EPA

Office of Air Quality

Pla nnin g a nd S ta nd a rds

C Air

lean

United States Office Of Air Quality EPA-453/R-99-007

Environmental Protection Planning And Standards July 2000

Agency Research Triangle Park, NC 27711

Air

NATIONAL AIR TOXICS 

PROGRAM: THE INTEGRATED 

URBAN STRATEGY

Report to Congress
EPA-453/R-99-007 

NATIONAL AIR TOXICS PROGRAM:

THE INTEGRATED URBAN STRATEGY

Report to Congress

U.S. ENVIRONMENTAL PROTECTION AGENCY

Office of Air and Radiation

Office of Air Quality Planning and Standards

Research Triangle Park, North Carolina 27711

July 2000
ACKNOWLEDGEMENTS

 This Report was prepared by the U.S. Environmental Protection Agency’s (EPA’s) Office

of Air Quality Planning and Standards (OAQPS) with input and review by other EPA Offices and

Regions. The Project Leads were Mr. Jaime Pagán and Ms. Laura Mc Kelvey.

We would like to acknowledge the contributions of the Agency work group members and

others involved in the development of the report, including staff (too numerous to name) in

OAQPS, the Offices of Transportation and Air Quality; Research and Development; Solid Waste

and Emergency Response; Prevention, Pesticides, and Toxic Substances; and General Counsel, as

well as EPA Regions I, II, IV, and V.

Also, special thanks to the group of external scientific experts that conducted the peer

review of Chapter 6 of this Report. These experts are:

Dr. Viney Aneja Department of Marine, Earth and Atmospheric

Sciences, North Carolina State University

Dr. Gail Charnley Health Risk Strategies

Dr. Merrill Jackson Consultant

Dr. Daland Juberg International Center for Toxicology and Medicine

Dr. Petros Koutrakis Harvard School of Public Health

Dr. Ron Wyzga Electric Power Research Institute
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

-iTable of Contents

Page

Executive Summary ....................................................... ES-1

1. Introduction ......................................................... 1-1

1.1 Characterization of Urban Air Pollution (Chapter 2) ..................... 1-2

1.2 Emissions Inventory and Selection of the Urban Pollutants (Chapter 3) ...... 1-2

1.3 Regulatory Programs and Activities to Reduce Air Toxics Emissions

(Chapter 4) ..................................................... 1-3

1.4 Assessment of Progress Toward the Goals (Chapter 5) ................... 1-4

1.5 Research Needed to Address Knowledge Gaps (Chapter 6) ............... 1-5

2. Characterization of Urban Air Pollution .................................. 2-1

2.1 Introduction .................................................... 2-1

2.2 What Do We Know About HAP? ................................... 2-1

2.3 What Do We Know About HAP Emissions? .......................... 2-2

2.4 What Do Monitoring Data Tell Us? .................................. 2-4

2.5 What Do We Know About Urban Populations? ........................ 2-5

2.6 Characterization of Air Toxics in Urban Areas ......................... 2-6

2.7 Why Is the Urban Strategy Needed? ................................ 2-17

2.8 References .................................................... 2-18

3. Emissions Inventory and Selection of the Urban Pollutants .................. 3-1

3.1 Introduction .................................................... 3-1

3.2 Baseline Emissions Inventory for the Integrated Urban Air Toxics Strategy . . 3-2

3.2.1 Development of the Baseline Inventory ......................... 3-3

3.2.2 Baseline Inventory Results ................................... 3-5

3.2.3 Allocating Emissions Between Locations and Source Types ........ 3-7

3.2.4 Limitations of the Emissions Inventory ......................... 3-9

3.3 Ranking the Urban Hazardous Air Pollutants ......................... 3-11

3.3.1 Exposure/Toxicity Indicators Ranking Analysis ................. 3-13

3.3.2 Risk Assessment/Hazard Ranking Studies in Urban Areas ......... 3-18

3.3.3 CEP Ranking Analysis ..................................... 3-19

3.4 Selection of the Urban Hazardous Air Pollutants ...................... 3-21

3.5 References .................................................... 3-26

4. Regulatory Programs and Activities to Reduce Air Toxics Emissions .......... 4-1

4.1 Introduction .................................................... 4-1

4.2 List of Area Source Categories ..................................... 4-1
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

-iiTable of Contents (Continued)

Page

4.3 Regulatory Activities for Area Sources ............................... 4-3

4.3.1 Tier 1 – MACT Standards ................................... 4-4

4.3.2 Tier 2 – Source Category-Specific GACT Standards .............. 4-4

4.3.3 Tier 3 – Flexible GACT Process .............................. 4-4

4.3.4 Issues on the National Versus Local Scope of Area Source Standards . 4-5

4.3.5 Schedule for Area Source Standards ........................... 4-6

4.4 Regulatory Activities for Mobile Sources ............................. 4-6

4.4.1 Urban HAP Emitted from Mobile Sources ...................... 4-6

4.4.2 Diesel Exhaust ............................................ 4-7

4.4.3 Mobile Source Emission Control Programs ..................... 4-9

4.4.4 Mobile Source Air Toxics Assessments and Controls ............. 4-10

4.5 Other Hazardous Air Pollutant Emission Sources ...................... 4-12

4.6 Other Programs and Authorities ................................... 4-13

4.6.1 Federal Regulatory Activities – CAA Section 112 Authorities ..... 4-16

4.6.2 Other CAA Authorities .................................... 4-17

4.6.3 Other Authorities, Laws, Rules, and Programs to Help Reduce

HAP Emissions .......................................... 4-18

4.7 State, Local, and Tribal Activities .................................. 4-21

4.7.1 Why are State, Local, and Tribal Programs Integral to the 

Strategy? ................................................ 4-22

4.7.2 What are the Objectives of State, Local, and Tribal Activities? ..... 4-23

4.7.3 How Can State, Local or Tribal Agencies Participate in the 

Strategy? ................................................ 4-24

4.7.4 What Elements Should a State, Local or Tribal Program Contain? ... 4-25

4.8 References .................................................... 4-25

5. Assessment of Progress Toward Goals .................................... 5-1

5.1 Overview of Health Risks ......................................... 5-1

5.2 The EPA Risk Assessment Paradigm ................................ 5-2

5.2.1 Exposure Assessment ....................................... 5-3

5.2.2 Dose-Response Assessment .................................. 5-6

5.2.3 Risk Characterization ...................................... 5-13

5.3 Methods, Tools, and Data to Estimate Risk ........................... 5-18

5.3.1 Assessing Exposures and Characterizing Risks .................. 5-18

5.3.2 Summary ............................................... 5-21

5.4 The Overall Risk Assessment Approach for the Strategy ................ 5-22

5.4.1 Designing the Assessments ................................. 5-22

5.4.2 Addressing Disproportionate Risks ........................... 5-23
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

-iiiTable of Contents (Continued)

Page

5.5 Designing Future Assessments .................................... 5-23

5.5.1 Initial Assessments – National ............................... 5-24

5.5.2 Initial Assessments – Urban ................................. 5-25

5.5.3 Periodic Assessments ...................................... 5-25

5.6 References .................................................... 5-26

6. Research Needed to Address Knowledge Gaps ............................. 6-1

6.1 Exposure Assessment ............................................. 6-2

6.2 Health Effects and Dose-Response Assessment ....................... 6-13

6.3 Risk Assessment/Characterization .................................. 6-22

6.4 Risk Management .............................................. 6-24

6.5 References .................................................... 6-26

Appendix

Overview ........................................................... A-1

Acetaldehyde ........................................................ A-3

Acrolein ............................................................ A-9

Acrylonitrile ........................................................ A-15

Arsenic Compounds .................................................. A-21

Benzene ........................................................... A-29

Beryllium Compounds ................................................ A-35

1,3-Butadiene ....................................................... A-43

Cadmium Compounds ................................................ A-49

Carbon Tetrachloride ................................................. A-55

Chloroform ......................................................... A-63

Chromium Compounds ............................................... A-71

Coke Oven Emissions ................................................ A-81

1,2-Dichloroethane (Ethylene Dichloride) ................................. A-85

1,2-Dichloropropane (Propylene Dichloride) .............................. A-93

1,3-Dichloropropene ................................................. A-99

Ethylene Dibromide (1,2-Dibromoethane) ............................... A-107

Ethylene Oxide ..................................................... A-113

Formaldehyde ...................................................... A-119

Hexachlorobenzene ................................................. A-127

Hydrazine ......................................................... A-133

Lead Compounds ................................................... A-139

Manganese Compounds .............................................. A-147

Mercury Compounds ................................................ A-153

Methylene Chloride ................................................. A-163

Nickel Compounds .................................................. A-169
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

-ivTable of Contents (Continued)

Page

Polychlorinated Biphenyls (PCBs) ..................................... A-177

Polycyclic Organic Matter (POM) ...................................... A-185

Quinoline ......................................................... A-193

2,3,7,8-Tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) ...................... A-197

1,1,2,2-Tetrachloroethane ............................................ A-201

Tetrachloroethylene (Perchloroethylene) ................................. A-207

Trichloroethylene ................................................... A-215

Vinyl Chloride ..................................................... A-223
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

-vList of Exhibits

Page

Exhibit ES-1 List of Urban HAP for the Integrated Urban Air Toxics Strategy

(“Urban HAP List”) ....................................... ES-4

Exhibit ES-2 Area Source Categories Already Subject to Standards or

Which Will Be Subject to Standards .......................... ES-5

Exhibit ES-3 New Area Source Categories Being Listed ..................... ES-5

Exhibit 2-1 HAP Baseline NTI Emissions by Source ........................ 2-3

Exhibit 2-2 HAP Emissions by State Based on 1993 NTI .................... 2-3

Exhibit 2-3 Risk-Based Assessments Covering Urban Areas ................. 2-10

Exhibit 2-4 Overview of Assessments .................................. 2-11

Exhibit 3-1 Baseline Emissions Inventory Estimates for Each of

the 40 Candidate Urban HAP (1990 – 1993) ..................... 3-6

Exhibit 3-2 Sources of Baseline Emissions from the Candidate Urban HAP ...... 3-7

Exhibit 3-3 Spatial Allocation of Baseline Emissions of the

Candidate Urban HAP ...................................... 3-7

Exhibit 3-4 40 Highest Priority Pollutants Identified by Exposure/Toxicity

Indicators Ranking ........................................ 3-15

Exhibit 3-5 Priority HAP Identified by Studies in Urban Areas ............... 3-18

Exhibit 3-6 HAP with Modeled Concentrations Higher than an RBC in

at Least 50 Urban Census Tracts ............................. 3-20

Exhibit 3-7 HAP Ranking Analysis for the Integrated Urban Strategy ......... 3-22

Exhibit 3-8 Results of the Three Ranking Analyses ........................ 3-23

Exhibit 3-9 List of Urban HAP for the Integrated Urban Air Toxics Strategy .... 3-25

Exhibit 4-1 Area Source Categories Already Subject to

Regulation or Which Will Be Subject to Regulation ............... 4-2

Exhibit 4-2 New Area Source Categories As Listed ......................... 4-3

Exhibit 4-3 1990 National Emission Estimates for Urban HAP Emitted from

Mobile Sources ........................................... 4-8

Exhibit 4-4 Completed Rules from Section 112 of the CAA

(MACT Standards) ........................................ 4-14

Exhibit 5-1 EPA Paradigm for Risk Assessment and Risk Management ......... 5-3

Exhibit 5-2 Sources of Information for Hazard Identification ................. 5-7

Exhibit 5-3 Summary of Major Differences Between EPA’s 1986 Guidelines 

(U.S. EPA, 1986b) and 1996 Proposed Guidelines for Carcinogen

Risk Assessment (U.S. EPA, 1996b) .......................... 5-13

Exhibit 5-4 Guiding Principles with Respect to Risk Descriptors ............. 5-15

Exhibit 6-1 Status of Fiscal Year 1999 IRIS Activities for HAP .............. 6-16
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

-viAcronym List

AEGL acute exposure guidance level

AIHA American Industrial Hygiene Association

AIRS Aerometric Information Retrieval System

ARE acute reference exposure

ASPEN Assessment System for Population Exposure Nationwide

ATSDR Agency for Toxic Substances and Disease Registry

BCF bioconcentration factor

BMD benchmark dose

CAA Clean Air Act

CAS Chemical Abstract Services

CASAC Clean Air Scientific Advisory Committee

CEP Cumulative Exposure Project

CERCLA Comprehensive Environmental Response, Compensation, and Liability Act

CFR Code of Federal Regulations

CHAD Consolidated Human Activity Database

CMAQ Community Multi-Scale Air Quality

C/MSA consolidated metropolitan statistical area

CO carbon monoxide

CWA Clean Water Act

DNA deoxyribonucleic acid

DOT Department of Transportation

EMPACT Environmental Monitoring for Public Access and Community Tracking

EPA Environmental Protection Agency

EPCRA Emergency Planning and Community Right-to-Know Act

ERPG emergency response planning guideline

ES Executive Summary

FIFRA Federal Insecticide, Fungicide and Rodenticide Act

FR Federal Register

GACT generally available control technology

GIS geographic information systems

GLC ground-level concentration

HAP hazardous air pollutant

HAPEM Hazardous Air Pollutant Exposure Model

HASTE Houston Area Source Toxic Emissions

HC hydrocarbon

HEAST Health Effects Assessment Summary Tables

HEC human equivalent concentration

HI hazard index

HQ hazard quotient

IEM Integrated Exposure Methodology
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

-viiAcronym List (Continued)

I/M inspection and maintenance

IRIS Integrated Risk Information System

ISC3 Industrial Source Complex

km kilometers

Kow octanol-water partition coefficient

LCA Life Cycle Analysis

LOAEL lowest-observed-adverse-effect level

LOC level of concern

LIDAR Light Detecting and Ranging

MACT maximum achievable control technology

MEASURE Mobile Emissions Assessment System for Urban and Regional Evaluation

MMT methylcyclopentadienyl manganese tricarbonyl

MOU memorandum of understanding

MPCA Minnesota Pollution Control Agency

MPO Metropolitan Planning Organizations

MRL minimal risk level

MSA metropolitan statistical area

MTBE methyl tertiary butyl ether

MWC municipal waste combustor

MWI municipal waste incinerator

NAAQS national ambient air quality standard

NAC National Advisory Committee

NERL National Exposure Research Laboratory

NESHAP national emission standards for hazardous air pollutants

NHAPS National Human Activity Pattern Survey

NHEXAS National Human Exposure Assessment Survey

NOAEL no-observed-adverse-effect level

NOx nitrogen oxide

NTI National Toxics Inventory

PAH polycyclic aromatic hydrocarbons

PAMS Photochemical Assessment Monitoring Stations

PBPK physiologically based pharmacokinetic (model)

PBT persistent, bioaccumulative, and toxic

PCB polychlorinated biphenyls

PCDD polychlorinated dibenzo-p-dioxin

PCDF polychlorinated dibenzofuran

PM particulate matter

PMx particulate matter (x microns or smaller)

PNGV Partnership for a New Generation of Vehicles

POM polycyclic organic matter

PPA Pollution Prevention Act
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

-viiiAcronym List (Continued)

PSI pollutant standard index

QSTR quantitative structure-toxicity relationship

RBC risk-based concentration

RBD risk-based dose

RCRA Resource Conservation and Recovery Act

RDDR regional deposited dose ratio

REL reference exposure level

RfC reference concentration

RfD reference dose

RFG reformulated gasoline

RMP Risk Management Program

SAB Science Advisory Board

SAR structure-activity relationship

SARA Superfund Amendments and Reauthorization Act

SIC Standard Industrial Classification

TCDD 2,3,7,8-tetrachlorodibenzo-p-dioxin

TCDF 2,3,7,8-tetrachlorodibenzofuran

TEAM Total Exposure Assessment Methodology

TEF toxic equivalency factor

TMDL total maximum daily load

TNRCC Texas Natural Resources Conservation Commission

TRI Toxics Release Inventory

TRIM Total Risk Integrated Methodology

TSCA Toxic Substance Control Act

TSD treatment, storage, and disposal

UF uncertainty factors

U.S. United States

U.S.C. United States Code

VMT vehicle-miles of travel

VOC volatile organic compounds

WMPT Waste Minimization Prioritization Tool
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

1

64 FR 38705. National Air Toxics Program: The Integrated Urban Strategy (Notice). July 19, 1999.

ES-1

Executive Summary

On July 19, 1999, we published a notice in the Federal Register entitled “National Air

Toxics Program: The Integrated Urban Air Strategy” (Strategy) that outlined the U.S.

Environmental Protection Agency’s (EPA’s) plans for addressing cumulative health risks in

urban areas1. The Strategy presented our plan for future actions to reduce emissions of air toxics

and improve our understanding of the health risks posed by toxics in urban areas.

Section 112(k) of the Clean Air Act (CAA) requires the EPA Administrator to submit

two Reports to Congress on actions taken under the CAA that reduce the risk to public health

posed by the release of hazardous air pollutants (HAP) from area sources. This Report to

Congress (Report), originally due in 1998, was prepared to meet the first part of that

requirement. In addition, it expands on much of the information provided in the Strategy, such as

the methodology for developing the emissions inventory, identifying the 33 urban HAP and

identifying the area source categories that will be subject to regulation. Furthermore, this Report

summarizes existing information on risk assessments that have been conducted in various urban

areas. These studies were performed by EPA and various States over the last several years. 

Taking into consideration the uncertainties and limitations of each study, these assessments

provide useful information on the potential nature and magnitude of exposures and health risks in

urban areas. Finally, this Report also provides a very detailed discussion of 13 research needs to

address in achieving the goals of the Strategy. These needs were identified in the following

areas: exposure assessment, health effects, dose-response assessment, risk assessment, risk

characterization and risk management. In addition, Chapter 6 of this Report provides a summary

of ongoing EPA activities to address those needs.

Section 112(k) also requires EPA to identify specific metropolitan areas that continue to

experience high risks to public health as the result of emissions from area sources. Since we

have only recently begun to work toward implementing the Strategy, we are unable to identify in

this first Report the metropolitan areas that continue to experience high risks to public health as

the result of emissions from areas sources. However, in the next few years, as we make progress

toward the goals of the Strategy, we will be better able to identify those metropolitan areas with

high risks due to air toxics.

The following sections provide an overview of the Strategy and describe the four

components of the Strategy and explain their role in achieving its goals. The four components

are: Standard Setting Activities, National and Local Initiatives, Air Toxics Assessments, and

Education and Outreach. These components also form the framework of our National Air Toxics

Program. Finally, Chapter 1 of this Report summarizes the contents of each chapter and their key

points. Important health and other general information about each one of the 33 urban HAP is

provided in the Appendix.
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

ES-2

Overview of the Strategy

The Strategy presents a framework for further reducing HAP emissions from all types of

sources found in urban areas, including major industrial sources, smaller stationary sources, and

cars and trucks. Air toxics can pose special threats in urban areas because of the large number of

people and the variety of sources that emit HAP. Individually, some of these sources may not

emit large amounts of toxic pollutants. However, all of these pollution sources combined can

potentially pose significant health threats. We are also concerned about the impact of toxics

emissions on minority and low income communities which are often located close to industrial

and commercial urbanized areas. Accordingly, there are three goals for the Strategy: 

1. Reduce, by 75 percent, the incidence of cancer associated with air toxics from both large

and small industrial/commercial sources. This is relevant to all HAP from both major and

area stationary sources in all urban areas nationwide. Reductions can be the result of

actions by Federal, State, local and/or Tribal governments achieved by any regulations or

voluntary actions. 

2. Substantially reduce noncancer health risks (e.g., birth defects and reproductive effects)

associated with air toxics from small industrial/commercial sources. This includes health

effects other than cancer posed by all HAP. Reductions can be the result of actions by

Federal, State, local and/or Tribal governments achieved by any regulations or voluntary

actions.

3. Address disproportionate impacts of air toxics hazards across urban areas, such as those

in areas known as “hot spots,” and minority and low-income communities in urban areas.

This will necessarily involve consideration of both stationary and mobile source

emissions of all HAP, as well as sources of HAP in indoor air. We intend to characterize

exposure and risk distributions both geographically and demographically. This will

include particular emphasis on highly exposed individuals (such as those in geographic

“hot spots”) and specific population subgroups (e.g., children, the elderly, and lowincome communities).

To accomplish these goals, the Strategy is comprised of four key components:

1. Standard setting activities addressing sources of air toxics at both the national and local

level; 

2. Initiatives at both the national and local level to address specific pollutants (e.g., mercury)

and to identify and address specific community risks (e.g., through pilot projects); 

3. Air toxics assessments (including expanded air toxics monitoring and modeling) to

identify areas of concern, to prioritize efforts to reduce risks, and to track progress; and 
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

ES-3

4. Education and outreach efforts to inform stakeholders about the Strategy and to get input

into designing programs to implement it.

Standard Setting Activities

This first component includes our regulatory tools and programmatic activities for sourcespecific and sector-based standard setting, as well as those of States, local agencies, and Tribes. 

These standards contribute to reductions in emissions of air toxics from major, area, and mobile

sources. This component includes activities such as selecting urban HAP, setting emission

standards, conducting studies, developing policies, and conducting enforcement and compliance

assistance activities. These actions result in emission reductions, as well as associated reductions

in risk. 

The CAA includes certain specific requirements for the Strategy. First, we must identify

at least 30 HAP, “which, as the result of emissions from area sources, present the greatest threat

to public health in the largest number of urban areas” (CAA § 112(k)(3)(B)(i)). To select these

HAP, we evaluated the health effects information available for 188 HAP, estimated emissions

from all known sources using a variety of techniques, assessed available air quality monitoring

data, reviewed existing studies, and produced a list of pollutants based on the relative hazards

they pose in urban areas, considering toxicity, emissions, and related characteristics. From this

effort, we established a list of 33 urban HAP which pose the greatest threats to public health in

urban areas, considering emissions from major, area and mobile sources (see Exhibit ES-1). This

list includes not only those that are emitted from area sources, but reflects the integrated nature of

the Strategy by including those posing public health concerns in urban areas regardless of

emissions source type. Included among the 33 urban HAP are the 30 HAP with greatest

emissions contributions from area sources (i.e., the “area source HAP”). The remaining three

urban HAP (i.e., coke oven emissions, 1,2-dibromoethane and carbon tetrachloride) have less

significant emissions contributions from area sources. Under section 112(k), there are no

specific regulatory implications of listing these three HAP, but we’ll use all 33 HAP in

prioritizing efforts to address risks.

Second, we’re required to assure that sources accounting for 90 percent of the emissions

of identified area source HAP are subject to standards (CAA § 112(c)(3) and (k)(3)(B)(ii)). We

adopted a two-step process for selecting the source categories which will be subject to regulation

under the Strategy. First, we identified those area source categories that emit one or more of the

30 area source HAP that are already listed for regulation under the CAA. For each of those

source categories, we identified the percentage contribution to the total area source emissions for

each of the 30 area source HAP. 

In the second step, we added area source categories that, based on inventory data,

contribute at least 15 percent of the national urban emissions of at least one of the 30 area source

HAP. We adopted this criterion to account for the uncertainties in our current emissions

inventory data. While we’ve been able to significantly improve our baseline emissions inventory 
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

ES-4

EXHIBIT ES-1

LIST OF URBAN HAP FOR THE INTEGRATED URBAN AIR TOXICS STRATEGY

(“URBAN HAP LIST”) 

HAP CAS No. + HAP CAS No. +

Acetaldehyde 75070 Formaldehyde 50000

Acrolein 107028 Hexachlorobenzene 118741

Acrylonitrile 107131 Hydrazine 302012

Arsenic compounds Lead compounds

Benzene 71432 Manganese compounds

Beryllium compounds Mercury compounds

1,3-butadiene 106990 Methylene chloride

(dichloromethane)

75092

Cadmium compounds Nickel compounds

Carbon tetrachloride* 56235 Polychlorinated biphenyls

(PCBs)

1336363

Chloroform 67663 Polycyclic organic matter (POM)

Chromium compounds Quinoline 91225

Coke oven emissions* 8007452 2,3,7,8-tetrachlorodibenzo-pdioxin (& congeners & TCDF

congeners)

1746016

1,2-dibromoethane* 106934 1,1,2,2-tetrachloroethane 79345

1,2-dichloropropane (propylene

dichloride)

78875 Tetrachloroethylene

(perchloroethylene)

127184

1,3-dichloropropene 542756 Trichloroethylene 79016

Ethylene dichloride

 (1,2-dichloroethane)

107062 Vinyl chloride 75014

Ethylene oxide 75218

+

 Chemical Abstracts Service number. *HAP with less significant contributions from area sources.

data, data gaps and uncertainty still remain. The list of source categories will be modified to

reach the 90 percent requirement by 2003.

As a result of this two-step approach, the Strategy identified and listed 29 area source

categories that emit significant amounts of one or more of the 30 area source HAP. Currently,

we have regulations under development or completed for 16 of these area source categories. We
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

ES-5

expect to develop regulations for the remaining 13 area source categories over the next five

years. Exhibit ES-2 shows those area source categories, as listed in the Strategy, that contribute

to emissions of the 30 area source HAP, and are either subject to existing standards, or will be

subject to standards that are currently being developed. Exhibit ES-3 shows the area source

categories listed in the Strategy for the first time, as required in section 112(c)(3). These are the 

area source categories that contribute at least 15 percent of the total area source emissions of at

least one of the 30 area source HAP.

EXHIBIT ES-2

AREA SOURCE CATEGORIES ALREADY SUBJECT TO STANDARDS

OR WHICH WILL BE SUBJECT TO STANDARDS

Chromic Acid Anodizing Industrial Boilers

Commercial Sterilization Facilities Institutional/Commercial Boilers

Other Solid Waste Incinerators (Human/Animal

Cremation)

Medical Waste Incinerators

Decorative Chromium Electroplating Municipal Waste Combustors

Dry Cleaning Facilities Open Burning Scrap Tires

Halogenated Solvent Cleaners Portland Cement

Hard Chromium Electroplating Secondary Lead Smelting

Hazardous Waste Combustors Stationary Internal Combustion Engines

EXHIBIT ES-3

NEW AREA SOURCE CATEGORIES BEING LISTED

Cyclic Crude and Intermediate Production Municipal Landfills

Flexible Polyurethane Foam Fabrication

Operations

Oil & Natural Gas Production

Hospital Sterilizers Paint Stripping Operations

Industrial Inorganic Chemical Manufacturing Plastic Materials and Resins Manufacturing

Industrial Organic Chemical Manufacturing Publicly Owned Treatment Works

Mercury Cell Chlor-Alkali Plants Synthetic Rubber Manufacturing

Gasoline Distribution Stage I
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

2

 65 FR 6698. Tier 2 Motor Vehicle Emission Standards and Gasoline Sulfur Control Requirements. 

February 10, 2000.

3

 65 FR 35430. Proposed Heavy-Duty Engine and Vehicle Standards and Highway Diesel Fuel Sulfur

Control Requirements. June 2, 2000.

ES-6

With respect to mobile sources, title II of the CAA provides several mechanisms to

achieve reductions in HAP. The most direct of these is section 202(l) which requires us to

identify the need for and consider regulations for control of HAP from motor vehicles and their

fuels. Those standards are to reflect the greatest degree of emissions reductions achievable

through the application of technology which will be available, taking existing standards,

availability and costs of the technology, noise, energy and safety factors into account. Section

202(l)(2) further specifies that, at a minimum, benzene and formaldehyde emissions must be

addressed. 

The section 202(l)(2) proposal will identify the HAP emitted by motor vehicles and their

fuels, assess the reductions achieved by our current and recently proposed title II regulations, and

evaluate the appropriateness of additional motor vehicle and fuel controls. With regard to

control strategies, several of the existing emission control programs developed under section

202(a) (motor vehicle controls) and section 211 (fuel controls) of the CAA already limit many

HAP emissions from motor vehicles and their fuels. In our assessment of whether additional

action is appropriate under section 202(l)(2), we’ll consider the impacts of these programs, our

recent and ongoing regulatory activities (such as our recent final rulemaking for new light-duty

“Tier 2” emission standards and gasoline sulfur controls2 and our recent proposal for heavy-duty

engine and vehicle standards and on-highway diesel fuel sulfur controls3), and such other mobile

source programs as are relevant to mobile source air toxics controls.

