healthy.
Many HAPs are naturally occurring substances to which people routinely receive trace exposures at
non-toxic levels.
Depending on whether a substance causes cancer and whether its dose-response curve is thought to
have a threshold, EPA may use either of two approaches in a dose-response assessment. One approach
produces a predictive estimate (e.g., inhalation cancer risk estimate), and the other produces a
reference value (e.g., RfC). Historically, the use of a predictive estimate has been limited to cancer
assessment. That is, dose-response assessments for cancer have been expressed as predictive cancer
risk estimates based on an assumption that any amount of exposure poses some risk. Assessments of
effects other than cancer usually have been expressed as reference values at or below which no harm is
expected. Many substances have been assessed both ways: the first for cancer and the second for
adverse effects other than cancer. While this use of predictive estimates for cancer and reference
values for other effects is still the practice for the vast majority of chemicals, EPA now recognizes that
there are chemicals for which the data support an alternate approach (see Volume 1, Chapter 12).
Epidemiologic and toxicologic data on air toxics typically result from exposure levels that are high
relative to environmental levels, therefore low-dose extrapolation (prediction) is necessary to derive
an applicable dose-response value. Low-dose extrapolation requires either information or assumptions
about the type of dose-response curve likely under low dose situations. Confidence in the toxicity
levels is indicated for noncarcinogens by applying uncertainty and modifying factors and by
discussion of the confidence level. Confidence for carcinogens is indicated by EPA's weight of
evidence evaluations. Volume 1, Chapter 12 provides a more detailed discussion of the derivation of
dose-response values.
April 2004 Page 35
-------
Derivation of Dose-Response Inhalation Values for Cancer Effects
The process for deriving a quantitative dose-response estimate for cancer (e.g., an IUR) involves the
following four steps:
1. Determination of the Point of Departure or POD. The POD may be the traditional no observed
adverse effect level (NOAEL) or lowest observed adverse effect level (LOAEL), or it may be a
benchmark concentration (BMC) for tumorigenic effects.(a) The BMC is derived by the use of a
mathematical curve-fitting model ("benchmark modeling") which uses the available dose-response
data set for the effect to predict an exposure level associated with a particular experimental
response level (e.g., observation of the effect in 10% of the experimental animals).
2. Duration adjustment of the POD to a continuous exposure. This step involves extrapolation of
the POD from a discontinuous exposure scenario (e.g., animal studies routinely involve inhalation
exposures of 6 hours per day, 5 days per week) to a POD for a continuous exposure scenario (as
applicable to the RfC and IUR). This is usually accomplished by applying, as a default, a
concentration-duration product (or C x t product) for both the number of hours in a daily exposure
period and the number of days per week that the exposures are performed. More refined methods,
such as physiologically-based pharmacokinetic (PBPK) modeling, may be used as data are
available for a chemical.
3. Extrapolation of the POD into its corresponding Human Equivalent Concentration (PODHEC).
This conversion is done using dosimetric adjustment factors derived either using default methods
specific to the particular chemical class of concern or more refined methods such as
physiologically-based pharmacokinetic (PBPK) modeling.
4. Extrapolation from the PODHEC to lower doses. Extrapolation from the PODHEC to lower doses
is usually necessary because observable cancer rates in laboratory or human occupational
epidemiologic studies tend to be several orders of magnitude higher than cancer risk levels that
society is willing to tolerate, and laboratory studies are conducted at exposures well above
environmentally relevant concentrations. In the absence of a data set rich enough to support a
biologically based model (i.e., a PBPK model), low-dose extrapolation is usually conducted using
linear extrapolation or nonlinear extrapolation using a margin of exposure (MOE) analysis or
derivation of an RfC.
A more detailed discussion is presented in Volume I (Chapter 12).
(a)'
While this is the general case for both cancer and non-cancer dose-response assessment, the LOAEL/NOAEL
. approach is not often used in cancer assessment. ,
April 2004 Page 36
-------
Derivation of Dose-Response Inhalation Values for Noncancer Effects'^1
The process for deriving a quantitative dose-response estimate for noncancer effects (e.g., an RfC)
involves the following five steps:
1. Determination of the critical effect. A critical effect is described as either the adverse effect that
first appears in the dose scale as dose is increased, or as a known precursor to the first adverse
effect. Underlying this designation is the assumption that if the critical effects are prevented, then
all other adverse effects observed at higher exposure concentrations or doses are also prevented.
Note that not all observed effects in toxicity studies are considered adverse effects. The
identification of the critical effect(s) depends on a comprehensive review of the available data with
careful consideration of the exposure conditions associated with each observed effect, so that
comparisons of effect levels or potential reference values are made on a common basis.
2. Determination of the Point of Departure or POD. This step is identical to the corresponding
step for cancer effects.
3. Duration adjustment of the POD to a continuous exposure. This step is identical to the
corresponding step for cancer effects.
4. Extrapolation of the POD into its corresponding Human Equivalent Concentration (PODHEC).
This step is identical to the corresponding step for cancer effects.
5. Application of Uncertainty Factors. The RfC is an estimate derived from the PODHEC for the
critical effect by consistent application of uncertainty factors (UF). The UFs are applied to account
for recognized uncertainties in the use of the available data to estimate an exposure concentration
appropriate to the assumed human scenario. An uncertainty factor of 10, 3, or 1 is applied for each
of the following extrapolations used to derive the RfC:
Animal to human;
Human to sensitive human populations;
Subchronic to chronic;
LOAEL to NOAEL; and
Incomplete to complete database.
A more detailed discussion is presented in Volume I (Chapter 12).
(a)While the Agency has historically limited this approach to the assessment of effects other than cancer, EPA
now recognizes that there are chemicals for which the data may support the use of this approach for all effects,
.including cancer (see Volume 1, Chapter 12) ,
The same chronic dose-response values (and range of acute dose-response values) can be used
for all three tiers of inhalation risk assessments. If no value is available for a given HAP, that
HAP is generally not quantitatively assessed for that effect (e.g., if there is no IUR, the HAP is
not quantitatively assessed for cancer risk). For such HAPs, the risk assessor is encouraged to
identify anything known qualitatively regarding the hazards posed by the HAP and its potential
to contribute significantly to overall risk, and discuss it as part of the assessment's uncertainty
analysis.
April 2004 Page 37
-------
5.0 Risk Characterization for Inhalation Exposure
Risk characterization for inhalation exposures is relatively straightforward because the
underlying dose-response values used are expressed in terms of exposure concentrations and take
into consideration the complex physical and pharmacokinetic processes that influence how the
chemical moves from the mouth/nose into the lungs, enters the blood stream, and reaches the
target organ. Therefore, in the exposure assessment, dispersion modeling is used to estimate air
concentrations, which are, in turn, used to estimate exposure concentrations (ECs) - ambient
air concentrations of air toxics at the exposure points. In the risk characterization, the ECs are
combined with the applicable dose-response values to generate the risk estimate. Tier 1 and Tier
2 assessments typically will assume that ambient concentrations and ECs are the same, but Tier 3
assessments will usually include separate exposure estimates developed by an exposure model.
Note that the risk and hazard estimates associated with a given EC are limited to the source(s)
and exposure(s) included in the exposure assessment. Depending on decisions made in the
planning, scoping, and problem formulation phase, background exposures and exposures
from other sources may or may not be considered in a given risk assessment.
5.1 Cancer Risk
Risk assessors estimate excess lifetime cancer risk by combining the applicable EC and IUR for
each HAP using the following equation:
Risk = ECLx IUR
where:
Risk = Individual cancer risk (expressed as an upper-bound risk of contracting cancer
over a lifetime);
ECL = lifetime estimate of continuous inhalation exposure to an individual HAP; and
IUR = the corresponding inhalation unit risk estimate for that HAP.
For inhalation cancer risk estimates, assessors assume some duration of exposure based on the
characteristics of the exposed population and the purpose of the assessment. A lifetime, assumed
by some air toxics risk assessments (e.g., for derivation of a MIR value), is 70 years by
convention. In such assessments, while the air quality model may be run for a shorter time
period (e.g., five years), and the emissions estimates also may be for a shorter time period (e.g.,
one year), the resulting EC is generally assumed to be representative of the entire exposure
duration of interest (e.g., 70 years). If the exposure duration is less than 70 years (e.g., 30 years),
then the EC would be adjusted proportionally (e.g., by multiplying the EC by 30/70). This is
done because the risk of cancer is generally assumed to be related to total lifetime dose (i.e., the
risk for an exposure of 100 g per year for 7 years is assumed to be equal to the risk for an
exposure of 10 g per year for 70 years), and the IUR is based on an assumed lifetime exposure
April 2004 Page 38
-------
(see Volume 1, Chapter 21, and EPA's carcinogen risk assessment guidelines(11) for a more
detailed discussion). (b)
In screening-level assessments of carcinogens for which there is an assumption of a linear dose-
response, the cancer risks predicted for individual chemicals may be added to estimate
cumulative cancer risk. This approach is based on an assumption that the risks associated with
individual chemicals in the mixture are additive. The following equation estimates the predicted
incremental individual cancer risk from multiple substances, assuming additive effects from
simultaneous exposures to several carcinogens:
RiskT = Ris^ + Risk2 + .... + Risk,
where:
RiskT = total individual cancer risk (expressed as an upper-bound risk of contracting cancer
over a lifetime)
Risk; = individual risk estimate for the ith HAP.
In more refined assessments, the chemicals being assessed may be evaluated to determine
whether effects from multiple chemicals are synergistic (greater than additive) or antagonistic
(less than additive), although sufficient data for this evaluation are usually lacking. In those
cases where lURs are available for a chemical mixture of concern, risk characterization can be
conducted on the mixture using the same procedures used for a single compound. Estimating
risks from chemical mixtures is a complex task that generally should be done by an
experienced toxicologist.
Estimates of cancer risk are usually expressed as a statistical probability represented in scientific
notation as a negative exponent of 10. For example, an additional upper bound risk of
contracting cancer of 1 chance in 10,000 (or one additional person in 10,000) is written as 1^10"
4. Sometimes an exponential notation is used; in this case it would be 1E-04. Because lURs are
typically upper-bound estimates, actual risks may be lower than predicted (see Volume 1,
Chapter 12).
In the risk characterization step, the weight-of-evidence for carcinogenicity is presented for each
HAP assessed, and a qualitative discussion generally is included for those HAPs for which a
quantitative assessment was not feasible (i.e., no IUR is available).
bEPA is currently reviewing methods for assessing cancer risk for less than lifetime exposures occurring in
childhood. EPA's Draft Document Supplemental Guidance for Assessing Cancer Susceptibility from Early-Life
Exposure to Carcinogens (http://www.epa.gov/sab/panels/sgacsrp.html') recommends a change to the current method
for strong mutagens. This document is undergoing public and Science Advisory Board review and will be
completed sometime in the future with consideration of that review. EPA's methods for air toxics assessments will
be consistent with the final document.
April 2004 Page 39
-------
Example Calculation to Estimate Cancer Risk (Hypothetical)
A Tier 1 modeling analysis was performed to estimate risk to the maximum exposed individual,
assumed to reside at the point of maximum concentration for ABC Factory. Four FฃAPs were
potentially of concern: benzene, dichloroethyl ether, formaldehyde, and cadmium compounds.
Cancer risk estimates were obtained for each FฃAP by multiplying the estimated annual average
Exposure Concentration (EC) by the Inhalation Unit Risk Estimate (IUR) for each FฃAP. The resulting
upper bound cancer risk estimates ranged from 2 x 10~6 (benzene, formaldehyde) to 8 x 10~4
(dichloroethyl ether). The cancer risk estimates for each FฃAP were summed to obtain an estimate of
total inhalation cancer risk (9 x 10~4). Note that 97 percent of the estimated total risk results from
dichloroethyl ether, and that more than 99 percent results from dichloroethyl ether and cadmium
compounds. In this hypothetical example, the risk assessor would need to decide which HAPs to carry
to higher tiers by weighing the small proportion of risk posed by benzene and formaldehyde against
the fact that these risks nevertheless exceeded 1 in 1 million.
HAP
Benzene
Dichloroethyl ether
Formaldehyde
Cadmium compounds
Total
EC
jig/m3
0.3
2.5
0.2
0.01
IUR
1/^g/m3)
7.8 x IQ-6
3.3 x IQ-4
1.3 x IQ-4
1.8 x IQ-3
Cancer Risk
Estimate'3'
2 x IQ-6
8 x IQ-4
2 x IQ-6
1 x IQ-5
9 x IQ-4
Percent of
Total Risk
<1%
97%
<1%
2%
(a) Standard rules for rounding apply which will commonly lead to an answer of one significant figure
in both risk and hazard estimates. For presentation purposes, hazard quotients (and hazard indices)
and cancer risk estimates are usually reported as one significant figure.
5.2 Chronic Noncancer Hazard
Risk assessors derive estimates of chronic noncancer hazard for each HAP by combining the
applicable exposure concentration (EC) and reference concentration (RfC) for the HAP to obtain
the chronic Hazard Quotient (HQ) for the HAP using the following equation:
HQ = ECr * RfC
where:
HQ = the chronic hazard quotient for an individual HAP;
ECC = estimate of continuous inhalation exposure to that HAP; and
RfC = the corresponding reference concentration for that HAP.
Note that, when calculating an HQ, it is very important to make sure that the EC and RfC are
expressed in the same units. Modeled results (EC) are usually expressed in units ofng/m3,
April 2004
Page 40
-------
while RfCs (e.g.,from IRIS) are usually expressed in units ofmg/m3. Note also that 1 mg/m3
is equal to 1,000 fig/m3.
For inhalation noncancer hazard estimates for facility/source-specific assessments, exposure
estimates derived from a single year's emissions estimates are commonly used to represent a
chronic exposure. Thus, if a model is run for a specified period (e.g., one year or five years), the
resulting EC is assumed to be representative of a chronic exposure duration for the purposes of
the chronic risk assessment.
Based on the definition of the RfC, a HQ less than or equal to one indicates that adverse
noncancer effects are not likely to occur. With exposures increasingly greater than the RfC,
(i.e., HQs increasingly greater than 1), the potential for adverse effects increases. However,
note the following:
The HQs should not be interpreted probabilistically because the overall chance of
adverse effects may not increase linearly as exposures exceed the RfC.
Non-cancer health effects data are usually available only for individual HAPs within a mixture.
In these cases, the individual HQs can be summed together to calculate a multi-pollutant hazard
index (HI) using the following formula:
where
HI = chronic hazard index; and
HQ = chronic hazard quotient for the ith HAP.
For screening-level assessments, a simple HI may first be calculated for all HAPs. This
approach is based on the assumption that even when individual pollutant levels are lower than
the corresponding reference levels, some pollutants may work together such that their potential
for harm is additive and the combined exposure to the group of chemicals poses greater
likelihood of harm. Some groups of chemicals can also behave antagonistically, such that
combined exposure poses less likelihood of harm, or synergistically, such that combined
exposure poses harm in greater than additive manner. Where the overall HI exceeds the criterion
of interest, a more refined analysis is warranted. However, note the following:
Interpretation of differences among HQs across substances may be limited by differences
among RfCs in their derivation and the fact that the slope of the dose-response curve above
the RfC can vary widely depending on the substance, type of effect, and subpopulation
exposed.
Because the assumption of dose additivity is most relevant to compounds that induce the same
effect by similar modes of action, EPA guidance for chemical mixtures(14) suggests subgrouping
pollutant-specific HQs by toxicological similarity of the pollutants for subsequent calculations,
April 2004 Page 41
-------
that is, to calculate a target-organ-specific-hazard index (TOSHI) for each subgrouping of
pollutants. This allows for a more refined estimate of overall hazard.(c)
Example Calculation to Estimate Chronic Noncancer Hazard (Hypothetical)
A Tier 1 modeling analysis was performed to estimate chronic noncancer hazard to the maximum
exposed individual, assumed to reside at the point of maximum concentration for ABC Factory. Four
FฃAPs were potentially of concern: benzene, dichloroethyl ether, formaldehyde, and cadmium
compounds. Noncancer hazard estimates were obtained for each FฃAP by dividing the estimated
Exposure Concentration (EC) by the Inhalation Reference Concentration (RfC) for each FฃAP (note
that the EC is expressed in units of mg/m3 for this analysis). The resulting Hazard quotient (HQ)
estimates ranged from 1 x 10~3 (formaldehyde) to 1 (cadmium compounds). Note that no RfC was
available for dichloroethyl ether. The HQs for each HAP were summed to obtain an estimate of the
Hazard Index (HI) of 1. Note that cadmium compounds account for 95 percent of the HI, suggesting
that the other HAPs may not need further consideration (although this determination should be made
in consideration of all relevant information, including uncertainties such as confidence in the exposure
concentration and uncertainty factors used to derive each RfC).
HAP
Benzene
Dichloroethyl ether(a)
Formaldehyde
Cadmium compounds
Hazard Index (HI)
EC
mg/m3
6 x ID'4
5 x 1Q-3
4 x ID'4
2 x ID'5
RfC
(mg/m3)
6 x ID'2
9.8 x ID'3
2 x ID'5
HQ
1 x 10-2
1 x ID'3
1
1
Percent of
HI
1%
4%
95%
(a) note that the absence of an RfC value means that we cannot quantitatively assess a HAP.
(b) Standard rules for rounding apply which will commonly lead to an answer of one significant figure in both risk
and hazard estimates. For presentation purposes, hazard quotients (and hazard indices) and cancer risk estimates
are usually reported as one significant figure.
Although the HI approach encompassing all chemicals in a mixture is commonly used for a
screening-level study, it is important to note that application of the HI equation to compounds
that may produce different effects, or that act by different mechanisms, could overestimate the
potential for effects. Consequently, in a refined assessment, risk assessors commonly calculate a
separate HI for each noncancer endpoint of concern those HAPs with toxicological similarity.
Descriptive information on the type of noncancer health hazards associated with each HAP may
be found at http ://www.epa. gov/ttn/atw/hapindex.html. Note that assessing hazards from
chemical mixtures (e.g., through calculation of a TOSHI) is a complex task that generally
should be done by an experienced toxicologist
cThe all-HAP HI generally is only used in screening-level (Tier 1) analyses to identify situations where the
risk assessor is confident that the estimate of hazard is unlikely to be greater than the risk management decision
criterion (e.g., a HI greater than 1). The all-HAP HI often is not used in more refined analyses.
April 2004
Page 42
-------
A qualitative discussion generally is included in the risk characterization for those HAPs for
which a quantitative assessment was not feasible (i.e., no RfC is available).
5.3 Acute Noncancer Hazard
Risk assessors can derive estimates of acute noncancer hazard for each HAP by combining the
applicable short-term exposure concentration (EC) and acute dose-response value (AV) for the
HAP to obtain the acute Hazard Quotient (HQ) for the HAP using the following equation:
HQA = ECST * AV
where:
HQA = the acute hazard quotient for an individual HAP;
ECST = estimate of short-term inhalation exposure to that HAP; and
AV = the corresponding acute dose-response value for that HAP.
Note that ambient air concentrations are calculated for an exposure duration compatible with the
acute dose-response value used.
Acute noncancer health effects data are usually available only for individual HAPs within a
mixture. In these cases, it may be possible to combine the individual acute HQs to calculate a
multi-pollutant acute hazard index (HI) using the following formula:
where
HIA = acute hazard index; and
HQAi = acute hazard quotient for the ith HAP.
Although this appears similar to the process for combining chronic HQs, the summing of acute
HQs is complicated by several issues that do not pertain to chronic HQs. First, acute dose-
response values have been developed for purposes that vary more widely than chronic values.
Some sources of acute values define exposures at which adverse effects actually occur, while
other sources develop only no-effect acute values. Second, some acute values are expressed as
concentration-time matrices, while others are expressed as single concentrations for a set
exposure duration. Third, some acute values may specifically consider multiple exposures,
whereas others consider exposure as a one-time event. Fourth, some sources of acute values are
intended to regulate workplace exposures, assuming a population of healthy workers (i.e.,
without children, seniors, or other sensitive individuals). Such occupational values may also
consider cost and feasibility, factors that EPA considers the province of the risk manager rather
than the risk assessor.
Given these differences among acute values with regard to their purposes, and the different types
of acute exposure characterization that may be performed, the acute HI analysis is most
informative when limited to acute values from the same source, the same level of effects, and the
same duration. Analyses that mix sources, effects levels, and durations are likely to be
misleading.
April 2004 Page 43
-------
Risk assessors commonly evaluate acute noncancer hazard using a variety of different acute
values from different sources, and discuss the resulting hazard estimates considering the purpose
for which each of value was developed. This kind of evaluation should only be done by an
experienced lexicologist The significance of these HQs and His would need to be
considered in the context of the purpose of the risk assessment and the characteristics of
the dose-response values, such as their purpose, averaging time, and health endpoints EPA
is working to provide more comprehensive guidance on what benchmarks to rely upon and plans
to develop a relevant acute benchmark methodology.
5.4 Assessment and Presentation of Uncertainty
The risk estimates used in air toxics risk assessments usually are not fully probabilistic estimates
of risk but conditional estimates given a considerable number of assumptions about exposure and
toxicity. Air toxics risk assessments make use of many different kinds of scientific concepts and
data (e.g., exposure, toxicity, epidemiology), all of which are used to characterize the expected
risk in a particular environmental context. Informed use of reliable scientific information from
many different sources is a central feature of the risk assessment process. Reliable information
may or may not be available for many aspects of a risk assessment. Scientific uncertainty is
inherent in the risk assessment process, and risk managers almost always must make decisions
using assessments that are not as definitive in all important areas as would be desirable. Risk
assessments also incorporate a variety of professional and science policy judgments (e.g., which
models to use, where to locate monitors, which toxicity studies to use as the basis of developing
dose-response values). Risk managers therefore need to understand the strengths and the
limitations of each assessment, and to communicate this information to all participants and the
public.(3) A critical part of the risk characterization process, therefore, is an evaluation of the
assumptions, limitations, and uncertainties inherent in the risk assessment in order to place the
risk estimates in proper perspective.
One of the key purposes of uncertainty analysis is to provide an understanding of where the
estimate of exposure, dose, or risk is likely to fall within the range of possible values. At lower
tiers of analysis, this often is expressed as a subjective confidence interval within which there is
a high probability that the estimate will fall. When a more quantitative understanding is
important to the risk management decision, a related analysis, termed "sensitivity analysis" or
"analysis of uncertainty importance," is often performed to identify the relative contribution of
the uncertainty in a given parameter value (e.g., emission rate, ingestion rate) or model
component to the total uncertainty in the exposure or risk estimate.(15) Often this is used either to
identify which parameter values should be varied to provide high-end vs. central-tendency risk
estimates, or to identify parameter values where additional data collection (or modeling effort)
can increase the confidence in the resulting risk estimate.
There are numerous sources of uncertainties in air toxics risk assessments, and each merits
consideration. The degree to which these sources of uncertainty need to be quantified, and the
amount of uncertainty that is acceptable, varies considerably on a study-specific basis. For a
screening-level (tier 1) analysis, a high degree of uncertainty is often acceptable, provided that
conservative assumptions are used to bias potential error toward protecting human health. The
use of conservative assumptions is intended to result in a health-protective estimate where the
risk assessor is confident that the risk estimate is unlikely to be greater than the point estimate of
April 2004 Page 44
-------
risk. In other words, the point estimate of risk is expected to be at the high end of the range of
possible values. The uncertainty characterization for a tier 1 analysis commonly is limited to a
qualitative discussion of the major sources of uncertainty and their potential impact on the risk
estimate. At higher tiers of analysis, sensitivity analysis to quantify the impact of varying input
parameter values (or model algorithms) on the risk estimate, or more complete quantitative
uncertainty analysis, commonly are performed to more fully describe the range of possible or
plausible values. There are three general approaches for tracking uncertainty through the risk
assessment:
Qualitative Approach. This approach , ~TT _, . _,
. , , , . . . Sources ot Uncertainty
involves developing a quantitative or
qualitative description of the
uncertainty for each parameter and
indicating the possible influence of
these uncertainties on the final risk
estimates given knowledge of the
models used.
Semi-Quantitative Approach. This
approach involves: (1) using . n ...
i ui j 4. 4. j -u 4.u 4^-1 v influence risk estimates
available data to describe the potential
Scenario uncertainty. Information to fully
define exposure or risk is missing or incomplete
Model uncertainty. Algorithms or assumptions
used in models may not adequately represent
reality
Parameter uncertainty. Values for model
parameters cannot be estimated precisely
Decision-rule uncertainty. Policy and other
choices made during the risk assessment may
range of values that the parameters
might assume; (2) performing sensitivity analysis to identify the parameters with the most
impact on the risk estimate; and (3) performing sensitivity analysis to compute the range of
exposure or risk estimates that result from combinations of minimum and maximum values
for some parameters and mid-range values for others.
Quantitative Approach. Probabilistic techniques such as Monte Carlo simulation analysis
can explicitly characterize the extent of uncertainty and variability in risk assessment,
especially in the exposure assessment step. Using these techniques, important variables in
the exposure assessment, as well as in the other parts of the risk assessment, are specified as
distributions (rather than as single values) according to what can be expressed about their
underlying variability and/or uncertainty. Values are sampled repeatedly from these
distributions and combined in the analysis to provide a range of possible outcomes. While
this technique can offer a useful summary of complex information, it must be noted that the
analysis is only as certain as the underlying data (and assumed forms of the distribution of
data values in the population). It is important that the risk assessor clearly expresses
individual modeled variables in a way that is consistent with the best information available.
Highly quantitative statistical uncertainty analysis is usually not practical or necessary for
most air toxics risk assessments. The general quantitative approach to propagating or
tracking uncertainty through probabilistic modeling is described in Volume 1, Chapter 31.
Highly quantitative statistical uncertainty analysis will generally be limited to situations where
the additional information (i.e., beyond a deterministic risk assessment) has some potential to
influence a risk management decision. Probabilistic analyses, from which the risk results can be
presented as valid probability distributions, require additional resources.
April 2004 Page 45
-------
Additional discussions of uncertainty analysis, including practical approaches to the assessment
and presentation of the principal sources of uncertainty in risk assessments are provided in
EPA's Risk Assessment Guidance for Superfund,(l6) guidance documents prepared by EPA and
other authors,(4) and in Volume 1 (Chapter 13) of this reference library.
6.0 Tier 1 Inhalation Analysis
6.1 Introduction
This section describes an example approach for performing a Tier 1 inhalation risk assessment.
Exhibit 11 provides an overview of this example approach. SCREENS or similar models are
used for both chronic and acute exposure estimates. Tier 1 analyses incorporate simplified
assumptions and default values for facility/source-specific modeling inputs that are not readily
available, and allow a simple, health-protective risk estimate to be calculated. The resulting
exposure estimates are likely to be higher than actual exposures. If the facility/source passes this
screening analysis, the risk manager can be reasonably confident that the likelihood for
significant risk is low. This example Tier 1 approach is not intended to prescribe a specific
approach that must be used by EPA or others in a particular risk assessment activity. In
particular, various modifications to this tiered approach may be both cost-effective and
appropriate, such as adding intermediate-level tiers that incorporate some features of the
higher and lower tiers, or conducting iterative, more refined analyses within a given tier.