As we review existing regulations for a number of motor vehicle and nonroad engine

categories, the Strategy’s goal of reducing disproportionate air toxics risks will be considered. In

addition, we envision that work done in the early stages of implementing the Strategy, such as

improving monitoring and inventories, will help us compare options related to the various

emissions sources in urban areas and control authorities to provide the best relative reduction of

risks to the urban public. To the extent possible, we will consider costs in the development of

regulations aimed at reducing those risks. Capital costs, fuel costs and incremental labor costs to

operate equipment are some but not all of the factors that may be considered in assessing the cost

effectiveness of a particular control strategy.

Overall, in meeting the Strategy’s goals, we’ll consider reductions in HAP resulting from

Federal actions both to address air toxics (e.g., maximum achievable control technology (MACT)

standards under section 112(d), residual risk standards, mobile source emission controls) and

attain the national ambient air quality standards (NAAQS) for particulate matter (PM) and ozone,

as well as State, local and Tribal measures. We’ll consider cumulative risks presented by

exposures to emissions of all HAP from all sources in a given area. Further, consistent with the
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direction of section 112(k)(4) to encourage and support areawide strategies developed by State or

local air pollution control agencies, we’ll work with State, local, and Tribal air pollution control

programs for additional progress toward these goals.

National and Local Initiatives

The second component of the Strategy involves local and community-based initiatives to

focus on multimedia and cumulative risks within urban areas. Developing the Strategy is a

challenge at the national level because urban air toxics problems vary significantly across the

country. Because of this variability, the Strategy is being approached as a partnership between

EPA and State, local and Tribal governments. These governments (including municipal offices

other than pollution control departments) have the most experience with local air pollution

issues, and can lend their expertise and knowledge to address and resolve air toxics concerns that

are unique to cities. Many of these governments also have existing air pollution control

programs that currently address, and can effectively continue to address, some or all of these

issues. In addition, these governments are often able to act much more quickly than we can to

address local concerns, which leads to less overall pollution, particularly in the areas where

pollution is of greatest concern.

At the Federal level, we can contribute Federal standards and requirements using our

authorities to develop and implement a national regulatory program. We also have the

knowledge base and expertise to evaluate, or to help other agencies evaluate, air pollution

problems. By integrating our relative strengths, we can provide a stronger, more efficient, and

more effective program to address toxic air pollution in urban areas. For example, as discussed

in Chapter 5 of this Report, once we’ve completed the initial assessment, we’ll have a better

understanding of our status with regard to the risk reduction goals of the Strategy. This will

inform us about additional Federal activities needed to meet those goals, and what additional

State, local and Tribal activities are needed to complement these activities. Periodic assessments

will continue to inform us about needed programs over time. 

Concurrent with the initial assessments, we plan to meet with our State, local and Tribal

partners. We’ll be reviewing the goals and the various components of the Strategy and how they

interrelate. In particular, we’ll focus on the assessment tools and their role in defining Federal,

State, local, and Tribal activities. These activities may include pilot projects to identify and

address risk and may rely on some of the assessment activities and tools described below. 

Air Toxics Assessments

The third component of the Strategy discussed in this Report is the urban component of

national air toxics assessments (NATA). NATA will provide us with meaningful information

and allow us to describe progress that we’ve made in meeting our overall program and strategyspecific goals. We’ll identify the pollutants and sources that contribute to any failures in meeting

our risk reduction goals and provide information to support regulatory and policy decisions

needed to move us closer to meeting these goals. These activities rely on improving our base of
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ES-8

knowledge (e.g., concerning health effects and exposure characteristics) and tools (e.g.,

emissions inventories, monitoring networks, and computer models), along with our plans for

their improvement and related research. 

Historically, EPA’s risk assessment and decisionmaking have focused on the likelihood

of health effects associated with exposure to individual environmental contaminants. In recent

years, our risk assessment emphasis has shifted increasingly to a greater consideration of multiple

pollutants, endpoints, pathways, routes of exposure, and holistic reductions of risks. This

complex analysis is often called “cumulative risk assessment.” It describes who or what is at risk

of adverse effects and identifies sources and stressors considering several different routes of

exposure over varied timeframes. Assessing progress in reducing cumulative risks from HAP

will require us to move away from a focus on assessing reductions in tons per year emitted 

toward a focus on estimating reductions in cancer and noncancer risks associated with lower

emissions.

In general, the choice of appropriate risk assessment approaches will be influenced by

both the availability of data to support exposure assessment, and the level of detail and resolution

needed to support the purpose of the assessment. Possible approaches span a wide range, from

simple weighting adjustments of emissions data or ambient concentrations, to detailed

multipathway risk assessments. Our assessment approaches will be iterative in nature to take

advantage of emerging science, new data, and improved tools that become available as future

assessments are performed. Beginning in early 2000, we’ll conduct an initial set of assessments

that will be based on final, updated emissions data for the 1990-93 and 1996 time periods and the

best available methods and tools. 

We’ll tailor each assessment to the purpose(s) it is to serve (e.g., measuring progress

against the 75 percent estimated cancer incidence reduction goal). Accordingly, assessments will

vary in scope, level of refinement, and, thus, data and resource requirements. The scope of each

assessment will generally be defined by the following characteristics:

C The number of HAP to be evaluated (all 188 or some subset);

C Types of sources included (area, major, mobile);

C Spatial resolution (e.g., aggregation of results on the national, State, or urban scale); and

C Pathways and media to be evaluated (inhalation and air only or multipathway and

multimedia).

Further, for each assessment, we will specify an appropriate approach for estimating

progress toward our risk reduction goals since it will not be possible to directly measure

reductions in cancer incidence or noncancer risks attributable to HAP emissions. Alternative

approaches will range from rough approximations to more precise risk estimates, depending on

data and resource requirements.
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Our risk assessment science has been extensively peer-reviewed, is widely used and

understood by the scientific community, and continues to expand and evolve as scientific

knowledge advances. We intend to use the most current and appropriate risk estimation methods

to track progress under the Strategy.

Education and Outreach

The fourth component of the Strategy, communicating about risks through education and

outreach to the public, ensures that the activities we undertake are responsive to stakeholder

concerns. Over the course of implementing the Strategy, we plan to work with State, local, and

Tribal governments and other stakeholders on developing the national assessments of the risks

from air toxics and the materials to communicate the findings with the public. We will include

State, local and Tribal authorities, and in particular mayors, in planning activities to assess and

address local air quality concerns and plan pilot project activities under the Strategy.

We will also explore the formation of groups such as roundtables and panels to involve

communities, small businesses and other stakeholders, including representatives from

universities and hospitals. These groups will explore issues related to rulemaking coordination,

risk assessments, and the process of defining roles and responsibilities for Federal and State,

local and Tribal agencies in implementing the Strategy. In addition, many of the activities

identified in the Strategy will require public notice and comment, which will provide further

opportunities for stakeholder input as the various activities are developed. We’ll also continue to

use the established Integrated Urban Air Toxics Strategy website on the Internet to update the

public on ongoing activities and opportunities to participate in implementation of the Strategy. 

This will include updates on rule development, assessment activities, and progress toward

meeting all of the Strategy goals.

As noted above, we’re required by the CAA to provide two Reports to Congress on

actions taken to reduce the risks to public health posed by the release of HAP from area sources. 

The CAA also requires that the reports identify specific metropolitan areas that continue to

experience high risks to public health as the result of emissions from area sources. This

document is our first Report to Congress. The second report is required to be submitted by 2002. 

We also expect to report to the public about air toxics emissions trends and air quality in urban

and other areas in our annual Air Quality and Emissions Trends Reports.

Research Needs

The Strategy describes the process we’ll use for identifying the various risks that may be

present in an urban environment. Part of that process is to determine gaps in our scientific

information and to identify the tools we’ll need to assess urban risks and to implement the risk

reduction elements of the Strategy. Chapter 6 of this Report describes the activities and research

needed to assist in our assessment and management of risks in urban environments and to

improve risk assessment and risk management of air toxics from all emission sources.
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We’re also developing an Air Toxics Research Strategy which will build on the research

needs presented in this Report, as well as other research strategies that our Office of Research

and Development has prepared that address specific air toxics research issues (e.g., the draft

Mercury Research Strategy, the draft Human Health Risk Assessment Research Strategy, and the

Ecological Research Strategy). The Air Toxics Research Strategy will identify the key scientific

questions that need to be answered for risk assessment and management of air toxics from all

emission sources and describe the research needed to answer them and, thereby, guide our

research efforts.
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1

Examples of area sources include hospital sterilizers, dry cleaners, and small publicly owned treatment

works.

1-1

1. Introduction

Since the enactment of the CAA Amendments of 1990, we have made considerable

progress in reducing emissions of air toxics from major stationary sources through regulatory,

voluntary and other programs. Our efforts to characterize, prioritize and address the impacts of

HAP on the public health and the environment have resulted, or are projected to result, in large

reductions in HAP emissions. However, the pollution sources addressed by our efforts so far

account for only part of the air toxics problem.

Recently, EPA announced a Strategy that aims at reducing the health risks associated with

air toxics exposures affecting populations in urban areas. In addition to addressing specific

statutory requirements for area sources as outlined in section 112(k), the Strategy has the

following goals:

• Attain a 75 percent reduction in incidences of cancer attributable to exposure to HAP

emitted by stationary sources in urban areas nationwide;

• Attain a substantial reduction in public health risks posed by HAP emissions from area

sources in urban areas nationwide;1 and

• Address disproportionate impacts of air toxics hazards across urban areas.

By integrating activities and programs under different parts of the CAA, we expect to

address more effectively the aggregate exposure to air toxics in areas where emissions and risks

are most significant.

This Report responds to a requirement in section 112(k)(5) of the CAA that calls for EPA

to submit a Report to Congress:

On actions taken under this subsection and other parts of this Act to

reduce the risk to public health posed by the release of hazardous

air pollutants from area sources. The reports shall also identify

specific metropolitan areas that continue to experience high risks to

public health as the result of emissions from area sources.

Even though this Report is being released shortly after the publication of the Strategy, it

provides further details on many of its key areas. For example, this Report contains a more

detailed discussion of the research needs to be addressed as part of the Strategy. Also, the

emissions inventory and methodology for the selection of the urban HAP are discussed more

thoroughly here. Since the Strategy has not been implemented yet, we’re unable, in this Report,
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2Major stationary sources are sources that emit more than 10 tons per year of any one HAP or 25 tons per

year of a combination of HAP. Examples include chemical plants, oil refineries, aerospace manufacturers and steel

mills.

3Mobile sources include motor vehicles (e.g., cars and trucks), and off-road equipment (e.g., construction

equipment and lawn mowers) and their fuels.

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to identify specific metropolitan areas that continue to experience high risks to public health. 

Nevertheless, we are providing, in this Report, a summary of recent risk-based assessments in

various urban areas. These assessments provide useful information on the potential nature and

magnitude of exposures and health risks in urban areas.

The following sections will provide a glimpse of the main issues discussed in each

chapter of this Report. Also, the Appendix gives key information about each of the urban HAP.

1.1 Characterization of Urban Air Pollution (Chapter 2)

The urban environment is very unique since the combination of high population densities

and large concentrations of commercial activity provide the conditions conducive to high

exposures and health risks as a result of the emissions of air toxics. Hazardous air pollutants are

emitted from thousands of sources ranging from small commercial facilities to large industrial

sources and also mobile sources. As the ambient concentrations of HAP in urban areas result

from a combination of different sources (e.g., area, major2, and mobile3) emitting many of the

same pollutants, we need to consider contributions from all types of sources in order to achieve

the reductions envisioned by Congress. The Strategy, described in detail in this Report, is that

part of the overall air toxics program that specifically focuses on the urban environment. The

Strategy will consider contributions from area, major, and mobile sources of HAP in addressing

reductions in public health risks.

Chapter 2 provides general information on our current understanding of the urban

environment and presents a summary of risk analyses that have been conducted over the past 10

years. Although it is not possible to draw any specific conclusions on current health risks, the

data that are available today support our concern that potential problems exist in urban areas and

suggest that we should continue our efforts to study the urban environment and to implement the

Strategy this Report presents.

1.2 Emissions Inventory and Selection of the Urban Pollutants (Chapter 3)

Chapter 3 presents two very important components of the Strategy. The first is the

baseline emissions inventory for 40 candidate HAP used to identify the final list of urban HAP. 

The baseline inventory quantifies the emissions of the candidate urban HAP and identifies the

source categories that emit them. The second is the ranking methodology used to identify the

final list of 33 priority urban HAP which are judged to present the greatest threats to public

health in the largest number of urban areas. 
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In developing the final HAP list, we estimated emissions from all known sources using a

variety of techniques, evaluated available health effects information for the 188 HAP, assessed

available air quality monitoring data, reviewed existing studies, and produced a list of pollutants

based on the relative hazards they pose in urban areas, considering toxicity, emissions, and

related characteristics. From this effort, we established a list of urban HAP which pose the

greatest threats to public health in urban areas, considering emissions from major, area and

mobile sources. Among these urban HAP are a subset of 30 HAP with the greatest emissions

contributions from area sources (the “area source HAP”). The analyses leading up to the

selection of these priority urban HAP are the focus of this chapter. 

1.3 Regulatory Programs and Activities to Reduce Air Toxics Emissions

(Chapter 4)

Chapter 4 presents the list of area source categories that were identified in the Strategy

and explains how we intend to ensure that, as required, we reach the goal of addressing the

source categories that represent 90 percent of the emissions of each of the 30 area source HAP. 

Also, this chapter describes the regulatory options that will be considered in order to address air

toxics from area sources. The role of mobile sources is also noted in this chapter, and the current

and future programs are described. Finally, a very important component of the Strategy is

described in this chapter – the role of State, local and Tribal programs in helping us address air

toxics and achieve the desired goals.

Chapter 4 describes the regulatory approaches to enable the emission reductions

necessary to achieve the goals of the Strategy. We plan to pursue a tiered approach that will

consider three standard-setting processes. The specific process selected for a particular source

category will depend on the criteria outlined below: 

C Tier 1 – Maximum achievable control technology (MACT) standard process;

C Tier 2 – Source category-specific generally available control technology (GACT)

standard process; and

C Tier 3 – Flexible GACT process.

The Strategy outlined a timeframe for the completion of area source standards, as shown

in the time line below:

C 2004 – Promulgate the area source standards newly listed in the Strategy; we’ll attempt to

meet this demanding schedule as expeditiously as practicable;

C 2006 – Promulgate some additional area source standards to meet the 90 percent

requirement;
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C 2009 – Promulgate all remaining area source standards necessary to meet the 90 percent

requirement; and

C 2012 – Expected compliance under all standards.

We’ll prioritize the order in which we regulate source categories to address those posing

the greatest risks first. 

Mobile sources and their role in the air toxics problem are also discussed in Chapter 4. 

Several of our existing emission control programs limit HAP emissions from mobile sources,

primarily through the regulation of hydrocarbon (HC), oxides of nitrogen (NOx) and particulate

matter (PM) emissions. We achieve mobile source controls through a range of programs under

various sections of the CAA, including motor vehicles controls, emission standards for nonroad

engines and vehicles and urban bus standards. In addition, section 202(l)(2) of the CAA directs

us to set standards for air toxics emissions from motor vehicles or their fuels, or both. Some of

the current and future regulations and programs aimed at reducing HAP emissions from mobile

sources are highlighted in this chapter.

1.4 Assessment of Progress Toward the Goals (Chapter 5)

The discussion of our assessment activities in this chapter first focuses on how we

generally intend to assess progress in meeting the goals of the Strategy. We then discuss in more

detail our methods and tools for estimating health risks and describe more specifically how we

intend to apply these risk assessment methods and tools in assessing progress and in supporting

implementation of the Strategy.

As we move from a focus on emissions reductions to a focus on estimated risks

reduction, we note that Agency risk assessment and decisionmaking have historically focused on

the likelihood of health effects associated with exposure to individual environmental

contaminants. In recent years, our risk assessment emphasis has shifted increasingly to a greater

consideration of multiple pollutants, endpoints, pathways and routes of exposure, and integrated

reduction of risks. This more complex assessment is often called “cumulative risk assessment,”

defined according to who or what is at risk of adverse effects, from identifiable sources and

stressors, through several routes of exposure over varied timeframes. While various integrated

approaches are now being used within the Agency, we realize that there are significant gaps in

methods, models and data that limit our ability to assess cancer and noncancer risks associated

with cumulative exposure to mixtures of pollutants having different endpoints. Progress toward

more refined assessments of cumulative risks will depend upon the pace and evolution of our

policy and guidance on cumulative risk and the underlying research.

We’ve identified four basic approaches that we plan to use for various assessments to

evaluate the progress of the Strategy in reducing estimated risks. Each of these approaches uses

the same dose-response information, but relies on different types of data to represent exposures. 

The four basic approaches that we intend to use are:
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C Emissions or ambient concentration weighting;

C Comparisons between ambient concentrations and risk-based concentrations (RBCs);

C Comparisons between estimated exposures and RBCs; and

C Quantitative estimates of carcinogenic risks for individuals and populations.

Each of these approaches is discussed in Chapter 5.

1.5 Research Needed to Address Knowledge Gaps (Chapter 6)

The purpose of Chapter 6 is to describe the types of scientific information and related

research needed to better inform future risk assessment and risk management judgments that will

be made in carrying out the Strategy. The research needs presented in this chapter are

categorized into both short-term (less than five years) and long-term (greater than five years). 

These needs are organized around the risk assessment/risk management paradigm, first

promulgated by the National Academy of Sciences in 1983. The needs are listed below:

Exposure Assessment Information Needs

Need 1. Improved ambient monitoring methods, characterization, and network design to

support a national ambient air toxics monitoring network.

Need 2. Improved area source emissions estimation methodologies and spatial allocation

methods.

Need 3. Methodologies that allow for identification and speciation of important HAP and

their combustion and transformation products.

Need 4. A more accurate nonroad mobile source emissions characterization.

Need 5. Improved characterization of air toxics from trucks and improvement of modal

emissions modeling capabilities for all vehicle classes.

Need 6. Development of source-based urban-scale air quality models for the urban HAP.

Need 7. An understanding of the distribution of human exposures (including susceptible

subpopulations) and the pathways by which HAP reach humans.

Health Effects Information Needs

Need 8. Use alternative sources of human health effects data (chronic and acute) for urban

HAP to develop and update dose-response assessments.

Need 9. Development of statistical and mode of action methods for developing acute and

chronic dose-response assessments.
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Risk Assessment and Risk Characterization Information Needs

Need 10. Improved risk assessment methods for mixtures.

Need 11. Development of better information for more effective techniques for

communicating the results of health risk assessments for urban HAP.

Risk Management Information Needs

Need 12. Identification of processes contributing to the HAP emissions from area source

categories, and listing of control options and pollution prevention alternatives for

these processes.

Need 13. Identification of pollution prevention alternatives for HAP emissions from mobile

sources.

Each of these needs for further research are discussed in Chapter 6.
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1Caprolactam was delisted on June 18, 1996 (61 FR 30816)

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2. Characterization of Urban Air Pollution

2.1 Introduction

The urban environment is unique in many ways. In urban areas, you will find a mix of

chemicals and their sources in close proximity to diverse populations, leading to large numbers

of people being exposed to the emissions of many HAP from many sources. While urban

exposures to some pollutants may be fairly similar across the country, studies in a number of

urban areas indicate that exposures and associated risks may vary significantly from one urban

area to the next. Recognizing this, Congress instructed us to develop a strategy for air toxics in

urban areas that includes specific regulatory actions addressing the large number of smaller,

stationary sources (i.e., area sources), and which also contains broader risk reduction goals

encompassing all stationary sources. Specifically, section 112(k)(1) of the CAA states:

The Congress finds that emissions of hazardous air pollutants from area sources may

individually, or in the aggregate, present significant risks to the public health in urban

areas. Considering the large number of persons exposed and the risks of carcinogenic

and other adverse health effects from hazardous air pollutants, ambient concentrations

characteristic of large urban areas should be reduced to levels substantially below those

currently experienced.

As the ambient concentrations of HAP in urban areas result from a combination of

different sources (i.e., area, major, and mobile) emitting many of the same pollutants, we need to

consider contributions from all types of sources in order to achieve the reductions envisioned by

section 112(k). The Strategy presented in the July 19, 1999 Federal Register (U.S. EPA, 1999a),

and discussed in this Report, is a part of our overall national effort to reduce toxics but with a

specific focus on the urban environment. The Strategy will consider contributions from area,

major, and mobile sources of HAP in addressing reductions in public health risks.

This chapter is intended to provide general information on our current understanding of

the air quality in the urban environment, to present a summary of risk analyses that have been

conducted over the past 10 years, and to provide the basis for our continuing support for an urban

program that will enhance our understanding of the urban environment and provide the strategy

for protecting the health of the public.

2.2 What Do We Know About HAP?

Section 112(b) of the CAA identifies 188 chemicals as HAP1. They include pollutants

like benzene, perchloroethylene, methylene chloride, heavy metals like mercury and lead,

polychlorinated biphenyls (PCBs), dioxins, and some pesticides. More than half of the HAP are

known or suspected to be human carcinogens. In addition, many are known to affect the
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Section 313 of the Emergency Planning and Community Right-To-Know Act (EPCRA) and section 6607

of the Pollution Prevention Act (PPA) mandate a publicly accessible database containing information on the release

and other waste management activities of toxic chemicals by facilities that manufacture, process, or otherwise use

them. The EPCRA specifically requires manufacturers to report releases of more than 600 designated toxic

chemicals to the environment. The reports are submitted to the EPA and State governments. The EPA compiles

these data in an on-line, publicly accessible national computerized TRI. More information about the TRI database

is available at the following website: http://www.epa.gov/opptintr/tri/.

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respiratory, neurologic, immune, reproductive, or developmental systems, particularly for more

susceptible or sensitive populations, such as children. Hazardous air pollutants are also known to

cause adverse effects in many species (e.g., toxicity in fish or reproductive decline in bird

species), including endangered species. These environmental effects may impact individual

species within a single level of the food chain or the entire ecosystem where multiple species are

affected.

Health concerns result from both short- and long-term exposures. Some health problems

occur very soon after a person inhales a toxic air pollutant (i.e., from a short-term exposure). 

These immediate effects may be serious, such as life-threatening lung damage, or they may be

minor. Health problems which are usually associated with long-term exposures may develop

slowly over time or may not appear until many months or years after a person’s first exposure to

the toxic air pollutants (e.g., cancer). Depending on their characteristics (e.g., vapor pressures

and atmospheric transformation rate), HAP may disperse locally, regionally, nationally, or

globally and may deposit in the environment and in some cases, bioaccumulate in the food chain.

2.3 What Do We Know About HAP Emissions?

Hazardous air pollutants are emitted from a variety of stationary sources of varying sizes

and from mobile sources. Emissions data, along with specific information about the emitting

sources (e.g., the height and location of the emissions release points, size of emitting facility,

local meteorology), may be used as inputs to computer models. These models generate estimates

of ambient HAP concentrations in areas surrounding a source. Although these concentrations are

not estimates of personal exposure and risk, an understanding of these emissions and their

sources is necessary when preparing a strategy for dealing with associated risks to public health

and the environment.

 For this reason, we developed the National Toxics Inventory (NTI). The NTI contains

emissions data for major, area and mobile sources. The data for the NTI have been gathered

from EPA (i.e., MACT development data and the Toxic Release Inventory, or TRI2), State, and
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3

The baseline NTI that we have compiled over the past few years is representative of the years 1990-93.

4

In estimating the amount of emissions from urban areas, we have totaled emissions from all U.S. counties

that include a metropolitan statistical area with a population greater than 250,000 or for which more than 50 percent

of the population has been designated “urban” by the U.S. Census Bureau. For a more detailed description of

emissions allocation among urban and rural areas, see the technical support document for the emissions inventory

which is available through the public docket (Docket No. A-97-44).

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EXHIBIT 2-1

HAP BASELINE NTI 

EMISSIONS BY SOURCE

Adapted from Trends Report (EPA, 1998)

Representative of 1990 - 1993 period

EXHIBIT 2-2

HAP EMISSIONS BY STATE BASED ON 1993 NTI

local studies and databases. A baseline year NTI3

has been developed and estimates emissions at

the county level. According to this inventory,

approximately 8.1 million tons of air toxics were

released annually (during the 1990 to 1993

timeframe) to the air nationwide with

approximately 6 million tons being released

annually into urban areas4. Exhibit 2-1 provides a

breakdown of the total, national emissions by

source. 

Although the level of specificity of this

inventory is insufficient for drawing conclusions

about population exposure levels in individual

urban areas versus rural areas, these data show

that the largest emissions are

found in those States which are

highly industrialized and contain

some of the largest urban areas in

the country. Exhibit 2-2 (taken

from 1997 Trends Report (EPA,

1998)) illustrates the distribution

of HAP baseline emissions by

State. While these national-level

emission estimates are useful for

describing general trends, they do

not necessarily reflect the specific

situation that may exist in specific

urban areas where a wider variety

of HAP are emitted. This is

particularly important because

some pollutants which

individually would not be

expected to present harm, may

work together as a mixture resulting in a potential for harm. Thus, depending on exposure levels
National Air Toxics Program: The Integrated Urban Strategy

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5An analysis of human activities published in 1996 reported that people spend as much as 69% of their

time in personal residences with an additional 18% of time being spent in other indoor environments (EPA, 1996).

6More information on indoor air quality may be obtained at the following website: http://www.epa.gov/iaq.

7

The concentration of HAP present in the ambient air that is not solely attributable to a specific or

identifiable source being studied. For example, a monitor may detect HAP emissions from stationary, mobile, or

nonanthropogenic sources while the source being modeled (i.e., the source of the emissions data being used) is a

stationary source.

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and characteristics of the pollutants, multiple pollutant exposures which may be more prevalent

in urban populations may pose increased public health risks.

An updated version of the NTI containing emission data from 1996 is currently being

developed. This 1996 NTI will be our first effort to estimate HAP emissions from all sources on

a national scale and to associate with them source-specific parameters necessary for modeling. 

Important modeling parameters include location and facility characteristics which describe the

emission points (e.g., stack heights, stack exit velocities, emission temperatures). This new

inventory will have greater utility for assessing trends in emissions, for providing data in

sufficient detail to perform regional, urban, and local level air quality and exposure modeling

assessments, and to monitor progress on risk reductions.

Emissions data such as the NTI provide useful estimates of emissions in outdoor air, but

they do not reflect the levels of HAP that exist in many indoor air environments. It is estimated

that most people spend as much as 80 to 90% of their time indoors5. This is of particular concern

because over the past several decades, exposure to indoor air pollutants is believed to have

increased due to a variety of factors, including the construction of more tightly sealed buildings,

reduced building ventilation rates (to save energy), the increased use of synthetic building

materials and furnishings, and the increased use of chemically formulated personal care products,

pesticides, and household cleaners. Our current lack of understanding of the nature of indoor

sources of HAP and our limited information on the movement of air between the outdoor and

indoor environments leave a gap in our ability to more completely characterize human exposures,

especially in urban areas6.

2.4 What Do Monitoring Data Tell Us?

Monitoring data provide information about the ambient levels of HAP in specific areas

and generally represent a snapshot of what HAP are present. These data, like modeled ambient

concentration data, may provide information about the potential for exposure and risk. When

monitoring data are used, however, the ability to identify the particular emitting source may be

lost unless the placement of the monitor allows for the detection of HAP contributions from

uniquely identifiable sources. Where the source or sources contributing to the monitored HAP

levels are not known, the monitored HAP levels may be considered to be a background

concentration7. In these cases, background concentration data may provide a comparison and/or
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8An air contaminant may undergo a chemical change in the atmosphere as it either breaks down or reacts

with other chemicals. The pollutants that are formed as a result of this transformation process may be more or less

toxic than the pollutants originally released.

9

The technical support documentation for this assessment analysis is available from the public docket

(Docket No. A-97-44) and includes a presentation of ambient monitoring data in 17 cities for a variety of HAP. 

Also presented are the upper bound estimates of excess cancer risks associated with continuous lifetime exposures

at those concentrations. 

2-5

a context concentration for ambient HAP levels estimated by modeling. In other cases,

background concentration data for a specific HAP may be added to the ambient HAP levels

estimated by modeling to account for known HAP sources not considered in the modeling

analysis. This may be done for HAP such as formaldehyde because of its ability to be formed by

the direct chemical transformation8 from other HAP in the air (see Section 2.6 of this Report for

more detailed discussion of transformation).

Currently, there is no national ambient air quality monitoring network designed to

measure the ambient levels of HAP in the environment. The data we have available nationally

come from monitoring that is done under programs like the Photochemical Assessment

Monitoring Stations (PAMS) program, the PM2.5 monitoring network, and from the many

voluntary State monitoring programs. The ambient air monitoring information collected by

States in certain metropolitan areas provides us with a limited understanding of HAP ambient

concentrations in urban areas. Data collected during the 1990's demonstrate elevated

concentrations of several HAP in urban areas across the country. For example, a limited

evaluation of the subset of HAP monitored indicate the presence of HAP in some cities which,

when evaluated cumulatively, is suggestive of upper bound estimates of additional, lifetime

cancer risks at or above 1 in 10,0009. Comparisons of estimated concentrations to RBCs can

provide indicators of a potential public health problem but should not be considered a

characterization of actual health risks. 

2.5 What Do We Know About Urban Populations?

A unique feature of urban areas is the proximity of many stationary and mobile sources

and their pollutants to each other and to the populations which live or work in these areas. 

According to a 1997 report on population (U.S. Department of Commerce, 1997), approximately

212 million people (including 57 million children) or 80% of the estimated 1996 U.S. population

live in metropolitan areas. This estimate represented a gain of 13 million people in these areas

since the 1990 census estimate. Given (as described earlier) that the largest levels of HAP

emissions are found in those States which contain some of the largest urban areas, we seem to

have mixtures of HAP and increasingly high density populations existing together in urban areas.

The issue becomes complex when other population factors such as age, socio-economic

status, proximity to emitting sources, decreased health and nutrition status, and lifestyles are

considered because it is known that these factors may lead to increased sensitivity and
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

10The movement of people through different daily micro-environments as they participate in various

activities. For example, being in an indoor or outdoor environment, or riding in a car are a few of microenvironments to consider in an exposure assessment.

2-6

susceptibility to the effects of HAP exposures. Within the general population, children, for

example, are likely to have additional susceptibility and vulnerability to HAP exposures because

of their daily activities, their immature or developing metabolic systems, or their developing

organ systems. In addition, the poverty factor (over 20% of the urban population consists of

children in poverty (U.S. Department of Commerce, 1997)) increases their vulnerability because

they are more likely than other children to lack sufficient nutrition and access to health care. 

In conducting an assessment that considers the population (i.e., an exposure assessment),

models are used to characterize population exposures based on ambient concentration data

(derived from modeling or monitoring). Specific population exposure factors such as the

location of various populations, population demographics, and group activity patterns10 when

coupled with HAP toxicity information provide a clearer picture of how, when, and for how long

people are exposed to HAP and what their potential risks may be. These are a few of the many

aspects that are considered when evaluating public health risks from HAP in urban areas. 

2.6 Characterization of Air Toxics in Urban Areas

As discussed above, different types of information may be useful for characterizing the

urban environment. In this Report, we have focused on nine risk-based assessments performed

by EPA and various States over the past ten years. Although some general similarities are

evident across these assessments, the identity and concentration of air toxics may vary

significantly from one city to the next depending on the particular sources present (or dominant),

the substances emitted, the local meteorology, and other factors. It should be noted that most of

these studies were based upon the situation that existed in urban environments up to ten years

ago. Given our current, national information, the situation is likely to have improved. That

notwithstanding, the summaries contribute to our understanding of the potential nature and

magnitude of exposures and health risks in specific urban areas and to the pollutants and sources

contributing to those exposures and risks.

To put these assessments in perspective, it is useful to first discuss some of the

uncertainties that were inherent in these assessments because of the lack of information at the

time or because of the way these assessments were designed. We can evaluate uncertainties from

the perspective of what we don’t know or what wasn’t considered in the analysis. For example,

most of these assessments did not consider risks from endpoints other than cancer, pathways

other than inhalation, or exposures other than long-term. The potential exposure to HAP for

which we have little or no health data was assumed to have resulted in no adverse health effects. 

These uncertainties are not quantifiable but are our reason to err on the side of conservatism

when it comes to interpreting the different assessments. The other side of the uncertainty

question (i.e., what we do know now that we didn’t know then) may have quantifiable effects. 
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

11The review and revision of data (resulting in revised unit risk and reference values) for the HAP in these

studies, (e.g., 1,3-butadiene) and for the other HAP not included in these studies is an ongoing process. It is likely

that the results of the studies described here would be different had these results been reevaluated. Future

assessments will have the benefit of the most current health effects data. 

12As described in Chapter 5 of this Report, our assessment approach will be generally iterative in nature, so

as to take advantage of emerging science, new data, and improved tools that become available at the time future

assessments are performed, (e.g., with better emissions and exposure data, our exposure estimates will be more

central tendency than upper bound). The resulting risk characterizations in these future assessments should reflect

this shift in data quality.

2-7

One HAP, 1,3-butadiene, was identified as a very common urban HAP responsible for much of

the estimated risk seen in these assessments. Currently, we are reevaluating the cancer potency

value, and it is likely that the potency value will decrease (i.e., the potency will likely be lower

than what was used in these assessments). This is important to keep in mind because many of

the assessments highlighted this HAP as being a major contributor to risk levels11.

Uncertainty is also present when various policy assumptions are used in deriving cancer

risk estimates. In most of these assessments (as well as many current screening assessments),

measurements and estimates of air concentrations are used, with the assumption of a lifetime

exposure to these concentrations, to calculate upper-bound estimates of an individual’s lifetime

increased cancer risk from each pollutant. Upper-bound estimates are used in order to avoid

underestimating the true value. The true value may, however, be lower than the estimate and

may, in fact, be zero. The upper-bound estimates for each HAP are summed to obtain a worstcase estimate of individual lifetime increased cancer risk resulting from exposure to the mixture

of HAP. For each of the studies described below, these worst-case estimates were on the order of

a 1 in 10,000 chance of getting cancer for someone exposed continuously over a 70-year

lifetime12. For substances that are not thought to cause cancer, air concentration estimates are

compared to concentrations considered unlikely to be harmful. These rough worst-case estimates

are used to identify those HAP posing the greatest likelihood of harm. For these nine

assessments, it must be kept in mind that other HAP which may have been present in the urban

air, and for which toxicity information was insufficient for the risk assessments, were excluded

from these calculations.

Additionally, not all possible HAP were considered in these assessments because HAP

selected usually met one or more of the following conditions: they were known or suspected to

be present in urban air, they were suspected to be important contributors to health risk based on

knowledge of their toxicity (most urban air studies to date have focused primarily on pollutants

either known to cause cancer in humans or for which test data are less conclusive yet provide an

indication of a potential to cause cancer), and/or there were available data on their emissions or

ambient concentrations. Pollutants that have been commonly studied in urban areas include

arsenic, benzene, 1,3-butadiene, cadmium, carbon tetrachloride, chromium, ethylene dichloride,

formaldehyde, methylene chloride, perchloroethylene, polycyclic organic matter (POM) (which
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

2-8

include polycyclic aromatic hydrocarbons and certain other chemicals that have multiple benzene

rings that are emitted as products of incomplete combustion), and trichloroethylene. Each of

these pollutants has been evaluated in multiple major studies of urban air, including the nine

assessments discussed below. Benzene and formaldehyde were evaluated in all nine of the

studies.

These assessments relied on source inventories that were created much earlier than the

assessments. Although a variety of sources were identified and assessed in different urban areas,

no attempt was made to identify all of the possible, specific sources of emissions. The particular

emission sources of concern can vary widely from one city to the next, and many of these

assessments concentrated only on what were thought to be the largest sources or only on one type

of source (e.g., area sources). Today’s inventories have reduced the potential uncertainty in this

area because more source data are available and have been included in the recent NTI (discussed

previously). These data which include area, major, and mobile source data will be used in future

urban risk assessments.

Emission estimates (i.e., inventories) do not consider that some HAP may disperse over

great distances (mercury, for example, may disperse globally). This type of HAP dispersion or

long-range transport would be of particular concern for HAP that have longer half-lives or which

may persist in the environment for a longer time. In the case of persistent HAP, re-volatilization

or resuspension of a deposited HAP may continue the transport of that HAP to more distant

locations. When developing an emissions inventory (i.e., a list of sources emitting HAP of

interest or concern), it is not always possible to consider sources that are too distant from the

geographic areas of interest. This may lead to an underestimate of the ambient HAP

concentrations predicted by modeling (dispersion models typically limit the ambient

concentration estimates calculated to a 50 kilometer (approximately 30 mile) radius around an

identified source). This is less of an issue when monitoring data are used as the basis for the

ambient HAP concentrations because monitors detect HAP regardless of their sources or their

distance from the monitor. The inventories developed for the urban assessments discussed below

did not consider the long-range transport of the HAP of interest into the geographic areas of

study.

The inventories developed for these assessments, also, did not consider the potential

effects of atmospheric transformation. An air contaminant may undergo a chemical change in the

atmosphere as it either breaks down or reacts with other chemicals. The pollutants that are

formed as a result of this transformation process may be more or less toxic than the pollutants

originally released. Just as some contaminants may degrade to less harmful chemicals,

sometimes relatively innocuous airborne chemicals may combine with other chemicals in the

atmosphere to form HAP (e.g., the formation of formaldehyde (a HAP) from the chemical

reaction among the components of “smog” and isoprene, a less harmful chemical). Transformation in the atmosphere may occur as the chemicals are dispersed and transported from an

emitting source. If the transformation process is not considered or only partially considered (by

adding some “background value,” as some of the urban assessments did), the significance of this
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

13The design of each of the studies discussed included assumptions described as conservative or worst case. In these

cases, the incidence values presented within the context of each study may overestimate the true incidence. Conversely, the

limitations of the study designs and assumptions (i.e., these studies did not consider pathways of exposure other than inhalation,

exposures other than long term, risks from other HAP present in these study areas or their potential synergistic interactions) leave

open the possibility that the incidence values presented may underestimate the true risk.

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on the final result must be part of the evaluation process when considering the results of these

assessments.

None of the urban assessments discussed below considered specific sub-populations (i.e.,

populations that may be more susceptible or vulnerable to HAP exposure) in their calculations of

potential risks. In addition, these assessments, with the exception of the Mobile Vehicle Study,

did not project changes in those aspects of daily lives that will continue to change the profile of

emissions and exposures especially in urban areas. For example, the number of miles traveled by

commercial and private vehicles nationally from 1990 to 1996 increased by approximately 310

billion miles (an average increase of 52 billion (2.5%) vehicle miles traveled (VMT) per year)

(U.S. Department of Transportation, 1998). If the change in the U.S. population during this time

is considered (248.7 to 265.3 million people, respectively (U.S. Department of Commerce,

1997)), the increase in VMT is not due solely to a population increase but to an increase in the

number of miles “each person” traveled. This becomes an important factor when the overall

results of many of the urban assessments point to mobile sources and their HAP as contributing

to potential urban area risks.

In general, for each of the assessments discussed below, outdoor HAP concentrations

(estimated using computer modeling projections or ambient air monitoring) were used to

represent potential human exposures. When combined with simplifying assumptions that can

lead to either under- or overestimates of risk, researchers were able to reach conclusions about

the chemicals, and in some cases the air pollution sources, that seem to contribute the most to

risks from urban air pollution. In these assessments (e.g., benzene, 1,3-butadiene, and

formaldehyde were consistently shown to be most responsible for the higher risk estimates), the

studies identified all three major source categories (area, major and mobile sources) as

contributing emissions and potential risks in urban areas, and they presented estimates of

increased individual lifetime cancer risks from air toxics from multiple sources across the studies

that ranged from 3 in 1,000 to 2 in 1,000,000 (with a median of 1 in 10,000) (although the true

risks could be higher or lower13). While providing useful information on the potential nature and

magnitude of health risks in urban areas, these assessments are limited by the lack of exposure

information and by the incompleteness of our knowledge regarding the range of health effects

associated with any additional HAP that may be found in urban environments. The nine

assessments listed in Exhibits 2-3 and 2-4 are summarized below.
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

2-10

EXHIBIT 2-3

RISK-BASED ASSESSMENTS COVERING URBAN AREAS

Risk-based Assessments Abbreviated

Name

U.S. EPA, 1989. Analysis of Air Toxic Emissions, Exposures, Cancer Risks and Controllability

in Five Urban Areas. This study was designed to define the multisource, multipollutant nature

of the urban air toxics problem and determine what control measures can best be employed to

mitigate the problem.

Five City Study

Engineering-Science, 1990. The Transboundary Air Toxics Study: Final Summary Report.

Risk assessment to evaluate the source types and pollutants which contribute to increased cancer

risk from air pollution in the Southeast Michigan/Windsor-Sarnia area.

Transboundary 

Study

MPCA, 1992. Estimation and Evaluation of Cancer Risks from Air Pollution in the

Minneapolis/St. Paul Metropolitan Area. Study by the Minnesota Pollution Control Agency to

analyze sources of HAP suspected or known to cause cancer, and to estimate the health risk

from exposure to these pollutants.

Twin Cities Study

U.S. EPA, 1993b. Staten Island/New Jersey Urban Air Toxics Assessment Project: Summary of

the Project Report. Assesses risk to Staten Island residents from ambient air pollutants and

generates an inventory of major, area and mobile sources to qualitatively examine sources of

high risk and high observed concentrations.

Staten Island

Study

U.S. EPA, 1993a. Motor Vehicle-Related Air Toxics Study. Summarizes what is known about

motor vehicle-related air toxics.

Motor Vehicle

Study

U.S. EPA, 1994. A Screening Analysis of Ambient Monitoring Data for the Urban Area Source

Program. Summarizes currently available ambient monitoring data sets for HAP from various

urban areas in the U.S. and estimates the risks associated with these HAP.

Ambient

Monitoring Study

ENSR, 1995a, b, c. Arizona Hazardous Air Pollution Research Program. Risk assessment to

determine which HAP and sources should be the focus of future research and control strategies

in Arizona. 

Arizona Study

TNRCC, 1996. Houston Area Source Toxics Emissions Project. Risk assessment to determine

which HAP from area sources should be focused on for future research and control strategies in

Houston.

HASTE Study

Woodruff et al., 1998. Cumulative Exposure Project. Assessment which compared modeled

ambient air concentration estimates with health benchmarks for 148 HAP nationwide.

CEP
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

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Five City Study

Time Period Covered: 1980 – 1987

Top HAP Contributing to Predicted HAPRelated Cancer Risk: POM, 1,3-butadiene,

formaldehyde, benzene, and chromium

Individual Lifetime Cancer Risk Estimates:

Ranged from 2 x 10-4 to 7 x 10 -4 (two to ten excess

cancer cases per year across the five cities)

EXHIBIT 2-4

OVERVIEW OF ASSESSMENTS

Study

Approach No. Air 

Contaminants

Studied

Location Health Effects

Hazard Evaluated

Assessment

Ambient

Monitoring

Five City Study U 23 5 unspecified cities Cancer

Transboundary U 57 Southeast Michigan/WindsorSarnia area Cancer

Twin Cities Study U 29 Minneapolis/St. Paul

metropolitan area Cancer

Staten Island Study U U 40 Counties in NJ and NYa Cancer,

Noncancer

Motor Vehicle Study U 4

b U.S. locations Cancer

Ambient Monitoring

Study U U 195c

40 U.S. locations Cancer,

Noncancer

Arizona Study U U 163d Phoenix, Tucson, Casa

Grande, and Payson, AZ 

Cancer,

Noncancer

HASTE Study U U 40 Harris County, TX Cancer,

Noncancer

CEP U 148 National assessment Cancer,

Noncancer

a

 Middlesex and Union Counties in New Jersey and Staten Island in New York for area and mobile sources, with

the addition of Monmouth, Essex, and Hudson Counties in New Jersey and Brooklyn (Kings County) in New York

for major sources.

b

 Study included four HAP and three mixtures (diesel and gasoline particulates and gasoline vapors).

c

 Monitoring data available for 195 air contaminants, but assessment focused on 93 HAP for which health effects

data were available. 

d

 Of the 163 possible contaminants, 25 chemicals of interest were selected for each of the four regions.

Five City Risk Assessment

This assessment, published in 1989,

was done to help characterize the

multisource, multipollutant nature of the

urban environment (U.S. EPA, 1989). A

base year emissions inventory was

compiled for each of five, unspecified

cities from a number of different data

sources and included inventories

representing point, area, and mobile source

emissions. The base year nominally

represents 1980 but selected source updates
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

14Modeled ambient concentrations were subtracted from ambient values derived from monitoring to yield

that portion of the ambient concentration due to the atmospheric transformation of other chemicals to formaldehyde.

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Transboundary Study

Time Period Covered: 1980 – 1989

Top HAP Contributing to Predicted HAPRelated Cancer Risk: Formaldehyde, coke oven

emissions, 1,3-butadiene, carbon tetrachloride,

chromium, POM, dioxins

Individual Lifetime Cancer Risk Estimates:

9 x 10-5 or five cancer cases per year over total study

area

were included so that the inventory was actually more reflective of the 1980 to 1985 timeframe. 

Emissions and source data were modeled to estimate annual average ambient HAP

concentrations for all 23 HAP included in this assessment. Monitoring data for formaldehyde

were included in order to calculate estimates of formaldehyde ambient concentrations that were

due to atmospheric transformation14. The ambient data for all HAP were then converted to

estimates of individual, lifetime cancer risks and incidence by applying the cancer unit risk

factors that were available at that time. The individual lifetime cancer risks ranged from 2 x 10-4

to 7 x 10-4 and provided an estimate of the multisource, multipollutant contribution to exposure

for the entire study area. This assessment did not consider routes of exposure other than

inhalation nor endpoints other than cancer. 

Transboundary Study

This assessment was initiated to

prepare an emissions inventory that through

risk assessment would help define the

relative contributions of various source

types to the risk estimated in the urban

transboundary area (Southwest Michigan/

Windsor-Sarnia area) (EngineeringScience, 1990). The pollutants chosen were

“generally substances known to be

atmospherically deposited in this region,

substances known to pose carcinogenic risk

or other substantial human health risk, or both.” Of the 57 pollutants chosen, inventories for 42

were identified. These inventories were not designed to cover all possible sources but rather only

the largest contributors to overall emissions for each of the pollutants. They did consider area,

point, and mobile sources. Only data between the years 1980 and 1989 were considered with the

target year being 1985. Background concentrations and local ambient concentrations due to

long-range transport were assumed to be zero, with two exceptions. The background

concentration levels for formaldehyde and carbon tetrachloride were assumed to be 2.2Fg/m3 and

0.8Fg/m3, respectively. These background concentration estimates were combined with modeled

ambient concentration estimates for these HAP.

The individual, lifetime excess cancer risks in this study was 9 x 10-5. This translates into

an estimated total cancer incidence of approximately 373 cases over 70 years or five cases per

year. Over 90% of these resulted from exposure to seven pollutants: formaldehyde, coke oven

emissions, 1,3-butadiene, carbon tetrachloride, chromium, POMs, and dioxin; with more than

50% being attributed to formaldehyde and carbon tetrachloride alone. The contribution of the

additional “background” concentrations to these latter results was not discussed, but the added
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

2-13

Twin Cities Study

Time Period Covered: Completed in 1992

Top Air Contaminants Contributing to Cancer

Risk: Diesel, gasoline, and wood-stove particulate

emissions, formaldehyde, benzene, 1,3-butadiene

Individual Lifetime Cancer Risk Estimates:

2x10-4 (2 cancer cases per year per million over

study area)

Staten Island Study

Time Period Covered: October 1987 – September 1989

for ambient air (plus July 1990 – March 1991 for indoor

air)

Top HAP Contributing to Risk: Benzene, arsenic,

chromium, nickel, cadmium, formaldehyde

Individual Lifetime Cancer Risk Estimates: 1 x 10-4

(1 excess cancer case per year per million)

Noncancer Effects: HI > 2 for both respiratory and

hematopoietic effects

background may have played a role in their higher contribution to overall incidence. No attempt

was made to include other routes of exposure or effects other than cancer in this assessment.

Twin Cities Study

The purpose of this assessment was

to analyze sources of HAP suspected or

known to cause cancer and to estimate the

cancer risks resulting from exposure to these

HAP (MPCA, 1992). Emission inventories

were developed for point, area, and mobile

sources, and modeled to estimate the

ambient concentrations of 29 pollutants and

three different POM mixtures (diesel, woodstove, and gasoline particulates). This

assessment developed estimates of increased

lifetime individual and population risks in the Minneapolis/St. Paul metropolitan area, but did

not estimate maximum risks. The results yielded an estimated individual lifetime cancer risk of 2

x 10-4 over the entire study area. This may result in an estimated two excess cancer cases per

year per million residents. Overall, 61% of the excess incidence may be attributed to road

vehicles which contributed gasoline and diesel particulates (including POMs) as well as

formaldehyde, benzene, and 1,3-butadiene. Wood stoves and fireplaces were also an important

source is this area, accounting for 17% of the incidence. It was concluded that mobile sources

and area sources were the dominant contributors to risk in this assessment, but it should be noted

that the assessment area did not include some of the major point sources that are present near the

study area. Noncancer endpoints, risks due to background concentrations, or risks due to routes

of exposure other than inhalation were not considered in this study.

Staten Island Study

This ambient monitoring-based

assessment estimated the increased risk

of cancer and noncancer effects in

Middlesex and Union Counties in New

Jersey, and in Staten Island (Richmond

County) in New York (U.S. EPA,

1993b). Monitoring data were collected

from October 1987 to September 1989. 

A total of 40 pollutants were monitored

but only 20 had adequate toxicological

data to use for the risk assessment. The

study found that lifetime cancer risk

estimate was approximately 1 x 10 -4 or

one to two excess cancer cases per year per million population. As in other studies, only
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

15The sum of hazard quotients (HQs) for multiple chemicals where the HQ is the ratio of a level of

exposure for a single substance to a reference level (e.g., a reference concentration) for that chemical derived from a

single exposure. An HQ or HI greater than one usually suggests that additional, more refined, analysis may be

warranted.

16It is important to note that since the completion of this study, EPA has promulgated or proposed a

number of programs that are expected to significantly reduce air toxics emissions in the future, including our

reformulated gasoline (RFG) program, the national low emission vehicle (NLEV) program, Tier 2 motor vehicle

emissions standards and gasoline sulfur control requirements, and our recently proposed heavy-duty engine and

vehicle standards and on-highway diesel fuel sulfur control requirements. As discussed in Chapter 4 of this Report,

EPA is updating estimates of motor vehicle toxic emissions and exposure (EPA, 1999b).

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 Motor Vehicle Study

Time Period Covered: 1990 projected to 2010

HAP Studied: Benzene, 1,3-butadiene,

formaldehyde, acetaldehyde, diesel particulates,

gasoline particulates

Estimated Cancer Deaths Per Year or Incidence:

For year: 1990 2000 2010

Benzene 70 35 35

Formaldehyde 44 21 22

1,3-Butadiene 304 176 204

Acetaldehyde 5 3 3 

inhalation risk was considered. This study did include an evaluation of noncancer effects as well. 

A hazard index (HI)15 of two was estimated for the respiratory tract as the target (chromium and

nickel) and also for the blood (hematopoietic) system (benzene). 

Motor Vehicle Study 

In 1993, EPA published the

assessment of risks due to motor vehicles

and their fuels beginning in 1990 and

projecting out to 2010 (U.S. EPA,

1993a)16. The assessment focused on the

emissions of benzene, formaldehyde, 1,3-

butadiene, acetaldehyde, and a group of

mixtures (diesel and gasoline particulates

and gasoline vapors) and on the assessment

of carcinogenic risk. It used exposure to

carbon monoxide (CO) as a tracer for toxic

exposures and used the relationship

between CO emission factors and toxic

emissions factors to estimate toxic

emissions. Monitoring data were used to evaluate the modeling results, and modeled

concentrations were adjusted to match the upper end of the monitored data. This assessment

focused on eleven urban areas and two rural areas, but the results were extrapolated to the entire

Nation using population data beginning in 1990. From 1990 to 2000 (projections), predicted

cancer incidence or deaths decreased for all HAP. During the years 2000 to 2010, the projected

estimates associated with 1,3-butadiene increased. Increases in the cancer incidence projected

for those later years were attributed to projected increases in the number of VMT for those later

years. It was also shown that for each HAP studied, the urban incidence accounted for over 80%

of the total (i.e., 80% of the total number of cancer deaths was due to exposure levels in urban vs.

rural areas). 
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

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Ambient Monitoring Study

Time Period Covered: 1986 – 1993 (individual

studies varied from a few months to multiple years)

Air Contaminants Studied: 195 detected, 93 with

health reference values: 1,3-butadiene, benzene,

formaldehyde, acrolein, 1,2-dibromoethene, and

manganese were more consistently ranked among the

top with respect to health concerns

Individual Lifetime Cancer Risk Estimates:

1,3-butadiene: 2 x 10 -3 to 5 x 10-4

benzene: 2 x 10-4 to 1 x 10-5

formaldehyde: 1 x 10-4 to 2 x 10-5

Noncancer Concern: Acrolein, 1,2-dibromoethene,

manganese

Ambient Monitoring Study

This assessment summarizes the

analyses of ambient monitoring data

obtained from 16 monitoring studies 

some of which were collecting data since

1987. They represented over 40 urban

areas and 195 air contaminants (U.S.

EPA, 1994). Risk was calculated for

only 93 contaminants (most of which are

listed as HAP in section 112(b) of the

CAA) for which health effects data

required for risk assessments were

available. For each site, a long-term

average concentration was calculated and

then applied to health reference values to

estimate lifetime excess cancer risks and

potential noncancer health effects for

each. Because the data were derived from monitoring studies rather than modeling, no

discussion of potential sources was included in the report. No estimates of population risks were

made nor were routes of exposure other than inhalation considered. 

With respect to cancer risks, 1,3-butadiene possessed the highest estimated individual risk

among all pollutants. Estimates for benzene and formaldehyde also ranked consistently near the

top. Acrolein, 1,2-dibromoethene, and manganese exhibited exceedances of noncancer reference

values more consistently than other contaminants. However, there were gaps in the data

presented. For example, not every contaminant was detected in every area due to variations in

the methodologies used in the different studies. The data, however, do provide a snapshot view

of urban areas with respect to contaminant concentrations and their potential to pose health risks

of concern.

Arizona Study

This assessment examined cancer and noncancer risks posed by air pollutants in four

areas of Arizona (Phoenix, Tucson, Casa Grande, and Payson) and was designed to evaluate the

existing risk to public health and to provide options and recommendations for programs to

control releases (ENSR, 1995a, 1995b, 1995c). These regions were assumed to represent a large

fraction of the State’s population and were characteristic of many of the types of communities in

the State. Monitoring of the selected HAP was done primarily in residential neighborhoods. 
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

2-16

Arizona Study

Time Period Covered: 1990 – 1995

Top HAP Contributing to Concern:

1,3-butadiene, benzene, formaldehyde, acrolein,

acetaldehyde, manganese, arsenic

Lifetime Cancer Risk Estimates:

1 to 5 x 10-4 (two to seven excess cancer cases

per year per million)

Noncancer HI: 6 to 15 for all endpoints 

HASTE Study

Time Period Covered: 1995 – 1996

Contributors to Predicted Cancer Risk:

Acrylonitrile, benzene, 1,3-butadiene, ethylene

dibromide, ethylene oxide, 2-nitropropane, vinyl

chloride

Contributors to Noncancer Risk: 

Acrolein (HQ = 5)

Individual Lifetime Cancer Risk Estimates:

 2 x 10-6 to 2 x 10-5

 About 25 HAP of “greatest concern”

were selected for each region. Half of the

estimated cancer risks for air pollutants was

caused by 1,3-butadiene. Other significant

contributors included benzene and

formaldehyde. Acrolein was identified in all

four regions as the HAP most likely to pose

health risks other than cancer. Smaller

likelihoods of noncancer risks were attributed

to acetaldehyde, benzene, and manganese. 

Motor vehicles were found to be the largest

contributor to estimates of cancer risks from

HAP in three of the four areas. Noninhalation pathway risk was determined not

to be of significance in any region studied.