Also, S/L/T agencies may have specific tiered assessment protocols and/or specific modeling
guidelines that must be followed. Therefore, consultation with appropriate regulatory
agencies is highly recommended.
Note that this example Tier 1 approach does not incorporate monitoring. While existing
monitoring data may be used as inputs to a Tier 1 analysis, if the Tier 1 results are not sufficient
for the risk management decision, it may be cost-effective to conduct additional analysis (Tier 2
or Tier 3) before implementing a new monitoring program.
April 2004 Page 46
-------
Exhibit 11. Example Approach for A Tier 1 Assessment
All HAPs Selected by
Toxicity-Weighted
Screening Analysis
Dispersion Modeling
SCREENS
Simple model inputs
High production year (or hour)
Highest offsite concentrations
Qualitative uncertainty analysis
Cumulative Cancer Risk Estimate
Sum across all carcinogens (generally
done during toxicity-weighting step)
Cumulative
Cancer Risk
Estimate At or Below
Target Level?
Cumulative Noncancer Hazard Estimates
Separate analysis of chronic and acute
Sum across all noncarcinogens - HI
Can sum separately by target organ - TOSHI
Go to Tier 2 or 3
Risk Targets Met
HI or TOSHI
At or Below
Target Level?
6.2 Fate and Transport Modeling
SCREENS can be used to predict maximum hourly ambient concentrations on the centerline of a
plume downwind from a source for all HAPs selected for Tier 1 during the toxicity-weighted
screening analysis (see Chapter II). The hourly concentrations are used directly for acute
exposure estimates and converted to maximum annual concentrations using a fixed screening
factor for chronic exposure estimates (see below). SCREENS uses generalized meteorological
data, some facility/source-specific information (e.g., terrain and building dimension
information), and facility/source-specific emissions data to estimate downwind ambient air
concentrations of HAPs within a user-specified radius from the source up to 50 km (30.8 miles).
Estimates of excess cumulative cancer risk and noncancer hazard can be calculated separately
from model outputs, or can be calculated by the model if emission rates are input in toxicity-
weighted form. Risk estimates are based on the concentrations at the point of maximum
concentration.
April 2004
Page 47
-------
6.2.1 Model Inputs
Input data for SCREENS fall into three categories: (1) emissions data; (2) release parameters
(e.g., source type, release temperature, etc.); and (3) building and terrain considerations (e.g.,
building downwash and simple or complex terrain). Note that several default parameters for
meteorological data are built into SCREENS. More detailed information is provided in the
SCREENS User's Guide.(8) Note that S/L/T agencies may have emissions and other source
information in documents such as state inventories and inspection reports.
General considerations. Many facilities have multiple emission sources (each with its
characteristic release height, emissions rate, etc.), and more than one type of emission source
within a single facility. Because SCREENS can model a single source per model run, and is
not able to aggregate the results of multiple model runs across different sources, it is most
efficient to combine all sources of each source type (e.g., point, volume) into a single source
for Tier 1 analysis (with the receptor assumed to be exposed to the highest concentration at
any location). The results for the combined sources of each type are then added together, as
if all the releases had occurred at the same point. Because this procedure is health-protective
screening (e.g., it pessimistically assumes that the highest hourly release rates from all
sources will occur simultaneously), it is appropriate for a Tier 1, screening-level analysis.
Exhibit 12 identifies health-protective default values to facilitate Tier 1 analyses. All
facility/source-specific information needs to be provided in the specific units required by
SCREENS (and therefore units may need to be converted). As noted earlier, S/L/T agencies
may have specific modeling guidelines that may differ from the default values presented in
Exhibit 12.
Emissions data. In this example approach, the total emissions is the sum of process and
fugitive emissions. Process emissions are discrete losses that occur at stacks or process vents
from reactors, columns, boilers, and other types of facility equipment. Fugitive emissions
result from facility equipment leaks, evaporation from waste products, losses from the raw
material feed, losses from in-process and final process storage tanks, loading and handling
losses, and losses from other non-discrete sources.
The risk assessor is encouraged to
use the best emissions data
available for the facility, including
chemical speciation information.
If speciated emissions data are not
readily available, an assumption
that all HAPs are emitted in the
most toxic form commonly is used
in Tier 1 assessments to ensure
that health-protective risk
estimates are produced.
Where to Find Source Emissions Information
Facility records or purpose-specific data collection
National Emissions Inventory
State and Federal risk assessment reports
Background Information Documents that support
Maximum Achievable Control Technology Standards
(MACT), available from EPA's MACT docket
State approved emission permits
Toxics Release Inventory
April 2004
Page 48
-------
Exhibit 12. Example Default Values for SCREENS Tier 1 Inputs'3'
Input Parameter
Source type
Emission rate (g/s)*-1
Stack height (m)
Stack diameter (m)
Stack temperature (degrees Kelvin)
Stack gas exit velocity (m/s)
Ambient temperature (degrees Kelvin)
Length of larger side of area source (m)
Length of smaller side of area source (m)
Receptor height above ground (m)
Urban/rural
Building downwash (Yes/No)
Building height (m)
Minimum horizontal width (m)
Maximum horizontal width (m)
Use simple terrain? (Yes/No)
Use complex terrain? (Yes/No)
Use simple elevated terrain? (Yes/No)
Meteorology
Automated distance array? (Yes/No)
Minimum and maximum distances (m)
Discrete distances (m)
Printout results
Stack/Vent
Health-protective
Default
Point
Actual
5
0.1524
293
1
293
n/a
n/a
0
Rural
Yes
5
30
30
Yes
No
No
1-Full
Yes
100; 5,000
No
Yes
Fugitive Source Health-
protective Default
Area
Actual (g/s/m2)
1
n/a
n/a
n/a
n/a
5
5
0
Rural
Yes
5
30
30
Yes
No
No
1-Full
Yes
100; 5,000
No
Yes
(a) S/L/T agencies may have specific modeling guidelines that may differ from these default values
(b) Use annual average for chronic exposure estimates and 1-hour maximum for acute exposure estimates
April 2004
Page 49
-------
One common Tier 1 approach is to use emissions data that are representative of maximum
annual emissions (e.g., a high-production year). For chronic exposures, the approach uses
the average hourly emissions rate for the high-production year. For acute exposures, the
approach uses the greater of (a) the maximum hourly rate, or (b) ten times the average hourly
rate. The ratio between a longer-term maximum concentration and a 1-hour maximum will
depend upon the duration of the longer averaging time, source characteristics, local
climatology and topography, and the meteorological conditions associated with the 1-hour
maximum. Because of the many ways in which such factors interact, it is not practical to
categorize all situations that will typically result in any specified ratio between the
longer-term and 1-hour maxima. EPA's Screening Procedures for Estimating the Air
Quality Impact of Stationary Sources, Revised*^ identifies ratios for a "general case," and the
risk assessor is given some flexibility to adjust those ratios to represent more closely any
particular point source application where actual meteorological data are used. Emissions of
multiple HAPs from a single source can be combined into a single emission using toxicity
weighting (see Section 6.2.2 below).
To obtain the estimated maximum concentration for a 3-, 8-, 24-hour or annual averaging
time, multiply the 1-hour maximum concentration by the indicated factor in the table below.
The numbers in parentheses are recommended limits to which one may diverge from the
multiplying factors representing the general case. For example, if aerodynamic downwash or
terrain is a problem at the facility, or if the emission height is very low, it may be necessary
to increase the factors (within the limits specified in parentheses). On the other hand, if the
stack is relatively tall and there are no terrain or downwash problems, it may be appropriate
to decrease the factors. If the risk assessment involves a regulatory action, the risk assessor
is encouraged to discuss these factors with the appropriate regulatory authorities.
Averaging Time
3 hours
8 hours
24 hours
Annual
Multiplying Factor
0.9 (ฑ0.1)
0.7 (ฑ0.2)
0.4 (ฑ0.2)
0.08 (ฑ0.02)
Note that some assessments may be based on permit limits (e.g., if their purpose is to
determine if those limits provide adequate protection).
The State of California has determined that the conversion multiplying factors noted above may not be
biased toward over-prediction when the source is not a continuous release. Appendix H of the Air
Toxics Hot Spots Program Guidance Manual for Preparation of Health Risk Assessments (August
2003; http://www.oehha.ca.gov/air/hot spots/pdf/HRAguidefinal .pdf) presents approaches for
developing multiplying factors for (a) non-standard averaging periods with a continuous release; (b)
intermittent releases (e.g., releases that occur only from 8 AM to 6 PM); (c) systematic releases (e.g., a
"clean-out" release once per day); and (d) random releases.
April 2004
Page 50
-------
Release type. SCREEN3 will prompt the user for source-specific characteristics. Point
sources are localized releases from stacks or vents. Flare sources are point sources that have
a high release rate (e.g., flames). Area sources are emissions that are spread over an area
(e.g., a landfill or lagoon). Volume sources are three-dimensional releases (e.g., fugitive
leaks from an industrial facility). When modeling a facility with multiple sources, assessors
typically model each source separately and sum the resulting maximum concentrations (see
below).
Physical release parameters. SCREEN3 will prompt the user for the release parameters
appropriate to the type of release. For example, SCREEN3 requires stack height, stack
diameter, stack gas exit velocity, and stack temperature in order to model a point source.
When available, it is preferable to use site- or source-specific release parameters. Example
default values for point, area, and volume sources (Exhibit 12) can be used when
facility/source-specific values are not available.
Meteorological data and building
and terrain considerations. For this
example approach, the following
inputs are selected: (1) the "actual"
urban/rural dispersion coefficient
Building Downwash
Volume 2 of the ISC User's Guide (Section 1.1.5.3)
provides a rule-of-thumb that a building is considered
,-> i ,, -, ,,- N /^\ ur-11 sufficiently close to a stack to cause wake effects
(based on the site setting); (2) "full j.
, , , . , . , , when the distance between the stack and the nearest
meteorology (which considers the , ,,,, , .,,. . , ,, , , P ,.
OJ ^ part ot the building is less than or equal to live times
the lesser of the height or the projected width of the
building. This relationship is obviously much more
complicated with complex building shapes. The ISC
User's guide is available on EPA's SCRAM website
(http://www.epa.gov/rtn/scram/).
effects of all atmospheric stability
classes); (3) building downwash
(using either the actual dimensions of
the largest building in the facility or
the default dimensions in Exhibit 12);
and (4) "simple terrain" (elevated
terrain can be entered if appropriate
for the facility/source being evaluated; otherwise, terrain should be assumed fiat). Note that
SCREEN3 uses built-in meteorological data (see Volume 1, Chapter 9).
6.2.2 Model Runs
SCREEN3 provides estimates of maximum one-hour ambient concentrations. If multiple model
runs are performed (e.g., separate runs for point sources and area sources), a conservative
approach is to sum the maximum predicted model results from each run across all sources. This
approach assumes that the maximum impact for each source occurs at the same location and the
same hour. These maximum one-hour concentrations can be used to evaluate acute noncancer
hazard as described in Section 6.5 below.
SCREEN3 models one HAP for each run of the model. For multiple chemicals, the modeler can
input 1 gram/year as the emission rate and run the model once (or once for each source type).
Ambient concentrations for each HAP can then be calculated by multiplying the model results by
the annual emission rate (in tons) for each HAP.
April 2004 Page SI
-------
6.3 Exposure Assessment
Tier 1 assessments will generally assume that the highest ambient concentrations predicted by
SCREEN3 are equivalent to exposure concentrations. As noted above, for chronic exposures, the
approach uses the average hourly emissions rate for the high-production year. For acute
exposures, the approach uses the maximum hourly rate, or 10 times the average hourly rate,
whichever is greater. If separate model runs were done for some sources (e.g., to separate point
sources from area sources), this example approach sums the maximum exposure concentrations
from each model run before characterizing risk. This procedure effectively treats all the releases
as occurring in the same place.
6.4 Risk Characterization
Risk characterization for Tier 1 is limited to estimating inhalation risk at the point of maximum
concentration (calculated separately for cancer risk, chronic noncancer hazard, and acute
noncancer hazard). The exposure concentrations described in Section 6.3 are used to calculate
risk and hazard according to basic equations presented in Section 5 above. Background
concentrations are often not explicitly considered in Tier 1.
Cancer risk. Excess cumulative cancer risk is calculated by multiplying the maximum
annual air concentration by the inhalation IUR for each HAP and summing across all HAPs.
Chronic noncancer hazard. Chronic cumulative noncancer hazard (the Hazard Index, or
HI) is calculated by dividing the maximum annual air concentration by the RfC for each HAP
and summing across all HAPs. If the resulting HI exceeds the noncancer target HI level of
regulatory interest, the HI results can be subdivided into a separate Target Organ Specific
Hazard Index (TOSHI) for each target organ of concern (see Volume 1, Chapter 13 for a
more detailed discussion on how to calculate a TOSHI.).
Acute noncancer hazard. As discussed in Volume 1, Chapter 13, available acute dose-
response values are more diverse than chronic values, because they were developed for
different purposes and considering different exposure durations. The most effective
characterization of acute risk often is to compare the maximum estimated hourly
concentrations with a range of acute dose-response values from sources described in Section
4 (see an example comparison in Exhibit 13). If the ambient concentration is lower than all
the acute benchmarks, it is generally reasonable to conclude that the potential for significant
acute risk is low. If the concentration exceeds some benchmarks but not others, the
assessment should describe the benchmark (e.g., is it a no-effect level, or a concentration at
which mild effects occur?) and discuss the implications of exceeding it.
6.4.1 Reporting Results
A relatively simple summary can be used to report results but should still ensure the results are
both transparent and reproducible. Examples of reports prepared for EPA's purposes can be
found in EPA's residual risk "test memos;" these may or may not be appropriate examples for the
specific purposes of other risk assessments. The summary generally will include the following
information:
April 2004 Page 52
-------
Documentation of input parameters, output spreadsheets, and risk characterization, with
special emphasis on comparing estimated risks to risk targets;
A simple presentation describing the assessment's purpose (e.g., to determine whether risk is
below levels of concern) and the outcome relative to that purpose (e.g., low risk is not
demonstrated).
Documentation of anything in the analysis that is discretionary (i.e., anything that is
facility-specific), such as emissions characteristics or choice of a meteorological station other
than the nearest.
Exhibit 13. Example Presentation of Risk Characterization Results for Acute Exposure
10000
E
a>
e
O
I
o
\J
01 t
ERPG-3
ERPG-2
IDlH/lQand ERPG-I
REL
e 1 i 1 w j 1 1 | I I
MRL
* * t
u'ul 1 1 1 1 1 ! 1 III
ABODE FGHI J
Facility
* = Exposure Concentration
This example illustrates one way to graphically compare estimated exposure concentrations (ECs) from
multiple facilities (or sources within a facility) to available acute dose-response values. In this
example, estimated ECs from facility A, C, D, E, and G were at or above MRLs but below all other
acute values. The risk characterization would need to clearly describe the significance of these results
in terms of potential health effects and related uncertainties.
April 2004
Page 53
-------
6.4.2 Assessment and Presentation of Uncertainty
Risk managers need to understand the strengths and the limitations of the Tier 1 assessment. A
critical part of the risk characterization process, therefore, is an evaluation of the assumptions,
limitations, and uncertainties inherent in the Tier 1 risk assessment in order to place the risk
estimates in proper perspective.(3) Tier 1 risk assessments will typically include a quantitative or
qualitative description of the uncertainty for each parameter and indicating the possible influence
of these uncertainties on the final risk estimates given knowledge of the models used (i.e., the
qualitative approach discussed in Section 5.4 above). The use of conservative assumptions in
Tier 1 is intended to result in result in a situation where the risk assessor is confident that the risk
estimate is unlikely to be greater than the point estimate of risk. In other words, the point
estimate of risk is expected to be at the high end of the range of possible values.
There may be situations where facility/source-specific information is so limited (e.g., emissions
estimates are based on industry-wide values rather than facility/source-specific data; many
facility/source-specific HAPs are lacking peer-reviewed dose-response values) that the risk
assessor may not be confident that the risk estimate is at the high end of possible values. In these
situations, additional data collection (e.g., to obtain facility/source-specific emissions estimates)
and/or a Tier 2 analysis may be appropriate.
6.5 Focusing Tier 2 on the Most Important HAPs/Sources
If cumulative cancer risk and/or noncancer hazard is above the level of concern, a Tier 2 analysis
may be needed. This analysis may focus on the particular HAPs and sources that account for a
high proportion of the estimated risk (at Tier 1) to reduce the Tier 2 analytical effort.
7.0 Tier 2 Inhalation Analysis
7.1 Introduction
This section describes an example approach for performing a Tier 2 inhalation risk assessment.
Exhibit 14 provides an overview of this example approach. This example approach uses HEM-3
for both chronic and acute exposures, with more facility/source-specific information for HAPs,
sources, and potentially exposed populations. Tier 2 analyses may often be limited to those
HAPs and sources that collectively account for a high proportion of the potential risk or hazard
that was estimated in Tier 1. If the facility/source database permits, risk assessors may be able
to skip Tier 1 entirely and start with Tier 2. For this example Tier 2 approach, HEM-3 provides
an estimate of ambient concentrations from all the facility's sources combined at multiple
Census block internal points, including the Census block with the highest ambient concentration.
In this approach to a Tier 2 assessment, these Census block concentrations are used as surrogates
for exposure concentrations for the people residing there. Note that more complex/advanced
exposure modeling is used in the example Tier 3 approach described in Section 7.
The most important differences from Tier 1 are: (1) the exposure surrogate shifts from the
maximum offsite ambient concentration to the concentrations within Census blocks (i.e., where
people actually reside); (2) individual modeling of release points is performed; and (3) average
April 2004 Page 54
-------
production year data are used for cancer risk estimates, while high-production year data are used
for noncancer hazard estimates.
Note that this example Tier 2 analysis focuses on current land use scenarios. It may be
appropriate to examine future land use scenarios.
Exhibit 14. Example Approach for A Tier 2 Assessment
HAPs/Sources Accounting for a
High Proportion of Tier 1
Cancer Risk and
Noncancer Hazard Estimate
Dispersion Modeling
HEM-3
Site-specific model inputs
High production year for noncancer
Census block concentrations
Qualitative uncertainty analysis
Average Production Year
High Production Year
Cumulative Cancer Risk Estimate
Sum risk across all carcinogens
Cumulative
Cancer Risk
Estimate At or Below
Target Level?
Cumulative Noncancer Hazard Estimates
Separate analysis of chronic and acute
Sum across all noncarcinogens - HI
Can sum separately by target organ - TOSHI
Monitoring to evaluate
modeled concentrations
and exposures
Go to Tier 3
Risk Targets Met
HI or TOSHI
At or Below
Target Level?
yes
April 2004
Page 55
-------
7.2 Fate and Transport Modeling
7.2.1 Model Inputs
Input data for HEM-3 falls into six categories: (1) source location; (2) emissions data; (3)
stack/vent parameter data; (4) pollutant specific data (reactivity and dose-response data); (5)
meteorological data; and (6) population data. Refinements for Tier 2 are described briefly
below. More detailed information is provided in the HEM-3 User's Guide.(7)
Source location. HEM-3 requires the geographical location (latitude and longitude) of each
source being simulated. Some of the above sources of geographic information may provide
coordinates in Universal Transverse Mercator (UTM) units. The HEM-3 contains a program
to convert UTM data into latitude and longitude (e.g., as provided by the use of a GPS
receiver). In many instances there is more than one emission source (each with its
characteristic release type, height, emissions rate, etc.) within a single facility. HEM-3 can
model each emission source individually within a single model run. HEM-3 also computes
the total ambient air concentrations resulting from facility emissions by summing the
individual estimates. The geographical location (latitude and longitude) of all sources being
simulated must be identified. The Tier 2 analysis often will not include a default option to
assume that all emission sources are located at single specified latitude and longitude within
the facility. The model requires that coordinate data be obtained for each emission source in
the analysis, and that each emission source is modeled individually. In other words, the
location of each source within the facility should be input to HEM-3.
X s.
The internal point is only an approximation of where people live. The Census Bureau(a) defines the
internal point as a set of geographic coordinates (latitude and longitude) that is located within a
specified geographic entity. A single point is identified for each entity; for many entities, this point
represents the approximate geographic center of that entity. If the shape of the entity causes this point
to be located outside the boundary of the entity or In a water body, It Is relocated to land area within
the entity. The term "centroid" (which is used interchangeably with internal point) is the term more
commonly used by risk assessors when referring to geographic or population-weighted centers. Note
that the internal point established by the Census Bureau is generally set to reflect the geographic center
of the entity in question, regardless of where people actually live in that entity. A population
weighted internal point is a modified point that is considered to better reflect the location of the
people living in the geographic entity.
(a)U.S. Department of Commerce, U.S. Census Bureau. 2000. Geographic Glossary (Census 2000).
Available at: http://www.census.gov/geo/www/tiger/glossrv2.pdf
> s
Emissions data. Depending on the source, the emissions being modeled may be process or
fugitive emissions. The risk assessor should use the best site-specific emissions data
available, including chemical speciation. As with Tier 1, HEM-3 requires emissions data in
the form of an annual emissions rate (e.g., tons/year). HEM-3 can be used to assess both
chronic and acute exposures. To do this, select "yes" for the "include hourly emissions
variations" choice, and provide a file of hourly emission rate factors (e.g., 10 times the
annual average) appropriate to the type of source for each HAP. Emission rate factors based
April 2004 Page 56
-------
on measured data are preferred, but if measurements are not available, engineering judgment
based on the nature of the process can be used. For infrequent releases (e.g., less than once a
month), the assessor may assume that the total annual emission rate is released during one
episode and use engineering judgment to determine the length of the episode.
Release parameter data. Release parameter data are necessary for dispersion modeling of
the chemical emissions. Facility/source-specific data generally are preferred for a Tier 2
analysis. When these are not available, surrogate data often can be found in the same data
sources as the emissions data. HEM-3 release parameter data requirements include:
- Stack or area source release height and diameter (meters);
- Dimensions of area source (meters);
- Stack diameter (meters);
- Gas discharge temperature (degrees Kelvin);
- Gas emission (exit) velocity (meters/second);
- Height of the initial plume (meters); and
- Building dimensions (meters, if relevant).
Atmospheric reactivity and deposition of chemicals. Because the highest inhalation
exposures are generally near the source, and little time passes between the release and the
exposures, atmospheric reactivity and deposition of fine particles generally do not need to be
considered in Tier 2.
Meteorology. HEM-3 uses meteorological data measured both at the surface and in the
upper atmosphere in its dispersion calculations. Surface data used by HEM-3 are pre-
processed hourly meteorological observations from a user library, or information from a
user-specified meteorological station. Upper atmosphere data are twice-daily mixing height
values. User-supplied data sets need to be pre-processed by the EPA RAMMET to fit the
HEM-3 input format. Surface and upper atmosphere data sets are available from the
National Climate Data Center in Asheville, NC or from the EPA SCRAM website
(www.epa.gov/scram001/index.htm).
Population. In this example of a Tier 2 analysis, modeling is focused on the locations where
people actually live. HEM-3 automatically identifies the exposed population using the
Census block internal points already included in the model. These locations are modeled
directly within a user-specified radius and are interpolated from locations on the polar
coordinate receptor grid for Census blocks outside the radius (Exhibit 15). For Tier 2
analyses, all people residing in a Census block are assumed to be continuously exposed to the
annual average concentration (and exposed for one hour to the maximum hourly
concentration) at the interior location within the Census block. Unless otherwise specified,
HEM-3 calculates concentrations for each Census block within 50 kilometers of the source's
location. If a Census block is exposed to emissions from more than one source, HEM-3
sums the impacts from each source for each Census block. The model outputs include the
risks posed by each HAP at each Census block internal point, the risks from all HAPs
combined, and the numbers of people living in Census blocks whose ambient levels fall
within specified risk ranges.
April 2004 Page 57
-------
Note that in some cases the Census block internal point may not represent the most exposed
individuals within the block (e.g., a large proportion of the population might live in an apartment
complex nearer to or farther from the facility/source). A different approach (e.g., more precisely
modeling receptor locations with a different model) may be more appropriate in certain situations.
Exhibit 15. Example of Interpolation to Calculate Concentrations at Census Block Internal
Points
Interpolation to Centroid
(beyond 3.5 km)
For polar grids, a two-step interpolation is used, starting with the modeled concentrations at the
nearest locations (e.g., al, a2, a3, and a4 in the graph above). The first interpolation is in the radial
direction (i.e., along the two adjacent radial lines [al,a2] and [a3, a4] in the graph). The
concentration is estimated at the intersection of each radial line with the concentric circle that
intersects the receptor location (i.e., at the same radial distance from the source as the internal point).
This interpolation is performed under the assumption that the logarithm of the concentration decreases
in proportion to the increase in the logarithm of the distance from the source (i.e., a log-log
interpolation). The second interpolation is in the azimuthal direction (i.e., along the concentric circle
that intersects the internal point). This interpolation is performed under the assumption that the
change in concentration is proportional to the distance around the circle between the two radial lines
(i.e., linear interpolation).
April 2004
Page 58
-------
7.2.2 Model Runs
The following input values can be used to set up HEM-3 model runs for a Tier 2 analysis:
On screen 1, select "inhalation," "yes" to both annual and acute concentrations, "1-hour" for
the length of acute exposure, and "rural" for the dispersion environment (unless the
facility/source is located in a densely-populated area).
Provide the names of the emissions file and the emissions location file, which should be in
the correct spreadsheet format (HEM-3 provides format guidelines).
Select "no" for the deposition and depletion choices.
Select "yes" for the terrain elevation choice if the facility/source is located in an area with
substantial elevation changes; otherwise select "no" for flat topography.
Select "no" to providing alternate lURs and RfCs.
Select dimensions of the area to be modeled that are appropriate to the facility. The
maximum radius is 50 kilometers, but for most facilities a radius of 30 kilometers will
capture virtually all important exposures. Select 0 as the minimum radius.
Select the "distance within which blocks are modeled individually" to capture the Census
blocks with the highest concentrations.
Choose the appropriate HEM-3 meteorological data file, or provide a facility/source-specific,
pre-processed file. Sources of meteorological data are provided in Volume 1, Appendix G.
7.3 Exposure Assessment
The Tier 2 assessment approach described here uses predicted ambient concentrations as
surrogates for exposure concentrations. HEM-3 provides estimates of annual average
concentrations within Census blocks and combines them with chronic dose-response values for
cancer and noncancer effects to estimate risk.