The urban centers, Phoenix, and to a lesser extent, Tucson, were found to have higher

estimates of cancer risk from HAP than the two areas that are more rural. Although emission

reduction mechanisms were expected to decrease the risk estimates in the near future, it was

stated that increases in population growth along with increases in motor vehicle use in these

urban areas would begin to erode any potential gains. The estimates of individual lifetime

increased cancer risks from air pollutants in all study areas ranged from one to 5 x 10-4. The total

HI for noncancer risks, calculated for young children, was six to fifteen for all endpoints. The HI

for respiratory effects was greater than one in all regions. Other HI greater than one were found

for neurological and blood effects but not across all regions studied.

HASTE Study

This project was conducted in three

phases: development of an emission inventory,

modeling of the inventory, and a risk analysis

(TNRCC, 1996). Only area sources of HAP

were studied. Health reference concentrations

(RfCs), when available, were used to compare

against the ground-level concentrations (GLCs)

estimated by modeling, for 87 air contaminants

for cancer and noncancer effects. With the

exception of acrylonitrile, benzene, 1,3-

butadiene, ethylene dibromide, ethylene oxide,

2-nitropropane, and vinyl chloride, the

estimated cancer risks for each of the

remaining air contaminants was less than 1 x 10-6. Individual lifetime cancer risks for the seven

ranged from 2 x 10-6 to 2 x 10-5. The acrolein GLC was the only one which exceeded its RfC (5

fold). 
National Air Toxics Program: The Integrated Urban Strategy

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17The estimated ambient concentrations were then compared to risk-based concentrations (termed

benchmarks by the authors) intended to represent either continuous exposure levels associated with a one-in-amillion upper bound estimate of excess lifetime cancer risk, or continuous lifetime exposure levels associated with

no significant risks of adverse noncancer effects (e.g., EPA’s Inhalation RfC).

2-17

CEP Analysis

Time Period Covered: 1990

Top HAP Contributing to Cancer Risk: 

Benzene, bis(2-ethylhexyl)phthalate, carbon

tetrachloride, chloroform, ethylene dibromide,

ethylene dichloride, formaldehyde, 1,3-butadiene

Top HAP Contributing to Noncancer Risk : 

Acrolein

Cumulative Exposure Project

(CEP)

The CEP is a recent effort by the EPA

to model ambient HAP concentrations on a

national scale (Woodruff et al., 1998). The

CEP suggests that HAP exposures are

prevalent nationwide, and that, in some

locations, concentrations are significantly

higher than the concentrations associated

with a one-in-one million excess cancer risk

(SAI, 1998; Woodruff et al., 1998)17. The

estimated outdoor concentrations, based on

1990 emission estimates, for 119 of the 148 HAP modeled in more than 60,000 census tracts

nationwide were compared to RBCs. The results suggest that HAP exposures are prevalent

nationwide, particularly in urban areas. For 75% of the HAP modeled, the average estimated

concentrations in urban areas were greater than the overall national average concentrations. The

emissions of three HAP (benzene, formaldehyde and 1,3-butadiene) appear to contribute to

concentrations above the associated one-in-one million excess cancer RBCs in at least 90% of

the census tracts. Estimated concentrations are generally higher in urban areas, and

concentrations of 28 HAP were greater than their RBCs in a larger proportion of urban areas as

compared to rural areas. In a smaller number of locations (both urban and rural), concentrations

of certain HAP were estimated to be more than a factor of 100 greater than the corresponding

RBCs (Woodruff et al., 1998). Estimated exceedances seen in this assessment suggest potential

public health problems especially in urban areas. 

2.7 Why Is The Urban Strategy Needed?

The overall findings of these nine assessments may be summarized as follows:

• Benzene, 1,3-butadiene, and formaldehyde were consistently shown to be most

responsible for the higher risk estimates;

• The studies identified all three major source categories (area, major and mobile sources)

as contributing emissions and potential risks in urban areas; and

• Estimates of increased cancer risks for air toxics from multiple sources across the studies

ranged from 3 in 1,000 to 2 in 1,000,000 with a median of 1 in 10,000. 
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

2-18

In addition, because many of these emission sources are area or mobile sources, their emissions

are likely to be released at ground level where people are more likely to be exposed to them. The

prevalence of minority and low income communities in urban industrial and commercial areas,

where ambient concentrations of HAP may be greater, increases the likelihood of elevated HAP

exposures among these subgroups. The potential for air toxics in urban areas, either directly or

indirectly, to contribute to elevated health risks among these and other subgroups (especially

children, the elderly and persons with existing illness or other potential vulnerabilities)

demonstrates the need to assess risk distributions across urban populations in order to address

disproportionate impacts of HAP.

As discussed earlier, each of these studies was limited in its scope and design (e.g.,

considered cancer effects from inhalation exposures only), and the results must be considered in

the context of conditions which existed up to ten years ago. Thus, many were performed prior to

the implementation of control strategies (including vehicle and fuel additive regulations, (e.g., 

HD2004 and Tier 2) and emission standards for numerous source categories) and do not reflect

the progress made in reducing emissions from air toxics through regulatory, voluntary, and other

programs at the State and Federal levels. For example, section 112(d), MACT standards

(adopted to date) are projected to yield yearly emission reductions of approximately 1.5 million

tons of HAP from stationary sources. Additional emission reductions are expected as the

remaining MACT standards are promulgated. Additionally, automobile emissions which

accounted for 20% of the total emissions of HAP in the baseline inventory mentioned earlier,

decreased by approximately 258,000 tons per year between the years 1993 and 1996 (U.S. EPA,

1998), possibly as result of regulations requiring the use of reformulated fuels which may have

contributed to the decreases seen in benzene emissions. Future assessments will be needed to

determine the impact of these reduced emissions on potential air toxics-related health risks.

In the meantime, these assessments adequately support our concern that a potential

problem exists in urban areas, and that we should continue with our efforts to study the urban

environment and to implement the urban strategy described earlier in the Federal Register (U.S.

EPA, 1999a) and presented again in this Report. 

2.8 References

Engineering-Science. 1990. The transboundary air toxics study, final summary report. Prepared

for U.S. EPA Region V, Air and Radiation Division. Fairfax, VA. December.

ENSR. 1995a. Arizona hazardous air pollution research program final report volume 1:

approach. Document number 0493-013-900. Phoenix, AZ. August.

ENSR. 1995b. Arizona hazardous air pollution research program executive summary. 

Document number 0493-013-920. Phoenix, AZ. December. 
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

2-19

ENSR. 1995c. Arizona hazardous air pollution research program volume 2: findings. Document

number 0493-013-920. Phoenix, AZ. December.

Minnesota Pollution Control Agency (MPCA). 1992. Estimation and evaluation of cancer risks

from air pollution in the Minneapolis/St. Paul metropolitan area. March.

Systems Applications, Inc. (SAI). 1998. Modeling cumulative outdoor concentrations of

hazardous air pollutants: final technical report. Prepared by SAI Division of ICF Kaiser

International. Prepared for U.S. Environmental Protection Agency. February.

Texas Natural Resources Conservation Commission (TNRCC). 1996. Houston area source

toxic emissions (HASTE) project, health effects evaluation. TNRCC Office of Air

Quality/Toxicology and Risk Assessment Section, Austin, TX. February.

U.S. Department of Commerce. 1997. Population profile of the United States. Current

population reports, special studies P23 – 194. Economic and Statistics Administration,

Bureau of the Census, Washington, DC.

U.S. Department of Transportation. 1998. Traffic volume trends, December 1997. Federal

Highway Administration report, publication number FHWA-PL-98-004.

U.S. EPA. 1989. Analysis of air toxic emissions, exposures, cancer risks and controllability in

five urban areas, volume I: base year analysis and results. Office of Air Quality Planning

and Standards, Research Triangle Park, NC. EPA-450/2-89-012a. July.

U.S. EPA. 1993a. Motor vehicle-related air toxics study. Office of Mobile Sources, Ann Arbor,

MI. EPA-420/R-93-005. April.

U.S. EPA. 1993b. Staten Island/New Jersey urban air toxics assessment project, summary of the

project report. U.S. EPA Region 2, New York, NY. EPA-902/R-93-002. January.

U.S. EPA. 1994. A screening analysis of ambient monitoring data for the urban area source

program, final report. Office of Air Quality Planning and Standards, Research Triangle

Park, NC. EPA-453/R-94-075. October. 

U.S. EPA. 1996. Analysis of the national human activity pattern survey (NHAPS) respondents

from a standpoint of exposure assessment. EPA/600/R-96/074. July.

U.S. EPA. 1998. National air pollutant emissions trends update, 1970-1997.

EPA-454/E-98-007. December.

U.S. EPA. 1999a. National air toxics program: the integrated urban strategy; notice. Federal

Register 64:38705. July 19.
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

2-20

U.S. EPA. 1999b. Analysis of the impacts of control programs on motor vehicle toxics emissions

and exposure in urban areas and nationwide (volumes I and II). Prepared for U.S. EPA

by Sierra Research, Inc. and Radian International Corporation/Eastern Research Group. 

EPA 420-R-99-029 and EPA420-R-99-030. November 30.

Woodruff, T.J., D.A. Axelrad, J. Caldwell, R. Morello-Frosh, and A. Rosenbaum. 1998. Public

health implications of 1990 air toxics concentrations across the United States. Envr.

Health Persp. 106(5):245-251.
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

3-1

3. Emissions Inventory and Selection of the Urban Pollutants

3.1 Introduction

Section 112(k)(3) of the CAA directs EPA to identify at least 30 HAP which, as the result

of emissions from area sources, present the greatest threat to public health in the largest number

of urban areas. In the Strategy, we identify 33 HAP (“urban HAP”) to meet this requirement. 

The Appendix of this Report details the physical properties, sources of exposure, health hazards,

and other pertinent information for each of the 33 urban HAP.

In developing the final HAP list, we estimated emissions from all known sources using a

variety of techniques, evaluated available health effects information for the 188 HAP, assessed

available air quality monitoring data, reviewed existing studies, and produced a list of pollutants

based on the relative hazards they pose in urban areas, considering toxicity, emissions, and

related characteristics. From these efforts, we established the list of urban HAP which pose the

greatest threat to public health in urban areas, considering emissions from major, area and mobile

sources. Among these urban HAP are a subset of 30 HAP with greatest emissions contributions

from area sources (the “area source HAP”). 

The first step we took toward developing both an emissions inventory and a HAP ranking

analysis was in 1997 when we conducted an initial screening analysis using a preliminary

methodology. In addition to identifying HAP for which we separately conducted a public review

of our emissions inventory information, this evaluation provided us with the opportunity for peer

review of our preliminary methodology. In the peer review, outside experts reviewed the ranking

methods and data used and offered suggestions on how the methodology could be used and

improved to select the priority urban HAP. The draft emissions inventory for the HAP identified

by the initial screening analysis was also made available for public comment. This was the first

of two public comment opportunities for the emissions inventory.

In the sections below, the results of the final analyses are described in detail. The initial

analyses are mentioned, as appropriate, primarily to give you a sense of how the final analyses

were developed in response to public comment and improvements made to the methodologies.

In section 3.2 of this chapter, the methods and data sources used to develop the baseline

emissions inventory are described. The baseline inventory quantifies the emissions of the

candidate urban HAP and identifies the source categories that emit them. The limitations of the

inventory are also discussed, and the final emissions estimates presented. In section 3.3, the

ranking methodology is described; the final selection criteria and the list of urban HAP are

presented in section 3.4. References are provided in section 3.5.
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3-2

Review of the Urban HAP Inventory

The Draft 1990 Emission Inventory of

Forty Section 112(k) Pollutants was made

available on EPA’s World Wide Web site in

1997 for review by individuals within and

external to the EPA (i.e., trade organizations,

environmental advocacy groups, academic

experts, and the general public). In addition,

EPA contacted individuals representing trade

organizations, industry, and environmental

groups by letter to announce the availability

of the inventory and to solicit review

comments. 

The technical comments related to

development of the inventory were

summarized in the EPA document Public

Comments Received About Technical Aspects

of the 1990 Emission Inventory of Forty

Pollutants in the Section 112(k). This

document can be obtained from the EPA’s

website: http:// www.epa.gov/ttn/uatw/

urban/112kfac.html. 

A few sections of the draft inventory were

revised based on new data provided by the

reviewers. The updated inventory was then

made available for public review for the

second time on September 14, 1998 as part of

the draft integrated urban strategy. During

this public review, a significant amount of

new data were provided which greatly

improved our facility-specific estimates for a

number of important source categories. All of

the changes made to the inventory subsequent

to the September 14, 1998 release are

reflected in the information presented in this

document.

3.2 Baseline Emissions Inventory for

the Integrated Urban Air Toxics

Strategy

One of the building blocks of the Strategy

is the baseline emissions inventory. The

inventory is critical in order to evaluate our

progress toward meeting the goals of the Strategy

as described in Chapter 1. Specifically, the

emissions inventory will help:

C Identify source categories that will be

subject to regulations under the Strategy,

as explained in more detail in Chapter 4;

C Evaluate progress toward the goal of

assuring those source categories are

subject to standards;

C Evaluate progress toward the goal of

reducing by 75 percent the incidence of

cancer associated with air toxics across all

urban areas; and

C Evaluate progress toward the goal of

substantially reducing noncancer health

risks associated with air toxics across all

urban areas.

To identify the required source categories

and to measure our progress toward the other

goals listed above, we developed a baseline

emissions inventory of HAP emissions

approximating emissions during the years 1990 to

1993. We believe the intention of the CAA is

that reductions occur from 1990 levels because

that was the year the CAA was amended to

include these requirements. However, since there

were very limited data for 1990, the inventory

spans a longer period of time. We believe that this is an appropriate timeframe because these

years represent HAP emissions prior to implementation of any MACT source category standards. 

The baseline inventory contains emissions estimates for major, area, and mobile sources of the

188 HAP and segregates according to whether the sources are located in urban or rural areas. A
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3-3

Documentation of the Inventory

For complete documentation of the inventory,

the reader is encouraged to refer to the 1990

Emissions Inventory of Forty Section 112(k)

Pollutants, Supporting Data for EPA’s

Proposed 112(k) Regulatory Strategy, Final

Report (U.S. EPA, 1999a). The Final Report

presents: emission estimates for each HAP by

source category; estimates of total national

emissions for each source category; separate

urban and rural emission estimates; specific

documentation for the subject pollutants of each

source category; the input data used to calculate

emissions; and the algorithms used to estimate

national emissions. The Final Report can be

obtained from the EPA’s Internet Web site

(www.epa.gov/ttn/uatw/urban/112kfac.html).

subset of the baseline inventory is information collected and publicly reviewed for 40 candidate

HAP to support the analysis of the Strategy, and an additional two HAP developed to support the

section 112(c)(6) efforts.

This section summarizes how the baseline emissions inventory was developed for each of

the candidate urban HAP. The first inventory of 40 HAP, which was a product of the screening

analysis described earlier, was the starting point for more intensive and refined inventory efforts. 

The final inventory estimates presented below in section 3.2.2 are the result of revisions made

after two public comment opportunities as described in the accompanying sidebar.

3.2.1 Development of the Baseline Inventory

The national estimates of the HAP

included in the NTI are calculated using

existing information; no source testing or

industry surveys were conducted specifically

for the purposes of generating the inventory. 

Existing emissions inventory data are obtained

from a variety of State and local databases and

EPA programs (such as the TRI, standards

development programs, and other studies

required by the CAA). Sometimes, emissions

information is available from direct

measurement of emissions at a source. For

logistical and financial reasons, direct

measurement, or stack testing, is usually

performed only at large point sources and is

far less common than the use of emission

factors. 

Many of the national emissions

estimates in the inventory (primarily for area

and mobile sources) were developed by applying an emission factor, or series of factors, to

activity data which are representative of source categories nationally. Emission factors are one

way to estimate emissions of various chemicals for a particular source category. To estimate

emissions, these factors were combined with information about the activity levels of a source,

such as the production capacity of the facility, the number of hours of operation, or the amount of

fuel consumed. Emissions for each source category were then allocated according to whether

they are emitted by major or area sources. 

The baseline NTI that was used in developing the Strategy is the first one compiled. New

NTI base year inventories will be compiled every three years (1996, 1999, 2001, etc.). Although

the inventory development methodology described below applies in general to all emissions
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3-4

inventories, the baseline and 1996 NTIs do differ in the level of detail they contain. Unlike the

baseline NTI, which includes emissions estimates from all counties by source category and

pollutant, the 1996 NTI will contain facility- and location-specific information that places

individual facilities within those counties and makes the emissions data suitable as input to

computer dispersion models that predict ambient air concentrations. The 1996 NTI data set was

compiled in cooperation with State and local agencies which submitted data they have gathered

during facility permitting and other regulatory activities.

Many estimates presented in the NTI (primarily for area and mobile sources) were

developed by using an emission factor in combination with appropriate activity data. The

emission factors were evaluated for age of the information, completeness and whether the data

adequately represent current practices. The EPA made judgments about the overall quality of the

information, and acceptable data were used to develop composite emission factors for use in the

national estimates.

The availability and overall quality of the activity data vary by source category. Most of

the activity data were obtained from published business/manufacturing sources, governmental

statistics publications, and background information from EPA regulatory programs. Other

sources of activity data were industrial trade associations, the Department of Transportation and

the Department of Energy’s Energy Information Administration.

 For many source categories, multiple methods were available to develop emission

estimates with some methods being preferable to others. The preferred approach was to use

national emissions estimates from existing inventories previously prepared by EPA. 

For pollutants where no EPA, State or local agency inventory was available, other sources

of information were used. In general, other sources of information were prioritized in the

following order.

1. National estimates available from other reference sources that were judged to be

reasonable, complete, and well documented. These estimates were used directly in the

inventories. Examples of these sources include air toxics inventories compiled by

individual State or local agencies, various regulatory projects for different source

categories, and Reports to Congress (e.g., the Utility Air Toxics Study). Estimates

obtained from such programs were generally accepted as the best available data for the

inventory. These estimates are based on recent test data, control information,

representative modeling scenarios, and input from informed industry and government

experts and are considered to be of higher quality than estimates derived through the use

of an overall emission factor and associated activity data.

2. Inventory data from TRI. These data sources received lower priority based on the

evaluation criteria. The TRI contains national inventory data only for sources that meet

certain reporting criteria, and the emission calculation methods cannot be confirmed. 
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While considered a relatively low-priority reference source, TRI data provide a significant

amount of emissions data for sources that might be missed completely by other inventory

compilation methods.

3. Calculated emission estimates. Emissions were calculated if national emissions estimates

were not directly available from a preferred reference source, and emission factors and

activity level data for a source category could be identified. The greatest influence on the

quality of these calculated estimates is the validity of the emission factor(s) used (in terms

of absolute accuracy), as well as representativeness for the processes to which they were

applied. The activity data also affect the quality of an emissions estimate; however, many

standardized and credible references for activity data preclude any large margin of error

being associated with the activity level.

Sometimes, data are available about the composition of emissions from a source category. 

This type of information, called a speciation profile, is a list of HAP on a percentage basis

that are the constituents of the emission plume. Thus, if the total concentration of the

plume is known, it can be multiplied by the speciation profile to determine the

concentration of the various HAP which comprise the mixture. In this analysis, suitable

speciation profiles were not available for most source categories in the inventory and

were generally not used. Significant limitations were identified which limited the use of

the speciation profiles, particularly the poor representation of source categories and the

age of the data on which most profiles are based. However, there were some exceptions. 

For example, mobile source categories emissions were calculated by first estimating total

HCs or particulates, then deriving the toxic components by using HAP profiles. In the

case of these mobile source categories, this approach is deemed to provide high quality

emissions estimates.

3.2.2 Baseline Inventory Results

Exhibit 3-1 summarizes the baseline inventory estimates developed for each candidate

urban HAP. Total national emissions for each HAP are presented, and emissions are reported for

major, area, and mobile sources. These data are also illustrated in Exhibits 3-2 and 3-3. 

Because there are multiple programs investigating HAP emissions in the United States,

emissions data and source activity data are continually changing and improving. The data

presented in this section reflect emissions estimates that have been developed according to the

input data and assumptions described above. The estimates are applicable for a specific time

period and may not necessarily agree with the national estimates from other published estimates 
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3-6

EXHIBIT 3-1

BASELINE EMISSIONS INVENTORY ESTIMATES FOR EACH OF THE 

40 CANDIDATE URBAN HAP (1990 – 1993)

HAP

Baseline

National Total

(tons)

Baseline

Major Sources

(tons)

Baseline

Area Sources

(tons)

Baseline

 Mobile Sources

(tons)

Benzene 390,000 36,000 74,000 280,000

Formaldehyde 350,000 32,000 140,000 180,000

Acetaldehyde 140,000 21,000 51,000 66,000

Tetrachloroethylene 130,000 22,000 100,000 0

Methylene Chloride 100,000 85,000 19,000 0

Trichloroethylene 75,000 61,000 14,000 0

1,3-Butadiene 72,000 4,000 20,000 48,000

Acrolein 68,000 750 55,000 12,000

Styrene 54,000 31,000 3,200 20,000

Chloroform 23,000 22,000 600 0

1,3-Dichloropropene 20,000 34 20,000 0

Methyl Chloride 6,400 6,300 89 0

Carbon Tetrachloride 5,500 5,400 110 0

1,4-Dichlorobenzene 5,100 735 4,400 0

Ethylene Dichloride 4,200 4,100 100 0

Lead Compounds 3,300 1,500 540 1,200

Manganese Compounds 2,800 2,100 650 52

Vinyl Chloride 2,700 2,100 570 0

Ethylene Oxide 2,600 1,200 1,300 0

Acrylonitrile 2,600 2,100 440 0

Coke Oven Emissions 1,800 1,800 0 0

Polycyclic Organic Matter as 7-PAH 1,300 250 1,000 48

Nickel Compounds 1,200 740 400 95

Chromium Compounds 930 490 390 54

bis(2-Ethylhexyl)phthalate 810 740 68 0

1,1,2-Trichloroethane 740 740 5 0

1,2-Dichloropropane 660 630 23 0

Arsenic Compounds 280 220 65 2.8

1,1,2,2-Tetrachloroethane 260 51 206 0

Methylene Diphenyl Diisocyanate 240 160 82 0

Vinylidene Chloride 220 170 48 0

Mercury Compounds 210 120 71 12

Cadmium Compounds 200 160 38 0.31

Ethyl Acrylate 160 140 20 0

Ethylene Dibromide 51 50 0.50 0

Acrylamide 35 32 3.3 0

Quinoline 26 24 1.6 0
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EXHIBIT 3-3

SPATIAL ALLOCATION OF BASELINE 

EMISSIONS OF THE CANDIDATE

URBAN HAP

Rural

Urban 67%

33%

EXHIBIT 3-2

SOURCES OF BASELINE EMISSIONS 

FROM THE CANDIDATE URBAN HAP

Major

Mobile

Area

35%

41%

24%

EXHIBIT 3-1 (Continued)

BASELINE EMISSIONS INVENTORY ESTIMATES FOR EACH OF THE 

40 CANDIDATE URBAN HAP (1990 – 1993)

HAP

Baseline

National Total

(tons)

Baseline

Major Sources

(tons)

Baseline

Area Sources

(tons)

Baseline

Mobile Sources

(tons)

Hydrazine 20 18 1.1 0

Beryllium Compounds 12 9.5 2.6 0.02

Dioxins/Furans as 2,3,7,8-TCDD TEQ 3.2e-03 2.2e-03 9e-04 1e-04

TOTAL 1,468,344 348,854 509,414 609,454

due to differences in base years, emission factors and activity data, and calculation assumptions. 

It should be recognized that some of the data presented here will likely change as more

information and improved estimation approaches are developed.

3.2.3 Allocating Emissions Between Locations and Source Types

For purposes of selecting the priority urban HAP, the emission estimates were further

refined in two ways. First, the emissions were allocated to either urban or rural areas so that it

could be determined which pollutants were potentially the most significant in the largest number

of urban areas. Second, the pollutants were allocated by source type including major sources,

area sources and mobile sources. The statutory language of section 112(k) focuses on area

sources, but as explained earlier, the Strategy will combine a number of statutory requirements

for both stationary and mobile sources to address the urban air toxics problem in the most

efficient and effective way. The subsections below describe these analyses. 

Urban/Rural Source Allocations

Section 112(k) of the CAA specifically addresses HAP that “present the greatest threat to

public health in the largest number of urban areas.” However, the CAA does not provide a

definition of “urban.” In other sections of the CAA, urban areas with populations greater than
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250,000 are singled out for air monitoring, although the possibility of monitoring other urban

areas is also mentioned. 

 Statistical data from the Bureau of the Census were used to spatially allocate emissions

on an urban and rural basis (U.S. Bureau of the Census, 1990). The Bureau of the Census has

designated urban and rural areas within every county in the United States based on population

density and total population. For this analysis, using population data and urban/rural

designations for 1990, every county in the United States was classified as either urban or rural

according to the following definitions:

C Urban counties are defined as those which include a metropolitan statistical area (MSA)

with a population greater than 250,000, or those counties that do not have an MSA with a

population greater than 250,000, but more than 50 percent of the county population has

been designated by the Bureau of the Census as “urban.” These counties include areas

with one or more central places and adjacent, densely settled, surrounding urban fringe

areas. The urban fringe consists of contiguous territory having a density of at least 1,000

persons per square mile.

C Rural counties do not have an MSA with a population greater than 250,000 and the

Bureau of the Census designates more than 50 percent of the county population as

“rural.”

For the purpose of defining “urban” and “rural” for the Strategy, if more than 50 percent

of the population was classified as rural, then that county was classified “rural.” All remaining

counties were classified as “urban.”

Emissions were assigned to counties by various methods. In some cases, such as with

TRI estimates and data obtained from regulatory programs studies, emissions could be assigned

to the actual county. Where facility-specific data were not available, emissions were assigned to

individual counties using surrogate approaches. Examples of these surrogate approaches include

proportioning national level emissions to counties based on population, proportioning emissions

from some industrial sectors to counties based on employment estimates, and assigning

emissions from forest fires to counties based on forested acres.

Major/Area Source Allocation

The national emission estimates for stationary source categories were also allocated

according to whether the emitting source category was classified as “major,” “area,” or could be

classified partially as both. According to section 112(a) of the CAA, a “major source” is any

stationary source (including all emission points and units located within a contiguous area and

under common control) of air pollution that emits or has the potential to emit, considering

controls, 10 tons or more per year of any single HAP or 25 tons or more per year of any

combination of HAP. An “area source” is any stationary source of HAP that does not qualify as
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a major source. The allocation of emissions for each source category on a major/area source

basis will be helpful in evaluating the effects of existing and future regulatory programs on

emissions reductions. 

The major/area allocation proportions were derived in a variety of ways. The primary

goal was to determine whether emissions from a category were predominantly emitted from

major or area sources so that sources accounting for 90 percent of the aggregate area source

emissions of each pollutant can be identified. The rationale used to make the major/area source

determinations varied depending on available information. The EPA report Documentation for

Developing the Initial Source Category List, which was used to identify major source categories

for standards development purposes, was a key reference (U.S. EPA, 1992). In some cases, the

accepted way that a source category is typically inventoried served as a guide for the

classification (e.g., residential wood burning is always assessed as an area source). In other

cases, technical analyses were conducted using actual and representative model plant data to

determine typical facility sizes and emissions. With the above information, the percentage of

facilities in a category likely to exceed the 10 or 25 ton-per-year HAP thresholds could be

estimated. Engineering judgment was used to assign an allocation in cases where data were

limited.

3.2.4 Limitations of the Emissions Inventory

In the development of emissions inventories, the quality of the final estimates varies

considerably among the different source categories. The data for some source categories will

have greater uncertainty and limited information especially if those categories have not been a

priority for previous evaluations of emissions. Despite these uncertainties, we feel that the

baseline inventory represents the best available data set for the 1990 to 1993 timeframe, and that

it meets the inventory needs of the Strategy at this time, and the 1996 NTI will represent

significant improvement because of its facility-level detail. Future NTI base year inventories are

expected to continue to improve in quality as data collection and estimation methodologies

improve. This section discusses some of the limitations of the data used to develop the

inventory. 

Consistency of Emissions Estimation Methods Within and Among Source

Categories

Because the NTIs, regardless of base year, are compiled in part by the collection of data

from other primary references (e.g., individual States, TRI, regulatory development programs,

etc.), the methods for developing those estimates vary. For example, TRI emissions are selfreported by individual facilities. Those facilities may estimate their emissions via different

technical approaches (e.g., mass balance versus stack testing) or report emissions on different

bases in scope or time (actual versus potential, or daily versus annual emissions). In developing

the NTI, we have made assumptions to allow us to standardize all of these reported emissions to

develop emissions on an ‘actual annual’ emissions basis.
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Emissions Inventories Continue to be Revised Over Time

Because there are multiple programs investigating HAP emissions in the U.S., emissions

data and source activity data are continually changing and improving. To develop emission

factors, extensive information about the different types of industrial processes is required. 

Research is always ongoing to update the emission factors so they reflect the most current

knowledge about the industrial sources. Because estimating emissions requires making various

assumptions, the estimates are applicable for a specific time period and may not necessarily agree

with the national estimates from other published estimates due to differences in base years,

emission factors and activity data, and calculation assumptions. It should be recognized that

some of the data presented in the baseline inventory used in developing the Strategy are likely to

change as more information and improved estimation approaches are developed. 

Source Category Specific Limitations

In some cases, categories are known or suspected to emit candidate urban HAP, but it was

not possible to develop emission estimates. At this time, the relative magnitude of these sources

is unknown. The majority of this type of uncertainty is in emissions from chemical

manufacturing facilities. In the baseline inventory, these emissions are reported in the baseline

NTI as “unspeciated organic HAP.” These emissions data were collected to develop the MACT

standard for this industry and could not be speciated into the individual chemical compounds. 

Thus, the emissions estimates for benzene and the other HAP that may be included in the

emissions from this source category may be underestimated.

Old or Limited Data

As described earlier, some of the emissions estimates in the NTI are based on calculations

made using emissions factors and activity data. We consider some of these estimates to be of

very high quality (e.g., mobile source estimates that are based on recently developed emissions

factors, VMT, and criteria pollutant inventory data). However, for some source categories,

primarily in the area source sector which has not been the focus of previous HAP studies,

emissions are based on emission factors that are either old (i.e., from the 1980's) and/or very

limited in terms of coverage. This means that for some source categories, a very limited number

of data points were available to characterize an entire category.

Assumptions Required to Divide Emissions into Urban Versus Rural Counties and

Major Versus Area Sources

As described in more detail below, for the sake of the Strategy, we had to allocate

emissions by urban/rural and major/area splits. These distinctions required some technical

assumptions. The major/area distinctions are generally a function of how the emissions estimates

were derived. For example, a facility reporting emissions of one HAP in an amount greater than
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10 tons would definitely be a ‘major’ source, but a similar facility that reports less than 10 tons

may not be major unless other HAP are emitted as well. 

For urban/rural designations, the distinction was simple if we knew the actual location of

a facility within a county that has been designated as urban or rural using U.S. Census Bureau

data. This was not so simple when no location was known, particularly for area sources. For

example, if the area source category emissions were calculated for the entire Nation and then

spatially allocated to urban and rural counties using a surrogate (e.g., population), an individual

county’s emissions may be skewed high or low, even though the national emissions estimate is

accurate.

3.3 Ranking the Urban Hazardous Air Pollutants

This section describes the ranking analyses used to select the priority urban HAP. The

analyses are described in more detail in an EPA technical support document (U.S. EPA, 1999b). 

As with the emissions inventory, the first step we took toward ranking the pollutants was the

development of an initial screening methodology. While the final ranking used to identify the

priority urban HAP is similar to that of the screening analysis, the methodology was revised to

address the comments of the January 1998 peer review panel and public comments. The analysis

was rerun using updated emissions, monitoring and toxicity information that became available in

the interim. The accompanying text box describes the screening analysis and its peer review. 

The purpose of these analyses was to identify which of the 188 HAP “present the greatest

threat to public health” in urban areas. In order to use the available data in the most robust

manner, we conducted three ranking analyses, each of which is described below. First, we

ranked the HAP by combining indicators of toxicity and exposure into four risk-related ranking

indices and then produced an overall ranking by combining each of the individual indices (i.e.,

the Exposure/Toxicity Indicators Ranking Analysis). Second, we reviewed a number of

previously conducted risk or hazard assessments concerning HAP in urban areas and produced a

list based on the results of these assessments (i.e., the Risk Assessment/Hazard Ranking Studies

Analysis). Third, we used information provided by EPA’s CEP which compares modeled

ambient concentrations of HAP in urban areas with health-based benchmarks (i.e., the CEP

Ranking Analysis). Each of these analyses have various limitations, but by assembling and

assessing this variety of analyses and types of information, a weight of evidence approach was

taken to provide a more sound identification of urban HAP than would be possible from a single
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Initial Screening Analysis and Peer Review

The screening analysis for the initial HAP ranking used various

types of information combined in five different rankings to

assess the relative potential health risks posed by each of the

188 HAP. For each method, contributions from major, area,

and mobile sources were considered. This approach accounted

for risks from multiple sources and minimizes the impact of

missing information for individual sources. The selection

process for the candidate HAP as well as the methods and data

used in the screening analysis are explained in detail in an EPA

document, “Prioritization of HAP for the Urban Air Toxics

Study - Peer Review Draft” (U.S. EPA, 1997a), which is

available in the Urban Strategy Docket. 

A technical review panel was convened on January 21, 1998 to

review the preliminary methodology used to select the candidate

list of HAP. Nine scientists from academia, government

agencies and an EPA/industry-supported research institute

participated as panel members. The panel was charged with

reviewing the ranking methodology for scientific accuracy,

objectivity, technical quality and validity. Reviewers were also

asked to comment on the general approach taken, the individual

ranking methods, the results of the ranking and other technical

aspects of the ranking method such as uncertainties and data

gaps, which were presented in the draft EPA report (U.S. EPA,

1997a).

In general, the reviewers agreed that the information available at

the time of the review had been appropriately incorporated into

the ranking approaches, and that the ranking results were

systematically evaluated and integrated. The various ranking

methods seemed to complement each other in that one method

filled in data gaps that the other ranking methods may have

missed. Overall, the ranking methodology appeared to result in

the highest rankings for pollutants with the most potential to

cause human health risks and lower rankings for those less

likely to be priorities. However, the reviewers expressed

concern that data gaps and the use of arbitrary cutoffs to select a

predetermined number of pollutants could result in some

priority pollutants being left off the list. The reviewers also

suggested that EPA explain how missing or uncertain data could

affect the ranking, that the analysis be updated periodically with

new science as appropriate, and that the reasons for selecting

each pollutant be illustrated more clearly. (The complete set of

written comments by the peer reviewers may be obtained from

the Urban Strategy Docket (A-97-44)).

analysis. The three separate analyses

and types of information are described

below along with their strengths and

limitations. 

Limitations Shared By All

Three Ranking Analyses

C The ranking analyses are

uncertain because there are

gaps and uncertainties

associated with the health

effects, monitoring and

emissions data for the 188

HAP.

C Although all three ranking

analyses used ambient

concentration data in the same

form, none considered

personal exposure. Personal

exposure, which includes

physiological and behavioral

factors that vary with

individuals, may vary

substantially from ambient

concentrations.

C Only HAP having both

toxicity data and emissions or

ambient concentration data

could be ranked. This could

lead to overlooking potentially

high-risk pollutants because of

sparse data.
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3.3.1 Exposure/Toxicity Indicators Ranking Analysis

The first analysis ranked HAP by combining surrogates for toxicity and exposure into

risk-related ranking indices. By considering short-term inhalation hazards and hazards posed by

ingestion of HAP with a potential to accumulate in foods, this analysis complemented the other

two ranking analyses described below, both of which considered only long-term inhalation

hazards or risks.

The surrogates for toxicity were the RBC for inhalation and the risk-based dose (RBD)

for ingestion. These are calculated by selecting a specified risk level (e.g., 1 in 1,000,000 excess

cancer risk) and calculating exposure concentration or dose of the HAP which will cause the risk

level to be exceeded, assuming the relevant acute or chronic exposure conditions. For effects

other than cancer, the RBC or RBD is the chronic RfC (or similar value from another source). If

available, the EPA’s inhalation RfC was chosen as the chronic noncancer RBC. If an RfC was

not available for a HAP, then a comparable value was obtained from another agency, such as the

minimal risk level (MRL) developed by the Agency for Toxic Substances and Disease Registry,

or the reference exposure level (REL) developed by the State of California Environmental

Protection Agency. Similarly, the EPA’s reference dose (RfD) was the first choice for the

noncancer RBD. Acute RBCs were set equal to risk management exposure guideline levels (e.g.,

Acute Exposure Guideline Levels (U.S. EPA, 1997b)) for mild, transient or no effects from short

exposure periods, when available. 

For HAP categorized as “known,” “probable,” or “possible” human carcinogens, rankings

were done separately for two risk levels. In the first case, the RBC or RBD was set at an

exposure associated with a one in one million upper-bound predicted lifetime cancer risk, or the

RfC/REL for noncancer effects (whichever was lower). In the second case, the RBC or RBD

was set at an exposure associated with a one in ten thousand upper-bound predicted lifetime

cancer risk, or the RfC/REL (whichever was lower). Two risk scenarios were selected because if

the cancer risk level was preset at only one in one million upper bound lifetime cancer risk, the

list of 30 substances selected likely would be dominated by carcinogens. This would in effect

give cancer preference over noncancer effects because the amount of pollutant needed to trigger

the one in one million cancer risk level would almost always be lower than the amount needed to

trigger the risk level based on noncancer effects. Thus, the lower of the cancer or noncancer

RBCs and RBDs is selected under two different risk scenarios to ensure that noncancer effects

are given appropriate consideration in the ranking.

Surrogates for exposure included measured ambient concentrations and emission

estimates from mobile, major and area sources. The Exposure/Toxicity Indicators ranking is

necessarily based on databases which are not complete and contain information that varies in

quality. While we believe that these databases contain the best available information, there is

still substantial uncertainty in this analysis. The results should be considered estimates of the

relative potential hazards of the various HAP and not a quantitative estimate of risks.
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Normalized Scores

A normalized score is prepared by listing the

score for each pollutant and dividing each score

by the value of the highest score. By

normalizing the scores, the magnitude of the

differences between the scores of each pollutant

is preserved. In addition, because each index is

normalized in the same way, each is given equal

weight, or importance, in the analysis.

Four separate ranking indices – three

of which had two separate risk scenarios (case

1 and case 2) as noted above – were prepared

for each HAP. The pollutants were ranked on

a normalized scale. To obtain the final

ranking, the normalized scores from each

index for each pollutant were averaged. The 

average normalized value for each pollutant

was then ranked in order from highest to

lowest. (If a score was not available for a

pollutant in a given index, the value was

treated as “missing,” not zero, so as not to

lower the average value.)

Toxicity is inversely related to the value of the RBCs and RBDs. For example, the more

toxic the HAP, the lower the concentration at which health effects would be realized. 

Consequently, the more toxic HAP would have lower RBCs and/or RBDs. In contrast, the

relative concern for exposure increases with increasing ambient measures or emissions (i.e.,

surrogates for exposure). Therefore, higher emissions (or ambient concentrations) are of greater

concern than lower emissions. In order to rank the HAP by toxicity and exposure, the exposure

surrogate is divided by the RBC (or RBD), as illustrated by the following equation:

Exposure Surrogate/RBC = Ranking Index

The ranking indices are used to estimate the relative concern for public health. The four

indices are:

C Index 1: Ambient/Acute. This index was intended to rank HAP by relative short-term

inhalation hazard. The ambient acute index for each HAP was calculated by dividing the

95th percentile 24-hour concentration of the database of 24-hour urban area ambient

concentrations by the RBC for acute inhalation exposure.

C Index 2: Ambient/Chronic. This index was intended to rank HAP by relative long-term

inhalation hazard. The ambient chronic index for each HAP was calculated by dividing

the average ambient long-term concentration for the urban areas monitored by the chronic

RBC. This was done separately for case 1 (RBC set at 1 x 10-6 upper bound cancer risk or

the RfC, whichever was lower) and case 2 (RBC set at 1 x 10-4 upper bound cancer risk or

the RfC, whichever was lower). 

C Index 3: Emission/Chronic/Inhalation. This index was intended to rank HAP by

relative long-term inhalation hazard. The emissions-based chronic inhalation index for

each HAP was calculated by dividing the national urban emissions estimate by the RBC

for chronic inhalation exposure. The emissions estimates were obtained from the
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baseline NTI (U.S. EPA, 1998a). As with the ambient chronic index, this was done

separately for case 1 (RBC set at 1 x 10-6 upper bound cancer risk or the RfC, whichever

was lower) and case 2 (RBC = 1 x 10-4 upper bound cancer risk or the RfC, whichever

was lower).

C Index 4: Emission/Chronic/Oral. This index was intended to rank HAP by relative

potential for oral toxicity and food-chain bioaccumulation. The emissions-based chronic

oral index for each HAP was calculated by multiplying the national urban emissions

estimate by the HAP’s bioconcentration factor (BCF) and then dividing by the oral RBD

for chronic oral exposure. As with the other chronic indices, this was done separately for

case 1 (RBD set at 1 x 10-6 upper bound cancer risk or the RfD, whichever was lower)

and case 2 (RBD = 1 x 10-4 upper bound cancer risk or the RfD, whichever was lower). 

With the exception of radionuclides, each HAP was carried through the index

calculations even if health benchmark, emission, or ambient data were not available. We believe

that this presentation will allow readers to see data gaps more clearly and will serve as a guide for

future efforts to prioritize data collection for the air toxics program. The results of the

Exposure/Toxicity Indicators ranking are shown in Exhibit 3-4.

EXHIBIT 3-4

40 HIGHEST PRIORITY POLLUTANTS IDENTIFIED BY 

EXPOSURE/TOXICITY INDICATORS RANKING

Acetaldehyde Chloroprene Formaldehyde 2-Nitropropane

Acrolein Coke oven emissions Heptachlor PCBs

Acrylonitrile Chromium compounds Hydrogen chloride POM

Arsenic compounds 1,2-Dibromomethane Hydrazine Propylene dichloride

Benzene 1,4-Dichlorobenzene Lead compounds Quinoline

Bromomethane

(methyl bromide)

1,3-Dichloroethane Manganese

compounds

1,1,2,2-Tetrachloro-ethane

1,3-Butadiene 1,1-Dichloroethylene Mercury compounds Tetrachloroethylene

Cadmium

compounds

1,3-Dichloropropene Methylene chloride Trichloroethylene

Carbon tetrachloride Dioxin (2,3,7,8-TCDD) Napthalene Vinyl chloride

Chloroform Ethylene oxide Nickel compounds Xylene
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For example, in the case of 1,3-butadiene, we determined that the EPA’s Integrated Risk Information

System (IRIS) risk estimate is no longer an appropriate basis from which to extrapolate human risk, and the updated

assessment has progressed to the point where it is appropriate for use here. Use of this new assessment, however,

does not affect the presence of 1,3-butadiene on the urban HAP list. In the case of vinyl chloride, we’ve chosen to

use the Agency consensus assessment currently in IRIS rather than a draft assessment that may yet change

significantly. However, we’ve confirmed that using the draft assessment for vinyl chloride wouldn’t change its

status on the final urban HAP list.

3-16

Data Sources for the Exposure/Toxicity Indicators Ranking

In order to rank each of the HAP in the indices described above, data on health-based

reference values, ambient air quality measurements, emissions, and bioconcentration factors were

collected. Each of these are described below.

Health-Based Reference Values. Dose-response assessments for health effects of HAP

were obtained from various sources, and prioritized according to: (1) applicability, (2) conceptual

consistency with EPA risk assessment guidance, and (3) level of review received. The

accompanying text box lists in priority order the health-based reference values which were used

in this analysis. For dose response estimates that are currently under review or being revised, we

reviewed current information to determine how potential changes to dose-response estimates

might affect the outcome of the analysis1. The Technical Support Document contains additional

details regarding these reference values (U.S. EPA, 1999b).

Estimates of Exposure. The second major part of the HAP ranking indices (the first part

being the dose-response data described above) was information on exposure. Actual data

describing human exposure to HAP are limited and lack the comprehensive geographic,

temporal, and multicontaminant coverage that this ranking exercise required. Therefore, we

chose to base the ranking on exposure surrogates – data related to, but not identical with,

exposure. The two types of exposure surrogates chosen were long- and short-term ambient air

quality measurements from urban areas, and estimated annual emissions of HAP from major,

area, and mobile sources in urban areas.

The ambient air quality data set used in this analysis was created by combining all

available monitoring data from EPA’s Aerometric Information Retrieval System (AIRS) and

Toxics Data Archive (12/31/97 version) databases for the 188 HAP. The analysis was restricted

to data from 1990 through 1997, for 24-hour sampling intervals only from counties designated as

“urban1” or “urban2.” A minimum of 20 observations during a year were required for inclusion

of that year’s data, and for volatile and semi-volatile compounds it was further required that at

least five observations were from the spring or summer and five from the fall or winter. 

Concentration data that were below the method detection limit were used as reported in the

calculations, while data values designated only as “below detection limits” (i.e., without a

reported concentration) were assumed to be present at one-half the detection limit (instead of
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Data Sources and Health-Based Reference

Values Used in the Exposure/Toxicity

Indicators Ranking Analysis

For chronic exposure (cancer and noncancer

reference values, in order of preference):

1. EPA IRIS

2. Agency for Toxic Substances and Disease

Registry (ATSDR) MRLs

3. EPA Health Effects Assessment Summary

Tables (HEAST)

4. California EPA inhalation unit risks 

5. EPA estimates of cancer risk from oral

exposure converted to inhalation units (IRIS

or HEAST)

For short-term exposure (noncancer effects):

1. National Advisory Committee (NAC)

Guideline Level (1-hr Level I)

2. NAC Acute Exposure Guideline Level (1-hr

Level II)

3. California EPA acute RELs

4. American Industrial Hygiene Association

(AIHA) Emergency Response Planning

Guidelines (ERPG) (1-hr Level I)

5. AIHA ERPG (1-hr Level II)

6. 10 percent of National Institute for

Occupational Safety and Health

Immediately Dangerous to Life or Health

levels

7. ATSDR acute MRL

omitting the observation). For HAP having

fewer than 10 percent of observations above the

detection limit, the data were omitted

altogether.

For input to the chronic exposure

indices, selected ambient air quality data were

first averaged arithmetically for each year, by

HAP and monitoring site. The annual average

concentrations from 1990 to 1997 for each sitepollutant combination were next averaged

across years. Finally, the resulting multiyear

average concentrations were averaged across

monitoring sites into a single national long-term

average concentration for each HAP for which

data met the selection criteria. 

To simulate acute exposure for each

HAP, the 95th percentile concentration of the

database of 24-hour ambient concentrations at

all locations was selected. We judged that this

concentration represented a reasonable

maximum short-term exposure.

The second type of data used in this

ranking analysis as a surrogate for exposure was

the estimated emissions of HAP from major,

area, and mobile sources in urban areas (U.S.

EPA, 1998b).

Bioconcentration Data. Measured and

estimated BCFs for HAP were obtained from

EPA’s draft Waste Minimization Prioritization

Tool (WMPT). The BCF provides an estimate of how much a pollutant will accumulate in

tissues and be concentrated throughout the food web (U.S. EPA, 1998c). 

Limitations of the Exposure/Toxicity Indicators Ranking

In addition to the general limitations of all three ranking analyses, the Exposure/Toxicity

Indicators ranking relied heavily on emissions data. Emissions-based indices do not consider

dispersion or transformation of HAP and are, therefore, likely to be less reliable surrogates for

exposure than are ambient concentrations. As a result, there are two limitations of this analysis:
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(1) the ranking is relative rather than absolute, and (2) the results cannot be inferred as

quantitative risk estimates.

3.3.2 Risk Assessment/Hazard Ranking Studies in Urban Areas

Much of the current information that has been collected to characterize urban air toxic

exposures and potential risks comes from 14 major studies in urban areas. These studies were

conducted by EPA and various State air pollution control agencies. All 14 included emissions

inventory analyses, although seven studies also included air monitoring data. Eleven of the

studies had a risk assessment component, while three studies were hazard rankings only and did

not have a risk assessment component. The number of pollutants studied varied from 11 to 34. 

Most studies focused on carcinogens, but six of the 14 also assessed noncancer risks. Eleven of

the 14 studies included major, area and mobile sources, and three evaluated area sources only.

These 14 studies were reviewed to determine which pollutants contributed the most to the

total risk or hazard reported for the study area. For example, if the total excess cancer risk was

estimated to be three cases per year and pollutant X contributed 0.3 cases per year, then pollutant

X would receive a score of 0.10 because it accounted for 10 percent of the risk. This was done

for each pollutant in each study. The scores for each pollutant were then added together, and the

pollutants ranked from the highest aggregate score to the lowest. Two rankings (one for cancer

as an endpoint and one for noncancer effects) were produced for the 11 studies that included

major, area, and mobile sources. Similarly, two rankings were produced based on the three

studies of area sources only. We used these four HAP rankings to select 27 HAP that appeared

to contribute substantially more risk or hazard than the rest. The 27 HAP identified from this

analysis are shown in Exhibit 3-5.

EXHIBIT 3-5

PRIORITY HAP IDENTIFIED BY STUDIES IN URBAN AREAS

Acrolein Coke oven emissions Methylene chloride

Acrylonitrile Cyanide compounds 2-Nitropropane

Arsenic compounds Ethylene dichloride Nickel compounds

1,3-Butadiene Ethylene oxide POM

Benzene Formaldehyde Tetrachloroethyene

Cadmium compounds Glycol ethers Trichloroethylene

Carbon tetrachloride Hexane Toluene

Chloroform Lead compounds Vinyl chloride

Chromium compounds Manganese compounds Xylene
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In the CEP, emissions from manufacturing point

sources are represented by data from the 1990

TRI. For the other five source categories, the

CEP estimates HAP emissions by applying

speciation profiles to inventories of VOC and

PM. Speciation profiles were specific to

industries or industrial processes. They

provided estimates, on a percentage basis, of the

amount of individual chemical constituents that

comprise VOC or PM emissions.

Sources of Emissions Data

In addition to the general limitations shared by all three analyses, the urban studies

summarized in this hazard ranking analysis studied only 11 to 34 HAP, substantially less than the

188 HAP listed in section 112 of the CAA. Thus, it is possible that high-risk HAP may have

been overlooked. Despite these limitations, however, these studies represent high quality

analyses which identified priority pollutants in a variety of urban areas in the United States. As a

result, the analysis of these studies was a critical component of the overall ranking methodology

and HAP selection process. 

3.3.3 CEP Ranking Analysis

The third ranking analysis was based on EPA’s CEP, initiated in 1994, with the objective

of using existing data and methods to evaluate the combined exposures to multiple pollutants

through three different routes of exposure – air, food and drinking water. In the air toxics

component (the only component completed), long-term air concentrations of HAP (but not

personal exposure) are estimated on a national scale (SAI, 1998).

In the CEP, the Assessment System of

Population Exposure Nationwide (ASPEN)

model was used with preliminary estimates of

1990 HAP emissions (see text box) to predict

long-term average concentrations at the census

tract level for 148 HAP. For some pollutants,

modeled concentrations were augmented with

estimates of background levels that were

intended to represent contributions from

natural sources as well as historic emissions of

persistent pollutants. The estimated ambient

concentrations were then compared to RBCs

(termed benchmarks by the authors) intended

to represent either continuous exposure levels

associated with a one in one million upper bound estimate of excess lifetime cancer risk, or

continuous lifetime exposure levels associated with no significant risk of adverse noncancer

effects (e.g., EPA’s inhalation RFC) (Caldwell et al., 1998). As stated earlier, estimated

concentrations greater than RBCs should be viewed as indicators of a potential health problem

and not as a characterization of health risks. 

As we wanted to focus the analysis on modeled concentrations resulting from controllable

sources, and we are currently using updated RBCs which, in some cases, differ from those used

in the CEP analysis, we took some additional steps. Prior to using this analysis as part of our

final methodology, we repeated the analysis for the subset of HAP for which concentrations had

been augmented with background concentrations or for which the health reference values needed

to be updated. For this small re-analysis, we used the modeled concentrations resulting only
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from current area, major and mobile sources (i.e., without addition of a background value) and an

updated set of RCBs.

From these analyses, we identified those HAP for which the modeled concentrations

exceeded RBCs in the greatest number of urban census tracts. There were 36 HAP for which

modeled concentrations were greater than an RBC in at least 50 urban census tracts (see Exhibit

3-6). These 36 HAP are those of greatest potential concern based on our use of the CEP

modeling analysis.

EXHIBIT 3-6

HAP WITH MODELED CONCENTRATIONS HIGHER THAN 

AN RBC IN AT LEAST 50 URBAN CENSUS TRACTS

Acetaldehyde 2,3,7,8-Tetrachlorodibenzo-p-dioxin (&

congeners & TCDF congeners 

Acrolein Ethyl acrylate

Acrylamide Ethylene oxide

Acrylonitrile Formaldehyde

Arsenic and compounds Heptachlor

Benzene Hexachlorobenzene

Benzotrichloride Hexachlorocyclopentadiene

Beryllium and compounds Hydrazine

1,3-Butadiene Lead and lead compounds

Cadmium and compounds Manganese and compounds

Carbon tetrachloride Methylene chloride (Dichloromethane)

Chloroform Nickel and compounds

Chromium VI and compounds PCBs

1,2-Dibromomethane Quinoline

1,4-Dichlorobenzene 1,1,2-Trichloroethane

1,2-Dichloropropane (Propylene dichloride) Tetrachloroethylene (Perchloroethylene)

Ethylene dichloride (1,2-dichloroethane) Trichloroethylene

1,3-Dichloropropene Vinyl chloride
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Limitations of the CEP

In addition to the general limitations of all three ranking analyses, the modeling

performed for this analysis was subject to the following uncertainties and limitations:

• The ASPEN model, as it had been run, may under- or over-estimate some HAP. Such a

tendency could then lead to an under- or over-estimation of the number of census tracts

with air concentrations higher than an RBC.

• This analysis prioritized HAP according to how frequently a modeled air concentration

was higher than an RBC; how much higher was not examined. Thus, a HAP whose

modeled concentration is slightly higher than the RBC in many census tracts would be

listed as a higher priority than a HAP whose modeled concentration is higher than the

RBC by a large margin in a smaller number of census tracts. 

• A majority of the RBCs were for cancer effects, rather than noncancer effects. This

reflects the fact that the cancer benchmarks set at a one in one million risk level are

generally much lower concentrations that the noncancer benchmarks. Consequently,

cancer as a health effect was emphasized over other health effects. 

While we recognize certain limitations associated with this initial attempt at modeling

HAP concentrations nationwide, and its inappropriateness for use in drawing conclusions at

small geographic scales, this modeling effort is useful as a national screening tool.

3.4 Selection of the Urban Hazardous Air Pollutants

Exhibit 3-7 summarizes the three ranking methodologies and illustrates how the results of

these analyses were considered to produce one listing of priority urban HAP. Results for all three

ranking analyses are summarized in Exhibit 3-8.

For the final HAP list, we selected those HAP for which the baseline inventory data were

publicly reviewed (through EPA’s public request in September 1997 for additional information

on 40 candidate compounds or during development of inventories for the specific HAP listed in

section 112(c)(6) of the CAA) and which had been either:

C Identified by two of the ranking analyses (regardless of area source contribution), or 

C Identified by at least one of the three analyses and had an area source contribution to total

emissions of at least 25 percent.

Exhibit 3-9 summarizes the final integrated list. This list of 33 urban HAP includes not

only those with emissions from area sources, but reflects the integrated nature of the Strategy by
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

3-22

Risk Assessment/Hazard Ranking Studies

14 urban studies reviewed.

Risk results normalized by pollutant and numerically ranked.

Cumulative Exposure Project

Modeled ambient concentrations of HAP were

compared to health benchmarks.

Exposure/Toxicity Indicators Ranking

Seven indices prepared for 188 pollutants.

Each pollutant numerically ranked within each index.

Acute Inhalation Hazard

95th percentile 24 hour conc.

divided by acute RBC

Ambient Chronic Index

Avg. long-term conc.

divided by chronic RBC

Emission/Chronic/Inhalation

NTI emission rate

divided by chronic RBC

Emission/Chronic/Oral

NTI emission rate X BCF

divided by oral chronic RBD

Case 1

Lower of

RBC=1x10-6 or

RfD

Case 2

Lower of

RBC=1x10-4 or

RfD

Case 1

Lower of

RBC=1x10-6 or

RfC

Case 2

Lower of

RBC=1x10-4 or

RfC

Case 1

Lower of

RBC=1x10-6 or

RfC

Case 2

Lower of

RBC=1x10-4 or

RfC

TRI emissions data or speciated

PM/VOC inventory was

apportioned to every census

tract in the U.S.