7.3.1 Chronic Exposures
HEM-3 provides ambient concentrations for the Census block with the highest annual average
levels, by individual HAP and emission point. HEM-3 also calculates the upper-bound lifetime
cancer risk and noncancer HQs associated with continuous exposure to those ambient
concentrations, and it sums cancer risk across all HAPs and noncancer HQs by target organ.
These results can be presented in summary tables (e.g., Exhibits 16 to 19, below).
April 2004 Page 59
-------
7.3.2 Acute Exposures
HEM-3 also provides estimates of the highest average ambient concentration predicted anywhere
within the assessment area. To estimate the maximum 1-hour ambient concentration, this
example approach multiplies the average concentration by the same screening factor used in Tier
1 (discussed in section 7.2, above, e.g., 10-fold). These maximum 1-hour concentration
estimates for each HAP are used as surrogates for acute exposures, to characterize acute
noncancer hazard as described in Section 7.5. Note that the maximum hourly concentrations for
different HAPs may occur in different locations; however HEM-3 automatically sums across
pollutants, thereby addressing this issue.
7.3.3 HEM-3 Outputs
HEM-3 produces six different output tables that make the following presentations of ambient
concentrations and risks:
The maximum individual risk table contains the upper bound lifetime cancer risk, total
hazard index, and target organ-specific hazard indexes for the Census block with the highest
ambient concentrations (including Census ID and location information).
The maximum offsite impacts table provides the same information as the maximum
individual risk table, except the location is the offsite point of highest ambient concentration,
whether populated or not.
The cancer risk/exposure table shows the numbers of people living in Census blocks whose
annual mean concentrations correspond to specified risk ranges (e.g., greater than or equal to
1 in 1 million, 10 in 1 million).
The noncancer risk/exposure table provides similar information regarding numbers of people
living in Census blocks whose concentrations correspond to specified TO SHI ranges.
The risk breakdown table provides the incremental contribution to individual cancer risk and
hazard quotient in the most exposed Census block by each HAP from each source.
The incidence table presents the incremental contribution to total estimated cancer incidence
within the modeled duration by each HAP from each source.
These presentations overlap substantially, and often may be condensed, as for the four example
summary tables in Exhibits 16 to 19 below.
Exhibits 16 and 17 illustrate estimates of individual cancer risk and noncancer hazard to a typical
resident of the most exposed Census block, using the modeled ambient concentration within the
block as a surrogate for exposure concentration. These tables are sorted to show the contribution
of each source in the assessment, and the combination of all sources. Note that the highest
exposure associated with different sources, and the total of all sources, may occur in different
Census blocks. Therefore, the subtotals in these tables may not be additive across sources.
April 2004 Page 60
-------
Exhibits 18 and 19 illustrate estimates of the aggregate cancer risk and noncancer hazard to all
Census block residents within the modeling domain. Receptor populations have been placed in
risk categories, and are shown as the numbers of people who live in Census blocks where the
modeled ambient concentration (if inhaled continuously), corresponds to specific levels of risk
or hazard. For example, the assessment predicts Census blocks where 36,599 people reside have
ambient concentrations equivalent to upper-bound lifetime cancer risk levels between 1 and 10
in 1 million. For characterizing acute risks, HEM-3 calculates the maximum average annual
offsite concentrations. These can be adjusted by the appropriate screening factors, and
graphically compared with acute benchmarks (as illustrated earlier in Exhibit 13).
7.3.4 Monitoring Data
It may be helpful to conduct a monitoring program to evaluate or further characterize exposure
concentrations at key locations (e.g., in the Census blocks where HEM-3 indicates relatively
high exposures). Volume 1 (Chapter 10) provides an overview of available approaches for
assessing air quality via monitoring.
7.4 Risk Characterization
Risk characterization for this example Tier 2 assessment focuses on inhalation risk to a receptor
at the point of maximum concentration (calculated separately for cancer risk, chronic noncancer
hazard, and acute noncancer hazard). This example approach uses the exposure concentrations
noted in Section 7.4 to calculate risk and hazard according to basic equations presented in
Section 5 above. Note that the maximum concentrations for cancer risk, chronic noncancer
hazard, and acute noncancer hazard may occur at different locations.
Although background concentrations (i.e., ambient levels originating from sources other than the
facility/source) are not explicitly considered in this example Tier 2 approach, situations may
exist where background is a potential concern. In such cases, monitoring data and/or modeled
results from community-wide assessments can be used to support a risk assessment for
background concentrations, and for the comparison of risk/hazard associated with facility/source
emissions with that associated with background concentrations.
April 2004 Page 61
-------
Exhibit 16. Example Presentation of HEM-3 Individual Cancer Risk Estimates
Receptor: Individual at Census Block Internal Point with Highest Cancer Risk Estimate
Upper-bound Lifetime Cancer Risk
Source
1
1
1
1
1
1
1 Total
2
2
2
2 Total
3
3
3
3 Total
All
All
All
All
All
All
Pollutant
1,3 -Butadiene
Arsenic compounds
Benzene
Cadmium compounds
Chromium (VI) compounds
Polycyclic Organic Matter
Arsenic compounds
Cadmium compounds
Chromium (VI) compounds
Emission
Type
volume
point
volume
point
point
volume
point
point
point
Risk
8e-07
8.E-07
8e-08
3.E-07
6.E-09
2.E-09
2.E-06
5.E-08
2.E-08
l.E-09
7.E-08
Concentration
(M-g/m3)
0.03
0.0002
0.01
0.0001
0
0.00002
0.00001
0.00001
0
Emissions
(tons/yr)
20
0.1
7
0.1
0.0003
0.01
0.0005
0.0005
0
: : : :
Arsenic compounds
Cadmium compounds
Chromium (VI) compounds
point
point
point
8.E-08
3.E-08
2.E-09
l.E-07
0.00002
0.00002
0
0.0008
0.0008
0
: : : :
1,3 -Butadiene
Arsenic compounds
Benzene
Cadmium compounds
Chromium (VI) compounds
Polycyclic Organic Matter
All Total
combined
combined
combined
combined
combined
combined
8.E-07
2.E-06
8.E-08
6e-07
5.E-08
l.E-11
0
0.03
0.004
0.01
0.0004
0
0
(a) Standard rules for rounding apply which will commonly lead to an answer of one significant figure
in both risk and hazard estimates. For presentation purposes, hazard quotients (and hazard indices)
and cancer risk estimates are usually reported as one significant figure.
April 2004
Page 62
-------
Exhibit 17. Example Presentation of HEM-3 Individual Noncancer TOSHI Estimates
Receptor: Individual at Census Block Internal Point with Highest Noncancer Hazard Estimate
Respiratory System TOSHI
Source
1
1
1
1
1
1 Total
2
2
2
2
2 Total
3
3
3
3
3 Total
All
All
All
All
All
Pollutant
Acrolein
Arsenic compounds
Cadmium compounds
Chromium (VI) compounds
Manganese compounds
Emission
Type
volume
point
point
point
point
HQ(a)
3.E-02
6.E-03
7.E-03
5.E-06
9.E-05
5.E-02
Concentration
(Hg/m3)
0.0007
0.0002
0.0002
0
0.000005
Emissions
(tons/yr)
0.4
0.1
0.001
0.0003
0.003
Arsenic compounds
Cadmium compounds
Chromium (VI) compounds
Manganese compounds
point
point
point
point
4.E-04
5.E-04
l.E-06
3.E-03
3.E-03
0.00001
0.00001
0
0.0001
0.0005
0.0004
0
0.005
Arsenic compounds
Cadmium compounds
Chromium (VI) compounds
Manganese compounds
point
point
point
point
6.E-04
9.E-04
2.E-06
4.E-03
0.01
0.00002
0.00002
0
0.0002
0.0008
0.0008
0
0.009
Acrolein
Arsenic compounds
Cadmium compounds
Chromium (VI) compounds
Manganese compounds
All Total
combined
combined
combined
combined
combined
0.03
l.E-02
0.02
4.E-05
4.E-02
0.1
0.0007
0.0004
0.0004
0.00004
0.002
(a) Standard rules for rounding apply which will commonly lead to an answer of one significant figure
in both risk and hazard estimates. For presentation purposes, hazard quotients (and hazard indices) and
cancer risk estimates are usually reported as one significant figure.
April 2004
Page 63
-------
Exhibit 18. Example Presentation of HEM-3 Population Cancer Risk Estimates
Metric: Number of People Living in Census Blocks Corresponding to
Specific Estimates of Cancer Risk
Upper-bound Estimate of
Lifetime Cancer Risk
Greater than or equal to 1 in 1,000
Greater than or equal to 1 in 10,000
Greater than or equal to 1 in 20,000
Greater than or equal to 1 in 100,000
Greater than or equal to 1 in 100,000
Greater than or equal to 1 in 1,000,000
Population Living in Census Block
0
0
0
0
36599
1102010
Exhibit 19. Example Presentation of HEM-3 Population Noncancer TOSHI Estimates
Metric: Number of People Living in Census Blocks Corresponding to
Specific Estimates of Noncancer Hazard (TOSHI)
Estimate of Hazard Index
Greater than or equal to 100
Greater than or equal to 50
Greater than or equal to 10
Greater than or equal to 1 .0
Greater than or equal to 0.5
Greater than or equal to 0.2
Population Living in Census Block
Total HI
0
0
0
0
3163
100982
Respiratory HI
0
0
0
0
3163
100982
CNSHI
0
0
0
0
0
0
April 2004
Page 64
-------
7.4.1 Reporting Results
A relatively simple summary can be used to report results, consistent with the need to make the
results both transparent and reproducible. Examples of reports prepared for EPA's purposes can
be found in EPA's residual risk "test memos;" these may or may not be appropriate examples for
the specific purposes of other risk assessments.(d) The summary generally will include the
following information:
Documentation of input parameters, output spreadsheets, and risk characterization, with
special emphasis on comparing estimated risks to risk targets;
A simple presentation describing the assessment's purpose (e.g., to determine whether risk is
below levels of concern) and the outcome relative to that purpose (e.g., low risk is not
demonstrated); and
Documentation of anything in the analysis that is discretionary, such as facility-specific
emissions characteristics or choice of meteorological station. In particular, the rationale used
to select specific receptor locations and methods or calculations used to identify the location
associated with the highest individual risk need to be documented.
7.4.2 Assessment and Presentation of Uncertainty
Risk managers need to understand the strengths and the limitations of the Tier 2 assessment. A
critical part of the risk characterization process, therefore, is an evaluation of the assumptions,
limitations, and uncertainties inherent in the Tier 2 risk assessment in order to place the risk
estimates in proper perspective.(3) Tier 2 risk assessments commonly include a quantitative or
qualitative description of the uncertainty for each parameter and indicate the possible influence
of these uncertainties on the final risk estimates given knowledge of the models used. Tier 2
assessments also may include a semi-quantitative sensitivity analyses. These approaches are
described in Section 5.4 above. Sensitivity analyses are discussed in more detail in Volume 1
(Chapters 3 and 13) of this reference library.
7.5 Focusing Tier 3 on the Most Important HAPs/Sources
If cumulative cancer risk and/or noncancer hazard is above the level of concern, a Tier 3 analysis
may be needed. This analysis may include all the sources and HAPs assessed in Tier 1, or may
be reduced to only those HAPs and sources of primary concern.
dThe "test memos" for a particular source category can be found on the NESHAPs page of EPA's air toxics
web site (http://www.epa.gov/ttn/atw/mactfnlalph.html') by selecting the source category and going to the residual
risk section of that page.
April 2004 Page 65
-------
8.0 Tier 3 Inhalation Analysis
8.1 Introduction
This section describes an example approach for performing a Tier 3 inhalation risk assessment.
Exhibit 20 provides an overview of this example approach. Tier 3 analyses are generally limited
to those HAPs and sources that collectively account for a large proportion of the potential risk
or hazard estimated in Tier 2. The example Tier 3 assessment is significantly different than the
example Tier 1 and 2 approaches, in that it involves more complex dispersion modeling (e.g.,
with ISCST3 or AERMOD), specific consideration of population locations, the use of an
exposure model (TRIM.ExpoInhalation) to account for receptor behavior (e.g., time spent in
different microenvironments), and use of a risk model (TRIM.Riskjjjj) to provide a more refined
characterization of risk, including multiple estimates of risk (e.g., central tendency and high
end).
The Tier 3 analysis often involves considerable flexibility in analytical approach and detail. This
example includes the use of:
A dispersion model (ISCST3 or AERMOD) to calculate hourly and annual average
concentrations at user-specified exposure locations. ISCST3 allows considerable spatial
refinement in selecting exposure locations, and provides concentrations for user-specified
(actual) locations.
An exposure model (TRIM.ExpoInhalation) to combine air concentration information with
human activity patterns to develop more precise, population- and site-specific exposure
estimates. The user specifies the geographic area to be modeled, the number of individuals
to be simulated to represent the study area population, and the demographic unit of resolution
for the outputs. The model produces exposure estimates specific to modeled individual and
demographic unit (e.g., census tract or block, etc). Because the modeled individuals
represent a random sample of the population of interest, the distribution of modeled
individual exposures can be extrapolated to the larger population.
A risk model (TRIM.Riskjjjj) to calculate cumulative excess cancer risk and noncancer
hazard associated with the modeled exposures. TREVI.Riskjjjj calculates human health risk
metrics, documents model inputs and assumptions, and displays results.
Monitoring data may be used to evaluate or further characterize exposure concentration and
exposure estimates.
The Tier 3 analysis may incorporate probabilistic inputs and model outputs using the TRIM
modeling system. If a potential regulatory action is involved, the scope, method, and inputs for
probabilistic modeling should be agreed to in advance with the appropriate regulatory agencies.
It is recognized that there may be practical limitations that affect the scope, methods, inputs, or
outputs of the modeling:
April 2004 Page 66
-------
Exhibit 20. Example Approach for A Tier 3 Assessment
HAPs/Sources Accounting for
a High Proportion of Tier 2
Cancer Risk and
Noncancer Hazard Estimate
Dispersion, Exposure, and Risk Modeling
ISCST3; TRIM.Expolnhalation; Trim.RiskHH
No defaults - all site-specific inputs
Complex activity-based multiple exposure estimates
Central tendency and high-end exposures at each location
Deterministic or probabilistic analysis
Limited quantitative uncertainty analysis
Cumulative Cancer Risk Estimate
Sum across all carcinogens
Cumulative Noncancer Hazard Estimates
Separate analysis of chronic and acute
Sum across all noncarcinogens (HI)
Can sum by target organ (TOSHI)
Monitoring to evaluate
modeled concentrations
and exposures
Cumulative
Cancer Risk
Estimate At or Below
Target Level?
Potential
Risk
Reduction
HI or TOSHI
At or Below
Target Level?
Risk Targets Met
Because or computing and other practical constraints, it is considered unlikely that a
distribution of ambient air concentration estimates will be developed for each location of
interest.
Quantitative information sufficient to support probabilistic modeling of dose-response
parameters seldom exists.
With regard to individual risk, presentation of distributions that reflect variation in both
location as well as population characteristics can mask information that is important to
April 2004
Page 67
-------
decision making (e.g., locational variation is particularly relevant to source-specific
assessment). Consequently, presentation of specific risk estimates across locations (e.g.,
central tendency and high end estimates displayed via a geographical information system)
separate from presentation of any distributions of risk estimates for each location are
preferred.
8.2 Fate and Transport Modeling
This example Tier 3 approach uses the ISCST3 model for estimating air concentrations for both
chronic and acute exposures. An alternative would be to use similar air quality model, such as
AERMOD, when it becomes available. Other models may be appropriate for a specific
facility/source. The extent to which a specific air dispersion model is suitable for the evaluation
of air toxic source impacts depends upon several factors, such as the nature of the pollutants
(e.g., gaseous, particulate, reactive, inert), the meteorological and topographic complexities of
the area, the complexity of the source distribution, the spatial scale and resolution required for
the analysis, and the level of detail and accuracy required for the analysis. For example, because
of the assumption in Gaussian models of a steady wind speed and direction over the entire
modeling domain for each hour, the 50 km distance may be inappropriately long in many areas,
especially where complex terrain or meteorology is present. In such cases a non-steady state
model would be more appropriate.
Finer scale models, such as CAL3QHC and CALINE4, are most typically applied to exposure
studies from mobile sources. The UAM-TOX and CMAQ models are examples of models
which can simulate photochemically active air toxic species, including secondary formation of
pollutants like formaldehyde. Because the complex secondary formation processes are nonlinear
and can occur at locations far distant from the emission source, these models are designed to be
applied to an exhaustive set of sources over a large region, rather than to individual facilities or
small groups of facilities. The models more typically applied to single or multiple facilities
include SCREENS, ISCST3, ISCLT3, AERMOD, and CALPUFF. Brief descriptions of these
models are provided in Volume 1 (Chapter 9). Some modeling studies have combined the
application of a regional model with a neighborhood-scale model in order to address secondary
and background concentration contributions, while capturing finer spatial resolution for primary
pollutant predictions (see EPA's Air Toxics Community Assessment and Risk Reduction
Projects Database
http://yosemite.epa.gov/oar/CommunityAssessment.nsfAVelcome7OpenForm).
Where the assessment could support a regulatory decision, the use of an alternative model
commonly is agreed to in advance with the regulatory agency decision-maker. Alternative
models that conform to EPA's air quality modeling guidance(17) are more likely to be acceptable
to those decision-makers.
April 2004 Page 68
-------
8.2.1 Model Inputs
Input data for ISCST3 falls into the same six categories used by HEM-3: (1) source location; (2)
emissions data; (3) physical release parameters; (4) pollutant specific data (reactivity and dose-
response data); (5) meteorological data; and (6) population data. Additional details are provided
in the ISC model user's guide.(9)
Source location. ISCST3 requires coordinate data (latitude and longitude) for each emission
source in the analysis. Multiple sources can be modeled in the same ISCST3 run.
Emissions data. The analysis generally benefits from the use of the highest-quality,
site-specific emissions data available, including chemical speciation. With ISCST3, users
have many more options for characterizing emissions. For example, users have the option to
specify variable emission rate factors for sources whose emissions vary as a function of time
(e.g., month, season, hour-of-day). In addition, settling velocity categories, mass fractions,
and reflection coefficients may be specified for sources of large particulates that experience
settling and removal during dispersion. The emissions profile (s) used for Tier 3 modeling
commonly reflect the expected pattern(s) of emissions over a reasonable period of time (e.g.,
several years). Note that these profiles may differ for different sources within a single
facility.
Physical release parameters. Tier 3 assessments commonly use facility/source-specific
values for all stack/vent parameter data, as appropriate for the type of source. These values
commonly reflect the expected patterns of emissions used to develop the emissions profiles
for modeling.
Atmospheric reactivities of chemicals. Tier 3 assessments often are focused on a relatively
small number of HAPs and sources that collectively account for a large proportion of the risk
and/or hazard estimated in lower-tier analyses. Therefore, it may be worthwhile to consider
reactivity and deposition in Tier 3 assessments. However, because the highest inhalation
exposures are generally near to sources, these processes may not substantially influence
exposures unless they are very rapid. Exhibit 21 below provides a list of HAPs with
atmospheric half-lives of one hour or less, for which considering reactivity may be useful.
Volume I of this reference manual (Chapter 17) provides more data sources for half-life data.
Atmospheric degradation in ISTST3 is limited to a first order approximation. ISCST3 can
also consider wet and dry deposition, but requires source- and HAP-specific information
(e.g., on particle size and mass and solubility). As noted earlier, for HAPs with a significant
potential to form reaction products in the atmosphere, either a different model should be
used, or the analysis should note the added uncertainties in not modeling these reaction
products.
Meteorology. Tier 3 analyses commonly use the most recent consecutive 5 years of
facility/source-specific data from the nearest representative meteorological station.
"Representative" generally means that the sources being modeled and the weather station are
located in the same general environment with respect to significant terrain (e.g., valley vs.
plateau), significant geographic features (e.g., proximity to a large body of water), and
prevailing winds (i.e., similar wind rose/direction of dominant wind). Documentation
April 2004 Page 69
-------
demonstrating the representativeness of the meteorological data is encouraged. Sources of
meteorological data are provided in Volume 1, Appendix G.
Exhibit 21. Volatile HAPs with Atmospheric Half-lives of Less than One Hour
CAS Number
107-02-8
107-05-1
106-99-0
126-99-8
1319-77-3
68-12-2
140-88-5
111-76-2
80-62-6
90-12-0
91-20-3
108-95-2
123-38-6
100-42-5
121-44-8
108-05-4
1330-20-7
Chemical Name
Acrolein
Allyl chloride
Butadiene
Chloroprene
Cresols/Cresylic acid (isomers and mixture)
Dimethyl formamide
Ethyl acrylate
Ethylene glycol butyl ether
Methyl methacrylate
Methylnaphthalenes
Naphthalene
Phenol
Propionaldehyde
Styrene
Triethylamine
Vinyl acetate
Xylenes
Receptor Locations. In Tier 3 these are set with consideration of the demographic unit
resolution for the TRIM.Expo^j^a,;,,,, exposure estimates. These may be specified as a list of
receptor locations (e.g., census tract internal points). Alternatively, they may be specified as
arrays of receptors (e.g., radially or via grid), and TRIM.ExpoInhalation has the capability to
associate these air concentration locations with corresponding demographic units.
April 2004
Page 70
-------
8.2.2 Model Runs
Using one complete year of meteorological data, ISCST3 calculates an ambient concentration for
each receptor location (district) specified in a run, for each hour of a one-year run. The ISCST
model can be run for single or multiple years. To obtain results for multiple years of
meteorological data, separate ISCST3 model runs commonly are completed for each year. Based
on these results, ISCST3 can provide average ambient concentration for each modeled location
for the time periods of interest (e.g., 1 hour to 5 years).
These concentrations are used to prepare inventories of chemical concentrations at each specified
exposure location at selected time intervals (e.g., days, hours). The specific ISCST3 model
outputs used to prepare inventories of chemical concentrations may depend on how the analysis
is structured. As a general guideline:
For cancer effects, calculate an annual average concentration using the one-hour
concentrations for each of the five years;
For chronic noncancer effects, calculate an annual average concentration using the highest
rolling annual average of one-hour concentrations for the five years; and
For acute noncancer effects, identify the highest one-hour concentration in all five years.
8.3 Exposure Assessment
In this example Tier 3 approach, the exposure model (TRIM.ExpoInhalation) is used to combine the
air concentration estimates with human activity patterns to develop more precise, population-
and site-specific exposure estimates. The user specifies the geographic area to be modeled, the
number of individuals to be simulated to represent the study area population, and the
demographic unit of resolution for the outputs. TRIM.Expo^^^^ generates a personal profile
for each simulated person that specifies various parameter variables required by the model. The
model next uses diary-derived time/activity data matched to each personal profile to generate an
exposure event sequence (also referred to as an "activity pattern" or "composite diary") for the
modeled individual that spans a specified time period, such as one year. Each event in the
sequence specifies a start time, an exposure duration, a geographic location, a microenvironment,
and an activity. Probabilistic algorithms are used to estimate the pollutant concentration
associated with each exposure event. The estimated pollutant concentrations account for the
effects of ambient (outdoor) pollutant concentration, penetration factors, air exchange rates,
decay/deposition rates, and proximity to emission sources, depending on the microenvironment,
available data, and the estimation method selected by the user. The model produces a
distribution of exposure estimates for the individuals modeled for each demographic unit (e.g.,
census tract or block).
Major aspects of the set up and execution of the TRIM.ExpOjnj^.,,^ model are described in
separate subsections below. The TRIM.ExpoInhalation User's Document provides additional
details. (10) Where the assessment could support a regulatory decision, advance discussions with
the regulatory agency risk manager are encouraged to confirm the approach to be employed for
the exposure assessment.
April 2004 Page 71
-------
8.3.1 Characterization of the Study Area
The study area will have been considered in the design of the air quality modeling step,
including the resolution desired for the demographic unit for which exposure estimates are to be
generated. In the exposure modeling step, the user will confirm the extent of the study area for
which air quality estimates are available, and the demographic unit scale at which exposure
estimates are to be generated.
If the air quality modeling was designed to yield ambient concentration estimates associated with
the demographic units of interest for the exposure assessment (e.g., air concentration estimates at
census tract/block centroids), TRIM.Expo will use those locations directly for developing
population specific exposure estimates. Otherwise, TRIM.Expo will assign the air quality
estimates to demographic units based on the distance between the location of each air quality
estimate and the geographic center of each demographic unit.
In TRIM.ExpoInhalation, the geographic units for the demographic data are called sectors. The
model uses the demographic data to create personal profiles at the sector level. For each sector
the model requires demographic information representing the distribution of age, gender, race,
and work status within the study population. The initial release of TRIM.ExpOjnj^.,,^ has input
files that already contain this demographic and location data for all Census tracts in the 50
United States based on the 2000 Census. This database enables the user to model any study area
in the country without having to make any changes to these input files. Finer scales, such as
Census block groups and blocks may be used with correspondingly suitable population data files.
If fewer (thus larger) sectors were desired, the existing population data files could be aggregated
to larger regions.
The spatial units for the ambient air quality estimates are called districts. These are the areas
associated with each air quality estimate. As mentioned earlier, the air quality modeling may be
designed so that the districts are the same as the sectors. For example, the air quality modeling
may produce estimates for census tract centroids and census tracts may be the sectors to be used
in the exposure modeling. If, however, the air quality estimate locations are not synonymous
with the sector centers, TRIM.Expo will assign the air quality districts to sectors based on
distance between their geographic centers (or other user-specified point). Each sector is
assigned the air quality district for which this distance is shortest, yet within a user-specified
maximum distance. Sectors falling outside that distance are not modeled.
Another spatial unit in TRIM.Expo is the temperature zone, which may be used by the model to
assign activity diaries to personal profiles (e.g., summer activities in summer weather) for the
modeled individuals (see Section 8.3.2), and to specify parameters pertaining to
microenvironments (e.g., aspects of climate control systems). The demographic sectors are
assigned to temperature zones in similar fashion to the air quality district assignments (e.g., by
closest proximity of user-specified representative locations
In summary, the exposure assessment study area is composed of the demographic sectors for
which air quality estimates (and temperature values) can been assigned.
April 2004 Page 72
-------
8.3.2 Generation of Simulated Individuals
TRIM.ExpoInhalation probabilistically generates a user-specified number of simulated persons to
represent the population in the study area. Each simulated person is represented by a "personal
profile." TRIM.ExpoInhalation generates the simulated person or profile by probabilistically
selecting values for a set of profile variables (Exhibit 22). The profile variables include:
Demographic variables, which are generated based on the Census data;
Residential variables, which are generated based on sets of distribution data;
Daily varying variables, which are generated based on distribution data that change daily
during the simulation period; and
Physiological variables, which are generated based on age group-specific distribution data.
Exhibit 22. Profile Variables in TRIM.ExpoInhalation
Variable
Type
Demographic
variables
Residential
variables
Daily varying
variables
Profile Variables
Gender
Race
Age
Home sector
Work sector
Employment status
Gas stove
Gas pilot
Air conditioner
Car air conditioner
Window position
Daily average car speed
Description
Male or Female
White, Black, Native American, Asian, Other
Age of the simulated person (years)
Sector in which the simulated person lives
Sector in which the simulated person works
Indicates employment outside home
Indicates presence of gas stove
Indicates presence of gas pilot light
Indicates presence of air conditioning at home
Indicates presence of air conditioning in the car
Daily window position (open or closed) during the
simulation period
Daily average car speed during the simulation period
TRIM.ExpoInhalation first selects and calculates demographic, residential, and physiological
variables (except for daily values) for all the specified number of simulated individuals, and then
determines exposures for each simulated person. The exposure assessor should be sure to
simulate enough individuals to produce a stable exposure distribution (i.e., one that is not
sensitive to which specific types of individuals the model randomly selects). The
TRIM.ExpoInhalation User's Document provides additional details.(10)
April 2004
Page 73
-------
8.3.3 Construction of A Sequence of Activity Events
TRIM.ExpoInhalation probabilistically creates a composite diary for each of the simulated persons
by selecting a 24-hour diary record (a diary day) from an activity database for each day of the
simulation period. This diary is created based on the activity data in the Consolidated Human
Activities Database (CHAD).(18) CHAD data have been supplied with TRIM.ExpoInhalation for this
purpose. A composite diary is a sequence of events that simulate the movement of a modeled
person through geographical locations and microenvironments during the simulation period.
Each event is defined by geographic location, start time, duration, microenvironment visited, and
an activity performed. For the activity database, TRIM.Expo^^^^ currently provides a personal
information file and an events file to summarize the CHAD data. These composite diaries are
then used in exposure concentration calculations.
8.3.4 Calculation of Concentrations in Microenvironments
TRIM.ExpoInhalation calculates ambient air concentrations in the various microenvironments
visited by the simulated person by using the ambient air data for the relevant sectors and the
user-specified method and parameters that are specific to each microenvironment.
TRIM.ExpoInhalation defines microenvironments by grouping the more than 100 location codes
defined in the activity (CHAD) database into a smaller set of user-defined microenvironments
amenable to modeling. The user has control over how many microenvironments will be
modeled, how they are defined, and what CHAD (or other activity database) locations should be
grouped into each of microenvironment. The TRIM.ExpoInhalation User's Document(10) lists the
115 CHAD location codes included in TRIM.ExpoInhalation and the microenvironment to which
each currently is assigned.
TRIM.ExpoInhalation calculates concentrations of the subject air pollutant in all the
microenvironments at each time step (e.g., hour) of the simulation period for each of the
simulated individuals, based on the user-provided hourly ambient air quality data specific to the
geographic locations visited by the individual. TRIM.ExpoInhalation provides two methods for
calculating microenvironmental concentrations: a mass balance method and a factors method
(see Volume 1, Chapter 11). The user is required to specify a calculation method for each of the
microenvironments; some microenvironments can use one method while the rest use the other,
without restrictions. The parameters, algorithms, and probabilistic elements used in each of the
methods are explained in the TREVI.ExpoInhalation User's Document.(10)
8.3.5 Estimating Exposure
TRIM.ExpoInhalation calculates exposure as a time series of exposure concentrations that a modeled
individual experiences during the simulation period. TRIM.ExpoInhalation determines the exposure
based on the air concentration in and minutes spent in each of a sequence of microenvironments
visited according to the composite diary. The exposure concentration at any clock hour during
the simulation period is determined using the following equation:
April 2004 Page 74
-------
N
(f
^hourly(j)
>=i"
fc
where:
Ct = Hourly exposure concentration at clock hour / of the simulation period (|ig/m3 or
ppm)
N = Number of events (i.e., microenvironments visited) in clock hour / of the simulation
period.
Chouriyd) = Hourly concentration in microenvironmenty (|ig/m3 or ppm)
t& = Time spent in microenvironmenty (minutes)
T =60 minutes
From the hourly exposures, TRIM.ExpoInhalation calculates time series of 1-hour, 8-hour and daily
average exposure concentrations that a simulated individual would experience during the
simulation period. TRIM.ExpoInhalation then statistically summarizes and tabulates the hourly, 8-
hour, and daily exposures. TREVI.ExpoInhalation also calculates and tabulates an annual average
exposure concentration per individual. The average concentration over the entire simulation
period is used as an input to chronic risk calculations.
8.3.6 General Considerations
Regardless of whether a deterministic or probabilistic approach is used, this example Tier 3
exposure assessment provides a range of exposure estimates, as evidenced by the exposures
predicted for the multiple simulated individuals in each exposure district. This information
facilitates presentation of central-tendency and high-end exposure estimates.
Probabilistic analyses include frequency distributions of exposures that include central-
tendency and high-end exposures for all locations and population sub-groups.
Additionally, different estimates of ambient air concentrations (e.g., annual average vs. an
alternate estimate) might be considered.
8.3.7 Monitoring Data
It may be helpful to conduct a monitoring program to evaluate or further characterize exposure
concentrations, such as through the use of air measurements at key locations (e.g., to establish
indoor or outdoor air concentrations) or exposure concentrations associated with specific activity
patterns (e.g., through the use of personal monitors). Volume 1 (Chapter 10) provides an
overview of available approaches for assessing air quality via monitoring.
April 2004 Page 75
-------
8.4 Risk Characterization
For Tier 3, most risk estimates will be calculated automatically by TRIM.Riskjjjj, once the
modeling scenarios are set up and run. The initial release of TRIM.Riskjjjj will calculate several
inhalation cancer risk and non-cancer hazard metrics at the individual and population level.
This example Tier 3 risk characterization considers background concentrations as appropriate
(e.g., where the contribution of facility/source to risk is small compared to that of other sources.
Note that consideration of background may or may not be appropriate pursuant to the specific
legal and regulatory authorities under which the risk assessment is being conducted.
8.4.1 Reporting Results
The initial release of TRIM.Riskjjjj will provide a visualization tool for presenting analysis
results in various automated formats. The risk assessor may want to utilize this tool to assist
with development of the risk characterization summary, which generally will include the
following information:
Documentation of input parameters, outputs, and risk characterization, with special emphasis
on the range of risk or hazard estimates;
A simple presentation describing the assessment's purpose and the outcome relative to the
purpose (e.g., purpose: demonstrate that risk is below target levels; outcome: low risk not
demonstrated); and
Documentation of all key assumptions or other inputs used for the assessment, such as
emissions characteristics or choice of a nearby meteorological station. In particular, the
assessor is encouraged to document the rationale used to define personal profiles and how
they are modeled and analyzed.
8.4.2 Assessment and Presentation of Uncertainty
Risk managers need to understand the strengths and the limitations of the Tier 3 assessment. A
critical part of the risk characterization process, therefore, is an evaluation of the assumptions,
limitations, and uncertainties inherent in the Tier 3 risk assessment in order to place the risk
estimates in proper perspective.(3) Tier 3 risk assessments commonly include semi-quantitative
sensitivity analyses and quantitative uncertainty analysis (described in Section 5.4 above). The
general quantitative approach to propagating or tracking uncertainty through probabilistic
modeling is described in Volume 1 (Chapter 31) of this reference library.
April 2004 Page 76
-------
Chapter IV: Multipathway Risk Assessment
/" >
This section constitutes a snapshot ofEPA's current thinking and approach to the adaptation of the
evolving methods of multipathway risk assessment to the context of Federal and state control of air
toxics. While inhalation risk assessment has been increasingly used in regulatory contexts over the
last several years, multipathway risk assessment tools are less well developed and field tested in a
regulatory context. This section should be considered a living document for review and input. By
publishing this portion of Volume 2 in its current state of development, EPA is soliciting the
involvement of persons with experience in this field to help improve these assessment methods for
use in a regulatory context. EPA anticipates revisions to this draft section of Volume 2 on the basis
of this input.
\ ^
1.0 Introduction and Overview
This section describes an example approach for performing site-specific multipathway risk
assessments for air toxics. These include an assessment of human health risks via ingestion (and
perhaps other pathways/routes) as well as ecological risk assessment. Both types of assessments
consist of a tiered approach. A risk assessor may decide to complete only the lowest-tier
analysis that fits the purpose of the assessment (e.g., to determine that a facility's cumulative risk
is lower than a risk manager's level of concern). Conversely, an assessor may choose not to
complete a lower-tier analysis before completing a higher-tier analysis (e.g., the risk assessor
could go directly to Tier 3).
In this example approach, a multipathway risk assessment is conducted only ifPB-HAP
compounds are present in facility/source emissions (see Exhibit 23), and acute exposures are
not assessed for multipathway analyses (although they may be for inhalation analyses). The
focus is on exposure and risk/hazard once the PB-HAPs are deposited onto soils, into surface
waters, etc. Other situations may warrant a multipathway analysis, such as when there are
significant emissions of pollutants whose primary risk is through non-inhalation exposure
pathways, or when state or local regulations require such analyses.
The discussion in this chapter is divided into the following sections:
Section 2 provides an overview of the multipathway risk assessment and the tiered
approaches to the human health and ecological analyses;
Section 3 provides information for preparing the emissions inventory for the multipathway
assessment;
Section 4 describes an example approach for the multipathway human health risk
assessment; and
Section 5 provides an example approach for the ecological risk assessment.
April 2004 Page 77
-------
Exhibit 23. HAPs of Concern for Persistence and Bioaccumulation (PB-HAP Compounds)
PB-HAP Compound
Cadmium compounds
Chlordane
Chlorinated dibenzodioxins and furans
DDE
Heptachlor
Hexachlorobenzene
Hexachlorocyclohexane (all isomers)
Lead compounds
Mercury compounds
Methoxychlor
Polychlorinated biphenyls
Polycyclic organic matter
Toxaphene
Trifluralin
Pollution
Prevention
Priority PBTs
X
X(a)
X
X
X(0
X
X
X(d)
X
Great Waters
Pollutants of
Concern
X
X
X
X
X
X
X
X
X
X
X
TRI PBT
Chemicals
X
xoป
X
X
X
X
X
X
X(e)
X
X
(a) "Dioxins and furans"
^ "Dioxin and dioxin-like compounds"
(c) Alkyl lead
(d) Benzo[a]pyrene
(e) "Polycyclic aromatic compounds" andbenzo[g,h,i]perylene
April 2004
Page 78
-------
2.0 Tiered Approach and Models Used
The example multipathway risk assessment approach currently includes only two tiers of
analysis (Tier 2 and Tier 3, see Exhibit 24). EPA is investigating whether it is possible to
develop a Tier 1 methodology for multipathway analyses. Therefore, at this point in time, this
example multipathway analysis starts with a Tier 2-level approach.
Tier 1 is conceptualized as a simple look-up table or graph that identifies threshold emissions
rates (tons/year) for each PB-HAP compound below which multipathway risks are not of
concern. The objective would be to allow a facility/source that emits small amounts of PB-
HAP compounds to demonstrate that risk targets are met without the need for facility-
specific modeling (as, for example, in a Tier 2 analysis). However, at this point in time, EPA
does not have sufficient experience with multipathway air toxics risk assessments to develop
a Tier 1 approach.
The example Tier 2 approach uses ISCST3 and the Methodology for Assessing Health
Risks Associated with Multiple Pathways of Exposure to Combuster (MPE) to estimate
concentrations in air, water, soil, and biota. For the human health assessment, MPE is used
to estimate cancer risk and noncancer hazard to a hypothetical receptor characterized using a
conservative "subsistence farmer" scenario. For the ecological risk assessment,
concentrations in air, water, and biota are compared to media-specific ecological toxicity
reference values (i.e., a generic set of ecological receptors is assumed).
The example Tier 3 approach uses the Total Risk Integrated Methodology (TRIM) in a
deterministic or stochastic mode. TRIM Fate, Transport, and Ecological Exposure
(TRIM.FaTE) is used to estimate concentrations in air, water, soil, and biota. For the
human health risk assessment, TRIM.ExpoIngestion (coupled with a farm food chain model) is
used to derive estimates of ingestion exposure for a set of scenarios (e.g., resident, farmer,
fisher), and TRIM.RiskjjH is used to derive cancer risk and chronic noncancer hazard
estimates. For the ecological risk assessment, TREVI.RiskEco is used to derive estimates of
ecological risk by comparing estimated concentrations of PB-HAPs in abiotic media, dietary
intakes, and body burdens to corresponding ecological toxicity reference values.
Although it is possible to evaluate acute exposures for the ingestion pathway, EPA does not
generally recommend such assessments for substances released to the air because it is very
unlikely that acute ingestion threats could exist under typical release conditions and in the
absence of serious chronic ingestion risks. However, each assessment should consider the
available evidence in making this judgment. The risk assessor is encouraged to state the reasons
why an acute analysis for non-inhalation pathways was not performed.
April 2004 Page 79
-------
Exhibit 24. Example Approach for a Multipathway Risk Assessment
PB-HAP Compounds
Present in Emissions
Wo Tier 1 Analysis is
Currently Available
TIER 2
ISCST3 -> WIPE
High-end
Human
Receptor
Generic
Ecological
Receptor
Deterministic Analysis
Risk
Estimate
At or Below
Rule-Specific Human
Health Target Risk
Level
9
Risk
Estimate
At or Below
Rule-Specific Ecological
Target Risk
Level
TIER 3
TRIM.FaTE
Risk Targets
Met
Risk Targets
Met
Deterministic or Stochastic Analysis
Monitoring to evaluate
modeled concentrations
and exposures
Risk
Estimate
At or Below
Rule-Specific Ecological
Target Risk
Level
Risk
Estimate
At or Below
Rule-Specific Human
Health Target Risk
Level
Potential Risk Reduction
Potential Risk Reduction
April 2004
Page 80
-------
Overview of Models Cited in this Example Approach
MPE. MPE, formerly referred to as the Indirect Exposure Methodology (IBM), primarily consists of a
set of multimedia fate and exposure algorithms developed by EPA's Office of Research and
Development.1-19-"-6-1 'The Human Health Risk Assessment Protocol for Hazardous Waste Combustion
Facilities, under development by EPA's Office of Solid Waste, is an implementation of this
approach.1-20-1 The MPE approach includes procedures for estimating human exposures and health risks
resulting from the transfer of emitted pollutants from air to soil and surface water bodies and the
subsequent uptake by vegetation, animals, and humans. The methodology specifically addresses
exposures via inhalation; ingestion of food, water, and soil; and dermal contact. The MPE
methodology was designed to predict long-term, steady-state impacts from continuous sources, rather
than short-term, time-series estimates. It consists of a "one-way process" through a series of linked
models and algorithms, beginning with the modeling of the transport of pollutant emissions in air and
the subsequent deposition to soil and surface water and culminating in the uptake of the emitted
pollutant(s) into biota.
TRIM.FaTE. TRIM.FaTE is a spatially explicit, compartmental mass balance model that describes
the movement and transformation of pollutants over time, through a user-defined, bounded system that
includes both biotic and abiotic components (compartments).(21) The TRIM.FaTE module predicts
pollutant concentrations in multiple environmental media and in biota and pollutant intakes for biota,
all of which provide both temporal and spatial exposure estimates for ecological receptors (i.e., plants
and animals). The output concentrations from TRIM.FaTE can also be used as inputs to a human
ingestion exposure model, such as TRIM.ExpoIngestlon, to estimate human exposures.
TRIM.ExpoIngestion. TRIM.ExpoIngestlon calculates the ingestion exposure to human receptor groups
from media and food concentrations estimated using TRIM.FaTE output data (or other pollutant
concentration data) for media and biota. A farm food chain module provides livestock and produce
contaminant estimates from air and soil concentrations and air deposition estimates provided by
TRIM.FaTE or from an external file.
TRIM.Riskjjjj. In TRIM.RiskHH, estimates of human exposures are characterized with regard to
potential risk using the corresponding exposure- or dose-response relationships. The output from
TRIM.RiskHH includes documentation of the input data, assumptions in the analysis, and the results of
risk calculations and exposure analysis.
TRIM.RiskEco. In TRIM.RiskEco, estimates of ecological exposures are characterized with regard to
potential risk using the corresponding exposure- or dose-response relationships. The output from
TRIM.RiskEco includes documentation of the input data, assumptions in the analysis, and the results of
risk calculations and exposure analysis.
Note: As of the publication of this document, Trim.Expo and Trim.Risk are not yet available.
Documentation for the current versions of all of these models may be found on the Fate, Exposure, and
Risk Analysis (FERA) page (http://www.epa.gov/ttn/fera/).
e Note that the MPE model and many of its variations are conceptual models used to describe fate and
transport, not "ready-to-run" computer models. Typically, users incorporate these conceptual models into
spreadsheets or other computer frameworks to create a usable model.
April 2004 Page 81
-------
3.0 Developing the Emissions Inventory for Multipathway Analyses
As with the inhalation analysis, developing the emissions inventory involves (1) quantifying
emissions rates; (2) quantifying other emissions parameters important for the exposure
assessment (e.g., temperature, stack height); (3) identifying the chemical species of the emitted
HAPs (where applicable); and (4) identification of background concentrations of the HAPs being
released (in some instances).
As with inhalation, the risk assessor is encouraged to use its highest quality, most detailed
emissions data. Acceptable data, in order by preference, include (1) actual measured emissions
from a recent high-activity, high-emission year, (2) measured emissions extrapolated to a high-
activity, high-emission year, (3) facility/source-specific engineering estimates of a high-activity,
high emission year (with documentation); and (4) permitted emissions, (e.g., the maximum
allowed under MACT, or under a permit) with documentation that the permitted limits are not
exceeded.
In general, if lower quality data (i.e., of types (3) and (4) above) are used, these data commonly
represent high-end estimates of emissions in order to ensure the assessment will produce health-
protective results. The inventories commonly include the following release parameters for each
HAP released from each source: volume, schedule, emission factors, and applicable time
periods. Emissions commonly represent conditions typical of a high-activity, high-emission
year.
In this example approach, the risk assessments consider emissions controls in use at the
facility/source. At the least, the default assumption is that the facility's sources are in
compliance with the appropriate MACT standards and permit requirements, although it may be
reasonable to modify this assumption if additional emissions controls are in place. The
documentation for the assessment includes the specific emissions inventories used.
4.0 Multipathway Human Health Risk Assessment
4.1 Introduction and Overview
The multipathway human health risk assessment is divided into two tiers, beginning with Tier 2:
This example Tier 2 analysis uses the ISCST3 model and the MPE methodology(19) to
estimate risk/hazard at the most impacted location via several ingestion pathways. The
Human Health Risk Assessment Protocol for Hazardous Waste Combustion Facilities
(HHRAP),(20) under development by EPA's Office of Solid Waste, is an implementation of
the MPE approach. Modeled deposition rates (from ISCST3) are converted by MPE into
chemical concentrations in media and biota. MPE then uses exposure scenarios (e.g.,
resident, farmer, fisher) to estimate exposure. Monitoring is not included explicitly in this
example Tier 2 analysis because it is intended as a health-protective analysis.
This example Tier 3 analysis uses TRIM.FaTE, TRIM.ExpoIngestion, and TRIM.Riskjjjj, to
estimate ingestion risk/hazard (see Exhibit 25). The initial version of TRIM.ExpOjng^^ uses
a scenario-based approach to model exposure. In TRIM Risk^, estimates of human
April 2004 Page 82
-------
ingestion exposures (intake rates) are characterized with regard to potential risk using the
corresponding dose-response relationships. As noted in Exhibit 25, measured concentrations
from monitoring programs can be used as inputs to TRIM.Expo and thus can be incorporated
into the Tier 3 analysis.
Exhibit 25. Role of the TRIM Modeling System
AIR-only IMPACTS
AQ Model
Or
AQ Data
Inputs:
e.g., Activity data,
population data,
indoonoutdoor
concentrations, etc)
Alternative
Exposure Model
(e.g., HAPEM)
HH Tox Database -
Inputs:
human health
-dose-response
assessments
- (e.g., RfC, URE)
MULTI-MEDIA IMPACTS -
TRIM.FaTE
(Fate, Transport &
Ecological Exposure)
Farm
Food Chain
TRIIVf.Expo
|(Human Exposure Event)
Event) i'
Inhalation II Ingestion
/TRIM. Risk
(Risr Characterization)
1 1 Eco 1^ '
n Risk] [Ingestion Risk] [Eco Risk]
Eco Tox
Database
Inputs:
Ecological
effects
Assessments
(e.g.,
endpoints,
criteria)
[Inhalation |
Quantitative risk & exposure characterization, U/V, assumptions, limitations, ...
The Total Risk Integrated Methodology (TRIM) modeling system can be used to assess human
inhalation, human ingestion, and ecological risks. TRIM.FaTE accounts for movement of a chemical
through a comprehensive system of discrete compartments (e.g., media and biota) that represent
possible locations of the chemical in the physical and biological environments of the modeled
ecosystem and provides an inventory, over time, of a chemical throughout the entire system. In
addition to providing exposure estimates relevant to ecological risk assessment, TRIM.FaTE generates
media concentrations relevant to human ingestion exposures that can be used as input to the ingestion
component of the Exposure-Event module, TRIM.Expo. Measured concentrations also can be used as
inputs to TRIM.Expo. In the inhalation component of TRIM.Expo, human exposures are evaluated by
tracking randomly selected individuals that represent an area's population and their inhalation and
ingestion through time and space. Trim.ExpoInhalatlon can accept ambient air concentration estimates
from an external air quality model or monitoring data. In the Risk Characterization module,
TRIM.Risk estimates of human exposures or doses are characterized with regard to potential risk using
the corresponding exposure- or dose-response relationships. The TRIM.Risk module is also designed
to characterize ecological risks from multimedia exposures. The output from TRIM.Risk is intended to
include documentation of the input data, assumptions in the analysis, and metrics of
uncertainty/variability, as well as the results of risk calculations and exposure analysis.
Both of these tiers of analysis require significant effort and input data, with many facility/source-
specific considerations and parameter values. This document provides a brief description of the
general modeling approaches and required input data, but a detailed discussion is beyond the
April 2004
Page 83
-------
scope of this document. Such information can be found in user's guides and related
documentation on EPA's Fate, Exposure, and Risk Analysis (FERA) web page
(http://www.epa.gov/ttn/fera/). Where the risk assessment involves a regulatory decision, the
risk assessor is encouraged to discuss the scope, modeling/monitoring approach, and input data
with the appropriate regulatory authorities prior to conducting the analysis.
4.2 Pathways Evaluated
The example multipathway exposure assessment in this technical resource document focuses on
two general categories of ingestion pathways. Incidental ingestion pathways consider exposures
that may occur from ingestion of soils or surface water while engaged in other activities (e.g.,
ingestion of soil while gardening or playing outside; ingestion of surface water while
swimming). Food chain pathways consider exposures that may occur if PB-HAP compounds
accumulate in the food and water people consume. Exhibit 26 provides some examples of which
specific pathways could be evaluated for each PB-HAP compound in a multipathway human
health assessment. As a general guideline, all of the pathways identified in the conceptual model
for the assessment should be evaluated in the multipathway analysis. Note also that state and
local agencies may have other recommended compounds and pathways required for analysis.
The focus of this example multipathway assessment is on ingestion pathways. Other exposure
pathways may be important for particular risk assessments, including dermal exposures (i.e.,
direct contact with contaminated soils, surface waters, or surface water sediments during outside
activities such as gardening or swimming); resuspension of dust (e.g., from wind blowing across
contaminated soils) and subsequent inhalation of the dust particles; and ingestion of
contaminated groundwater. However, EPA does not have sufficient experience with
multipathway air toxics risk assessments to identify the circumstances for which exposures via
these additional pathways may represent a potential concern. Each assessment may consider the
available evidence in determining whether the risk assessment should include dermal exposure,
resuspension of dust, and ingestion of groundwater. At a minimum, the risk characterization
should state the reasons why an acute analysis for non-inhalation pathways was not performed.
If facility/source-specific circumstances suggest that dermal pathways may be of concern,
EPA's Risk Assessment Guidance for Superfund (RAGS), PartE, Supplemental Guidance for
Dermal Risk Assessment ,(22) includes a relatively straightforward methodology for dermal
exposure and risk assessment, starting with soil concentrations. The Planning Tables in the
document are simple to use and incorporate into the multipathway analysis.
Relative to the direct inhalation pathway, inhalation of soil resulting from dust resuspension
by wind erosion generally is not a significant pathway of concern for air toxics risk
assessments. If facility/source-specific circumstances suggest that resuspension of dust may
represent a potential concern, EPA's MPE methodology(19) discusses the methods for
evaluating this pathway.
If facility/source-specific circumstances suggest that groundwater may represent a potential
concern (e.g., the presence of extremely shallow aquifers used for drinking water purposes,
or a karst environment in which the local surface water significantly affects the quality of
ground water used as a drinking water source) the TRIM.FaTE library includes a
April 2004 Page 84
-------
groundwater compartment that can and has been used to assess the groundwater pathway.
EPA's Human Health Risk Assessment Protocol for Hazardous Waste Combustion
Facilities(20) and Draft Technical Background Document for Soil Screening Guidance(73)
discuss the methods for evaluating the groundwater pathway.
Exhibit 26. Examples of Specific Pathways to be Analyzed for Each PB-HAP Compound
PB-HAP Compound
Cadmium compounds
Chlordane
Chlorinated dibenzodioxins and furans
DDE
Heptachlor
Hexachlorobenzene
Hexachlorocyclohexane (all isomers)
Lead compounds'^
Mercury compounds
Methoxychlor
Polychlorinated biphenyls
Polycyclic organic matter
Toxaphene
Trifluralin
^o
-ป ป
VI
O
*
'o
00
tซ
00
00
CL>
T3
s3
^
'a
tf
CL>
%
Fish ingestion
_o
% ป
tซ
CL>
00
Jฃ
x>
S3
-4 ป
CL>
00
CL>
T3
S3
-4 ป
PH
^0
-M
W
W
.s
o
1
o
60
0
-t ป
O
ฃ
o
'+-ป
VI
*
1
^
ฃH
^0
-M
W
W
*
^ฃ
1
+-ป
VI
c3
S
03
(b)
(a)EPA suggests assessing effects of lead exposures with the Integrated Uptake/Biokinetic (IEUBKK)
model, which predicts blood lead levels in children exposed to lead concentrations in air, water, soil, and
house dust.
(b)Most POM compounds do not tend to accumulate to high levels in breast milk. Polybrominated biphenyl
ethers (PBDEs), which fit within the POM group definition in the CAA and are therefore HAPs, are a
significant exception. When assessing PBDEs, breast milk should be included.
April 2004
Page 85
-------
4.3 Estimating Dietary Intake
The following generic equation is used calculate dietary chemical intake:(24) Volume 1 of this
Reference Library (Chapter 20) provides a more detailed discussion of this equation.