Emissions data modeled to

provide long-term ambient

levels in each census tract.

Background levels added.

Total concentration compared

to 1x10-6 excess cancer risk or

RfC.

HAP ranked by number of

census tracts in which modeled

concentration is greater than a

health benchmark.

Integrated Urban HAP List: 33 HAP with publicly reviewed emissions data prioritized by 2 of 3 analyses (regardless

of area source contribution).

A subset of 30 HAP were selected for the urban HAP list based on the following criteria: (1) availability of publicly

reviewed emissions data; and (2) at least 25 percent of national urban emissions are from area sources.

Seven rankings for each HAP were normalized, then

HAP were ranked by average normalized score.

EXHIBIT 3-7 

HAP RANKING ANALYSIS FOR THE INTEGRATED URBAN STRATEGY
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

3-23

EXHIBIT 3-8

RESULTS OF THE THREE RANKING ANALYSES 

Contaminant

Risk

Assessment

Hazard

Ranking

CEP Urban

Analysis

(All Sources)

Exposure

Toxicity

Ranking

System

Ratio of

Area/Total

Emissions

Urban

Strategy

Lista

Tetrachloroethylene X X X 81.4% X

Acrolein X X X 66.9% X

Ethylene oxide X X X 53.0% X

Chromium VI and

compounds

X X X 44.2% X

Nickel and compounds X X X 33.0% X

Manganese and compounds X X X 26.1% X

Formaldehyde X X X 23.7% X

Vinyl chloride X X X 20.2% X

Trichloroethylene X X X 19.3% X

Cadmium and compounds X X X 19.1% X

Methylene chloride X X X 17.7% X

Acrylonitrile X X X 16.8% X

Arsenic and compounds X X X 16.4% X

1,3-Butadiene X X X 13.3% X

Benzene X X X 11.2% X

Chloroform X X X 3.8% X

1,2-Dichloroethane X X X 2.9% X

Carbon tetrachloride X X X 2.7% X

1,3-Dichloropropene X X 99.8% X

Carcinogenic PAHs: 7-PAH X X 61.8% X

2,3,7,8-TCDD (dioxin) X X 23.5% X

Hexachlorobenzene X X 22.3% X
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

3-24

EXHIBIT 3-8 (Continued)

RESULTS OF THE THREE RANKING ANALYSES 

Contaminant

Risk

Assessment

Hazard

Ranking

CEP Urban

Analysis

(All Sources)

Exposure

Toxicity

Ranking

System

Ratio of

Area/Total

Emissions

Urban

Strategy

Lista

PCBs X X 19.9% X

Acetaldehyde X X 18.8% X

Lead and lead compounds X X 16.7% X

Hydrazine, hydrazine sulfate X X 8.0% X

Quinoline X X 6.3% X

1,2-Dichloropropane 

 (propylene dichloride)

X X 3.6% O

1,2-Dibromoethane X X 1.5% O

Coke Oven Emissions X X 0.0% O

1,1,2,2-Tetrachloroethane X 79.5% X

Mercury and compounds X 34.5% X

Beryllium and compounds X 27.7% X

1,1-Dichloroethylene X 19.3%

Ethyl acrylate X 12.5%

Acrylamide X 9.1%

1,1,2-Trichloroethane X 1.0%

a HAP to be used in selecting area sources for regulation under the Strategy are marked with an “X.” HAP selected

for the Strategy, but not for area source selection, are marked with an “O.”
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

3-25

EXHIBIT 3-9

LIST OF URBAN HAP FOR THE INTEGRATED URBAN AIR TOXICS STRATEGY

Acetaldehyde Formaldehyde 

Acrolein Hexachlorobenzene

Acrylonitrile Hydrazine

Arsenic compounds Lead compounds

Benzene Manganese compounds

Beryllium compounds Mercury compounds

1,3-Butadiene Methylene chloride (dichloromethane)

Cadmium compounds Nickel compounds

Carbon tetrachloride* PCBs

Chloroform POM

Chromium compounds Quinoline

Coke oven emissions* 2,3,7,8-tetrachlorodibenzo-p-dioxin (&

congeners & TCDF congeners)

1,2-Dibromoethane* 1,1,2,2-Tetrachloroethane

1,2-Dichloropropane (propylene dichloride) Tetrachloroethylene (perchloroethylene)

1,3-Dichloropropene Trichloroethylene

Ethylene dichloride

(1,2-dichloroethane)

Vinyl chloride

Ethylene oxide

* These 3 HAP are identified mainly due to emissions from major sources, and therefore are not

considered urban area source HAP at this time.

including those posing public health concerns in urban areas regardless of emissions source type. 

Included among the 33 urban HAP are the 30 HAP with greatest emissions contributions from

area sources (i.e., the “area source HAP”). The 3 HAP noted with an asterisk are listed mainly

due to major source emissions. Nonetheless, they are included in the Integrated Urban Air

Toxics Strategy (which considers emissions in urban areas from all source types) based on the

criteria presented in this chapter. Under section 112(k), there aren’t any specific regulatory

implications of listing the other three HAP, and we’ll use all 33 HAP in prioritizing efforts to

address risk.

It is important to note that the HAP list in Exhibit 3-9 was generated based on our best

estimates representing national baseline air toxics emissions and ambient concentrations for
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

3-26

urban areas. For example, implementation of technology-based standards for coke ovens has

reduced the benzene, coke oven gases, and POM from these sources by 80 percent (or 1,408 tons

per year) since 1993. In addition, certain urban areas have reduced other benzene emissions by

as much as 30 or 40 percent. Much of this reduction is attributable to the implementation of

mobile source reformulated gasoline requirements. To ensure that we appropriately target

reductions of urban air toxics to support the protection of public health, it will be important to

reevaluate our priorities as we develop emissions estimates and obtain more comprehensive

monitoring information covering more recent years.

3.5 References

Caldwell, J.C., T.J. Woodruff, R. Morello-Frosch, and D.A. Axelrad. 1998. Application of 

health information to hazardous air pollutants modeled in the Environmental Protection

Agency’s Cumulative Exposure Project. Toxicology and Industrial Health, Vol.14, No. 3,

pp. 429-454.

Systems Applications, Inc. (SAI). 1998. Modeling cumulative outdoor concentrations of 

hazardous air pollutants: final technical report. Prepared by SAI Division of ICF Kaiser

International. Prepared for U.S. Environmental Protection Agency. February.

U.S. Bureau of the Census. 1990. Summary tape file 1A, 1990 decennial census of population 

and housing. Washington, D.C.

U.S. EPA. 1992. Documentation for developing the initial source category list, final report. 

EPA-450/3-91-030. Office of Air Quality Planning and Standards, Research Triangle

Park, North Carolina. 

U.S. EPA. 1997a. Prioritization of HAP for the Urban Air Toxics Study - peer review draft. 

Office of Air Quality Planning and Standards, Research Triangle Park, North Carolina. 

December 29.

 

U.S. EPA. 1997b. National Advisory Committee for Acute Exposure Guideline Levels for 

Hazardous Substances; notice. Federal Register 62:58839-58851. October 30.

U.S. EPA. 1998a. 1993 National Toxics Inventory, version 9702.

U.S. EPA. 1998b. Inventory of Emissions Estimates for HAP Emitted from MACT Source 

Categories. Prepared by the Emission Factor and Inventory Group and the Emission

Standards Division, Research Triangle Park, North Carolina. 

U.S. EPA. 1998c. Waste Minimization Prioritization Tool spreadsheet document for the RCRA 

waste minimization PBT chemical list docket (#F-98-MMLP-FFFFF). Office of Solid

Waste and Emergency Response, Washington, D.C. Available on-line at

www.epa.gov/wastemin.
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

3-27

U.S. EPA. 1999a. 1990 Emissions inventory of forty section 112(k) pollutants, supporting data 

for EPA’s proposed 112(k) Regulatory Strategy, final report. Office of Air Quality

Planning and Standards, Research Triangle Park, North Carolina. May 21.

U.S. EPA. 1999b. Ranking and selection of hazardous air pollutants proposed for listing under 

section 112(k) of the Clean Air Act Amendments of 1990. Technical Support Document. 

Office of Air Quality Planning and Standards, Research Triangle Park, North Carolina. 

April 12.

U.S. EPA Docket A-97-44. Urban Air Toxics Strategy.
National Air Toxics Program: The Integrated Urban Strategy

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National Air Toxics Program: The Integrated Urban Strategy

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1

The Hazardous Waste Combustor source category combines the following: hazardous waste incinerators,

hazardous waste-burning cement kilns, and hazardous waste lightweight aggregate kilns. 

2We have recently promulgated MACT standards for hazardous waste combustors (U.S. EPA, 1999a) and

will be using the support information for that rule to update our information on this source category.

4-1

4. Regulatory Programs and Activities to Reduce Air Toxics

Emissions

4.1 Introduction

The Strategy describes many of the programs and regulatory activities that will help

achieve the goals of reducing cancer and noncancer risks. One of the key aspects described by

the Strategy is that national regulatory programs are but one of the many tools that we will use to

address emissions of air toxics. Other authorities and laws will, directly or indirectly, also allow

us to address these pollutants. Furthermore, by working collaboratively with State, local, and

Tribal governments, we will ensure that localized air toxics issues are addressed as well.

Section 4.2 presents the list of area source categories that were identified in the Strategy

and explains how we intend to ensure that, as required, we reach the goal of addressing the

source categories that represent 90 percent of the emissions of each of the 30 area source HAP. 

Section 4.3 describes the regulatory options that will be considered in order to address air toxics

from area sources. The role of mobile sources is noted in section 4.4, and current and future

programs are described. Other emission sources which may be affected by the Strategy are

described in section 4.5, while other programs and authorities which may also account for

emissions reductions are described in section 4.6. A very important component of the Strategy is

described in section 4.7 – the role State, local, and Tribal programs will play in helping us

address air toxics and achieve the Strategy goals. References are listed in section 4.8.

4.2 List of Area Source Categories

Our selection of the area source categories was a two-step process. First, we identified

area sources that contribute to emissions of the area source HAP and that are subject to existing

standards or will be subject to standards that are currently being developed. These area source

categories have already been listed for regulation under the CAA. For each of these source

categories, we identified the percent contribution to the total area source emissions for each of

the 30 area source HAP. These source categories are provided in Exhibit 4-1. We have included

hazardous waste combustors1 on this list, despite the fact that information related to the

percentage contribution of emissions from this area source category was not known at the time

that the list was developed. Once we determine the percentage of urban area emissions from the

area source categories affected by this rule, their emissions will be counted toward the 90 percent

requirement for the appropriate HAP2.
National Toxics Air Program: The Integrated Urban Strategy

Report to Congress

3

1,1,2,2-tetrachloroethane, 1,2-dichloropropane, POM, acetaldehyde, acrolein, benzene, dioxins/furans,

ethylene oxide, formaldehyde, quinoline, and tetrachlorethylene.

4

1,3-butadiene, 1,3-dichloropropene, acrylonitrile, beryllium compounds, chloroform, hydrazine, mercury

compounds, methylene chloride, trichloroethylene, and vinyl chloride.

4-2

EXHIBIT 4-1

AREA SOURCE CATEGORIES ALREADY SUBJECT TO REGULATION

OR WHICH WILL BE SUBJECT TO REGULATION

Chromic Acid Anodizing Industrial Boilers

Commercial Sterilization Facilities Institutional/Commercial Boilers

Other Solid Waste Incinerators (Human/Animal

Cremation)

Medical Waste Incinerators

Decorative Chromium Electroplating Municipal Waste Combustors

Dry Cleaning Facilities Open Burning Scrap Tires

Halogenated Solvent Cleaners Portland Cement

Hard Chromium Electroplating Secondary Lead Smelting

Hazardous Waste Combustors Stationary Internal Combustion Engines

In the second step, we added to the list those area source categories that contribute at least

15 percent of the total area source emissions of any of the individually-listed HAP. This criterion

was adopted to account for uncertainties in our current inventory data. Although the baseline

emissions inventory data have improved, data gaps and uncertainty still remain. By listing only

those additional sources contributing 15 percent of the area source emissions of at least one of

the area source HAP, we can be fairly certain that, despite the gaps in our inventory data, a listed

source category genuinely contributes to emissions of that HAP. Once listed, we counted the

percent contribution, even if less than 15 percent, to emissions of any other listed HAP because

once the source is subject to regulation, its emissions of any of the 30 listed HAP can be counted

toward the 90 percent goal for each of the listed HAP. Exhibit 4-2 includes those new area

source categories listed under section 112(c)(3) for the first time. 

The result of these criteria for the source selection process is that the current list of 29

source categories does not, at this time, contain area source categories representing 90 percent of

the emissions of each individual HAP. The current list meets the 90 percent or greater

requirement for 11 of the 30 area source HAP3. For 10 other HAP, the list accounts for at least

80 percent of the emissions4, and for ethylene dichloride the list accounts for approximately 78

percent of the emissions. Improved inventory data may demonstrate that the current list of area

sources already meets the 90 percent requirement for some of these HAP. For the remaining

HAP on the list, less than 75 percent of their emissions are accounted for in the list of source
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

4-3

EXHIBIT 4-2

NEW AREA SOURCE CATEGORIES AS LISTED

Cyclic Crude and Intermediate Production Municipal Landfills

Flexible Polyurethane Foam Fabrication

Operations

Oil & Natural Gas Production

Hospital Sterilizers Paint Stripping Operations

Industrial Inorganic Chemical Manufacturing Plastic Materials and Resins Manufacturing

Industrial Organic Chemical Manufacturing Publicly Owned Treatment Works

Mercury Cell Chlor-Alkali Plants Synthetic Rubber Manufacturing

Gasoline Distribution Stage I

categories: arsenic compounds, cadmium compounds, chromium compounds,

hexachlorobenzene, lead compounds, manganese compounds, nickel compounds and PCBs. 

It’s important to clarify that we still intend to meet our statutory obligation to list area

sources accounting for 90 percent of the emissions of each of the 30 area source HAP. We have

chosen to complete this list in stages by keeping the option to add or delete source categories

from the list as we gather more and improved data. This first stage lists those area sources that

we are reasonably confident add real contributions to the total area source emissions of a

particular area source HAP. We anticipate to begin evaluating the source categories for the HAP

for which we haven’t reached a 90 percent emission reduction, including the six metal HAP,

PCBs, and hexachlorobenzene, when we conduct an initial risk assessment by the end of 2000

(discussed in Chapter 5 of this Report). That initial assessment will use the updated 1996 NTI. 

We’ll use this information as part of our process to reevaluate the source categories listed in the

Strategy. Based on this updated information, we may decide to remove an area source category

listed here if, for example, the reason for the listing was inaccurate (e.g., faulty reporting to the

TRI) or if no urban area sources exist. We’ll also use this assessment to evaluate area source

categories to be added and will complete the list by 2003.

4.3 Regulatory Activities for Area Sources

We plan to pursue a tiered approach that will consider three standard-setting processes. 

The specific process selected for a particular source category will depend on the criteria outlined

below. We intend to determine which one of these approaches is most appropriate when we

conduct rulemaking. The three tiers of standard setting processes that will be considered are:

• Tier 1 – MACT standards;

C Tier 2 – Source category-specific GACT standards; and

C Tier 3 – Flexible GACT.
National Toxics Air Program: The Integrated Urban Strategy

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4-4

4.3.1 Tier 1 – MACT Standards

We’ll develop MACT standards in accordance with section 112(d)(3) for those area

sources whose emissions pose the greatest threat to human health and the environment, and for

which the technology to achieve maximum reductions in HAP emissions is appropriate. Section

112(d)(3) requires the standards to reduce HAP emissions as much as is achievable, considering

the cost of these reductions, effects on health or the environment (other than air), and energy

requirements. 

Section 112(d)(3) requires us to use a minimum statutory baseline (“floor”) when setting

MACT standards. For new sources, the MACT standards for a source category or subcategory

must be at least as stringent as the emission control achieved in practice by the best controlled

similar source. The standards for existing sources can be less stringent than standards for new

sources, but they can’t be less stringent than the average emission limitation achieved by the

best-performing 12 percent of existing sources (excluding certain sources) for categories or

subcategories with 30 or more sources, or by the best-performing five sources for categories or

subcategories with fewer than 30 sources.

We’ve issued MACT standards for area sources in previous cases. For example, in the

chromium electroplating national emission standards for hazardous air pollutants (NESHAP), we

developed MACT standards for area sources because of the high toxicity of chromium. 

Similarly, in the Portland Cement NESHAP, we determined that MACT controls were

appropriate because of the quantity and toxicity of the HAP being emitted from area sources. In

addition, both of these source categories have numerous, widespread sources. We’ve also

determined in a recent rulemaking that air toxic emissions from area source hazardous waste

combustors present a threat of adverse effects to human health and, thus, will be required to meet

MACT controls.

4.3.2 Tier 2 – Source Category-Specific GACT Standards

While we may develop MACT standards for some area sources, we expect most sources

will be subject to GACT standards developed in accordance with section 112(d)(5). As with

MACT standards, GACT standards would be developed for a specific source category, but they

would be based on the use of GACT rather than MACT. This approach will be used to address

source categories that present a human health risk or environmental concern, but where GACT is

a more appropriate approach for reducing HAP emissions than MACT. To make these decisions,

we’ll consider economic feasibility and other factors that could lead us to GACT.

4.3.3 Tier 3 – Flexible GACT Process

Considering the large number and diversity of area sources and limitations in the data and

information currently available for many of them, it may be appropriate to develop flexible

requirements that would apply to several area source categories where more flexibility is

appropriate (e.g., where there are very few area sources, they are confined to a limited geographic
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

5

“Urban 1” areas are those counties that have a population of more than 250,000. “Urban 2” areas are

counties where at least 50 percent of the population is considered to be urban.

4-5

area, or they contribute to localized public health or environmental risks). Under this option, we

might develop general requirements, such as a process rule similar to the one developed under

section 112(g) of the CAA, which would be applicable to area sources in several source

categories. These general requirements could outline procedures for determining what

constitutes “generally available control technology.” In this context, by following these

procedures, States, local governments, and Tribal agencies could elect to develop GACT for the

area sources. We would review these resulting standards to ensure they were developed

following the procedures contained within the general requirements and, if appropriate, we

would adopt the standards as GACT for these area sources. 

We believe this approach presents several advantages. It could be implemented in a

manner that permits States, local and Tribal agencies to address cumulative risk posed by

exposures to HAP emissions from many different source categories. It also permits greater

flexibility in tailoring GACT to individual area sources or area source categories which may

contribute to an undue public health risk in a particular area. For example, a State, local or

Tribal agency could tailor GACT to a particular source by requiring potentially more stringent

controls when the source contributes emissions that, when aggregated with emissions from other

sources in the area, pose health risk concerns. They could also require less stringent controls

when the source is in an area where exposures to aggregated emissions don’t present significant

concern. 

 To supplement our general requirements, we may choose to issue control technique

guidelines or alternative control technology documents to provide information on generally

available control technologies for controlling HAP emissions. The CAA gives us flexibility in

deciding which level of control to apply to a given source category. As long as the result of the

rulemaking is that sources use enforceable GACT or management practices, we have the

flexibility in choosing between the adoption of numerical emission limits and the promulgation

of other requirements that result in sources applying GACT.

4.3.4 Issues on the National Versus Local Scope of Area Source Standards

Section 112(k) requires that listed area source categories be subject to standards under

section 112(d). Section 112(d) standards are national standards that generally apply everywhere

in the country. Consistent with this approach, we expect, in general, to apply area source

standards developed under section 112(k) nationally; however, for those area source categories

where the standards only apply in urban areas, we’ll look to the consolidated metropolitan

statistical area (C/MSA) boundaries as a starting point to define the urban area. Although we

used the “urban 1” and “urban 2” definitions5 for the development of the inventory to support the

HAP and the source category analysis, we believe the C/MSAs are more appropriate for defining
National Toxics Air Program: The Integrated Urban Strategy

Report to Congress

6As part of the air toxics rulemaking currently under development pursuant to the requirements of section

202(l) of the CAA, described below, we will be preparing a more comprehensive list of air toxics emitted by motor

vehicles and their fuels.

4-6

applicability of area source standards, because the C/MSAs better reflect the nature of population

density, commercial development, area growth, and air emissions that represent urban areas.

Although we generally believe that urban areas are those C/MSAs with populations of

more than 50,000, we recognize that the appropriate area in which standards should apply may

vary among area source categories. Consequently, we believe the determination of the

appropriate urban area size for where standards apply should be made separately for each

category. 

4.3.5 Schedule for Area Source Standards

The Strategy outlined a timeframe for the completion of area source standards, as shown

in the time line below:

C 2004 – Promulgate the area source category standards listed in Exhibit 4-2; we expect to

meet this demanding schedule as expeditiously as practicable;

C 2006 – Promulgate some additional area source standards to meet the 90 percent

requirement;

C 2009 – Promulgate all remaining area source standards necessary to meet the 90 percent

requirement; and

C 2012 – Expected compliance under all standards.

We’ll prioritize the order in which we regulate source categories to address those posing

the greatest risks first. This will be a part of our initial assessments which will be done in the

spring of 2000. We’ll be developing standards between now and 2009. Compliance with these

standards is required within 3 years of promulgation. Therefore, compliance with all standards is

anticipated by no later than 2012. 

4.4 Regulatory Activities for Mobile Sources

4.4.1 Urban HAP Emitted from Mobile Sources

There are hundreds of different compounds and elements that are known to be emitted

from passenger cars, on-highway trucks, and various nonroad equipment. Using emission

speciation data from several sources, we have determined that 15 of the compounds included in

the list of 33 urban HAP may be emitted from mobile sources6. These are listed in Exhibit 4-3,
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

7

These metals are arsenic compounds, beryllium compounds, cadmium compounds, chromium compounds,

lead compounds, manganese compounds, mercury compounds, and nickel compounds. It is worth noting that: (1)

hexavalent chromium, a known human carcinogen, is the carcinogenic compound of interest among chromium

compounds; (2) nickel has been classified as a known human carcinogen; (3) while lead in gasoline has been

phased-out for use in cars, it is still used in aircraft and in racing fuel; (4) recent studies have not been able to detect

mercury compounds in measurable amounts in light-duty gasoline or heavy-duty diesel mobile source emissions

(Ball, 1997; Truex et al., 1998); however, we are presently undertaking further study of mercury emissions from

vehicles, and the Ball (1997) and Truex et al. (1998) studies should not be viewed as conclusive; and (5) we are

investigating the potential health impact of manganese in fuels under our section 211 testing programs, described

below; and (6) while mobile source emissions of beryllium compounds and cadmium compounds are reported in our

baseline inventory, these emission estimates are derived from data that are more than 10 years old and thus may not

be representative of current emissions.

4-7

along with their absolute and relative contributions as determined by our baseline emissions

inventory.

The inventory estimates presented in Exhibit 4-3 are 1990 estimates. As we continue to

improve our inventories for urban HAP from mobile sources, these values may change. For

example, the 1996 NTI is incorporating new information based on improved data and methods. 

Based on information in EPA’s Integrated Risk Information System (IRIS) database, four

of the urban HAP listed in Exhibit 4-3 are VOCs considered to be known or probable human

carcinogens (acetaldehyde, benzene, 1,3-butadiene, and formaldehyde), and a fifth VOC,

acrolein, is considered to be a possible human carcinogen (U.S. EPA, 1999b). POM includes a

number of carcinogenic compounds such as benzo(a)pyrene. While 2,3,7,8-TCDD (& congeners

& TCDF congeners) has a very high potency, it is emitted in only trace amounts by mobile

sources (Truex et al., 1998; Gertler et al., 1997; U.S. EPA, 1998a). The eight remaining HAP

listed in Exhibit 4-3 are metals that may be contained in very small quantities in particulate

emissions from gasoline and/or diesel engines7.

4.4.2 Diesel Exhaust 

Diesel exhaust is one of the pollutants under consideration for inclusion on a

comprehensive list of air toxics emitted by motor vehicles and their fuels in the section 202(l)

rulemaking, described below. Diesel exhaust was not included by Congress on the list of 188

HAP under section 112(b) of the CAA and consequently was not included in the group of

pollutants that were considered for inclusion on the urban HAP list. Because diesel exhaust

emissions come almost exclusively from mobile sources, we are investigating the health risks

associated with diesel exhaust and assessing its role in the urban air toxics problem as part of the

section 202(l) rulemaking process. 

Diesel exhaust includes components in the gas and particle phases. Gaseous components

of diesel exhaust include at least one organic compound known to cause cancer in humans (e.g.,

benzene) while possible or probable human carcinogens and compounds causing noncancer

effects are also present in the gas-phase (e.g., formaldehyde, acetaldehyde, 1,3-butadiene,
National Toxics Air Program: The Integrated Urban Strategy

Report to Congress

4-8

EXHIBIT 4-3

1990 NATIONAL EMISSION ESTIMATES 

 FOR URBAN HAP EMITTED FROM MOBILE SOURCES†

HAP Mobile Source

Tons/year

Total Emissions

Tons/year

Percent Mobile

Source

Contribution

Acetaldehyde 65,535 137,476 47

Acrolein 12,315 67,901 18

Arsenic compounds 3 284 1

Benzene 281,170 390,615 72

Beryllium compounds 0.02 12.15 0.16

1,3-butadiene 47,822 71,870 66

Cadmium compounds 0.31 203.34 0.15

Chromium compounds 54 927 6

Formaldehyde 177,031 350,617 50

Lead compounds 1,199 3,270 37

Manganese compounds 52 2,846 2

Mercury compounds 12 208 6

Nickel compounds 95 1,245 8

POM ‡ 48 1,318 4

2,3,7,8-TCDD (&

congeners & TCDF

congeners)

0.0001 0.0032 2.9844

†Emissions and percentages for most of these compounds are rounded to the nearest whole unit. However, due to

the small amount of emissions of beryllium and compounds and cadmium and compounds, these emissions

and percentages are reported to 2 decimal places. Similarly, values for 2,3,7,8-TCDD (& congeners &

TCDF congeners) emissions and percentages are reported to four decimal places.

‡ POM represents the 7-polycyclic aromatic hydrocarbons (7-PAH) group from the baseline emissions inventory.

acrolein). Because diesel exhaust is a mixture of particles and gases, the choice of a measure of

exposure (i.e., dosimeter) is important. The EPA believes that exposure to whole diesel exhaust

is best described, as many researchers have done over the years, by diesel particulate

concentrations expressed in units of mass concentration (e.g., Fg/m3). This does not imply that

mass is the only toxicologically important aspect of PM since other parameters such as particle
National Air Toxics Program: The Integrated Urban Strategy

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4-9

number, particle size, surface area, and chemical composition can influence toxicity. The choice

of this dosimeter implies that the contribution of the gaseous components and diesel particulate

constituents to toxicity are related by diesel particulate mass. This assumption is consistent with

historic practice, but can only be validated when there is a better understanding of the

toxicological mode of action for diesel exhaust.

While some gaseous components of diesel exhaust may play a role in the cancer hazard

attributed to diesel exhaust exposure, studies suggest that the particulate component plays a

substantial role in carcinogenicity and other noncancer effects. Diesel PM typically consists of a

solid core, composed mainly of elemental carbon, which has a coating of various organic and

inorganic compounds. The characteristically small particle size (on average 0.2 microns in

diameter) increases the likelihood that the particles and the attached compounds will reach and

lodge in the deepest and more sensitive areas of the human lung. Diesel PM may be influential

in contributing to potential human health hazards from long term exposure.

Our draft health assessment for diesel emissions identifies lung cancer and several other

adverse respiratory health effects (including respiratory tract irritation, immunological changes,

and changes in lung function) as possible concerns for long term exposure to diesel exhaust (U.S.

EPA, 1999c). The evidence for these health effects comes from occupational exposures and high

exposure animal studies. The draft health assessment finds that diesel exhaust is a likely human

carcinogen in the lung at environmental levels of exposure, and that exposure to diesel exhaust

can pose a noncancer health risk. The draft health assessment document is currently being

revised to address comments from a peer review panel of the Clean Air Scientific Advisory

Committee (CASAC) (U.S. EPA, 2000a) and will be reviewed by CASAC again in late 2000.