ECx CR EFx ED
l~ BW X AT
where
/ = Chemical intake rate, or the amount of pollutant ingested per unit time per unit body
mass, expressed in units of mg/kg-day. For evaluating exposure to noncarcinogens,
the intake is referred to as Average Daily Dose (ADD}; for evaluating exposure to
carcinogenic compounds, the intake is referred to as Lifetime Average Daily Dose
(LADD)
Chemical-related variable:
EC = Exposure concentration of the chemical in the medium of concern for the time period
being analyzed, expressed in units of mg/kg for soil and food or mg/L for surface
water or beverages (including milk)
Variables that describe the exposed population (also termed "intake variables"):
CR = Consumption rate, the amount of contaminated medium consumed per unit of time or
event (e.g., kg/day for food items and L/day for water)
EF = Exposure frequency (number of days exposed per year)
ED = Exposure duration (number of years exposed)
BW = Average body weight of the receptor over the exposure period (kg)
Assessment-determined variable:
AT = Averaging time, the period over which exposure is averaged (days). For carcinogens,
the averaging time is 25,550 days, based on an assumed lifetime exposure of 70
years; for noncarcinogens, averaging time equals ED (years) multiplied by 365 days
per year
The exposure concentration (EC) for a chemical is calculated separately for each food item
and environmental medium of concern. The value of these variables is determined primarily
by modeling; however, monitoring data may be used to evaluate or further characterize
exposure concentrations at key locations considered (as noted earlier, where the risk
assessment involves a regulatory decision, the risk assessor is encouraged to discuss the
scope and approach for collecting monitoring data with the appropriate regulatory authorities
prior to conducting the analysis).
Consumption rate (CR) is the amount of contaminated food or medium consumed per event
or unit of time (e.g., amount offish consumed per meal or per day). Note that consumption
April 2004 Page 86
-------
rate changes with age (e.g., children and adults eat different amounts of the same food items).
The consumption rate is usually calculated by first estimating the amount of a given medium
consumed per unit time and then multiplying by a fraction of the total dietary intake for this
type of food or medium (e.g., 25 percent), representing the amount consumed from the study
area. The specific fraction applied depends on the assumptions used for the analysis and can
range from zero to 100 percent. For example, if the analysis assumed an individual
consumed 6 grams offish per day and obtained 25 percent of the fish from the contaminated
area, CR would be 6 x .25 = 1.5 g/day.
The specific exposure frequency (EF) specifies the number of days exposed each year,
which generally ranges from a weekly or seasonal basis to 350 days/year (i.e., a person is
resident in an area but spends two weeks each year in a different location, such as on
vacation).
Exposure duration (ED) is the length of time that a particular assessment represents (e.g., a
lifetime or a particular residence time). This is specified for each analysis.
The choice of body weight (BW) for use in the exposure assessment depends on the
definition of the person at potential risk. Because children have lower body weights, typical
ingestion exposures per unit of body weight, such as for soil, milk, and fruits, are
substantially higher for children. If a lifetime exposure duration (or an exposure duration
over the childhood and adult years) is being evaluated, it needs to be based on differing
values for the different age groups. If less than a lifetime exposure estimate is being
evaluated, it is important to include the children's age group in the specific scenarios or
cohorts used (see Volume 1, Chapter 20).
Averaging time. When evaluating exposure to noncarcinogenic toxicants, intake is
averaged over the period of exposure. For carcinogens, intakes are traditionally calculated
by prorating the total cumulative dose over a lifetime (i.e., chronic daily intakes, also called
lifetime average daily intakes).
4.4 Ingestion Toxicity Assessment
As noted in Volume 1 of the reference library (Chapter 12), toxicity assessment is accomplished
in two steps: hazard identification and dose-response assessment. Dose-response values (e.g.,
CPFs, RfDs) are used to estimate the potential for adverse impacts resulting from exposure to a
given concentration of a PB-HAP. Identifying critical human health endpoints (cancer vs.
noncancer) and target organs is critical for structuring the multipathway risk assessment,
including determining what ingestion exposure pathways are of potential concern and how to
sum the risks from exposure to multiple HAPs. Volume 1 describes this process in greater
detail. For each PB-HAP included in a risk assessment, the risk assessor should identify the
critical human health endpoints and target organs to ensure that cumulative risk across all HAPs
is estimated in a manner consistent with risk assessment principles.
EPA/OAQPS has developed a set of recommended screening-level chronic human health dose-
response values for many HAPs. This information is presented in Appendix C of Volume 1,
which provides information on the type of hazard associated with each HAP (e.g., cancer,
April 2004 Page 87
-------
non-cancer) and the applicable dose-response values for each HAP (e.g., RfCs, ITJRs). The most
up-to-date list of default screening level dose-response values recommended by EPA for the 188
HAPs is provided at http://www.epa.gov/ttn/atw/toxsource/summary.html. Other dose-response
values that have undergone independent peer review may also be acceptable, but generally
should be consistent with EPA risk assessment guidelines and agreed upon in advance for
assessments that have regulatory implications. Descriptive information on the type of health
hazards associated with each HAP (e.g., cancer, noncancer) may be found at
http ://www. epa. gov.ttn/atw/haptindex.html.
The oral cancer slope factor (CSF) is used to estimate ingestion cancer risk. It is derived in a
similar way as the inhalation unit risk estimate (IUR) (see Volume I of this reference library).
The CSF is defined as the upper-bound excess lifetime cancer risk estimated to result from
continuous exposure to an agent. The true risk to humans, while not identifiable, is not likely to
exceed the upper-bound estimate (the CSF). The CSF is presented as the risk of cancer per mg
of intake of the substance per kg body weight per day (i.e., [mg/kg-day]"1).
The oral Reference Dose (RfD) is used to estimate hazard. The RfD is expressed as a chronic
dietary intake level (in units of mg/kg-day). The RfD is an estimate (with uncertainty spanning
perhaps an order of magnitude) of a continuous exposure to the human population (including
sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a
lifetime. In other words, exposures at or below the RfD will probably not cause adverse health
effects, even to sensitive subgroups. This generally is used in EPA's health effects assessments
for effects other than cancer.
/\
Definition of Terms in Ingestion Dose-Response Values
Oral Cancer Slope Factor (CSF): An upper bound, approximating a 95% confidence limit, on the
increased cancer risk from a lifetime exposure to an agent. This estimate is usually expressed in units
of proportion (of a population) affected per mg/kg-day.
Reference Dose (RfD): An estimate (with uncertainty spanning perhaps an order of magnitude) of a
daily oral exposure to the human population (including sensitive subgroups) that is likely to be without
an appreciable risk of deleterious effects during a lifetime.
V s
4.5 Risk Characterization for Ingestion Analysis
The process for characterizing cancer risks and noncancer hazards in this example multipathway
analysis approach can be thought of as developing information to fill in a matrix similar to that
shown in Exhibit 27 in addition to the discussion of assumptions, limitations, and uncertainties
that are an essential part of risk characterization. A table like this would be developed for each
receptor being evaluated (e.g., a scenario-based receptor or simulated individual) in the study
area. This type of presentation format shows the aggregate risk for each chemical across
multiple pathways, the cumulative risk for each pathway across chemicals, and the overall
cumulative cancer risk. In addition, this format allows one to quickly identify both the
individual chemicals and pathways that contribute most to the total risk estimate.
April 2004 Page,
-------
Exhibit 27. Example Matrix for Estimating Excess Cancer Risks for Multiple Chemical
Exposure through Multiple Ingestion Pathways for a Particular Exposure Scenario
Chemical 1
Chemical 2
Chemical 3
Chemical 4
Cumulative
Ingestion
Pathway
Risk
Estimate ฐฐ
Pathway 1
(Vegetable
Ingestion Risk
Estimate)00
1 x 1Q-6
4 x ID'7
4 x ID'9
9 x ID'7
3 x 1Q-6
Pathway 2
(Fish
Ingestion Risk
Estimate)00
3 x 1Q-4
4 x ID'6
7 x ID'7
1 x 1Q-6
3 x 1Q-4
Pathway 3
(Egg Ingestion
Risk
Estimate)00
9 x ID'8
4 x ID'8
3 x 1Q-8
6 x ID'7
7 x ID'7
Pathway 4
(Beef
Ingestion Risk
Estimate)00
8 x ID'5
4 x ID'7
9 x ID'9
6 x ID'7
8 x ID'5
Aggregate
Chemical
Ingestion
Risk Estimate ฐฐ
4 x ID'4
5 x 1Q-6
8 x ID'7
3 x 1Q-6
4 x ID'4
00 Standard rules for rounding apply which will commonly lead to an answer of one significant figure
in both risk and hazard estimates. For presentation purposes, hazard quotients (and hazard indices) and
cancer risk estimates are usually reported as one significant figure.
4.5.1 Cancer Risk Estimates
Estimated individual cancer risk is expressed as the probability that a person will develop cancer
as a result of the estimated exposure over a lifetime. This predicted risk is the incremental risk
of cancer from the exposure being analyzed (i.e., it does not take into account cancer risk from
other factors). Due to default assumptions in their derivation, oral cancer slope factors (CSFs)
are generally considered to be "plausible upper-bound" estimates, regardless of whether they are
based on statistical upper bounds or best fits. Risks may be estimated for both the central
tendency (average exposure) case and for the high end (exposure that is expected to occur in the
upper range of the distribution) case, or probabilistic techniques can be used to develop a
distribution of estimated risks.
4.5.1.1 Characterizing Individual Pollutant Risk
The first step in characterizing individual pollutant risk for an exposure scenario (e.g., a
recreational fisher) is to quantify risk for each ingestion exposure pathway being evaluated. In
this step, cancer risks for individual pollutants are estimated by multiplying the estimate of the
lifetime average daily dose (LADD) for each ingestion exposure pathway by the appropriate CSF
to estimate the potential incremental cancer risk:
Risk = LADD x CSF
where:
April 2004
Page 89
-------
Risk = Individual cancer risk (expressed as an upper-bound risk of contracting cancer
over a lifetime) for each pollutant via the ingestion pathway being evaluated
(unitless);
LADD = Lifetime Average Daily Dietary Intake rate for the pollutant via the
ingestion pathway being evaluated (mg/kg-d); and
CSF = Oral Cancer Slope Factor for the pollutant via the ingestion pathway being
evaluated [(mg/kg-d)"1]
Estimates of cancer risk are usually expressed as a probability represented in scientific notation
as a negative exponent of 10. For example, an additional upper bound risk of contracting cancer
of 1 chance in 10,000 (or one additional person in 10,000) is written as IxlO"4. Because CSFs
are typically upper-bound estimates, actual risks may be lower than predicted - note that "the
true value of the risk is unknown and may be as low as zero."(25)
In this example approach, risks are evaluated initially for individuals within the potentially
exposed population. Population risks for the exposed population may also be estimated, which
may be useful in estimating potential economic costs and benefits from risk reduction. Sensitive
subpopulations should also be considered, when possible. Estimates of incidence also are
possible, although in small populations, even a very high individual risk estimate may not yield
an estimated incidence above one case of cancer.
For carcinogens being assessed based on the assumption of nonlinear dose-response, for which
an RfD was derived that considers cancer as well as other effects, the hazard quotient approach
is appropriate for risk characterization (see below). Where detailed information on carcinogenic
mechanisms exists it may also be possible to estimate risk directly from a nonlinear low-dose
extrapolation. This approach is supported by EPA's Guidelines for Carcinogen Risk
Assessment.,(11)
4.5.1.2 Characterizing Risk from Exposure to Multiple Pollutants
By each exposure pathway of a scenario, exposure may be to multiple chemicals at the same
time rather than a single chemical; however, CSFs are usually available only for individual
compounds within a mixture. Consequently, a component-by-component approach is usually
employed.(14) The following equation estimates the predicted cumulative incremental individual
cancer risk from multiple substances for a single exposure pathway, assuming additive effects
from simultaneous exposures to several carcinogens:
RiskT = Risk,, + Risk2 + .... + Risk,
where:
RiskT = Cumulative individual ingestion cancer risk (expressed as an upper-bound risk of
contracting cancer over a lifetime); and
Risk; = Individual ingestion risk estimate for the ith substance.
In screening-level assessments of carcinogens for which there is an assumption of a linear dose-
response, the cancer risks predicted for individual chemicals may be added to estimate
cumulative cancer risk for each pathway. This approach is based on an assumption that the risks
April 2004 Page 90
-------
associated with individual chemicals in the mixture are additive. In more refined assessments,
the chemicals being assessed may be evaluated to determine whether effects from multiple
chemicals are synergistic (greater than additive) or antagonistic (less than additive), although
sufficient data for this evaluation are usually lacking. In those cases where CSFs are available
for a chemical mixture of concern, risk characterization can be conducted on the mixture using
the same procedures used for a single compound.
For carcinogens being assessed based on the assumption of nonlinear dose-response, for which
an RfD considering cancer as well as other effects has been derived, the hazard quotient
approach will be appropriate (see Volume 1, Chapter 12).
4.5.1.3 Combining Risk Estimates across Multiple Ingestion Pathways
To evaluate risks associated with the aggregate exposure to a single PB-HAP across multiple
pathways of a given scenario, the individual pollutant cancer risk estimates may be summed for
each chemical across the multiple ingestion pathways assessed. Additionally, a cumulative
multi-pathway risk estimate may be derived by summing cumulative (multiple pollutant) cancer
risk estimates across the multiple ingestion pathways.
4.5.1.4 Evaluating Risk Estimates from Inhalation and Ingestion Exposures
Depending on the ingestion scenario, the inhalation pathway may also have been assessed. In
such cases, it may be possible to obtain an overall estimate of risk across all pathways by
combining the inhalation exposures with the ingestion exposures. It is important to note,
however, that the methods and assumptions used to derive the inhalation and ingestion risks may
not always yield compatible exposure scenarios. Consequently, it may be sufficient to simply
qualitatively consider any potential cumulative risk across routes. This is particularly important
when population-level (versus individual) risk estimates are being developed. For example, a
scenario-based ingestion exposure assessment will not be easily amenable to producing estimates
of numbers of people at different risk levels, while a population-based inhalation assessment
may be more appropriate. For example, it would generally not be appropriate to add an
inhalation risk that presumes a 70-year exposure duration with an ingestion pathway that
presumes a 30-year exposure duration. Any mismatching of exposure durations among
pathways in a multipathway assessment should be carefully considered. For this reason,
combining any risk estimates across the ingestion and inhalation pathways is commonly done
only by an experienced toxicologist.
4.5.2 Noncancer Hazard
For noncancer effects (as well as carcinogens being assessed based on the assumption of
nonlinear dose-response), ingestion exposure concentrations are compared to RfDs, which are
estimates (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure to
the human population (including sensitive subgroups) that is likely to be without an appreciable
risk of deleterious noncancer effects during a lifetime.
As with carcinogens, the development of hazard quotients (HQs) for ingestion typically is
performed first for individual air toxics, then hazard indices (His) may be developed for multiple
April 2004 Page 91
-------
pollutant exposures, and may be summed across pathways to develop multiple pathway
cumulative hazard estimates. An additional step in the multipathway analysis is to evaluate both
ingestion and inhalation hazard estimates. These steps are described in separate subsections
below.
4.5.2.1 Characterizing Individual Pollutant Hazard
The first step in characterizing individual pollutant hazard for an exposure scenario (e.g., a
recreational fisher) is to quantify hazard for each pollutant being evaluated. For ingestion
exposures, noncancer hazards are estimated by dividing the estimate of the Average Daily Dose
(ADD) by the chronic oral RfD to yield a hazard quotient (HQ) for individual chemicals:
HQ = ADD * RfD
where:
HQ = The Hazard Quotient for the pollutant via each ingestion pathway being evaluated
(unitless);
ADD = Estimate of the Average Daily Dietary Intake rate for the pollutant via the
ingestion pathway being evaluated (mg/kg-d); and
RfD = the corresponding reference dose for the pollutant via the ingestion pathway being
evaluated (mg/kg-d)
In screening assessments, which are routinely built around a particular year's estimate of
emissions, the chronic exposure estimate may be based on a somewhat shorter than "chronic"
exposure concentration estimate (e.g., the average annual concentration estimated by modeling),
employing the simplifying assumption of continued similar conditions for a long-term period. A
more refined assessment might then include an estimate of exposure derived using information
for the full chronic period of exposure time period (e.g., a lifetime or substantial portion of a
lifetime, refined emissions estimates over the long-term period).
Based on the definition of the RfD, an HQ less than or equal to one indicates that adverse
noncancer effects are not likely to occur. With exposures increasingly greater than the RfD (i.e.,
HQs increasingly greater than one), the potential for adverse effects increases. However, the HQ
should not be interpreted as a probability, because the overall chance of adverse effects does not
increase linearly as exposures exceed the RfD.
4.5.2.2 Multiple Pollutant Hazard
Noncancer health effects data are usually available only for individual compounds within a
mixture. In these cases, the individual HQs can be summed together to calculate a multi-
pollutant hazard index (HI):
+ HQ2 + ...+ HQi
where:
HI = Hazard index; and
HQ; = Hazard quotient for the ith air toxic.
April 2004 Page 92
-------
For screening-level assessments, a simple HI may first be calculated for all chemicals of concern
(Exhibit 28). This approach is based on the assumption that even when individual pollutant
levels are lower than the corresponding reference levels, some pollutants may work together
such that their potential for harm is additive and the combined exposure to the group of
chemicals poses greater likelihood of harm. Some groups of chemicals can also behave
antagonistically, such that combined exposure poses less likelihood of harm, or synergistically,
such that combined exposure poses harm in greater than additive manner. Where this type of HI
exceeds the criterion of interest, a more refined analysis is warranted. However, note that
interpretation of differences among HQs across substances may be limited by differences among
RfDs in their derivation and the fact that the slope of the dose-response curve above the RfD can
vary widely depending on the substance, type of effect, and exposed population.
Exhibit 28. Example Matrix for Characterizing Hazard for Multiple Chemical Exposure
through Multiple Ingestion Pathways for a Particular Exposure Scenario
Chemical 1
Chemical 2
Chemical 3
Chemical 4
Cumulative
Ingestion
Pathway HI (a)
Pathway 1
(Vegetable
Ingestion
HQ)(a)
2 x ID'1
3 x ID'1
1 x ID'1
9 x ID'2
7 x ID'1
Pathway 2
(Fish
Ingestion
HQ)(a)
2 x ID'1
7 x ID'1
4 x ID'1
1 x ID'2
1
Pathway 3
(Egg Ingestion
HQ)(a)
4 x ID'2
3 x ID'2
2 x ID'1
1 x ID'1
4 x ID'1
Pathway 4
(Beef
Ingestion
HQ)(a)
2 x ID'1
2 x ID'1
4 x ID'1
2 x ID'2
9 x ID'1
Aggregate
Chemical
Ingestion
HQ(a)
7 x ID'1
1
1
3 x ID'1
3
(a) Standard rules for rounding apply which will commonly lead to an answer of one significant figure
in both risk and hazard estimates. For presentation purposes, hazard quotients (and hazard indices) and
cancer risk estimates are usually reported as one significant figure.
The assumption of dose additivity is most appropriate to compounds that induce the same effect
by similar modes of action. Thus, EPA guidance for chemical mixtures(14) suggests subgrouping
pollutant-specific HQs by toxicological similarity of the pollutants for subsequent calculations;
that is, to calculate a target-organ-specific-hazard index (TOSHI) for each subgrouping of
pollutants. This calculation allows for a more appropriate estimate of overall hazard.
The HI approach encompassing all chemicals in a mixture may be appropriate for a screening-
level study. However, it is important to note that applying the HI equation to compounds that
may produce different effects, or that act by different mechanisms, could overestimate the
potential for effects. Consequently, in a refined assessment, it is more appropriate to calculate a
separate HI for each noncancer endpoint of concern when mechanisms of action are known to be
similar.
April 2004
Page 93
-------
4.5.2.3 Evaluating Hazard Estimates From Inhalation and Ingestion Exposures
As with carcinogenic assessments, in some cases it may be possible to combine estimates of
inhalation hazard with ingestion hazard estimates to provide an estimate of total hazard across all
exposure pathways for a receptor. As noted earlier, this is a complex analysis that generally is
conducted by an experienced toxicologist.
4.5.3 Consideration of Long-Range Transport and Background
Although the example approach presented here focuses on populations located close to a
facility/source, the contribution of a facility/source to deposition of PB-HAPs in more distant
environmentally sensitive areas (e.g., the Great Lakes, Chesapeake Bay, the Florida Everglades)
through long-range transport may also be a potential concern. Even small contributions from a
single facility may become significant over time. In addition, while local residents may not eat
fish from bodies of water around a facility/source, fish caught from the large, productive lakes
and bays in the U.S. are known to be eaten by significant numbers of people. Risk assessors are
encouraged to discuss the contribution by an evaluated facility/source to the potential risks
associated with this exposure route.
Similarly, the study area around a specific facility/source may be subject to deposition of PB-
HAPs resulting from long-range transport from more distant sources. Risk assessors are
encouraged to discuss the contribution of these background levels of deposition as appropriate.
Note, however, that the local impacts of PB-HAP emissions may be of greatest potential concern
for many facilities/sources. Therefore, whether or not to include a detailed assessment of long-
range transport and/or background generally is an analysis-specific decision (often determined
by legal and regulatory requirements).
4.5.4 Assessment and Presentation of Uncertainty
In the final part of this example risk characterization, estimates of cancer risk and noncancer
hazard are presented in the context of uncertainties and limitations in the data and methodology.
Exposure estimates and assumptions, toxicity estimates and assumptions, and the assessment of
uncertainty and variability commonly are discussed.
The risk estimates used in multipathway toxics risk assessments are unlikely to be fully
probabilistic estimates of risk because of the numerous pathways, potential receptors, and
potential parameter values involved in the assessment. Rather, such risk estimates are likely to
be conditional estimates that incorporate a considerable number of assumptions about exposure
and toxicity. Multipathway air toxics risk assessments are subject to additional sources of
uncertainty and variability as compared to inhalation risk assessments. The multimedia
modeling effort is both more complex and less certain due to many factors. For example: (1)
there are many more chemical-dependent and chemical-independent variables involved as input
values to the models; (2) the models involve analysis of the transfer of air toxics from the air to
other media (e.g., soil, sediment, water), the subsequent movement of the air toxics between
these media (e.g., soil runoff to surface water), and uptake and metabolism by biota; and (3)
many variables affect the ingestion of food, water, and other media by humans and wildlife, and
April 2004 Page 94
-------
the exposure and risk estimates may differ considerably as a consequence of the assumptions
used to derive intake estimates. Sampling of biota and abiotic media also may be more complex
and uncertain. Additional uncertainties are incorporated in the risk assessment when exposure
estimates to multiple substances across multiple pathways are summed.
As a result of the increased complexity and uncertainty of the analytical approach, multipathway
risk assessments commonly include semi-quantitative sensitivity analyses and may include
quantitative uncertainty analysis. These approaches to uncertainty analysis are discussed in
greater detail in Section III-5.4 and in Volume 1 (Chapters 3 and 13) of this reference library.
4.6 Tier 1 Multipathway Human Health Analysis
(reserved)
April 2004 Page 95
-------
4.7 Tier 2 Multipathway Human Health Analysis
4.7.1 Introduction
This section describes an example approach for performing a Tier 2 multipathway risk
assessment. Exhibit 29 provides an overview of this example approach. In this example
approach, ISCST3 is used to provide deposition rates to soils and surface waters. The MPE
methodology is used to estimate human exposure at the most impacted location via several
ingestion exposure pathways. Because EPA has not yet identified a Tier 1 approach, this
example Tier 2 analysis incorporates simplified assumptions that allow a conservative
risk/hazard estimate to be calculated with a relatively modest analytical effort. If the
facility/source passes this screening analysis, the risk manager can be reasonably confident that
the likelihood for significant risk/hazard is low. As a consequence, monitoring is not explicitly
included in this example Tier 2 analysis (although available monitoring data can be used as
inputs to the exposure analysis).
4.7.2 Fate and Transport Modeling
This example Tier 2 approach uses the ISCST3 model for estimating air concentrations for both
chronic and acute exposures (an alternative would be to use AERMOD). Other models may be
relevant for a specific facility/source. For example, if the facility/source is located in complex
terrain and/or near a large body of water, other models may be more applicable (e.g., Cal-Puff
for complex terrain; non-Gaussian models for sources close to large bodies of water). Similarly,
if the exposure point of concern is very near source (< 100-m) or very distant (> 50-km), other
models would need to be applied (e.g., CALPUFF for > 50-km). However, where the
assessment could support a regulatory decision, the use of an alternative model commonly is
agreed to in advance with the regulatory agency decision-maker. Alternative models that
conform to EPA's air quality modeling guidance(17) are more likely to be acceptable to those
decision-makers.
4.7.2.1 Model Inputs
The modeling for the multipathway analysis commonly is executed in about the same way as
would be done for a Tier 2 inhalation analysis. For example, sources are characterized the same
way regarding stack/vent height and diameter, release temperature and velocity, flow rate, etc.
The ISCST3 model requires the speciation profile of the emissions for ISCST3 in order to
calculate deposition rates properly. The risk assessor would have addressed deposition and these
properties in the Tier 2 inhalation analysis if he/she executed the ISCST3 inhalation runs "with
depletion" (i.e., telling the model to subtract out the mass of chemical deposited). This is a
concern for emissions of chemicals that are predominantly particulates instead of vapors and/or
are predominantly bound to particles (e.g., metals). However, the inhalation runs may not have
been done with depletion, because it takes longer to do this. If the inhalation runs were done
without depletion, they should be done again with depletion for the multipathway analysis.
April 2004 Page 96
-------
Exhibit 29. Example Approach for a Tier 2 Multipathway Assessment
All PB-HAP Compounds
Multimedia Modeling
ISCST3
Site-specific model inputs
High production year
Resident Farmer Scenario (including childhood)
Qualitative uncertainty analysis
Cumulative Cancer Risk Estimate
Sum risk across all pathways
Sum risk across all carcinogens
Cumulative
Cancer Risk
Estimate At or Below
Target Level?
Cumulative Noncancer Hazard Estimates
Sum hazard across all pathways - HQ
Sum hazard across all noncarcinogens - HI
Can sum separately by target organ - TOSHI
Monitoring to evaluate
modeled concentrations
and exposures
Go to Tier 3
Risk Targets Met
HI or TOSHI
At or Below
Target Level?
yes
Inputs for ISCST3
Input data for ISCST3 fall into seven general categories: (1) source location; (2) emissions data;
(3) stack/vent parameter data; (4) pollutant-specific data (reactivity); (5) wet and dry deposition
parameters; (6) meteorological data; and (7) population data. The ISC user's guide(9) provides
more detailed information on the deposition algorithms and required input data. There also is
guidance for application of ISC for multipathway assessment in the latest MPE
documentation.(19) This example approach assumes that all input data are at a level of detail
equivalent to the Tier 2 inhalation analysis.