4.4.3 Mobile Source Emission Control Programs 

We regulate mobile sources emissions through a wide range of programs under the

authority contained in several sections of the CAA. These include the motor vehicles provisions

contained in section 202(a), the fuel requirements contained in section 211, the nonroad engine

and vehicle provisions contained in section 213, and the urban bus standards contained in section

219. While many of our programs are designed primarily for control of criteria pollutants,

especially ozone and PM, they also achieve important reductions in air toxics through VOC and

HC controls. For example, vehicle- and engine-based control programs reduce benzene, 1,3-

butadiene, formaldehyde, and acetaldehyde that are produced during the combustion process

when there is incomplete combustion. Overall, vehicle- and engine-based HC controls have

dramatically reduced exhaust emissions of gaseous air toxics emitted by mobile sources. 

Similarly, we have several programs that reduce diesel exhaust emissions from diesel engines

and equipment. Finally, our evaporative control programs are designed to further reduce

emissions of volatile air toxics due to engine design or faulty components that allow fuel vapors

to escape into the atmosphere. 

We also address mobile sources air toxics through fuel requirements. Our fuel control

programs have resulted in significant reductions in the emissions of toxic substances from motor
National Toxics Air Program: The Integrated Urban Strategy

Report to Congress

8Chapter 3 of the Regulatory Impact Analysis for this rule assesses the impacts of the Tier 2 program on

air toxics (U.S. EPA, 1999e).

4-10

vehicles. The phase-out of lead in gasoline has essentially eliminated mobile sources emissions

of this highly toxic substance. More recently, the reformulated gasoline (RFG) program has

assisted areas of the country with the worst ozone problems to help improve their air quality. By

controlling fuel benzene content and vehicle emissions of air toxics, ozone-forming HC and NOx,

Phase I of the RFG program has removed thousands of tons of air pollutants for the 17 States and

the District of Columbia currently participating in the program. Phase II of the RFG program

began on January 1, 2000 and contains even more stringent emissions reductions requirements

than Phase I. 

In addition to vehicle and fuel control programs, we have established several programs to

make sure vehicle emission controls are functioning properly in actual use. At the national level,

vehicle manufacturers are required to install computerized diagnostic systems that alert drivers

and mechanics to malfunctioning emission controls. We also follow up with manufacturers by

performing selective engine testing as engines leave the assembly line to make sure they are

manufactured as designed and meet the mandatory exhaust emission limits. At the State level,

we have developed programs that States can adopt to require vehicle owners to have their

vehicles periodically inspected. In addition, we follow up on in-use performance by testing or

requiring that manufacturers test vehicles that have been in service.

In continuing our progress in controlling emissions from mobile sources, there are four

major recent and ongoing mobile source rulemaking activities that have the potential to achieve

additional reductions of health risks from air toxics. First, in October of 1999, we proposed to

reconfirm heavy-duty diesel engine emission standards for the 2004 model year and proposed

heavy-duty gasoline vehicle emission standards for the 2004 model year (U.S. EPA, 1999d). 

Second, we recently promulgated stringent new “Tier 2” emission standards and gasoline sulfur

controls that will reduce NOx and HC emissions from light-duty vehicles and light-duty trucks8

(U.S. EPA, 2000b). The Tier 2 program also contains new PM limits that will reduce PM

emissions from the diesel versions of these vehicles. Third, we recently proposed heavy-duty

engine and vehicle standards for the 2007 model year and highway diesel fuel sulfur controls

beginning in 2006 (U.S. EPA, 2000c). The proposed diesel fuel sulfur controls would enable the

use of a new generation of emission control technologies for diesel engines to decrease diesel PM

and other emissions. Fourth, we are conducting a technology review, to be concluded in 2001,

for land-based compression ignition nonroad engines (U.S. EPA, 1998b). 

4.4.4 Mobile Source Air Toxics Assessments and Controls

In addition to the general emission control provisions mentioned above, title II of the

CAA contains provisions that call more directly for reductions in HAP from motor vehicles and

their fuels. These provisions are contained in section 202(l) of the CAA. The first of these

requirements, outlined in section 202(l)(1), requires us to study the need for and feasibility of
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

9

This assessment is currently being revised based on comments from the EPA Science Advisory Board

(SAB) and others.

10The test requirements for fuels containing oxygenates include short and long term animal health effects

testing, as well as human microenvironmental exposure measurement studies to determine how much of certain

compounds we breathe in our everyday lives. The list of compounds includes, but is not limited to, air toxics such

as benzene, 1,3-butadiene, formaldehyde, and acetaldehyde. The MMT testing program includes pharmacokinetic

4-11

controlling emissions of toxic air pollutants associated with motor vehicles and their fuels that

are otherwise unregulated under the CAA. 

Pursuant to section 202(l)(1), in 1993 we released the Motor Vehicle-Related Air Toxics

Study (U.S. EPA, 1993). The study summarized information on emissions of toxic air pollutants

associated with motor vehicles and motor vehicle fuels, as well as estimated exposures and

potential risks. The study also provided predictions of cancer risks associated with continuous

lifetime exposure to motor vehicle emissions of several air toxics in the years 1990, 1995, 2000,

and 2010 under various control scenarios. We have recently updated the emissions and exposure

analyses done for the study to account for new information (U.S. EPA, 1999f ). These analyses

include base scenarios for the years 1990, 1996, 2007, and 2020, and control scenarios in 2007

and 2020. We modeled toxics emissions and exposure for 10 urban areas (Atlanta, Chicago,

Denver, Houston, Minneapolis, New York, Philadelphia, Phoenix, Spokane, and St. Louis), and

nationwide. In addition, we developed emission estimates for 16 geographic regions. We

assessed emissions and exposure from benzene, formaldehyde, acetaldehyde, 1,3-butadiene,

methyl tertiary butyl ether (MTBE), and diesel PM. As part of our section 202(l)(2) proposal

(see below), we will outline the additional research and technical analysis we plan to conduct to

improve these analyses. 

We have several activities already under way to improve our understanding of the risks

associated with exposure to mobile source air toxics. We are developing and updating

information on health effects for some pollutants on the urban HAP list with contributions from

mobile sources including, for example, our recent benzene cancer risk assessment (U.S. EPA,

1998c; U.S. EPA, 1985) and our draft 1,3-butadiene risk assessment (U.S. EPA, 1998d)9. We are

also continuing our research on health effects of diesel exhaust through the development of our

diesel health assessment document, and through the support of research efforts by organizations

such as the Health Effects Institute. We are developing models of mobile source emissions as

inputs for emissions inventory and dispersion modeling efforts such as the NTI and ASPEN (see

discussion in Chapter 6 of this Report). In addition, we seek to better characterize emissions and

exposures to HAPutants through research and testing efforts at EPA facilities such as the

National Exposure Research Laboratory, as well as the National Vehicle Fuel and Emissions

Laboratory. We also have programs requiring manufacturer-run fuel and fuel additive health

effects testing programs under section 211(b) of the CAA, including testing of various fuels

containing oxygenates, such as MTBE or ethanol, as well as research focused on the gasoline

additive, methylcyclopentadienyl manganese tricarbonyl (MMT), and tailpipe emissions of

manganese particulates10. 
National Toxics Air Program: The Integrated Urban Strategy

Report to Congress

testing of manganese compounds and characterization of manganese emissions from vehicles utilizing fuels

containing MMT. 

4-12

Section 202(l)(2) of the CAA instructs us to set standards for HAP from motor vehicles

or their fuels, or both. Those standards are to reflect the greatest degree of emissions reductions

achievable through the application of technology which will be available, taking into

consideration existing standards, availability and costs of the technology, noise, energy, and

safety factors, and leadtime. The CAA also specifies that, at a minimum, benzene and

formaldehyde emissions must be addressed. We are currently working on a proposal in

compliance with section 202(l)(2). As indicated above, we are not limiting our examination of

toxic emissions from motor vehicles and their fuels to benzene and formaldehyde; rather, we are 

preparing a more comprehensive list of air toxics emitted by motor vehicles and their fuels for

consideration in the rulemaking. 

4.5 Other Hazardous Air Pollutant Emission Sources

As discussed previously, section 112(k)(3)(B) of the CAA requires that we ensure that

area sources accounting for 90 percent of the aggregate emissions of each of the 30 area source

HAP are subject to standards. However, in achieving required reductions in cancer incidences,

section 112(k)(3)(C) permits us to consider reductions in public health risks resulting from

actions to reduce emissions from “all stationary sources and resulting from measures

implemented by the Administrator or by the States under this or other laws.” Therefore, we’ll

consider emission reductions from a combination of major and area sources in conducting risk

assessments to address this requirement.

These assessments will support regulatory efforts under the CAA and other authorities, as

necessary, to address the identified risk. For example, any reductions resulting from MACT, the

NAAQS, and other programs that achieve reductions in HAP can be included in the assessment

of reductions in risks. Therefore, if we determine that a source category or an individual source

is presenting a significant health risk, then we’ll address it using the appropriate regulatory

authority. For example, if needed to provide an ample margin of safety to protect human health,

section 112(f) residual risk standards will be developed for source categories currently subject to

MACT. Additionally, if our analyses reveal a major source category that is currently unregulated

or unlisted but poses a public health risk, we’ll list that source category under the authority of

section 112(c) and develop the necessary regulations under section 112(d), or we may address it

through other activities like pollution prevention or voluntary programs. Similarly, if a specific

source is contributing to a local risk problem, then the State, local or Tribal program may be

more appropriate for addressing that risk.

We also intend to coordinate our authorities in addressing cumulative risks posed by

exposures to aggregate emissions from multiple source types. For example, during the

development of the Strategy, many commenters raised concerns about the risks from airports to

the communities that surround them. Airports can be viewed as “mini-cities,” which produce
National Air Toxics Program: The Integrated Urban Strategy

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4-13

numerous pollutants from multiple sources and are governed by many different authorities. 

We’ll need to have an integrated plan to reduce air emissions and the many other environmental

impacts associated with aviation activities.

Although airports don’t meet the definition of “area” or “major” source under section 112

of the CAA, we’re involved with numerous efforts to better understand and reduce the

environmental impacts of aviation-related activities and their associated human health risks. For

example, we co-chair the EPA/Federal Aviation Administration Voluntary Aircraft Emissions

Reduction Initiative, a multistakeholder process designed to identify and evaluate technically

feasible and cost-effective voluntary measures to reduce aviation emissions. We’re actively

involved in the International Civil Aviation Organization, which is the forum for evaluating and

establishing international aircraft engine standards. We’re also participating with other

stakeholders in the development of the South Coast Ground Service Equipment memorandum of

understanding (MOU) in California to identify ways to achieve additional emissions reductions

from the commercial aviation community. Implementation of the MOU should yield emissions

reductions through increased use of cleaner engines, electrification, and alternative fuels. In

addition, we’re developing a Green Airport Initiative to demonstrate innovative strategies for

reducing the environmental impacts of aviation-related activities at an airport undergoing

expansion. In April 1999, we released a report that assesses the current and potential impact of

aircraft emissions on local air quality at ten selected airports (U.S. EPA, 1999g ). The regulatory

and voluntary actions under way for aviation will produce data that can inform the Strategy and

begin to address the environmental impacts of aviation-related activities and their associated

risks to the communities that surround them.

4.6 Other Programs and Authorities

We’ve already made progress in addressing air toxics emissions using existing programs.

To put the problem in perspective, we estimate that approximately 8.1 million tons of 188 HAP

were released in the United States in 1993 (U.S. EPA, 1998c). We’ve already issued at least 43

MACT and GACT standards and two section 129 standards with post-1993 compliance dates,

which will address many sources of these emissions. Exhibit 4-4 lists the MACT standards that

we have finalized as of June 2000. Emission controls for the Nation’s cars, trucks and off-road

equipment, and standards for fuels add even more to these reductions. In this section, we’ll

discuss the utility of these programs and others to achieve additional air toxics emissions

reductions.
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Report to Congress

4-14

EXHIBIT 4-4

COMPLETED RULES from SECTION 112 of the CAA (MACT STANDARDS)a

Source Category Final Rule

Publication Date

(Citation)b

Source Category Final Rule

Publication Date

(Citation)b

Dry Cleaning 09/22/93

(58 FR 49354)

Hazardous Organic

NESHAP (HON)

04/22/94

(59 FR 19402)

Aerospace Industry 09/01/95

(60 FR 45956)

Asbestos 11/30/95 

(60 FR 61550)

Chronium Electroplating 01/25/95

(60 FR 4948)

Coke Ovens 10/27/93

(58 FR 57898)

Commercial Sterilizers 12/06/94

(59 FR 62585)

Degrease Organic Cleaners 12/02/94

(59 FR 61801)

Gasoline Distribution 12/14/94

(59 FR 64303)

Industrial Cooling Towers 09/08/94

(59 FR 46339)

Magnetic Tape 12/15/94

(59 FR 64580)

Marine Vessel Loading

Operations 

09/19/95

(60 FR 48399)

Off-site Waste and

Recovery Operations

07/01/96

(61 FR 34140)

Petroleum Refineries 08/18/95

(60 FR 43244)

Polymers & Resins I 09/05/96

(61 FR 46906)

Polymers & Resins II 03/08/95

(60 FR 12670)

Polymers & Resins IV 09/12/96

(61 FR 48208)

Printing/Publishing 05/30/96

(61 FR 27132)

Secondary Lead Smelters 06/23/95

(60 FR 32587)

Shipbuilding & Ship Repair 12/15/95

(60 FR 64330)

Wood Furniture 12/07/95

(60 FR 62930)

Chromium Chemicals

Manufacturing

06/04/96

(61 FR 28197)

Electric Arc Furnace:

Stainless & Non-stainless

Steel

06/04/96

(61 FR 28197)

Ferralloys Production 05/20/99

(64 FR 27450)

Flexible Polyurethane Foam

Production

10/07/98

(64 FR 34853)

Generic MACT 06/30/99

(64 FR 34853)

Mineral Wool Production 06/01/99

(64 FR 29490)

Nylon 6 Production 02/12/98

(63 FR 7155)
National Air Toxics Program: The Integrated Urban Strategy

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4-15

EXHIBIT 4-4 (Continued)

COMPLETED RULES from SECTION 112 of the CAA (MACT STANDARDS)a

Source Category Final Rule

Publication Date

(Citation)b

Source Category Final Rule

Publication Date

(Citation)b

Oil & Natural Gas

Production, Transmission & 

Storage

06/17/99

(64 FR 32610)

Pesticide Active Ingredient

Production

06/23/99

(64 FR 33549)

Pharmaceuticals Production 09/21/98

(63 FR 50280)

Phosphoric Acid/ Phospate

Fertilizers

06/10/99

(64 FR 31358)

Polyether Polyols

Productions

06/01/99

(64 FR 29420)

Portland Cement

Manufacturing

06/14/99

(64 FR 31897)

Primary Aluminum

Production

10/07/97

(62 FR 52383)

Primary Lead Smelting 06/04/99

(64 FR 30194)

Pulp & Paper (Noncombust) MACT I04/15/98

(63 FR 18504)

Pulp & Paper Cluster Rule

(Non-chem) MACT III

03/08/96

(61 FR 9383)

Steel Pickling - HCL

Process Facilities &

Hydrochloric Acid

Regeneration Plants

06/22/99 

(64 FR 33202)

Tetrahydrobenzaldehyde

Manufacture

05/12/98

(63 FR 26078)

Wood Treatment MACT 06/04/96

(61 FR 28197)

Wood Fiberglass

Manufacturing

06/14/99

(64 FR 31695)

Cyanuric Chloride

Production

02/12/98

(63 FR 7155)

Lead Acid Battery

Manufacturing

06/04/96

(61 FR 28197)

Secondary Aluminum 03/23/2000

(65 FR 15689)

Publicly Owned Treatment

Works (POTW)

10/26/99

(64 FR 57572)

Polymers & Resins III 01/20/2000

(65 FR 3275)

Antimony Oxides

Manufacturing

11/18/99

(64 FR 63025)

Aerosol Can-Filling

Facilities

11/18/99

(64 FR 63025)

a Current as of June, 2000. 

b Citation identifies the Federal Register (FR) volume and page number (e.g., 58 FR 49354 can be found in FR

volume 58, page 49354).
National Toxics Air Program: The Integrated Urban Strategy

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4-16

4.6.1 Federal Regulatory Activities – CAA Section 112 Authorities

Section 112 of the CAA provides several authorities for us to use in meeting our air

toxics goals. We’ve promulgated section 112(d) MACT and GACT standards that are projected

to reduce air toxics emissions by approximately one million tons per year once fully

implemented. Within the next ten years, as we complete more MACT and GACT standards, the

air toxics program is projected to reduce emissions of toxic air pollutants by well over 1.5

million tons per year. These nationwide emissions reductions will contribute significantly to

reductions needed in urban areas.

The need for section 112(f) standards, or “residual risk” standards, is under consideration

for some of the early source categories covered by MACT standards. Where justified, these

standards will address remaining public health and environmental impacts of HAP to ensure an

ample margin of safety to protect public health and, in consideration of other factors, to prevent

adverse environmental effects. Consistent with the requirements of the CAA, we’ll consider

such evaluation for those area source categories for which GACT standards have been

promulgated.

The chemical accident prevention regulations (“Risk Management Program

requirements,” or “RMP rule”) were promulgated under section 112(r). These regulations

require owners and operators handling more than a threshold quantity of any substance on the list

of regulated toxic substances and threshold quantities for accidental release prevention (40 CFR 

68.130) to develop risk management plans to prevent and address accidental releases. Eighteen

of these listed substances are HAP.

We’ve already received several requests for permits under the section 112(g) construction

and reconstruction rule. This rule applies to new or reconstructed major sources and requires

them to install MACT to reduce HAP emissions. In addition, the section 112(i)(5) rule (early

reductions) provides incentives for sources to reduce emissions by up to 95 percent from 1990

levels prior to proposal of MACT for that source category. Approximately 27 title V permit

applications have been received, representing HAP reductions of over 6,800 tons.

Section 112 (n)(1)(A) requires us to conduct a study of the hazards to public health

reasonably anticipated to occur as a result of HAP emissions from fossil fuel-fired electric utility

steam generating units (i.e., utilities) and on the alternative control strategies for HAP emissions

which may warrant regulation. In addition, section 112 (n)(1)(A) requires us to regulate HAP

emissions from utilities if we find such regulation is appropriate and necessary after considering

the results of study. In February 1998, we published a report describing the results of the study

described above (U.S. EPA, 1998h). The primary components of the report are: (1) a description

of the industry, (2) an analysis of emissions data, (3) an assessment of hazards and risks due to

inhalation exposures to 67 HAP, (4) assessments of risks due to multipathway (inhalation plus

non-inhalation) exposures to 4 HAP (radionuclides, mercury, arsenic, and dioxins), and (5) a

discussion of alternative control strategies. The overall conclusion of the 1998 Utility Study is as

follows:
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Based on available information and current analyses, the EPA believes that mercury

from coal-fired utilities is the HAP of greatest potential concern and merits additional

research and monitoring. There are uncertainties regarding the extent of risks due to

mercury exposures, including those from utility emissions. Further research and

evaluation are needed to gain a better understanding of the risks and impacts of utility

mercury emissions. In addition, further research and evaluation of potential control

technologies and strategies for mercury are needed. 

For a few other HAP, there are still some remaining potential concerns and uncertainties

that may need further study. First, the screening multipathway assessments for dioxins

and arsenic suggest that these two HAP are of potential concern (primarily from coalfired plants); however, further evaluations and review are needed to better characterize

the impacts of dioxins and arsenic emissions from utilities. Second, nickel emissions

from oil-fired utilities are of potential concern, but significant uncertainties still exist

with regard to the nickel forms emitted from utilities and the health effects of. those

various forms. The impacts due to HAP emissions from gas-fired utilities are negligible

based on the results of this study; therefore, the EPA feels that there is no need for

further evaluation of the risks of HAP emissions from natural gas-fires utilities (U.S.

EPA, 1998h). 

We plan to make the regulatory determination in December 2000. In the interim, we are

collecting additional information on mercury emissions and potential control technologies as well

as conducting various analyses to increase our understanding of the impact of HAP emissions

(especially mercury) from utilities and the feasibility of reducing those emissions.

4.6.2 Other CAA Authorities 

Other programs under the CAA also contribute to the reductions of HAP in urban areas. 

For example, section 109 requires States to develop State implementation plans to attain

compliance with the NAAQS. Many of the activities that are designed to address criteria

pollutants (e.g., ozone, PM, and lead) and attain the NAAQS also achieve reductions in air

toxics. For example, many of the VOCs that form ozone are also air toxics, such as benzene and

1,3-butadiene. In addition, some VOCs can react in the atmosphere to form HAP, such as

formaldehyde. Thus, controlling VOCs leads to reductions in air toxics. Similarly, compliance

with the PM standards will provide incidental, but potentially significant, reductions in HAP that

are either emitted in the form of PM or condense to form particles in the atmosphere. These

include POM, chromium, mercury, and other metals. In addition, lead is a criteria pollutant and

lead compounds are listed as a HAP, so reducing lead emissions through the lead NAAQS also

reduces HAP.

With regard to mobile sources, in addition to authority under section 202(l) to address

hazardous air toxics, other sections of title II that address mobile sources, including other parts of

section 202 (motor vehicles), section 211 (fuel requirements), section 213 (emission standards
National Toxics Air Program: The Integrated Urban Strategy

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4-18

for nonroad engines and vehicles), and section 219 (urban bus standards), are resulting in

reductions in urban air toxics by limiting VOCs, oxides of nitrogen, and PM.

We’ve established section 129 performance standards for two source categories for

combustion sources. These are expected to result in over 50,000 tons per year in HAP

reductions, much of which may be in urban areas. Finally, Title IV, The Acid Rain Program, and

Title VI, Stratospheric Ozone Protection, also reduce or eliminate urban air toxics emissions.

4.6.3 Other Authorities, Laws, Rules, and Programs to Help Reduce HAP 

Emissions

There are a number of other authorities, laws, rules, and programs that will help reduce

emissions of HAP and consequent exposures and risks. Some of these are discussed below.

We're currently evaluating the appropriateness of these statutes for controlling emissions of HAP

as described under section 112(k)(3) and intend to take further actions under these statutes as

appropriate.

 As discussed previously, the Strategy involves collaboration between offices within the

air program to assess the risks from exposures to air toxics indoors and to assimilate nonregulatory, voluntary programs developed to address those risks. Title IV of the Superfund

Amendments and Reauthorization Act (SARA) provides EPA with the authority to perform

research and provide information to the public on the health problems associated with air

pollutants in the indoor environment. 

Under the Toxic Substances Control Act (TSCA), chemicals produced or imported into

the United States are evaluated as to toxicity to human health and the environment. To prevent

adverse consequences of the many chemicals developed each year, TSCA requires that any

chemical that will reach the consumer marketplace be tested for possible toxic effects prior to

commercial manufacture. Any existing chemical that is determined to pose health and

environmental hazards is tracked and reported under TSCA. Procedures are also authorized for

corrective action under TSCA in cases of cleanup of toxic materials contamination. The TSCA

is a complementary authority to the CAA and has contributed to decreased emissions of several

HAP. For example, concern over the toxicity and persistence in the environment of PCB

compounds led Congress to include, in TSCA, prohibitions on the manufacture, processing, and

distribution in commerce of PCBs (TSCA section 6(e), 15 U.S.C. 2605(e)). In 1990, TSCA

authority was relied upon to eliminate chromium use in, and emissions from, comfort cooling

towers (i.e., industrial process cooling towers used exclusively for cooling, heating, ventilation,

and air conditioning systems). 

There are several provisions of the Resource Conservation and Recovery Act (RCRA)

and its amendments which may yield reductions of urban air toxics. One impact evidenced in the

1990's was increased recycling and recovery of hazardous waste, including solvents which

through volatilization contribute to HAP emissions. Section 3004(n) of RCRA has been the

basis of a three-phased regulatory program to control air emissions from hazardous waste
National Air Toxics Program: The Integrated Urban Strategy

Report to Congress

1163 FR 18504. National Emission Standards for Hazardous Air Pollutants for Source Category: Pulp and

Paper Production; Effluent Limitations Guidelines, Pretreatment Standards, and New Source Performance

Standards: Pulp, Paper, and Paperboard Category. April 15, 1998. 

4-19

treatment, storage and disposal facilities. The third phase would address any risks remaining

after implementation of the control regulations issued in 1990 and 1994, which were estimated to

reduce organic emissions by more than one million tons per year. Any resulting reductions in

emissions and risk can be considered in assessing progress toward the 75 percent reduction in

cancer incidence from the baseline.

Under the Comprehensive Environmental Response, Compensation and Liability Act

(CERCLA), commonly known as Superfund, the clean-up of abandoned hazardous waste sites

may also reduce emissions of HAP. Where significant health risks from chemical releases to the

air have been identified at Superfund sites in urban areas, clean-up will reduce risks from urban

air toxics.

Under the Clean Water Act (CWA), controls on the discharge of pollutants to surface

water can also reduce the amount of HAP entering the environment. These controls may take the

form of national technology-based standards under the effluent guidelines program or sitespecific water quality-based controls to achieve State water quality standards. In addition to

providing control by establishing discharge limitations on pollutants (including HAP) in the

wastewater, process changes made in order to comply with these limitations may also reduce

fugitive emission sources. 

As part of the effluent guidelines program under the CWA, we've issued effluent

limitations for the pharmaceuticals industry. Human health benefits from these guidelines

include reductions in excess cancer risk through inhalation. The regulatory impact assessment

prepared for these guidelines estimates that the number of excess cancer cases avoided per year

nationwide ranges from 0.02 to 0.35. These reductions are due to reductions in VOC emissions,

including 10 carcinogens (principally chloroform and methylene chloride). We can also point to

air toxics benefits from the effluent guidelines for the pulp, paper, and particle board industry. 

These guidelines, coupled with the associated NESHAP, are expected to decrease background

emission of HAP by 139,000 megagrams (152,900 tons) annually11.

If a water body isn't meeting water quality standards even after all technology-based

controls under the effluent guidelines program are in place, the State, local agency, or Tribe must

list the water as “water quality limited” and prepare a total maximum daily load (TMDL)

calculation that allocates the maximum amount of pollution, with a margin of safety, that the

water body can absorb from point and nonpoint (including air deposited) sources. A plan must

then be developed to implement the TMDL, which might include provisions to address air

sources under Federal or State (or local or Tribal) programs. We're conducting a pilot project in

two waterbodies to study models which can be used to identify the relative contributions of air

pollutants deposited from various air pollution sources. This project will also examine how
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Federal and State water programs can work together to reduce contamination of water due to air

deposition.

 The Federal Insecticide, Fungicide and Rodenticide Act (FIFRA) provides Federal

control of pesticide distribution, sale, and use. Several HAP listed in CAA section 112(b) have

been used as pesticides. An EPA registration is required of all pesticides sold in the United

States and is intended to ensure that pesticide use, when in accordance with label specifications,

doesn't cause unreasonable harm to people or the environment. It's a violation of FIFRA to use a

pesticide in a manner inconsistent with its label. Registered pesticides classified as “restricted

use” may only be used by registered applicators who have passed a certification exam. This

restricted use requirement minimizes the number of persons having access to certain pesticides. 

The FIFRA regulations may also reduce emissions and exposures by banning (canceling or

denying registration) or severely restricting pesticide use. Seven individual HAP and members

of three HAP compound groups have been banned or severely restricted in their use as pesticides. 

Two other Federal laws discussed earlier in Chapter 2 of this Report, EPCRA and PPA,

while not directly regulating air emissions of HAP, may influence decisions regarding chemical

usage and storage and yield significant reductions in air toxics risks in urban areas. The goal of

EPCRA is to reduce risks to communities through informing communities and citizens of

chemical hazards in their areas. Sections 311 and 312 of EPCRA require certain facilities to

report the locations and quantities of chemicals stored at their facilities to State and local

governments. This information is used by State and local agencies in preparing for, and

responding to, chemical spills and similar emergencies. 