Source location. ISCST3 requires coordinate data (latitude and longitude) for each emission
source in the analysis. Multiple sources can be modeled in the same ISCST3 run.
April 2004
Page 97
-------
Emissions data. In this example approach, the risk assessor uses the best site-specific
emissions data available, including chemical speciation. With ISCST3, users have many
options for characterizing emissions. For example, users have the option to specify variable
emission rate factors for sources whose emissions vary as a function of time (e.g., month,
season, hour-of-day). In addition, settling velocity categories, mass fractions, and reflection
coefficients may be specified for sources of large particulates that experience settling and
removal during dispersion. Therefore, this example approach assumes that the emissions
profile(s) used for modeling reflect the expected pattern(s) of emissions over a reasonable
period of time (e.g., several years). Note that these profiles may differ for different sources
within a single facility.
Stack/vent parameter data. Facility/source-specific values commonly are used for all
stack/vent parameter data. These values commonly reflect the expected patterns of emissions
used to develop the emissions profiles for modeling.
Atmospheric reactivities of chemicals. Atmospheric reactivities generally are not needed
for PB-HAP compounds.
Wet and dry deposition parameters. The ISCST3 models requires the particulate/
particle-bound/vapor fractions of the emissions in order to calculate wet and dry deposition
of vapors and particles. These would probably be considered source-related, since although
they are chemical-dependent, they also vary by source (i.e., the industrial process affects the
emissions profile).
For dry deposition of particles, the user needs to supply the following inputs (in addition to
the normal ISC inputs), including the:
- Array of particle diameters of the emissions;
- Array of mass fractions corresponding to the different particle diameters; and
- Array of particle densities corresponding to the different particle diameters.
For wet deposition of particles, the user needs to supply the following inputs (in addition to
the normal ISC inputs), including the:
- Particle scavenging coefficients for liquid precipitation corresponding to the different
particle diameters; and
- Particle scavenging coefficients for frozen precipitation corresponding to the different
particle diameters.
For wet deposition of gases, the user needs to supply the following inputs (in addition to the
normal ISC inputs), including the:
- Gaseous scavenging coefficient for liquid precipitation; and
- Gaseous scavenging coefficient for frozen precipitation.
Meteorology. Tier 2 multipathway analyses commonly use the most recent consecutive five
years of facility/source-specific data from the nearest representative meteorological station.
"Representative" generally means that the sources being modeled and the weather station are
located in the same general environment with respect to significant terrain (e.g., valley vs.
plateau), significant geographic features (e.g., proximity to a large body of water), and
April 2004 Page 98
-------
prevailing winds (i.e., similar wind rose/direction of dominant wind). Documentation
demonstrating the representativeness of the meteorological data is encouraged. Sources of
meteorological data are provided in Volume 1, Appendix G.
Population. Population is not defined for the ISCST3 model runs (population is defined
using MPE (see Section 4.7.3 below).
Inputs for the MPE Methodology
The MPE methodology requires air concentrations and deposition rates for the appropriate
locations as inputs. These are provided by ISCST3. A variety of additional chemical- and/or
facility/source-specific parameters are needed for MPE to calculate concentrations in various
media (e.g., soil, surface water) and biota (e.g., plants, fish). These are identified and described
in detail in the MPE documentation.(19)
4.7.2.2 Model Runs
Using one complete year of meteorological data, ISCST3 calculates annual deposition rates (or
fluxes) for each receptor location specified in a run. Results for each of the five years of
meteorological data are obtained using separate ISCST3 model runs for each year. ISCST3 can
model all sources at the facility simultaneously; however, only one chemical can be modeled at a
time. Therefore, for each PB-HAP compound, all sources of that compound could be modeled in
the same ISCST3 model run.
Defining receptor locations
For this example Tier 2 analysis, the subsistence farmer is assumed to occur at the modeling
location ("node") with the maximum deposition rate. Several iterations of the ISCST3 model
may be required to locate this point. The risk assessor is encouraged to clearly document the
process used to identify this point.
If multiple PB-HAPs are present, the point where maximum deposition occurs for each
individual PB-HAP may not be in the same location. This example approach assumes that
these are all co-located (see Section 4.7.4 below).
For this example approach, the point where maximum deposition occurs is used for all soil
pathways and for the drinking water pathway.
For surface water pathways, this example Tier 2 analysis is based on the surface water body
within the assessment area where maximum concentrations occur. This will depend on the
location of the surface water bodies with respect to sources, characteristics of the surface
water body (e.g., size, depth, flow rate), and characteristics of the watershed (e.g., size,
runoff, erosion potential). Several water bodies/watersheds within the assessment area may
need to be characterized in order to identify this water body. The risk assessor is encouraged
to clearly document the process used to identify this water body.
April 2004 Page 99
-------
For this example approach, the subsistence farmer is assumed to fish in the water body where
maximum concentrations occur.
Defining the duration of emissions
Because the concentrations of PB-HAP compounds often will slowly accumulate in soil,
sediment, and biota over time, the total deposition over time (and the resulting media
concentrations) will depend on the specific duration of emissions selected for the analysis.
For a Tier 2 analysis, the duration of emissions used in the analysis commonly reflects the
expected duration of emissions from the facility/source being evaluated. A common duration is
30 or 40 years (e.g., the expected lifespan of many facilities or processes). However, facilities
may continue to operate beyond their expected lifespan. Therefore, the risk assessor is
encouraged to document the rationale for selecting a duration of emissions. In the absence of
clear rationale for another value, a conservative value (e.g., 100 years) can be selected.
Defining deposition/flux rates for estimating media concentrations
This example approach uses the average deposition/flux rates from the five years of ISCST3
modeling and assumes these rates are constant over the duration of emissions.
Model outputs to use
The modeled deposition rates and duration of deposition are used as inputs to the MPE
methodology to estimate PB-HAP concentrations in soil, water, and biota. This example
approach uses the average annual deposition rates as inputs to the MPE methodology.
4.7.3 Exposure Assessment
For this example Tier 2 assessment, the exposure assessment includes both central tendency and
high end exposure estimates.
4.7.3.1 Characterization of the Study Population
For this example Tier 2 assessment, the study population is limited to a hypothetical subsistence
farmer assumed to reside at the point of maximum deposition and to fish in the water body with
the highest modeled concentrations. For assessments for which information of local farming
practices is available, the location of actual farms can be used as the basis for a more realistic
exposure scenario.
4.7.3.2 Defining the Point of Maximum Exposure
This example Tier 2 assessment defines the point of maximum exposure as follows:
For a single PB-HAP compound, the point of maximum exposure is defined as the modeled
location (node) at which the highest deposition rate occurs (soils) and the surface water body
April 2004 Page 100
-------
with maximum modeled concentrations. Exposure estimates from these two locations are
summed to calculate total maximum exposure.
For multiple PB-HAP compounds, the point of maximum exposure is defined by assuming
that the point of maximum exposure occurs at the same location for each PB-HAP compound
(i.e., exposure for each compound is added to calculate total exposure).
4.7.3.3 Defining the Exposure Scenario
This example Tier 2 assessment is based on a single exposure scenario designed to provide a
conservative estimate of risk/hazard via all ingestion pathways. This scenario is termed the
subsistence farmer. This scenario reflects an individual living on a farm and consuming meat,
dairy products, and vegetables that the farm produces. All drinking water is obtained from a
surface water body on the farm (or if no surface water is present, from collected rainfall). The
animals raised on the farm subsist primarily on forage that is grown on the farm. This scenario
also assumes that the farm family fishes in the surface water body with the highest
concentrations within the study area. They fish at a recreational level and eat the fish they catch.
The maximum exposed individual is assumed to be exposed to PB-HAP compounds through the
following exposure pathways:
Direct inhalation of vapors and particles (assessed during the inhalation analysis);
Incidental ingestion of soil and house dust;
Ingestion of drinking water from surface water sources;
Ingestion of homegrown produce;
Ingestion of home-produced meat, milk, and eggs; and
Ingestion offish; and
Ingestion of breast milk (evaluated separately for an infant [for PCBs, dioxins, and furans]).
Within this general scenario, the specific exposure routes evaluated for a given facility/source
may depend on the particular PB-HAP compounds in the emissions being assessed (see Exhibit
26).
4.7.3.4 Calculation of Exposure Concentration
This example Tier 2 approach calculates exposure concentration as follows:
Exposure concentrations in soil, drinking water, and food items are calculated using the
equations provided in the MPE methodology(19) or the HHRAP.(20)
The maximum concentration (via each exposure pathway) reached during the modeling
period is used as the exposure concentration. For a constant emissions scenario, this usually
will be the final year of the modeling simulation (e.g., the last year the facility/source is
expected to operate).
Note that existing monitoring data may be used to evaluate or refine the exposure estimates
based on multimedia modeling.
April 2004 Page 101
-------
4.7.3.5 Determining Exposure
This example Tier 2 approach assumes that the subsistence farmer is exposed to this
concentration during his/her entire lifetime, from birth to the age of 70 years. This entails the
use of variable exposure factors (e.g., body weight, consumption rate) as the subsistence farmer
ages from birth to age 70. Additionally, for the derivation of chronic hazard estimates, a child
(e.g.,
0-7 years old) may be included to address the potential for substantially higher pollutant intake
(in mg/kg-day) during those ages.
4.7.3.6 Determining Intake
For this example approach, the risk assessor calculates a central tendency and high end intake.
EPA's Exposure Factors Handboott26) provides default central tendency and high-end values for
intake and other exposure factors (e.g. body weight). Equations used to calculate intake are
found in the MPE methodology.(19) EPA's Guidance on Selecting the Appropriate Age Groups
for Assessing Childhood Exposures to Environmental Contaminants(21) and Child-Specific
Exposure Factors Handbooti2^ provide guidance on selecting the appropriate age groups to
include for children and the exposure factors to use that are specific to each age group.
4.7.4 Risk Characterization
Risk characterization for this example Tier 2 approach is limited to estimating ingestion risk for
the subsistence farmer (calculated separately for cancer risk and chronic noncancer hazard). The
estimates of intake rates described in Section 4.7.3.6 are used to calculate risk and hazard
according to the basic equations presented earlier in Section 4.5. Background concentrations are
not explicitly considered.
As noted earlier, the points of maximum deposition rates for multiple PB-HAPs are assumed to
be co-located, and the subsistence farm family is assumed to eat fish from the surface water body
with the highest modeled concentrations.
4.7 A.I Reporting Results
A relatively simple summary can be used to report results, as long as it is consistent with the
need to make the results both transparent and reproducible. Examples of reports prepared for
EPA's purposes can be found in EPA's residual risk "test memos;" these may or may not be
appropriate examples for the specific purposes of other risk assessments. The summary
generally will include the following information:
Documentation of input parameters, output values, and risk characterization, with special
emphasis on comparing estimated risk/hazard to risk targets;
A simple presentation describing the assessment's purpose (e.g., to determine whether risk is
below levels of concern) and the outcome relative to that purpose (e.g., low risk is not
demonstrated); and
April 2004 Page 102
-------
Documentation of anything that is discretionary (i.e., anything that is facility-specific), such
as emissions characteristics or choice of a meteorological station other than the nearest.
4.7.4.2 Assessment and Presentation of Uncertainty
Risk managers need to understand the strengths and the limitations of the Tier 2 multipathway
risk assessment. A critical part of the risk characterization process, therefore, is an evaluation of
the assumptions, limitations, and uncertainties inherent in the Tier 2 assessment in order to place
the risk estimates in proper perspective.(3) Tier 2 assessments commonly include a quantitative
or qualitative description of the uncertainty for each parameter and indicating the possible
influence of these uncertainties on the final risk estimates given knowledge of the models used.
Tier 2 assessments also may include a semi-quantitative sensitivity analyses. These approaches
are described in Section III-5.4. Sensitivity analyses are discussed in more detail in Volume 1
(Chapters 3 and 13) of this reference library.
4.7.5 Potential Refinements of a Tier 2 Approach
If the results of the Tier 2 assessment indicate that risk targets are not met, the risk assessor has
the option of conducting a much more facility/source-specific, refined Tier 2 assessment using
the ISCST3 model and MPE methodology. Refinements might include characterizing the
modeling region in much greater detail and using exposure scenarios that are more realistic for
the facility/source setting (the exposure assessment for each scenario could still be based on the
basic equations found in the MPE methodology). Potential refinements might include:
Defining and assessing a "resident" scenario based on modeled deposition rates at locations
where people actually live (e.g., census tract internal points);
For the "subsistence farmer," (a) use an actual location of a farm within the study area (rather
than assuming it is located at the point of maximum deposition), (b) more realistically
incorporate only a subset of the potential pathways, and/or (c) assume that the farmer obtains
some of his/her food from other sources.
When summing exposures over multiple pathways, use high-end concentrations for some
pathways and central tendency concentrations for others.
Incorporating a limited monitoring program to evaluate key exposure estimates (e.g.,
concentrations of PB-HAPs in various food items).
A more complete listing of potential exposure scenarios is presented in Volume 1 (Part III) of
this reference library. EPA's Guidelines for Exposure Assessment discusses how to develop
these types of exposure scenarios.
April 2004 Page 103
-------
4.8 Tier 3 Multipathway Human Health Analysis
Note that the discussion in this section is based on information about the design of
TRIM.ExpoIngestion and might need to be modified in future versions of this document.
4.8.1 Introduction
This section describes an example approach for performing a Tier 3 multipathway risk
assessment. Exhibit 30 provides an overview of this example approach. This example Tier 3
assessment is significantly different than the Tier 2 example approach, in that it involves the use
of TRIM.FaTE for multimedia modeling, specific consideration of population locations, and the
use of an exposure model (TRIM.ExpoIngestion).
This example Tier 3 analysis allows considerable flexibility in analytical approach and detail.
For example:
TRIM.FaTE is used for multimedia modeling. This component of the TRIM modeling
system accounts for the movement of a chemical through a comprehensive system of discrete
compartments (e.g., media and biota) that represent possible locations of the chemical in the
physical and biological environments of the modeled ecosystem and provides an inventory,
over time, of a chemical throughout the entire system. TRIM.FaTE generates media
concentrations relevant to human ingestion exposures that can be used as input to
TRIM.ExpoIngestion. TRIM.FaTE allows considerable spatial refinement in selecting exposure
locations, and provides concentrations for user-specified (actual) locations.
TRIM.ExpoIngestion is used to estimate the ingestion intake rates used for the risk
characterization. Estimated media and fish concentrations needed by TRIM.ExpOjng^n are
provided by TRIM.FaTE. A farm food chain model (employing MPE equations(19)) will also
be available to provide livestock and produce contaminant estimates from air and soil
concentrations and air deposition estimates provided by TRIM.FaTE or from an external file.
A risk model (TRIM.Riskjjjj) is used to calculate cumulative excess cancer risk and
noncancer hazard associated with the modeled dietary intake estimates. TRIM.Riskjjjj
calculates human health risk metrics, documents model inputs and assumptions, and displays
results.
Monitoring data may be incorporated into the exposure assessment as inputs to
TRIM.Riskjjjj.
This example Tier 3 analysis is highly facility/source-specific and requires careful planning.
Where the assessment could support a regulatory decision, advance discussions with the
regulatory agency risk manager are strongly encouraged.
April 2004 Page 104
-------
Exhibit 30. Example Approach for a Tier 3 Multipathway Assessment
All PB-HAP Compounds
Multimedia Fate, Transport, Exposure, and Risk
Modeling
TRIM.FaTE; TRIM.Expolngestion; Trim.RiskHH
Site-specific inputs, if available
Central tendency and high-end exposures at each location
Deterministic or probabilistic analysis
Limited quantitative uncertainty analysis
Cumulative Cancer Risk Estimate
Sum across all carcinogens
Cumulative Noncancer Hazard Estimates
Separate analysis of chronic and acute
Sum across all noncarcinogens (HI)
Can sum by target organ (TOSHI)
Monitoring to evaluate
modeled concentrations
and exposures
Cumulative
Cancer Risk
Estimate At or Below
Target Level?
Potential
Risk
Reduction
Risk Targets Met
HI or TOSHI
At or Below
Target Level?
yes
April 2004
Page 105
-------
4.8.2 Fate and Transport Modeling
This example Tier 3 approach uses TRIM.FaTE for fate and transport modeling. Other models
could be used. Where the assessment could support a regulatory decision, the use of an
alternative model commonly is agreed to in advance with the regulatory agency decision-maker.
4.8.2.1 Model Inputs
The only facility-related/source term data points required by TRIM.FaTE are chemical emission
rate, location (i.e., latitude/longitude, UTM), and emission height, all of which should be
available from modeling performed for the inhalation risk assessment. TRIM.FaTE does all the
calculations internally for determining vapor/particle fractions and deposition rates based on
chemical-specific (vs. source-specific) properties. TRIM.FaTE also requires a number of input
variables which fall into the following general categories:
Source, meteorological, and other input parameters;
Chemical-dependent parameters for biotic compartment types;
Chemical-dependent parameters for abiotic compartment types;
Chemical-dependent parameters independent of compartment type;
Chemical-independent parameters for biotic compartment types; and
Chemical-independent parameters for abiotic compartment types.
These variables are described in Module 16 of the TRIM.FaTE User's Guide.(21) Note that the
values provided with the public Reference Library are to assist users in learning how to use
TRIM.FaTE and set up TRIM.FaTE scenarios. It remains each user's responsibility to confirm
or identify alternate values that are appropriate for their application and customize the library for
their use accordingly.
4.8.2.2 Model Runs
This subsection provides an overview of what's involved in performing a TRIM.FaTE
simulation. A more detailed description of how set up and run a TRIM.FaTE scenario is
provided in the TRIM.FaTE User's Guide.(21) Exhibit 31 illustrates the general process for
TRIM.FaTE modeling, including five general steps: (1) definition of scenario components; (2)
specification of links and algorithms; (3) specification of scenario and other property values; (4)
performing the simulation; and (5) analyzing results.
Definition of scenario components includes identifying the chemicals and sources to be
included (i.e., the facility/sources and PB-HAPs), determining the modeling region, and
specifying parcels, volume elements, and compartment types. Information to assist TRIM.FaTE
users in all aspects of designing the scenario is provided in the TRIM.FaTE User's Guide.,(21)
Additionally, the user will need to consider facility/source-specific information sources for each
application (e.g., National Land Cover Data at http://www.epa.gov/mrlc/nlcd.html - for parcel
set up).
April 2004 Page 106
-------
Exhibit 31. Developing and Executing a TRIM.FaTE Simulation
PROCESS FLOW
PRIMARY TOOLS
Define Scenario Components
Specify chemicals and sources
to be modeled
Specify modeling region
Specify volume elements
Specify compartments
Specify simulation period
Q.
2
Q.
Q.
re
V)
re
Specify Links and Algorithms
Specify links between
compartments
Specify algorithms where
required
Specify input data for links
Specify Scenario and
Other Properties
Set initial and boundary
conditions
Specify input data (i.e.,
properties for all objects)
Set simulation and output
time steps
INPUT VALUES
Spatial data
Meteorological and other
environmental setting data
Chemical properties
Source terms and
"background" data
Data pre-processors
ALGORITHM LIBRARY
Transfer factors
Perform Simulation
MODEL:
Updates property values for each
simulation or data time step
Calculates transfer factor for each link
Calculates moles distribution in
compartments at simulation time steps
Coverts moles to mass and concentration
Saves moles, masses, and
concentrations for output time steps
GENERAL CALCULATION TOOLS
Differential equation solver
Partial differential equation solver
Analyze Results
POST-PROCESSING TOOLS
Results averagers, aggregators
Visualization tools
April 2004
Page 107
-------
TRIM.FaTE Terminology
The modeling region encompasses the
geographical extent of the area to be modeled.
A parcel is a two-dimensional, horizontal
geographical area used to subdivide the modeling
region. Parcels can be virtually any size and
shape, are the basis for defining volume elements,
and do not change for a given scenario. There can
be separate parcels for air and for the land surface
(soil or surface water).
A volume element is a bounded, three-
dimensional space that defines the location of one
or more compartments.
A compartment is a unit of space within which it
is assumed that all chemical mass is
homogeneously distributed and is in phase
equilibrium.
The modeling region encompasses
the geographical extent of the area to
be modeled. The user should consider
factors such as the mobility of the PB-
HAPs, location of the facility/source,
location of sensitive populations, and
background concentrations of the PB-
HAPs. The results of inhalation
modeling may be helpful in evaluating
the predicted spatial pattern of
deposition.
Parcels are defined for the air and
land surface (soil and surface water).
Their individual and combined
boundaries do not need to line up. A
larger number of parcels in a given
scenario can provide higher spatial v '
resolution and/or greater aerial
coverage, but more parcels correspond to greater resource requirements for model set-up,
data collection, and model runs. There are three principal technical considerations for
determining the parcels:
- The likely pattern of transport and transformation of each PB-HAP (i.e., where
significant concentration gradients are likely to occur);
- The locations of natural and land use boundaries (e.g., airsheds and watersheds); and
- The locations of important environmental or biological receptors (e.g., human or
ecological cohorts, landscape components such as lakes or farms).
As noted in Volume 1 (Chapter 6), there are a number of EPA and other sources of
landscape, elevation, climate, and GIS data that can be used to help structure modeling runs.
Volume elements corresponding to each parcel are specified. Examples include air, surface
soil, root zone soil, vadose zone soil, surface water, and sediment. Volume elements add the
component of depth to each two-dimensional parcel. The volume elements are determined
based on various factors (e.g., mixing heights in air, average depth of and approximate
stratification of water bodies, typical demarcations of the soil horizon).
Compartments are determined and their property values set. Abiotic compartments are
assigned as appropriate to each volume element (e.g., each air volume element is assigned
one or more air compartments). Biotic compartments are assigned based on their occurrence
within the volume element as well as their influence on overall mass balance in the modeled
scenario and concentration in the compartments of interest in the assessment. The user has
flexibility in assigning biotic compartments (e.g., a single species can represent an entire
trophic group, or the user can specify a particular species of concern such as an endangered
species).
April 2004
Page 108
-------
The simulation period is determined. As noted with the Tier 2 analysis, this commonly
reflects the expected duration of emissions from the facility/source being evaluated. Note,
however, that the rate at which a modeled chemical accumulates in all compartments slows
with time, and for chemicals that degrade there may likely be a leveling off of concentration
by 30-40 years. Therefore, the duration selected also should reflect the time necessary for
the rates of accumulation in the media/biota of interest to slow to a negligible rate of increase
or cease. If information on accumulation rate is not available, the steady-state solution may
be an acceptable output. Some additional thought is required for this option during set-up,
but run time and the time needed to process results is reduced.
Specification of links and algorithms is the step in which links between compartments and sinks
are specified for a given scenario. Generally, adjacent abiotic compartments are linked to each
other, and compartments at the edge of the modeling region are linked to advection sinks. Biotic
compartments generally need to be linked to the appropriate abiotic and biotic compartments.
For example, each biotic compartment should be linked to all compartments that comprise its
diet or in any way provide it a source of chemical mass and all to which it passes mass. The
system of links is very important, because the links provide for the assignment of the algorithms
describing the processes that drive chemical transfer and transformation (e.g., with the current
set of library algorithms, TRIM.FaTE cannot simulate bioconcentration in benthic invertebrates
if that biotic compartment is not linked to the abiotic sediment compartment).
Specifying the scenario and other properties involves providing the remaining relevant input
values needed for the simulation. This involves specifying the chemical properties of each PB-
HAP being modeled, any initial distribution of chemical mass in the compartments, the data for
each modeled source, environmental data needed by the selected algorithms, and the simulation
and output time steps. A list of all the parameters associated with the current Reference Library
algorithms, which, to date, have been set to constant or time-varying numeric values (e.g., as
compared to equations or functions) is presented in Appendix D of Volume II of the TRIM.FaTE
Technical Support Document (http://www.epa. gov/ttn/fera/trim_fate.html).
Chemical-specific properties include molecular weight, melting point, half-life or
degradation rates, chemical transformation rates, and elimination rates.
Initial and boundary conditions (e.g., initial concentrations in specific media) can be
specified.
Source data include location, height, and emission rate.
Environmental setting data include meteorological data (at any or various time intervals),
data needed to define the characteristics of the biotic and abiotic compartments being
evaluated (e.g., soil density, current flow velocity, biomass per area, food ingestion rate), and
data needed to define properties of links between compartments (e.g., fraction of total surface
runoff from a soil compartment to an adjacent water compartment). Collecting these data
may be difficult and time-consuming.
The simulation time step specifies a minimum frequency at which the model will calculate
transfer factors and chemical mass exchange between (and transformed within)
April 2004 Page 109
-------
compartments. The output time step determines the points in time at which the amount of
chemical in each compartment will be reported as output as moles, mass, or concentration.
Performing the simulation is the actual running of the model.
Analyzing results is facilitated with several TRIM.FaTE tools:
The Averager can generate averages of TRIM.FaTE outputs in any multiple of the output
time step as well as in monthly and annual increments. It can also limit the compartments
included in the averaged file.
The Graphical Results Viewer presents model results (moles, mass, or concentration) on a
map of the parcels by using different colors to represent incremental gradients in the results
for a specific chemical.
The Aggregator can produce tables in HTML, text, or comma-delimited formats that
combine columns of output data in different ways for producing combined or comparative
statistics. Functions available for combining results include sum, average, difference, ratio,
and percent difference.
4.8.3 Exposure Assessment
This example Tier 3 exposure assessment
requires careful planning. Where the
assessment could support a regulatory
decision, advance discussions with the
regulatory agency risk manager are
encouraged. TRIM.ExpoIngestion provides a
more flexible way to assess exposure
scenarios for multipathway assessments.
.Expolngestlon is not available, risk
assessors can use TRIM.FaTE to calculate PB-
FIAP concentrations in media and biota and then
use the basic intake equations in the MPE
methodology to estimate exposure for each
specific scenario evaluated.
The initial version of TRIM.ExpoIngestion incorporates a scenario-based approach to exposure
assessment. It calculates dietary intake using the output from TRIM.FaTE modeling (e.g.,
concentrations) to calculate ingestion intake using the generic intake equation presented in
Section 4.3 above. TRIM.ExpoIngestion currently supports 13 exposure scenarios (Exhibit 32).
Within each scenario, TRIM.ExpOjng^n provides the flexibility to incorporate a variety of
assumptions regarding exposure duration (ED), exposure frequency (EF), and varying age
groups within the ED period (e.g., an individual exposed as both a child and an adult).
April 2004 Page 110
-------
Exhibit 32. Scenarios'3' Currently Supported by TRIM.ExpOj tion
Resident: Ingestionof soil and water
Resident Gardener: Ingestion of soil, water, home-grown fruits, vegetables and grains
Resident Fisher: Ingestion of soil, water, local fish
Resident Gardener Fisher: Ingestion of soil, water, home-grown fruits, vegetables and grains, and
local fish
Beef Farmer Fisher: Ingestion of soil, water, locally-produced fruits, vegetables and grains,
locally-produced beef, and local fish
Dairy Farmer Fisher: Ingestion of soil, water, locally-produced fruits, vegetables and grains,
locally-produced dairy, and local fish
Beef Farmer: Ingestion of soil, water, locally-produced fruits, vegetables and grains,
locally-produced beef
Dairy Farmer: Ingestion of soil, water, locally-produced fruits, vegetables and grains,
locally-produced dairy
Poultry Farmer: Ingestion of soil, water, locally-produced fruits, vegetables and grains,
locally-produced poultry
Egg Farmer: Ingestion of soil, water, locally-produced fruits, vegetables and grains,
locally-produced eggs
Pork Farmer: Ingestion of soil, water, locally-produced fruits, vegetables and grains,
locally-produced pork
Subsistence Beef Farmer: Same as beef farmer but fractions contaminated for fruits, vegetables,
grains, and beef is set to 1 rather than applying the "locally-produced" fractions contaminated
Subsistence Dairy Farmer: Same as dairy farmer but fractions contaminated for fruits, vegetables,
grains, and dairy is set to 1 rather than applying the "locally-produced" fractions contaminated
(a)Additionally, TRIM.Expo has the capability to assess infant exposures via the breast milk pathway for each/any
of the listed scenarios.
TRIM.ExpoIngestion can incorporate measured concentrations (from monitoring data) as inputs.
Because multimedia modeling involves many uncertainties, it may be helpful to implement a
monitoring program to evaluate or further characterize key concentrations (e.g., those that drive
the exposure estimate). Volume 1 (Chapter 19) provides an overview of multimedia modeling.
TRIM.ExpoIngestion provides outputs in the form of pollutant intake rate, oral intake rate, or
Average Daily Dose (ADD) for each exposure scenario modeled. A future version of
TRIM.ExpoIngestion will employ a population-based (vs. scenario-based) approach.
4.8.4 Risk Characterization
For this example Tier 3 approach, most risk estimates are calculated automatically by
TRIM.Riskjjjj, once the modeling scenarios are set up and run. The initial release of
TRIM.Riskjjjj will calculate a deterministic ingestion cancer risk and non-cancer hazard metrics
for the scenarios of interest.
This example Tier 3 approach considers background concentrations if these are a significant
potential concern for a particular assessment. Again, note that consideration of background may
April 2004 Page 111
-------
or may not be appropriate pursuant to the specific legal and regulatory authorities under which
the risk assessment is being conducted.
4.8.4.1 Reporting Results
The initial release of TREVI.Riskjjjj will provide a visualization tool for presenting analysis
results in various automated formats. The risk assessor may want to utilize this tool to assist
with development of the risk characterization summary, which generally will include the
following information:
Documentation of input parameters, outputs, and risk characterization, with special emphasis
on the range of risk or hazard estimates;
A simple presentation describing the assessment's purpose and the outcome relative to the
purpose (e.g., purpose: demonstrate that risk is below target levels; outcome: low risk not
demonstrated); and
Documentation of all key assumptions or other inputs used for the assessment, such as
emissions characteristics or choice of a nearby meteorological station. In particular, the
rationale used to define personal profiles and how they are modeled and analyzed, need to be
documented.
4.8.4.2 Assessment and Presentation of Uncertainty
Risk managers need to understand the strengths and the limitations of the Tier 3 multipathway
risk assessment. A critical part of the risk characterization process, therefore, is an evaluation of
the assumptions, limitations, and uncertainties inherent in the Tier 3 assessment in order to place
the risk estimates in proper perspective.(3) Tier 3 multipathway risk assessments may be
deterministic or probabilistic and commonly include semi-quantitative sensitivity analyses and
quantitative uncertainty analysis (described in Section III-5.4 above). The general quantitative
approach to propagating or tracking uncertainty through probabilistic modeling is described in
Volume 1 (Chapter 31) of this reference library.
April 2004 Page 112
-------
5.0 Ecological Risk Assessment
This section constitutes a snapshot of EPA's current thinking and approach to the adaptation of the
evolving methods of ecological risk assessment to the context of Federal and state control of air
toxics. While inhalation risk assessment has been increasingly used in regulatory contexts over the
last several years, ecological risk assessment tools are less well developed and field tested in a
regulatory context. This section should be considered a living document for review and input. By
publishing this portion of Volume 2 in its current state of development, EPA is soliciting the
involvement of persons with experience in this field to help improve these assessment methods for
use in a regulatory context. EPA anticipates revisions to this draft section of Volume 2 on the basis
of this input.
This section describes an example approach for performing facility/source-specific ecological
risk assessments. In this example approach, ecological risk assessments are performed when air
toxics that persist and which also may bioaccumulate or biomagnify in food chains (e.g., the PB-
HAP compounds) are present in emissions; however, other factors such as state and local
regulations may need to be considered in determining whether an ecological risk assessment is
appropriate for a particular facility/source. Readers unfamiliar with ecological risk assessment
are encouraged to consult the more general description of ecological risk assessment that is
presented in Part IV of Volume 1.
5.1 Introduction and Overview
The ecological risk assessment process has three main phases that correspond to the three phases
of the human health risk assessment methodology:(30)
Planning, scoping, and problem formulation, which focuses on identifying the ecological
risk management goals, ecological receptors of concern, and assessment endpoints (explicit
expression of the environmental value that is to be protected, operationally defined by an
ecological entity and its attributes).
Analysis includes characterization of ecological effects for the PB-HAPs present in
emissions from the facility/source. A distinction is made between assessment endpoints,
which are the environmental values to be protected, and measures of effects, which are the
specific metrics used to evaluate risk to the assessment endpoints. Common measures of
effects include ecological toxicity reference values (Exhibit 33), which are discussed in more
detail in Volume 1, Chapter 25. Analysis also includes characterization of direct exposures
(e.g., estimated concentrations in abiotic media) or indirect exposures (based on dietary
intake). Quantification of exposure via ingestion is similar to that for human health ingestion
analyses, except that different food items may be involved, and the appropriate ecological
exposure factors (e.g., diet, body weight) will be different.
For this example approach, ecological effects analysis is limited to primary effects (e.g.,
lethality, reduced growth, neurological/behavioral and impaired reproduction) result from
exposure of aquatic and terrestrial organisms to air toxics. An example of a chronic primary
April 2004 Page 113
-------
effect would be reduced reproduction in a fish species exposed to air toxics in a surface water
body or mortality in a terrestrial bird eating contaminated fish from a small pond. Secondary
effects (e.g., loss of prey species in the community) resulting from the action of air toxics on
supporting components of the ecosystem are not included in this example approach.
However, such effects could be examined in a Tier 3 analysis.
Ecological risk characterization generally involves integration of exposure and
stressor-response profiles with a summary of assumptions, scientific uncertainties, and
strengths and limitations of the analyses. The final product is a risk description presenting
the results of the integration, including an interpretation of ecological adversity and
descriptions of lines of evidence. For the present purposes, risk characterization is often
done more narrowly, comparing estimated media concentrations, dietary intake levels, or
body burdens to ecological toxicity reference values using the hazard quotient or hazard
index approach. Ecological risk characterization is described in more detail in Section 5.2
below.
Exhibit 33. Commonly Used Point Estimates
Median effect concentrations or doses (acute exposures)
LC50 Concentration (food or water) resulting in mortality in 50 percent of the exposed organisms
LD50 Dose (usually in dietary studies) resulting in mortality in 50 percent of the exposed organisms
EC50 Concentration resulting in a non-lethal effect (e.g., growth, reproduction) in 50 percent of the
exposed organisms
ED50 Dose resulting in a non-lethal effect (e.g., growth, reproduction) in 50 percent of the exposed
organisms
Low- or no-effect concentrations or doses (chronic exposures)
NOAEL no-observed-adverse-effect-level, the highest dose for which effects are not statistically
different from controls
LOAEL lowest-observed-adverse-effect level, the lowest dose at which effects are statistically
different from controls
NOEC no-observed-effect-concentration, the highest ambient concentration for which adverse
effects are not statistically different from controls
LOEC lowest-observed-effect concentration, the lowest ambient concentration at which adverse
effects are statistically different from controls
MATC maximum acceptable toxicant concentration, the range of concentrations between the
LOEC and NOEC
GMATC geometric mean of the MATC, the geometric mean of the LOEC and NOEC
April 2004
Page 114
-------
5.2 Ecological Risk Characterization
A common approach for characterizing ecological risks is the Hazard Quotient (HQ) approach
(also referred to as the "quotient method"), which is similar to that used for human noncancer
health risk assessment. In this approach, modeled or measured concentrations of the chemical in
each environmental medium are divided by the appropriate ecological toxicity reference value
(TRV) to yield a HQ for an individual chemical.
Oral Intake EEC BB
or H=- or
where:
HQ = hazard quotient.
Oral Intake = estimated or measured contaminant intake relevant to the oral intake-based
ecological toxicity reference value (usually expressed as mg/kg-day).
TRV = ecological toxicity reference value. This may be in terms of oral intake,
media concentration, or body burden. As described elsewhere, it may be a
result of a single study (e.g., NOAEL) or the result of integration of multiple
studies (e.g., water quality criterion).
EEC = estimated or measured environmental media concentration at the exposure
point (usually expressed as mg/L for water and mg/kg for soil and sediment).
BB = estimated or measured body burden (usually expressed as mg/kg wet weight).
As with human health assessments, it is important that the measure of oral intake, EEC, or BB be
in the same units as the ecological toxicity reference value to which the measure is being
compared.
When ecological toxicity data for complex mixtures are unavailable, the hazard index (HI)
approachฎ may be used, as scientifically appropriate, to integrate the ecological risks due to
simultaneous exposure to multiple air toxics.
If the HI approach is used, the assumptions and associated limitations concerning air toxic
interactions should be clearly documented. It may often be the case that a single chemical is
responsible for the HI exceeding one, and the assessment can then focus on that chemical. In
more refined assessments, the scientific integrity of assumptions inherent in the use of the HI
will need to be carefully evaluated.
More complex approaches are available for characterizing ecological risks, as noted in Volume 1
(Part IV) of this reference library. If the risk assessment involves a regulatory decision, the risk
assessor is encouraged to discuss any of these proposed approaches with the appropriate
regulatory authorities prior to the analysis.
The HI approach is termed the "quotient addition approach" in EPA's Guidelines for Ecological Risk
Assessmentฎ^
April 2004 Page 115
-------
Some Important Differences Between Ecological Risk Assessment and
Multipathway Human Health Risk Assessment
Planning and scoping. The ecological risk assessment requires more preliminary analysis and
deliberation regarding endpoints to be assessed and toxicity reference values to be used, because
ecological systems are more complex and not as well understood biologically as are human health
systems. The planning and scoping team should include individuals with specific expertise in
ecological risk assessment.
Assessment area. It may be necessary to evaluate additional portions of the assessment area that
are not of concern from a human health perspective.
Potentially exposed populations. The focus shifts from potentially exposed groups of humans to
potentially exposed populations and species of ecological receptors of concern. In many cases, the
exposure assessment may need to address multiple species and life-stages, many of which have
physiological and biochemical processes that differ significantly from humans. (When threatened
or endangered species are present, the assessment may also include an evaluation of those
organisms as individuals).
Exposure pathways and exposure routes. It may be necessary to assess different exposure
pathways and routes that are not of concern for human health.
Ecological effects assessment. Ecological systems have traits and properties that are different
from humans and, thus, the ecological effects assessment (comparable to hazard assessment for
human health) may consider a wider range of potential causal relationships.
Risk characterization. While risks may be assessed at multiple levels of ecological organization
(i.e., organism, population, community, and ecosystem), they generally are assessed at the
population level in air toxics assessments. (Nevertheless, when appropriate, consideration should
be given to assessments as high levels of ecological organization, such as at the landscape level).
Ecological risk assessments are subject to additional sources of uncertainty and variability as
compared to multipathway human health risk assessments. In addition to the uncertainties
associated with multimedia modeling and sampling, the ecological risk assessment involves
many decisions regarding choice of ecological receptors of concern and associated assessment
endpoints and measures of effects. Some of these receptors may be at levels of organization
above individual species (e.g., communities, ecosystems), where stressor-response relationships
are poorly defined, characterized, and/or understood (e.g., air toxics effects on loss of
community prey species mentioned in Section 5.1). Because many different species and higher
taxonomic groups may be included in the assessment, selection of many parameter values such
as bioconcentration factors, dose-response values, and dietary intake is more complex and
uncertain for the ecological risk assessment as compared to the human health multipathway risk
assessment.
April 2004 Page 116
-------
5.3 Tier 1 Ecological Analysis
(reserved)
5.4 Tier 2 Ecological Analysis
5.4.1 Introduction
This section describes an example approach for performing a Tier 2 ecological risk assessment.
Exhibit 34 provides an overview of this example approach. In this example approach, ISCST3 is
used to provide deposition rates to soils and surface waters, and the MPE methodology is used to
estimate PB-HAP concentrations in abiotic media (soils, surface waters, sediments) and wildlife
food items (fish) at the most impacted location. These concentrations are compared to applicable
ecological toxicity reference values to provide a conservative estimate of ecological risk to be
calculated. If the facility/source passes this screening analysis, the risk manager can be
reasonably confident that significant ecological risk is unlikely. As a consequence, monitoring is
not included explicitly in this example Tier 2 ecological analysis (although available monitoring
data can be used as inputs to the ecological exposure analysis)
5.4.2 Fate and Transport Modeling
This example approach uses the ISCST3 model for the Tier 2 fate and transport modeling.
5.4.2.1 Model Inputs
This example approach uses the same model inputs that were used for the example Tier 2 human
health multipathway assessment.
5.4.2.2 Model Runs
This example approach uses the same model runs that were used for the example Tier 2 human
health multipathway assessment.
Defining receptor locations
For this example Tier 2 analysis, terrestrial ecological receptors are assumed to occur at the
modeling location ("node") with the maximum deposition rate as determined in the example Tier
2 human health multipathway assessment.
If multiple PB-HAPs are present, the point where maximum deposition occurs for each
individual PB-HAP may not be in the same location. This example approach assumes that
these are all co-located (see Section 5.4.4 below).
The point where maximum deposition occurs is used for terrestrial exposure pathways.
April 2004 Page 117
-------
For surface water pathways, this Tier 2 analysis is based on the surface water body within the
assessment area where maximum concentrations occur. This was determined in the example
Tier 2 human health multipathway analysis described earlier.
Exhibit 34. Example Approach for a Tier 2 Ecological Assessment
All PB-HAP Compounds
Multimedia Modeling
ISCST3
Site-specific model inputs
High production year
Ecological Risk Estimate
Surface waters (fresh and/or salt)
Sediments
Soils
Wildlife
Terrestrial plants
Qualitative uncertainty analysis
Ecological
Hazard Quotient
or Hazard Index
At or Below
Target Level?
Go to Tier 3
>
yes
f
1 Risk Targets Met
April 2004
Page 118
-------
Defining the duration of emissions
This example approach uses the same duration of emissions that was used for the example Tier 2
human health multipathway analysis.
Defining deposition/flux rates for estimating media concentrations
This example approach uses the same deposition/flux rates that were used for the example Tier 2
human health multipathway analysis.
Model outputs to use
This example approach uses the same average annual deposition rates that were used for the
example Tier 2 human health multipathway analysis as inputs to the MPE methodology.
5.4.3 Exposure Assessment
5.4.3.1 Characterization of Ecological Receptors
This example Tier 2 assessment uses generic ecological receptors. In other words, modeled
concentrations of PB-HAPs in abiotic media and biota are compared to ecological toxicity
reference values protective of the following groups of organisms: soil-dwelling biota, terrestrial
plants, terrestrial animals, aquatic organisms, and sediment-dwelling biota. Note that EPA's
ambient water quality criteria are protective of aquatic ecosystems (see Exhibit 35 below).
5.4.3.2 Defining the Point of Maximum Exposure
This example approach uses the same exposure locations used for the example Tier 2 human
health multipathway analysis.
For a single PB-HAP compound, the point of maximum exposure is defined as the modeled
location (node) at which the highest deposition rate occurs (soils) and the surface water body
with maximum modeled concentrations.
For multiple PB-HAP compounds, the point of maximum exposure is defined by assuming
that the point of maximum exposure occurs at the same location for each PB-HAP compound
(i.e., exposure for each compound is added to calculate total exposure).
5.4.3.3 Calculation of Exposure Concentration
This example approach uses the following concentrations estimated for the example Tier 2
multipathway human health assessment:
Maximum concentrations in soil, surface water, and sediment; and
Maximum concentration in fish.
April 2004 Page 119
-------
Note that existing monitoring data may be used to evaluate or refine the exposure estimates
based on multimedia modeling. Volume 1 provides an overview of multimedia monitoring
(Chapter 19) and additional discussion of monitoring for ecological exposure analysis (Chapter
24).
5.4.3.4 Determining Intake
Ecological toxicity reference values for some PB-HAPs incorporate assumptions about wildlife
intake. For those substances, no additional calculations are required to determine intake. For
the remaining PB-HAPs, it will be necessary to determine intake. Equations and exposure
factors used to calculate intake are found in EPA's Wildlife Exposure Factors Handbook.^
5.4.4 Risk Characterization
This example approach considers three types of comparisons:
Comparison of modeled concentrations in soils, surface waters, and sediments to ecological
toxicity reference values for each medium;
Comparison of dietary intake levels for terrestrial birds and mammals to ecological toxicity
reference values for wildlife ingestion; and
Comparison of estimated body burdens in fish to ecological toxicity reference values that
relate body burdens to adverse ecological impacts.
For these comparisons, three general types of ecological toxicity reference values are applicable
(Exhibit 3 5):
Toxicity reference values that relate concentrations of PB-HAPs in abiotic media (e.g., soil,
sediment) to adverse effects (these may be available at the species- or community-level);
Toxicity reference values that relate dietary intake levels of PB-HAPs to adverse effects
(e.g., in birds and mammals); and
Toxicity reference values that relate concentrations of PB-HAPs in biota (i.e., body burdens)
to adverse effects in those biota. These generally have to be derived based on oral toxicity
data and assumptions about wildlife exposure factors.
April 2004 Page 120
-------
Exhibit 35. Sources of Ecological Toxicity Reference Values (TRVs) or Benchmarks
Data Source
Freshwater
Saltwater
Sediment
Soil/
Terrestrial
Reference
TRVs or benchmarks based on ambient concentrations
EPA
Ambient
Water
Quality
Criteria
X
X
EPA has developed national recommended water quality criteria for
the protection of aquatic life for approximately 150 pollutants. These
criteria are published pursuant to Section 304(a) of the Clean Water
Act (CWA) and provide guidance for States and Tribes to use in
adopting water quality standards under Section 303(c) of the CWA.
Source: http://www.epa.gov/waterscience/criteria/aqlife.html
Sediment
Quality
Criteria
X
EPA and other agencies have developed sediment quality criteria for
the protection of benthic communities. These criteria are highly
specific to regions and bodies of water in the U.S. Regional experts
are the recommended source for appropriate facility/source-specific
criteria.
NOAA
Screening
Quick
Reference
Tables
(SQuiRTs)
X
X
X
X
NOAA has developed a set of Screening Quick Reference Tables, or
SQuiRTs, that present screening concentrations for inorganic and
organic contaminants in soil, sediment, and surface water. The
SQuiRTs also include guidelines for preserving samples and
analytical technique options. Note that sediment SQuiRTs may not
be appropriate to facility/source-specific bodies of water; consultation
with regional experts is recommended.
http://response.restoration.noaa.gov/cpr/sediment/squirt/squirt.html.
April 2004
Page 121
-------
Exhibit 35. Sources of Ecological Toxicity Reference Values (TRVs) or Benchmarks
Data Source
Freshwater
Saltwater
Sediment
Soil/
Terrestrial
Reference
Great Lakes
Criteria
X
The GLWQI Tier II criteria and SCV have received some peer review
prior to publication, and 12 of them are included in the HWIR, which
underwent public comment before promulgation. The GLWQI Tier II
methodology calculates SCV in a similar way to FCV, but uses
statistically derived "adjustment factors" and has less rigorous data
requirements.
Tier II Criteria are designed to be protective of aquatic
communities
SCV are designed to measure chronic toxicity to aquatic
organisms
Source: Ecotox Thresholds ECO Update (volume 3, No. 2, January
1996, EPA/540/F-95/038).
EPA Soil
Screening
Levels
X
EPA has developed a methodology and initial soil screening levels
protective of ecological receptors. Source: United States
Environmental Protection Agency. 2000. Ecological Soil Screening
Guidance (Draft). Office of Emergency and Remedial Response,
Washington, D.C., July 2000.
http://www.epa.gov/superfund/programs/risk/ecorisk/ecossl.htm.
EPA Region
4 Soil
Screening
Levels
X
Source: U.S. Environmental Protection Agency 1995. Supplemental
Guidance to RAGS: Region 4 Bulletins No. 2. Ecological Risk
Assessment. Region IV, Waste Management Division.
http://www.epa.gov/region04/waste/ots/ecolbul.htm
April 2004
Page 122
-------
Exhibit 35. Sources of Ecological Toxicity Reference Values (TRVs) or Benchmarks
Data Source
Netherlands
target values
Freshwater
Saltwater
Sediment
Soil/
Terrestrial
X
Reference
The Netherlands bases the prevention and remediation of
contaminated soil on its Soil Protection Act. Target, limit, and
intervention values have been established for soil and groundwater as
part of a general framework of risk-based environmental quality
objectives. Target values represent background concentrations in
which risk is considered negligible. If target values are currently not
met, limit values may be applied to define general concentrations
which must be attained. Source:
http : //www .contaminatedland . co .uk/std-2uid/dutch-l .htm
TRVs or benchmarks based on body burdens (tissue concentrations)
USAGE/
EPA ERED
X
X
The U.S. Army Corps of Engineers/U.S. Environmental Protection
Agency Environmental Residue-Effects Database (ERED) is a
compilation of data, taken from the literature, where biological effects
(e.g., reduced survival, growth, etc.) and tissue contaminant
concentrations were simultaneously measured in the same organism.
Currently, the database is limited to those instances where biological
effects observed in an organism are linked to a specific contaminant
within its tissues. Source: http://www.wes.army.mil/el/ered/index.html
April 2004
Page 123
-------
Exhibit 35. Sources of Ecological Toxicity Reference Values (TRVs) or Benchmarks
Data Source
Freshwater
Saltwater
Sediment
Soil/
Terrestrial
Reference
Toxicity data that can be used to derive TRVs or benchmarks for dietary intake
ECOTOX
CAL-Ecotox
X
X
X
X
X
X
X
X
ECOTOX is a source for locating single chemical toxicity data for
aquatic life, terrestrial plants and wildlife. ECOTOX was created and
is maintained by EPA's Office of Research and Development and the
National Health and Environmental Effects Research Laboratory's
Mid-Continent Ecology Division. ECOTOX is a source for locating
single chemical toxicity data from three EPA ecological effects
databases: AQUIRE, TERRETOX, and PHYTOTOX. AQUIREand
TERRETOX contain information on lethal, sublethal and residue
effects. AQUIRE includes toxic effects data on all aquatic species
including plants and animals and freshwater and saltwater species.
TERRETOX is the terrestrial animal database. It primarily focuses on
wildlife species but the database does include information on domestic
species. PHYTOTOX is a terrestrial plant database that includes
lethal and sublethal toxic effects data.
Source: http://www.epa.gov/ecotox.
The California Wildlife Biology, Exposure Factor, and Toxicity
Database (Cal/Ecotox) is a compilation of ecological, physiological
data, and toxicity data for a number of California mammals, birds,
amphibians and reptiles, http : //www . oehha. ca. gov/cal_ecotox
April 2004
Page 124
-------
Exhibit 35. Sources of Ecological Toxicity Reference Values (TRVs) or Benchmarks
Data Source
Freshwater
Saltwater
Sediment
Soil/
Terrestrial
Reference
ORNL
Toxicity
databases
X
Oak Ridge National Laboratory has developed toxicity reference
values for soils protective of terrestrial plants, soil and litter
invertebrates, and terrestrial wildlife. Sources:
Efroymson, R.A., M.E. Will, G.W. Suter II, and A.C. Wooten. 1997.
Toxicological Benchmarks for Screening Contaminants of Potential
Concern for Effects on Terrestrial Plants: 1997 Revision. Prepared for
the U.S. Department of Energy, Office of Environmental
Management. Oak Ridge National Laboratory, Oak Ridge, TN.
ES/ER/TM-85/R3.
http://www.hsrd.ornl.gov/ecorisk/tm85r3.pdf
Efroymson, R.A., M.E. Will, and G.W. Suter II. 1997. Toxicological
Benchmarks for Contaminants of Potential Concern for Effects on Soil
and Litter Invertebrates and Heterotrophic Process: 1997 Revision.
Prepared for the U.S. Department of Energy, Office of Environmental
Management. Oak Ridge National Laboratory, Oak Ridge, TN.
ES/ER/TM-126/R2. http://www.hsrd.ornl.gov/ecorisk/tm 126r21 .pdf
Efroymson, R.A., G.W. Suter II, B.E. Sample, and D.S. Jones 1997.
Preliminary Remediation Goals for Ecological Endpoints. Prepared
for the U.S. Department of Energy, Office of Environmental
Management. Oak Ridge National Laboratory, Oak Ridge, TN.
ES/ER/TM-162/R2. http://www.hsrd.ornl.gov/ecorisk/tm 162r2.pdf
April 2004
Page 125
-------
Exhibit 35. Sources of Ecological Toxicity Reference Values (TRVs) or Benchmarks
Data Source
ECOSAR
Freshwater
X
Saltwater
X
Sediment
Soil/
Terrestrial
Reference
ECOSAR is a computer program that uses structure-activity
relationships (based on available data) to predict the acute and chronic
toxicity of organic chemicals to aquatic organisms. ECOSAR
provides quantitative estimates of chronic values (e.g., GMATC),
acute LC50 values, and acute EC50 values for industrial chemicals for
several aquatic species (e.g., fish, daphnia, green algae, mysids).
When the estimated aquatic toxicity reference value exceeds the water
solubility of the compound, the estimated value is flagged; this
situation generally is interpreted to mean that the chemical has no
toxic effects in a saturated solution.
Source: htto://www.epa.sov/oppt/newchems/2 lecosar.htm
April 2004
Page 126
-------
5.4.4.1 Reporting Results
For this example approach, a relative simple summary can be used to report results, as long as it
is consistent with the need to make the results both transparent and reproducible. The summary
generally will include the following information:
Documentation of input parameters, output values, and risk characterization, with special
emphasis on comparing estimated risk/hazard to risk targets;
A simple presentation describing the assessment's purpose (e.g., to determine whether risk is
below levels of concern) and the outcome relative to that purpose (e.g., low risk is not
demonstrated); and
Documentation of anything that is discretionary (i.e., anything that is facility-specific), such
as emissions characteristics or choice of a meteorological station other than the nearest.
5.4.4.2 Assessment and Presentation of Uncertainty
Risk managers need to understand the strengths and the limitations of the Tier 2 ecological risk
assessment. A critical part of the risk characterization process, therefore, is an evaluation of the
assumptions, limitations, and uncertainties inherent in the Tier 2 assessment in order to place the
risk estimates in proper perspective.(3) Tier 2 ecological assessments commonly include a
quantitative or qualitative description of the uncertainty for each parameter and indicating the
possible influence of these uncertainties on the final risk estimates given knowledge of the
models used. Tier 2 assessments also may include a semi-quantitative sensitivity analyses.
These approaches are described in Section III-5.4 above. Sensitivity analyses are discussed in
more detail in Volume 1 (Chapters 3 and 13) of this reference library.
April 2004 Page 127
-------
5.5 Tier 3 Ecological Analysis
5.5.1 Introduction
This section describes an example approach for performing a Tier 3 ecological risk assessment.
Exhibit 36 provides an overview of this example approach. This example Tier 3 assessment is
significantly different than the Tier 2 example approach, in that it involves the use of
TRIM.FaTE for multimedia modeling, specific consideration of ecological receptor locations,
and use of a risk model (TRIM.RiskEco) to provide a more refined characterization of risk,
including multiple estimates of risk.
This example Tier 3 analysis allows considerable flexibility in analytical approach and detail.
In this example approach, TRIM.FaTE is used for multimedia modeling and generates
concentrations in abiotic media, body burdens, and wildlife intake rates that feed directly into
TRIM.RiskEco for ecological risk characterization. TRIM.FaTE allows considerable spatial
refinement in selecting exposure locations, and provides concentrations for user-specified
(actual) locations.
In this example approach, a risk model (TRIM.RiskEco) is used to characterize ecological risk.
This module performs ecological risk characterization calculations for multimedia ecological
risk assessments of toxic air pollutants or other chemical contaminants. The output of
TRIM.RiskEco are hazard quotients (HQ) that can be processed with TRIM.Risk analysis
tools to prepare tables and charts that can be used in communicating the risk assessment
results.
In this example approach, monitoring data are used to evaluate or further characterize key
concentration data.
Exhibit 37 illustrates how the TRIM modules and data correspond to EPA's ecological risk
assessment framework as described in the Framework for Ecological Risk Assessment.(32)
Guidance for how to structure TRIM analyses for ecological risk assessment is provided in the
TRIM.RiskEco User's Guide.(33} This example Tier 3 analysis will be highly facility/source-
specific and will require careful planning.
April 2004 Page 128
-------
Exhibit 36. Example Approach for a Tier 3 Ecological Assessment
All PB-HAP Compounds
Multimedia Modeling
TRIM.FaTE
High production year
Site-specific model inputs
Abiotic concentrations, dietary intake, or
body burdens as outputs
Ecological Risk Estimate
TRIM.RiskEco
Hazard Quotient Approach
Consideration of Secondary Effects
Qualitative or quantitative uncertainty analysis
Ecological
Hazard At or Below
Target Level?
Monitoring to evaluate
modeled concentrations
and exposures
Potential Risk Reduction
Risk Targets Met
April 2004
Page 129
-------
Exhibit 37. TRIM Modules in the Context of EPA's Framework for Ecological Risk Assessment
Ecological Risk Assessment Using TRIM
Planning
Problem Formulation
(e.g., Conceptual Model, TRIM.FaTE Set Up Decisions)
v>
'
Characterization
It
3 <
O ฃ
o O
r: of Exposure
Characterization
of Ecological
Effects
TRIM.FaTE
(A 0)
ฃ t3
5
re
O
TRIM Ecological
Effects Database
Communicating Results
to the Risk Manager
Risk Management and
Communicating Results
to Interested Parties
Ecological
Risk Results
(Tables,
Charts,
Figures)
CD
O
CD
CD
*<
Q.
CD
CD
CO-
ST
T3
O
O
CD
O
3
o"
CD
April 2004
Page 130
-------
5.5.2 Identification of Potentially Exposed Populations
For this example approach, potentially exposed populations (ecological receptors of concern)
may be defined at the species and/or community level (Exhibit 38). Within these general
categories, users have considerable flexibility in defining ecological receptors. For example, the
analysis could focus on a particular species (e.g., a mink), or the species could be used as a
surrogate for an entire trophic group (e.g, terrestrial carnivores). Specific receptors may be of
concern for a variety of reasons, including:
The receptor (or one of it's life stages) is particularly vulnerable to or sensitive to one or
more PB-HAP compounds;
The receptor (usually a species or a community such as a wetland) is listed as endangered or
threatened or is otherwise given special legal protection by the state or federal government;
The receptor plays an important part in the overall structure or function of the ecological
community or ecosystem; and/or
The receptor is of particular economic or cultural value to local populations.
Exhibit 38. Potential Ecological Receptors of Concern
Species-level
Community -level
Terrestrial plants
Terrestrial invertebrates
soil -dwelling (e.g., earthworms)
surface-dwelling
Terrestrial vertebrates
birds
mammals
reptiles
amphibians
Aquatic plants
Aquatic invertebrates
sediment-dwelling
benthic
pelagic
Aquatic vertebrates
fish
(reptiles)
(amphibians)
Aquatic communities
Wetland communities
April 2004
Page 131
-------
Often it is important to understand the aquatic and terrestrial food webs in the habitats of
concern, because these can be important parts of ecological exposure pathways. Top predators
are often of special concern for exposure to PB-HAP compounds.
For this example approach, ecological receptors for each habitat potentially impacted are
identified to ensure (1) plant and animal communities representative of the habitat are
represented by the habitat-specific food web, and (2) potentially complete exposure pathways are
identified. Ecological receptor identification may need to include species both known and
expected to be present in a specific habitat being evaluated, and include resident and migratory
populations. Consultation with ecological experts is encouraged (see Volume 1, Chapter 23).
5.5.3 Assessment Endpoints and Measures of Effect
As discussed in Volume 1 of this reference library (Chapter 23), an assessment endpoint is an
explicit expression of the "actual environmental value that is to be protected" or is of concern. It
includes the identification of the ecological entity for the analysis (e.g., a species, ecological
resource, habitat type, or community) as well as the attribute of that entity that is potentially at
risk (e.g., reproductive success, production per unit area, surface area coverage, biodiversity) and
that is important to protect. Measures of effects are the metrics by which these endpoints are
assessed.(30) EPA has recently released guidance that describes a set of endpoints, known as
Generic Ecological Assessment Endpoints (GEAE), that can be considered and adapted for
specific ecological risk assessments (Exhibit 39).(34)
Where ecological effects information is available, TRIM.RiskEco allows the user to select (or
input) multiple measures of effects for a given ecological receptor. For example, different
toxicity reference values (TRVs) may be available for the same species that are associated with
different measures of effects (e.g., reproductive effects, respiration, mortality). Volume 1
(Chapter 25) provides a discussion on the selection of TRVs for a particular assessment.
Where available ecological toxicity reference values do not consider secondary effects (e.g., on
communities), it may be possible to use TRIM.RiskEco outputs as a starting point for evaluating
secondary effects, either qualitatively or quantitatively. For this example Tier 3 assessment, risk
assessors are encouraged to include secondary effects as assessment endpoints to the extent that
resources and information allows.
April 2004 Page 132
-------
Exhibit 39. Generic Ecological Assessment Endpoints(a)
Entity
Attribute
Organism-level endpoints
Organisms (in an assessment
population or community)
Kills (mass mortality,
conspicuous mortality)
Gross anomalies
Survival, fecundity, growth
Population-level endpoints
Assessment population
Extirpation
Abundance
Production
Identified EPA Precedents
Vertebrates
Vertebrates, shellfish, plants
Endangered species, migratory
birds, marine mammals, bald
and golden eagles, vertebrates,
invertebrates, plants
Vertebrates
Vertebrates, shellfish
Vertebrates (game/resource
species), harvested plants
Community and ecosystem-level endpoints
Assessment communities,
assemblages, and ecosystems
Taxa richness
Abundance
Production
Area
Function
Physical structure
Aquatic communities, coral reefs
Aquatic communities
Plant assemblages
Wetlands, coral reefs,
endangered/rare ecosystems
Wetlands
Aquatic ecosystems
Officially designated endpoints
Critical habitat for endangered
or threatened species
Special places
Area
Quality
Ecological properties that
relate to the special or legally
protected properties
e.g., National Parks, National
Wildlife Refuges, Great Lakes
(a)Generic ecological assessment endpoints for which EPA has identified existing policies and precedents (in
particular, the specific entities listed in the third column). Bold indicates protection by federal statute.
Source: EPA's Generic Ecological Assessment Endpoints (GEAE) for Ecological Risk Assessment
April 2004
Page 133
-------
5.5.4 Fate and Transport Modeling
This subsection provides an overview of TRIM.FaTE set up and execution. This is explained
more fully in section 4.8.2 and in the TRIM.FaTE User's Guide(2l)
The modeling region encompasses all areas where ecological receptors are known or likely
to occur, especially any important receptors such as wetlands, endangered/threatened species,
or areas that are particularly important to regional populations (e.g., wintering areas,
migration routes, breeding grounds).
Parcels are defined to adequately provide an assessment of exposures at the locations where
the ecological receptors identified above occur.
Volume elements are defined to include all potential routes of ecological exposure (e.g., root
zone soil for earthworms).
Compartments can be defined in a flexible manner depending on the level of detail in which
ecological receptors are characterized for the analysis. For example, a single species (e.g.,
lake trout) could be used as a surrogate for all higher-trophic level fish, or the analysis could
identify several multiple species of higher-trophic level fish.
Links and algorithms should incorporate the processes that drive chemical transfer and
transformation that are relevant to the ecological exposure assessment.
As noted above, the TRIM.FaTE model runs may be set up and performed along with the
Tier 3 human health model runs.
Results can be processed with TRIM.Risk analysis or other tools to prepare tables and charts
that can be used in communicating the risk assessment results.
5.5.5 Exposure Assessment
TRIM.FaTE provides three general metrics of ecological exposure (Exhibit 40): ambient
concentrations in abotic media, ingestion intake levels for specified receptors, and body burdens.
Each of these can be compared with a corresponding ecological toxicity reference value for risk
characterization. Intake and body burdens are calculated for specific ecological receptors
specified in the model setup, although these receptors may be matched with TRVs for surrogates,
as appropriate, in TRIM.RiskEco.
The user can specify the specific time points of interest of the TRIM.FaTE exposure simulation
to be compared with each type of ecological toxicity reference values.
April 2004 Page 134
-------
Exhibit 40. TRIM Metrics of Ecological Exposure and Metrics of Ecological Effects
Metrics of Ecological Exposure
Available from TRIM.FaTE
Ambient concentrations in abiotic compartments
of interest (i.e., soil, water, air, and sediment
concentrations)
Ingestion intake (on a mass per mass and time
basis) for ecological receptor(s) of interest
Whole-body concentrations in biotic
compartments of interest (i.e., body burdens)
Corresponding Ecological Toxicity reference
value Available in the TRIM Ecological
Effects Database
Abiotic media concentrations associated with
adverse effects
Biota oral intake (on a mass per mass and time
basis) associated with adverse effects
Body burden concentrations associated
with adverse effects
Because ecological exposure assessments are subject to many sources of uncertainty and
variability (e.g., uncertainties associated with multimedia modeling; choice of ecological
receptors of concern and associated assessment endpoints and measures of effects), it may be
helpful to incorporate a multimedia monitoring program to evaluate or refine the exposure
estimates based on multimedia modeling. Volume 1 provides an overview of multimedia
monitoring (Chapter 19) and additional discussion of monitoring for ecological exposure analysis
(Chapter 24).
5.5.6 Risk Characterization
TRIM.RiskEco quantifies the potential for ecological risk from exposure to PB-HAPs using a
hazard quotient (HQ) approach. The HQs calculated by TPJM.RiskEco are based on metrics of
ecological exposure calculated in TRIM.FaTE and the corresponding metrics of ecological
effects compiled in the TRIM Ecological Effects database (Exhibit 41). TRIM.RiskEco can also
estimate HQs based on ecological exposure estimates from models other than TRIM.FaTE,
assuming the data are provided in the TRIM.FaTE MySQL database format. Detailed
instructions on configuring this module are included in the TRIM.RiskEco User's Guided
Users can also calculate HQs for other ecological receptors whose TRVs are based on abiotic
media concentrations. For instance, the ecological TRVs database may include a TRV for
largemouth bass that is based on the pollutant concentration in surface water. If a user modeled
surface water concentrations in TRIM.FaTE, s/he could estimate the HQ for largemouth bass for
this chemical even if large mouth bass were not included in the TRIM.FaTE simulation. This
feature allows users to calculate HQs for a variety of receptors without including these receptors
in exposure modeling.
The TRIM Ecological Effects database contains a variety of ecological toxicity reference values
for PB-HAPs. Volume 1 of this reference library (Chapter 26) provides a listing of additional
sources of ecological toxicity reference value levels.
April 2004
Page 135
-------
5.5.6.1 Reporting Results
TRIM.Risk provides a visualization tool for presenting analysis results in various automated
formats. The risk assessor may want to utilize this tool to assist with development of the risk
characterization summary, which generally will include the following information:
Documentation of input parameters, outputs, and risk characterization, with special emphasis
on the range of risk or hazard estimates;
A simple presentation describing the assessment's purpose and the outcome relative to the
purpose (e.g., purpose: demonstrate that risk is below target levels; outcome: low risk not
demonstrated); and
Documentation of all key assumptions or other inputs used for the assessment, such as
emissions characteristics or choice of a nearby meteorological station.
5.5.6.2 Assessment and Presentation of Uncertainty
Risk managers need to understand the strengths and the limitations of the Tier 3 ecological risk
assessment. A critical part of the risk characterization process, therefore, is an evaluation of the
assumptions, limitations, and uncertainties inherent in the Tier 3 assessment in order to place the
risk estimates in proper perspective/3' Tier 3 ecological risk assessments may be deterministic or
probabilistic and commonly include semi-quantitative sensitivity analyses and quantitative
uncertainty analysis (described in Section ni-5.4 above). The general quantitative approach to
propagating or tracking uncertainty through probabilistic modeling is described in Volume 1
(Chapter 31) of this reference library.
April 2004 Page 136
-------
References (note that some numbered references include multiple citations)
1. U.S. Environmental Protection Agency. 2003. Framework for Cumulative Risk Assessment.
Risk Assessment Forum, Washington, DC 20460, May 2003, EPA/630/P-02/001F; available
at http://cfpub.epa.gov/ncea/raf/recordisplay.cfm?deid=54944.
2. U.S. Environmental Protection Agency. 1999. Residual Risk Report to Congress. Office of
Air Quality Planning and Standards, Research Triangle Park, NC 27711, March 1999, EPA-
453/R-99-001; available at http://www.epa.gov/ttn/oarpg/t3/reports/risk_rep.pdf.
3. U.S. Environmental Protection Agency. 1995. Policy for Risk Characterization at the U.S.
Environmental Protection Agency. Science Policy Council, Washington, B.C., March 1995,
available at: http://64.2.134.196/committees/aqph/rcpolicy.pdf.
4. Hattis. D.B. and D.E. Burmaster. 1994. Assessment of variability and uncertainty
distributions for practical risk analyses. Risk Analysis 14(5):713-730.
U.S. Environmental Protection Agency. 1999. Report of the Workshop on Selecting Input
Distributions for Probabilistic Assessments. Risk Assessment Forum, Washington, DC.
EPA/630/R-98/004.
U.S. Environmental Protection Agency. 1997. Guiding Principles for Monte Carlo Analysis.
Risk Assessment Forum, Washington, DC. March 1997. EPA-630/R-97-001; available at
http://www.epa.gov/NCEA/pdfs/montcarl.pdf.
U.S. Environmental Protection Agency. 1988. National Emission Standards for Hazardous
Air Pollutants. Federal Register 53(145):28496-28056, Proposed Rule and Notice of Public
Hearing, July 28, 1988.
Finkel, A.M. 1990. Confronting Uncertainty in Risk Management: A Guide for Decision-
Makers. Center for Risk Management, Resources for the Future. Washington, DC.
U.S. Environmental Protection Agency. 1997. Policy for Use of Probabilistic Analysis in
Risk Assessment. Office of the Administrator, Washington, DC. May 15, 1997; available at
http://www.epa.gov/osp/spc/probpol.htm.
National Council on Radiation Protection and Measurements. 1996. A Guide for Uncertainty
Analysis in Dose and Risk Assessments Related to Environmental Contamination. NCRP
Commentary No. 14; available at http://www.ncrp.com/comml4.html.
5. U.S. Environmental Protection Agency. 2001. Risk Assessment Guidance for Superfund
(RAGS). Volume III - Part A. Process for Conducting Probabilistic Risk Assessment. Office
of Emergency and Remedial Response, Washington, D.C.
(http://www.epa.gov/superfund/programs/risk/rags3a/index.htm).
April 2004 Page 137
-------
6. U.S. Environmental Protection Agency. 1992. Screening Procedures for Estimating the Air
Quality Impact of Stationary Sources, Revised. Office of Air Quality Planning and Standards,
Research Triangle Park, North Carolina, October 1992. EPA-454/R-92-019. Available at:
http://www.epa. gov/scramOO 17tt25 .htm#guidance.
7. U.S. Environmental Protection Agency. 2002. User's Guide for the Human Exposure Model
(HEM). Office of Air Quality Planning and Standards, Research Triangle Park, NC; current
version available at: http://www.epa.gov/ttn/fera/human_hem.html.
8. U.S. Environmental Protection Agency. 1995. SCREENS Model Users'Guide. Office of
Air Quality Planning and Standards, Research Triangle Park, NC. EPA-454/B-95-004.
(http://www.epa. gov/scramOO 1 /userg/screen/screen3 d.pdf).
9. U.S. Environmental Protection Agency. 1995. User's Guide for the Industrial Source
Complex (ISC3) Dispersion Models Volume I - User's Instructions. Office of Air Quality
Planning and Standards, Research Triangle Park, NC. September 1995. EPA-454/B-95-
0031; available at http://www.epa.gov/scramOO l/tt22.htm#isc.
10. U. S. Environmental Protection Agency. 2003. Total Risk Integrated Methodology
Trim.ExpoInhalation User's Document. Volume 1: Air Pollutants Exposure Model (APEX,
Version 3) User's Guide. Office of Air Quality Planning and Standards, Research Triangle
Park,NC. April 2003.
11. EPA's carcinogen risk assessment guidelines were first published in 1986, revisions were
proposed in 1996 and 2001, the July 1999 draft of the revisions were adopted as interim
guidance. A subsequent 2000 draft of the Guidelines has been released for public and
scientific review prior to adoption as final (see http ://cfpub.epa.gov/ncea/raf/rafguid.htm).
U.S. Environmental Protection Agency. 1999. Guidelines for Carcinogen Risk Assessment.
Review Draft. Risk Assessment Forum, Washington, DC. NCEA-F-0644.
U.S. Environmental Protection Agency. 1986. Guidelines for Carcinogen Risk Assessment.
Federal Register 51(185):33992-43003.
U.S. Environmental Protection Agency. 2003. Draft Final Guidelines for Carcinogen Risk
Assessment (External Review Draft), Risk Assessment Forum, Washington, DC
NCEA-F-0644A.
12. U.S. Environmental Protection Agency. Health Effects Information Used in Cancer and
Noncancer Risk Characterization for the NATA 1996 National-Scale Assessment, available at
http ://www.epa. gov/ttn/atw/nata/nettables .pdf.
13. U.S. Environmental Protection Agency. 1998. An SAB Report: Development of the Acute
Reference Exposure. Science Advisory Board, Washington, D.C., November 1998, available
at: http://www.epa.gov/sab/pdf/ehc9905.pdf.
April 2004 Page 138
-------
14. U.S. Environmental Protection Agency. 2000. Supplementary Guidance for Conducting
Health Risk Assessment of Chemical Mixtures. Risk Assessment Forum, Washington, B.C.
EPA/630/R-00/002, available at
http://www.epa.gov/ncea/raf/pdfs/chem_mix/chem_mix_08_2001 .pdf.
U.S. Environmental Protection Agency. 1986. Guidelines for the Health Risk Assessment of
Chemical Mixtures. EPA/630/R-98/002; published in the Federal Register 51 (185):34014-
34025, Sept 24, 1986, available at
http://www.epa.gov/ncea/raf/pdfs/chem_mix/chem_mix_08_2001 .pdf.
15. Morgan, G. and Henrrion. M. 1990. Uncertainty: A Guide to Dealing with Uncertainty in
Quantitative Risk and Policy Analysis. Cambridge University Press, Cambridge, U.K.
16. U.S. Environmental Protection Agency. 1989. Risk Assessment Guidance for Superfund:
Volume I. Human Health Evaluation Manual (Part A). Office of Emergency and Remedial
Response. Washington, D.C., EPA/541/1-89/002, available at:
http ://www. epa. go v/superfund/programs/risk/ragsa/index .htm
17. U.S. Environmental Protection Agency. 2003. Guideline on Air Quality Models. 40 CFR
Part 51, Appendix W, available at http://www.epa.gov/scramOO 17tt25.htm#guidance.
See also Procedures for Air Modeling of Superfund Sites and Dispersion Modeling of Toxic
Pollutants in Urban Areas, available at (http://www.epa.gov/ttn/scram/).
18. The CHAD database is available at http://www.epa.gov/chadnet 1 /.
19. U.S. Environmental Protection Agency. 1998. Methodology for Assessing Health Risks
Associated with Multiple Pathways of Exposure to Combustor Emissions. Update to
EPA/600/6-90/003 Methodology for Assessing Health Risks Associated With Indirect
Exposure to Combustor Emissions. National Center for Environmental Assessment. EPA-
600/R-98-137, available at: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=55525.
20. U.S. Environmental Protection Agency. 1998. Human Health Risk Assessment Protocol for
Hazardous Waste Combustion Facilities, Peer Review Draft. Office of Solid Waste and
Emergency Response, July 1998. EPA530-D-98-001 A, B, and C and subsequent Errata
(EPA Memo, July 1999), available at
http ://www. epa. gov/earth 1 r6/6pd/rcra_c/pd-o/comb_risk.htm.
21. U.S. Environmental Protection Agency. 2002. TRIM.FaTE Technical Support Document,
Volume 1: Description of Module. Office of Air Quality Planning and Standards, Research
Triangle Park, NC. EPA 453/R-02-01 la, available at http://www.epa.gov/ttn/fera/.
U.S. Environmental Protection Agency. 2002. TRIM.FaTE Technical Support Document,
Volume 2: Description of Chemical Transport and Transformation Algorithms. Office of Air
Quality Planning and Standards, Research Triangle Park, NC. EPA 453/R-02-01 Ib, available
at http://www.epa.gov/ttn/fera/.
The current version of the TRIM.FaTE User's Guide is available at
http://www. epa.gov/ttn/fer a/trim_fate.html.
April 2004 Page 139
-------
22. U.S. Environmental Protection Agency. 2001. Risk Assessment Guidance for Superfund
(RAGS): Volume I - Human Health Evaluation Manual (Part E, Supplemental Guidance for
Dermal Risk Assessment), Interim. Office of Emergency and Remedial Response,
Washington, D.C. 20460. EPA/540/R/99/005, OSWER 9285.7-02EP, September 2001,
available at http://www.epa.gov/oerrpage/superfund/programs/risk/ragse/index.htm.
23. U.S. Environmental Protection Agency. 1994. Draft Technical Background Document for
Soil Screening Guidance. Office of Solid Waste and Emergency Response, Washington,
D.C., December 1994. EPA/540/R-94/106.
24. U.S. Environmental Protection Agency. 1989. Risk Assessment Guidance for Superfund:
Volume I. Human Health Evaluation Manual (Part A). Office of Emergency and Remedial
Response. Washington, D.C., EPA/541/1-89/002, available at
http ://www. epa. go v/superfund/programs/risk/ragsa/index .htm
25. U.S. Environmental Protection Agency. 1986. Guidelines for Mutagenicity Risk Assessment.
Risk Assessment Forum, Washington, DC. EPA/630/R-98/003; published in the Federal
Register 51:(1185): 34006-34012, Sept 24, 1986, available at
http ://cfpub. epa. gov/ncea/raf/pdfs/mutagen2 .pdf.
26. U.S. Environmental Protection Agency. 1989. Exposure Factors Handbook. Office of
Research and Development, National Center for Environmental Assessment, Washington,
D.C., May 1989. EPA/600/8-89/043, available at
http ://cfpub. epa. gov/ncea/cfm/recordisplay.cfm?deid= 12464.
27. United States Environmental Protection Agency. 2003. Guidance on Selecting the
Appropriate Age Groups for Assessing Childhood Exposures to Environmental Contaminants
(External Review Draft). Risk Assessment Forum, Washington, D.C. September, 2003.
EPA/630/P-03/003A, available at www.epa.gov/ncea.
28. U.S. Environmental Protection Agency. 2002. Child-specific Exposure Factors Handbook
(Interim Report). Office of Research and Development, National Center for Environmental
Assessment, Washington Office, Washington, DC, September 1, 2002.
EPA-600-P-00-002B, available at
http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=55145.
29. U.S. Environmental Protection Agency. 1992. Guidelines for Exposure Assessment. Risk
Assessment Forum, Washington, DC, May 1992. EPA 600Z-92/001, available at
http ://cfpub. epa. gov/ncea/cfm/recordisplay.cfm?deid= 15263.
30. U.S. Environmental Protection Agency. 1998. Guidelines for Ecological Risk Assessment.
Risk Assessment Forum Washington, April 1998. EPA/630/R095/002F. Available at:
(http ://cfpub .epa. gov/ncea/cfm/recordisplay. cfm?deid= 12460)
31. U.S. Environmental Protection Agency. 1993. Wildlife Exposure Factors Handbook. Office
of Research and Development, Washington, D.C. EPA/600/R-93/187. Available at:
http ://cfbub. epa. gov/ncea/cfm/wefh. cfrn? ActType=de fault.
April 2004 Page 140
-------
32. U.S. Environmental Protection Agency. 1992. Framework for Ecological Risk Assessment.
Risk Assessment Forum, Washington, D.C., February 1992. EPA/63O/R-92/001.
33. The current version of the TRIM.RiskEco User's Guide is available at
http ://www. epa. gov/ttn/fera/trim_risk.html.
34. U.S. Environmental Protection Agency. 2003. Generic Ecological Assessment Endpoints
(GEAE) for Ecological Risk Assessment. Risk Assessment Forum, Washington, B.C.,
October 2003. Available at: http://cfpub.epa.gov/ncea/raf/recordisplay.cfm?deid=55131.
April 2004 Page 141
------- |