Through EPCRA, Congress mandated that TRIs be made public. The TRI provides

citizens with information about potentially hazardous chemicals stored, manufactured and used

in their community. Section 313 of EPCRA specifically requires certain manufacturers and all

Federal facilities to report to EPA and State governments all releases of any of more than 600

designated toxic chemicals to the environment (including most of the 188 HAP). Each year,

more than 20,000 manufacturing facilities and 200 Federal facilities submit information to us on

the releases of chemicals to the environment. We compile these data in an on-line, publicly

accessible national database, which is a significant source of information regarding HAP

emissions. Reporting requirements for TRI became more comprehensive in 1991, highlighting

the importance of pollution prevention. In 1997, we added seven industry groups (i.e., metal

mining, coal mining, RCRA subtitle C treatment, storage, and disposal (TSD) and solvent

recovery, petroleum distribution, electricity generating, and chemical distribution). We believe

that for the manufacturing sector, this public spotlight on releases and other waste management

of toxic chemicals has led to reductions in their environmental release. 

The passage of the PPA established an environmental hierarchy that establishes pollution

prevention as the first choice among waste management practices. Traditionally, much

environmental protection has involved controlling, treating or cleaning up pollution. Pollution

prevention, which eliminates or minimizes pollution at the source, is most effective in reducing

health and environmental risks because it: (1) eliminates any pollutant associated risks; (2)
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avoids shifts of pollutants from one medium (air, water or land) to another, which can result from

certain waste treatments; and (3) reduces the waste of natural resources. For waste that cannot be

avoided at the source, recycling is considered the next best option. A waste generator should turn

to treatment or disposal only after source reduction and recycling have been considered. 

Pollution prevention strategies include redesigning products, changing processes, substituting

raw materials for less toxic substances, increasing efficiency in the use of raw materials, energy,

water, land, and other techniques. The EPA implements the PPA by promoting voluntary

pollution reduction programs, engaging in partnerships, providing technical assistance, funding

demonstration projects and incorporating cost-effective pollution prevention alternatives into

regulations and other initiatives.

 In addition, we've developed the “Waste Minimization National Plan,” a voluntary, long

term effort to reduce the quantity and toxicity of hazardous waste through waste minimization. 

The plan was built on extensive stakeholder involvement and was released in 1994. The plan

focused on the following key objectives:

• Prioritize pollution prevention efforts based on risk;

• Promote source reduction over recycling;

• Adopt a multimedia approach and prevent cross media transfers;

• Provide flexibility in implementing pollution prevention activities;

• Provide accountability and measure progress; and

• Involve the public.

The plan calls for a 50 percent reduction in the presence of the most harmful persistent,

bioaccumulative, and toxic (PBT) chemicals in hazardous waste by 2005. 

The starting point for selecting chemicals for the national waste minimization list is

EPA's Waste Minimization Prioritization Tool (WMPT), which is a software program that

provides a screening-level assessment of the potential chronic risks that chemicals pose to human

health and the environment based on their persistence, bioaccumulative potential, and human and

ecological toxicity. This software program contains full or partial PBT data for approximately

4,200 chemicals. The draft WMPT was released for public comment on June 23, 1997 (U.S.

EPA, 1997). We made significant changes in response to public comment and published a

revised version on November 9, 1998 (U.S. EPA, 1998i). The revised software, in conjunction

with a publicly reviewed methodology, was used to generate a draft list of 53 PBT chemicals,

which is now in the process of being finalized.

4.7 State, Local, and Tribal Activities

This section describes the role of State, local and Tribal authorities in developing and

implementing the Strategy.
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4.7.1 Why are State, Local, and Tribal Programs Integral to the Strategy?

The CAA requires that the Strategy achieve the risk reduction goals considering control

of emissions of HAP from all stationary sources, using measures implemented by EPA under the

CAA, or by the States under the CAA, or other laws. By providing for State reductions in

achieving the goals, Congress acknowledged that there are many State programs achieving HAP

emissions reductions and, therefore, reducing the chances for exposure and health risks,

including cancer. For example, before the CAA was amended in 1990, many State, local and

Tribal governments developed their own programs for the control of air toxics from stationary

sources. Some of these programs have now been in place for many years and, for some of the

source categories, they may have succeeded in reducing air toxics emissions to levels at or below

those required by the Federal standards. It’s clear that Congress intended State and local

governments to be important partners in carrying out the mandates of the Federal air toxics

program, and the Strategy provides a mechanism to recognize the reductions made by them.

Because of the varied nature of the emissions sources, legislative structures, and other

factors, the State, local and Tribal government programs address air toxics in a number of ways. 

For example, some programs have enacted technology standards for source categories that

require controls for specific HAP, much like the MACT program. Other programs apply a risk

standard that prohibits emissions that result in exceedances of a certain level of risk, or they use

an ambient air standard for air toxics that is based on threshold or exposure levels. Still others

may rely on reductions achieved through VOC, PM, or lead regulations developed under section

110 or subpart D of the CAA to meet NAAQS. Regardless of the approaches used to address air

toxics, State, local and Tribal governments have accomplished and continue to accomplish

reductions in HAP. As we proceed to implement the Strategy, we’ll work with these

governments to better characterize these reductions in emissions and the resulting reductions of

public health risks, including risks of cancer.

Developing the Strategy at the national level is a challenge because urban air toxics

problems vary significantly across the country. Because of this variability, the Strategy works

best if approached as a partnership between EPA and State, local and Tribal governments. These

governments (including municipal offices other than pollution control departments) have the

most experience with local air pollution issues and can lend their expertise and knowledge to

address and resolve air toxics concerns that are unique to cities. Many of these governments also

have existing air pollution control programs that currently address, and can effectively continue

to address, some or all of these issues. In addition, these governments are often able to act much

more quickly than we can to address local concerns, which leads to less overall pollution.

At the Federal level, we can contribute Federal standards and requirements using our

authorities to develop and implement a national regulatory program. We also have the expertise

to evaluate, or to help other agencies evaluate, toxic pollution problems. By integrating our

relative strengths, we can provide a stronger, more efficient, and more effective program to

address air pollution in urban areas.
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4.7.2 What are the Objectives of State, Local, and Tribal Activities?

As indicated before, the Strategy will be a partnership between EPA and State, local and

Tribal governments to address the risks from air toxics in urban areas. Listed below are the

objectives that we’ve identified to guide the CAA taken by us and our governmental partners so

that those actions will be effective and efficient in achieving the goals of the Strategy:

C Establish appropriate national measures, through guidance, policies and

rulemaking, which enable State, local and Tribal agencies to be full partners. Many

of the State, local and Tribal agencies may be unable to do more than the Federal laws

and rules require. These agencies could benefit from Federal rulemaking guidance in

addressing local issues. As the same time, we recognize the need for flexibility for these

agencies to identify and address the local issues. We need State, local and Tribal

agencies’ help to reach the CAA’s goals for healthy air, and they’ll benefit by being able

to tailor the Strategy to their specific needs.

C Provide flexibility for strong State, local and Tribal programs. Many of these

governments have developed their own air programs. In fact, during the development of

the Strategy, we received many comments requesting that the Strategy acknowledge

programs that are already in place. Those governments that have been proactive in

controlling air toxics can benefit by tailoring the Strategy to their own needs, or by being

able to implement a program earlier than we can. 

C Provide incentives for State, local and Tribal action. Since enabling through

standards, policies and guidance and providing flexibility can result in more effective and

earlier controls of urban HAP, it will be beneficial to State, local, and Tribal

governments, to EPA, and to the public to facilitate State, local and Tribal actions.

C Set priorities among urban areas and source categories. Given the broad scope of the

Strategy and the time it may take to implement, it may be most effective to first identify

and address those areas and sources with the highest air toxics emissions or exposure

levels (including consideration of multipathway exposure where appropriate).

C Provide information to the public on HAP and potential risk in urban areas. The

public benefits by having a sound basis to use in setting their pollution control priorities

and communicating their priorities to us. Providing information to the public is also our

responsibility, and an informed public will be better equipped to help us set priorities for

appropriate State, local and Tribal HAP control actions. This public outreach will include

not only information on exposure to air toxics, but also information on the link between

water quality and the deposition of air toxics.

C Facilitate a focus on areas with disproportionate impacts and greatest risks. The

Strategy is intended to recognize the potential for disproportionate impacts of air toxics

hazards across urban areas. State, local and Tribal governments can be particularly
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effective in identifying and addressing disproportionate impacts of HAP. We’ll work

with our regulatory partners to provide technical and policy guidance to help identify and

address disproportionate impacts from HAP, including consideration of multipathway

exposure as appropriate.

4.7.3 How Can State, Local or Tribal Agencies Participate in the Strategy?

The Strategy needs to be a partnership between EPA and State, local and Tribal agencies

in order to focus on local urban air toxics concerns. But our relative roles may vary according to

the needs of particular urban areas and any limitations faced by State, local and Tribal

governments. With our regulatory partners, we’ll discuss and explore options for how the State,

local and Tribal agencies should participate in developing and implementing the Strategy to

address public and other environmental issues related to air toxics. 

We see a broad range of possibilities for State, local and Tribal agency participation. For

example, as indicated above, many regulatory agency programs are designed to implement

delegated Federal requirements. However, to provide additional flexibility, we may be able to

provide a Federal program that allows the agencies to either develop and substitute their own

requirements for an existing Federal program, or, if they wish, to simply adopt and implement a

risk reduction program designed by EPA. For example, we could promulgate a Federal rule

describing how we’d develop and implement a local risk reduction program. State, local or

Tribal agencies could then either develop and implement a program modeled on ours, or submit

an alternative program for our approval.

Alternatively, instead of promulgating a Federal rule setting out the details of an

acceptable risk reduction program, we could promulgate a set of minimum elements that any

local risk reduction program – whether implemented by EPA or a State, local or Tribal agency –

must contain. This would provide agencies with more flexibility to design and implement their

own risk reduction programs that we could approve.

The Federal role in developing additional risk reduction strategies for urban areas could

be smaller still. It may not be necessary for us to directly guide development of State, local and

Tribal programs. It may be enough for us to encourage them to meet the goals of the Strategy

and to provide necessary guidance. In the end, we (or the State, local or Tribal agency) would

still need to measure progress against the mandatory goals of the CAA. We might then need to

determine whether additional Federal action is warranted to meet the goals.

In evaluating and comparing the options we develop together, we and our regulatory

partners and other stakeholders will need to consider how well each option addresses our

objectives. We’ll also need to consider such other issues as practicality of implementation,

resource burden at each governmental level, and possible adverse impacts on other Federal, State,

local or Tribal programs.
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4.7.4 What Elements Should a State, Local or Tribal Program Contain?

No matter who develops and implements State, local or Tribal programs, they should

contain certain basic elements in order to meet the risk reduction goals of the Strategy. The

following list of elements should be considered:

C Locally-focused assessments using existing information and sufficiently refined tools

capable of identifying significant contributors to urban risk, problem chemicals and

sources, and toxic “hot spots” within an urban area, and characteristics of at-risk

populations;

C A process, regulatory or otherwise, to develop strategies aimed at reducing risks from

those sources;

C Opportunity for public review of both the baseline assessment and the proposed risk

reduction strategies;

C A process and schedule for implementing the risk reduction strategies;

C Evaluation of whether the goals of the Strategy have been met;

C Provisions to implement additional risk reduction strategies if the goals have not been

met; and

C A process to encourage public participation.

At this point, this list is fairly general because we don’t have enough information to more

fully develop this program structure. However, over the next couple of years, we’ll be working

to further develop this aspect of the Strategy, to develop and use information from assessments

and other tools to guide our thinking, and to get input from our stakeholders. Also, we’ve started

to develop the framework for a number of pilot projects in several urban areas. These pilot

projects will help us initiate and facilitate a broad partnership effort to get a better understanding

of the local urban health risks from air toxics and to identify actions that can be taken to improve

local air quality.

4.8 References

Ball, J. C. 1997. Emission rates and elemental composition of particles collection from 1995

ford vehicles using the urban dynamometer driving schedule, the highway fuel economy

test, and the US06 driving cycle. SAE Paper 97FL-376.
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Gertler, A.W., Sagebiel, J.C., Dippel, W.A., and L.H. Sheetz. 1997. A study to quantify on-road

emissions of dioxins and furans from mobile sources: phase 2. Prepared by the Health

and Environmental Sciences Department, Energy and Environmental Engineering Center,

Desert Research Institute, Reno, NV. Prepared for the American Petroleum Institute

(API). API Publication Number 4642.

Truex, T.J., Norbeck, J.M., Smith, M.R., Arey, J., Kado, N., Okamoto, B., Kiefer, K., Kuzmicky,

P., and I. Holcomb. 1998. Final report: evaluation of factors that affect diesel exhaust

toxicity. Prepared by the Center for Environmental Research and Technology and the

Statewide Air Pollution Research Center, University of California, Riverside, CA, and the

Department of Environmental Toxicology, University of California, Davis, CA. Prepared

for the California Air Resources Board, Contract No. 94-312. June 25.

U.S. EPA. 1985. Interim quantitative cancer unit risk estimates due to inhalation of benzene.

Prepared by the Office of Health and Environmental Assessment, Carcinogen Assessment

Group, for the Office of Air Quality Planning and Standards, Washington, DC.

U.S. EPA. 1993. Motor vehicle-related air toxics study. Office of Mobile Sources, Ann Arbor,

MI. EPA/420/R-93/005. April.

U.S. EPA. 1997. Notice of availability of waste minimization software and documents. Federal

Register 62:33868. June 23.

U.S. EPA. 1998a. The inventory of sources of dioxin in the United States. Office of Research

and Development, Washington DC. External Review Draft. EPA/600/P-98/002Aa. 

April. 

U.S. EPA. 1998b. Control of emissions of air pollution from nonroad diesel engines. Federal

Register 63:56968. October 23.

U.S. EPA. 1998c. Carcinogenic effects of benzene: an update. National Center for

Environmental Assessment, Washington, DC.

U.S. EPA. 1998d . Health risk assessment of 1,3-butadiene. EPA/600/P-98/001A. February.

U.S. EPA. 1998e. Study of hazardous air pollutant emissions from electric utility steam

generating units, final Report to Congress, vol. 1 and 2. EPA/453/R-98/004a (vol. 1) and

EPA/453/R-98/004b (vol. 2). February.

U.S. EPA. 1998f. Notice of availability of draft RCRA waste minimization PBT chemical list. 

Federal Register 63:60332. November 9.

U.S. EPA. 1999a. NESHAPS: Final standards for hazardous air pollutants for hazardous waste

combustors; final rule. Federal Register 64:52828. September 30.
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U.S. EPA. 1999b. Integrated Risk Information System (IRIS) at http://www.epa.gov/iris. 

Updated March 3.

U.S. EPA. 1999c. Health assessment document for diesel emissions. U.S. EPA Science

Advisory Board Review Draft. Office of Research and Development. Washington, DC. 

EPA/600/8-90/057D. November.

U.S. EPA. 1999d. Control of emissions of air pollution from 2004 and later model year

heavy-duty highway engines and vehicles; revision of light-duty truck definition;

proposed rule. Federal Register 64:58471. October 29.

U.S. EPA. 1999e. Regulatory impact analysis, control of air pollution from new motor

vehicles, tier 2 motor vehicle emissions standards and gasoline sulfur control

requirements. Office of Air and Radiation . EPA420-R-99-023.

U.S. EPA. 1999f. Analysis of the impacts of control programs on motor vehicle toxics

emissions and exposure in urban areas and nationwide (volumes I and II). Prepared for

U.S. EPA by Sierra Research, Inc. and Radian International Corporation/Eastern

Research Group. EPA 420-R-99-029 and EPA420-R-99-030. November 30.

U.S. EPA. 1999g . Evaluation of air pollutant emissions from subsonic commercial jet aircraft. 

Prepared by ICF Consulting Group, Fairfax, VA. Prepared for U.S. EPA, Office of

Mobile Sources, Engine Programs and Compliance Division, Ann Arbor, MI. 

EPA/420/R-99/013. April.

U.S. EPA. 2000a. Clean Air Scientific Advisory Council review of the draft diesel health

assessment document. U.S. EPA Science Advisory Board, Washington DC. EPA-SABCASAC-00-004.

U.S. EPA. 2000b. Tier 2 motor vehicle emission standards and gasoline sulfur control

requirements. Federal Register 65:6698. February 10. 

U.S. EPA. 2000c. Proposed heavy-duty engine and vehicle standards and highway diesel fuel

sulfur control requirements. Federal Register 65:35430. June 2.
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5. Assessment of Progress Toward Goals

This discussion of our assessment activities first focuses on how we generally intend to

assess progress in meeting the goals of the Strategy. We then discuss in more detail our methods

and tools for estimating health risks and describe more specifically how we intend to apply these

risk assessment methods and tools to assess progress and support implementation of the Strategy.

As we move from a focus on emissions reductions toward a focus on estimated risk

reduction, we note that Agency risk assessment and decisionmaking have historically focused on

the likelihood of health effects associated with exposure to individual environmental

contaminants. In recent years, our risk assessment emphasis has shifted increasingly to a greater

consideration of multiple pollutants, endpoints, pathways and routes of exposure, and integrated

reduction of risks. This more complex assessment is often called “cumulative risk assessment,”

defined according to who or what is at risk of adverse effects, from identifiable sources and

stressors, through several routes of exposure over varied timeframes. While various integrated

approaches are now being used within the Agency, we realize that there are significant gaps in

methods, models, and data that limit our ability to assess cancer and noncancer risks associated

with cumulative exposure to mixtures of pollutants having different endpoints. We’ve identified

both short-term and long-term research needs to fill these gaps, as highlighted in Chapter 6 of

this Report. Progress toward more refined assessments of cumulative risks will depend upon the

pace and evolution of our policy and guidance on cumulative risks and the underlying research. 

5.1 Overview of Health Risks

Assessing progress in reducing cumulative risks from HAP will require us to move away

from a focus on assessing reductions in tons per year emitted, toward a focus on estimating

reductions in cancer and noncancer risks associated with lower emissions. 

“Cancer” describes a group of related diseases that affect a variety of organs and tissues. 

Cancer results from a combination of genetic damage and non-genetic factors that favor the

growth of damaged cells. Cancer currently causes approximately one fourth of all deaths in the

U.S. (American Cancer Society, http://www.cancer.org/statistics/index.html). Cancer is

associated with a wide range of factors, of which exposure to HAP is only one. Other causes of

cancer, including genetic susceptibility, background radiation, diet, smoking, and other lifestyle

factors, are thought to be the dominant factors determining total cancer incidence. Against the

very high total cancer mortality rate of about one in four from all risk factors, the rate of cancer

incidence associated with HAP alone cannot be observed directly. Attributing cancer to HAP is

also complicated by the fact that many cancers do not appear for years or decades after exposure

and, therefore, may have been caused by exposures long past and in different locations. In order

to distinguish cancer risks associated with HAP from cancer risks due to other factors, we’ll need

to rely on modeled estimates of cancer risk rather than on direct measurements for assessing the

Strategy’s progress toward the goal of 75 percent reduction in cancer incidence associated with

HAP.
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1Some HAP that cause cancer may also cause adverse noncancer health effects at environmentally relevant

doses. Thus, when we discuss “noncarcinogens,” we mean substances that may potentially cause noncancer effects in

humans. Some of the same substances may also be evaluated as carcinogens.

5-2

Adverse health effects other than cancer (“noncancer risks”) include a wide range of

health endpoints in all organ systems (e.g., cardiovascular, immune, liver, or kidney)1. As with

cancer, other factors such as genetics, diet, lifestyle, and other exposures (e.g., smoking) may

exert a dominant influence over incidence of adverse noncancer health effects. Therefore, as

with carcinogens, we expect to rely primarily on risk estimates to assess progress, rather than on

direct measurements of changes in the incidence of adverse noncancer health impacts due to

reductions in emissions.

The CAA sets a clear numerical goal for reductions in cancer incidence, but specifies

only a “substantial” reduction in public health risks for effects other than cancer. We see a need

to define and clarify this goal more fully as we work to implement this Strategy, but we haven’t

yet developed a specific numerical goal for risk reductions for various noncancer effects. One

major purpose of our noncancer risk assessments will be to provide a sound technical basis for

developing and defining noncancer goals that are quantifiable, attainable, and consistent with the

CAA.

5.2 The EPA Risk Assessment Paradigm

Because cancer and noncancer health impacts can’t be directly isolated and measured, we

and others have spent more than two decades developing an extensive set of risk assessment

methods, tools, and data that serve the purpose of estimating health risks for many of our

programs. Our risk assessment science has been extensively peer-reviewed, is widely used and

understood by the scientific community, and continues to expand and evolve as scientific

knowledge advances. We intend to use the most current and appropriate risk estimation methods

in tracking progress under the Strategy.

Our framework for assessing and managing risks reflects the risk assessment and risk

management paradigm set forth by the National Academy of Sciences in 1983, shown in diagram

form in Exhibit 5-1. The inner circle of the figure divides the risk assessment and management

process into four general phases. The first three phases (exposure assessment, dose-response

assessment, and risk characterization) comprise risk assessment. The fourth phase (risk

management, shown shaded) involves evaluation of information provided by the risk assessment

by the environmental manager who makes a risk management decision. The outer circle of the

figure depicts a cycle of specific milestones or information produced during each phase of the

process. This figure is intended to present a generalized model of our framework, but readers

should realize that the framework is always applied in a flexible way to fit unique factors of

specific environmental problems.
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EXHIBIT 5-1

EPA PARADIGM FOR RISK ASSESSMENT AND RISK MANAGEMENT

5.2.1 Exposure Assessment

Our 1992 guidelines for exposure assessment (U.S. EPA, 1992) establish a broad

framework for exposure assessments by describing the general concepts of exposure assessment,

including definitions and associated measurement units, and by providing broad guidance on the

planning and conduct of an exposure assessment. The guidelines also provide information on

presenting the results of the exposure assessment and characterizing uncertainty. Although the

guidelines focus on exposure of humans to chemical substances, much of the guidance also

pertains to assessing ecological exposure to chemicals, or to human exposures to biological,

radiological, or other agents.

The guidelines define human exposure as contact with a chemical or agent at the visible

external boundary of a person, including skin and openings into the body such as mouth and

nostrils (but not necessarily contact with exchange boundaries where absorption may take place,

such as skin, lung, and gastrointestinal tract). Therefore, an exposure assessment is the

quantitative or qualitative evaluation of contact and includes such characteristics as intensity,
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frequency, and duration of contact. Often, an assessment will also evaluate the rate and route at

which a chemical crosses the external boundary (dose) and the amount absorbed (internal dose). 

The numerical output of an exposure assessment may be either exposure or dose, depending on

the purpose of the evaluation and available data. 

An exposure assessment has three major components: source characterization,

environmental fate and transport characterization, and characterization of personal exposure. 

These components are discussed individually below.

Source Characterization

In the first step of exposure assessment for air toxics, the specific HAP emitted and the

sources of their airborne emissions are determined. Data are collected on the emission rates of

the pollutants and parameters of the sources. Knowledge of the emission rate and release

characteristics enables the pollutant fate and transport to be estimated. 

Ideally, the emission estimates are from direct measurements of source emissions. 

Although direct measurement is likely to provide the most accurate data for an emission source,

these data are typically not available, as such sampling is often time- and resource-intensive. 

When specific emission measurements are not feasible or available, other emission estimation

methods, including material balances and emission factors, are sometimes used as alternate

methods. Emission factors indicate the quantity of a pollutant typically released to the

atmosphere for a particular source operation and are usually considered to be representative of an

industry or emission type as a whole. Each approach to estimating emissions, including use of

direct measurement data, has an inherent level of uncertainty, which adds to the overall

uncertainty of a risk analysis.

Depending on the analysis, source and emissions data can be derived from broad-scale

emission inventories, specific data collection efforts with particular industries, or information

from Regional, State, or local air toxics agencies. Other information, such as the geographic

location of release points, the temporal pattern of emissions (e.g., periodic "puffs" vs. constant

emission rates), and the release height may be necessary depending on the level of detail needed

or types of exposure examined in the assessment.

Environmental Fate and Transport Characterization

After the pollutants of interest and their sources and emission rates are defined, the

exposure assessment process continues with estimation of pollutant fate and transport. This step

describes how the pollutant is transported, dispersed, and transformed over the area of interest.

Initially, the fate of the emitted pollutants is largely determined by the source release

characteristics. After pollutants are released to the atmosphere, their transport, dispersion, and

transformation are governed by meteorological principles, terrain characteristics, wet and dry

deposition rates, and certain chemical properties of the HAP (e.g., aqueous solubility, vapor

pressure, molecular diffusivity, melting point, and adsorptivity). For a limited subset of HAP, it
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is important to consider deposition from air to soil, vegetation, or waterbodies. For others, such

deposition is not important.

A variety of mathematical models, each with specific data needs, has been developed or

are under development to describe the transport and fate of pollutants released to the atmosphere. 

The model chosen must be appropriate for the intended application and may vary among

estimates of short-term peak concentrations immediately adjacent to a facility, long-term

concentrations over a city-wide area, or deposition over hundreds or even thousands of miles. 

The HAP’s reactivity and persistence will influence its fate as well and can be important factors

in estimating exposure for certain pollutants. Additionally, secondary transformation products of

some HAP may need to be identified for consideration in risk assessment. High quality,

representative meteorological information is crucial to a valid exposure assessment for air toxics,

as well as information on local topography. Any available HAP monitoring data can be used

either to check the validity of modeled concentration estimates or as a primary or supplemental

source of information for the exposure assessment itself. 

For a limited subset of HAP, greater human and ecological exposures to the HAP occur

through non-inhalation exposures than through inhalation exposures. These HAP typically are

persistent in the environment, have a strong tendency to bioaccumulate, and exhibit moderate to

high toxicity. Exposure assessments can consider exposures that occur through routes other than

inhalation by using multipathway models. The simplest multipathway exposure assessments

require chemical-specific data (e.g., octanol-water partition coefficient (Kow)) to model the

partitioning of the chemical in the environment and uptake rates (e.g., 2 liters water/day) to

predict intakes. Combining this information yields general predictions of non-inhalation

exposure.

Characterization of Personal Exposure

After ambient concentrations have been derived, human exposures to these

concentrations are determined. In this component, the study population is defined in terms of

geographic distribution and other characteristics relevant to the exposure pathways of concern.

For the more frequently performed human inhalation exposure analyses, the locations of

resources, homes, workplaces, schools, and other receptor points will partially determine the

extent of actual exposure. Factors such as age, sex, and activity patterns affect the amount of

pollutant actually inhaled by an individual, while mobility of the subject affects the concentration

levels to which an individual is exposed over time. Depending on the focus of the analysis, 5 to

10 percent output of the exposure assessment may vary. In some cases, the most highly exposed

five to ten percent of the population may need to be well-characterized, while for others, the

distribution of exposures across a wider area is needed. Information on specific sensitive

populations, such as children or the elderly, is another layer of detail that may often be needed in

refined analyses. 
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As with inhalation, assessing non-inhalation exposure to human populations involves

combining pollutant concentration information with relevant information concerning the study

population. After identification of the relevant exposure pathways, information such as soil,

drinking water, and food ingestion rates (often including specific foods, such as fish, beef, pork,

eggs, root vegetables, grains, and fruit), generally for both adults and children, as well as contact

frequencies with soil and surface water, may be needed. Some activities of particular interest for

non-inhalation modeling are subsistence farming and subsistence fishing because of the unique

dietary habits of these two groups (i.e., eating much more garden vegetables and fish,

respectively). Also, as with inhalation exposure, the extent to which these factors are included in

the risk assessment depends on the purpose of the assessment, available resources, uncertainties

in the assessment, and data quality and quantity. Not only are the data requirements often

extensive, particularly when many different pathways are being assessed, but the computational

demands also can be quite large in a multimedia, multipathway assessment.

5.2.2 Dose-Response Assessment

The dose-response assessment phase of the risk assessment produces two sequential

analyses (Exhibit 5-1, outer circle). The first analysis is the hazard identification, which

identifies contaminants that may pose health hazards at environmentally relevant concentrations

and qualitatively describes the effects that may occur in humans. The second analysis is the

human health dose-response, which generally describes the relationship between exposure

received and likelihood of effects in quantitative terms.

Hazard Identification

The dose-response assessment phase begins with hazard identification, in which we

identify contaminants that are suspected to pose health hazards, describe the specific forms of

toxicity (neurotoxicity, carcinogenicity, etc.) that they may cause, and evaluate the conditions

under which these forms of toxicity might be expressed in exposed humans. The types of effects

that are relevant to a particular chemical (e.g., cancer, noncancer) are determined as part of the

hazard identification. The current approaches for dose-response assessment and risk

characterization can differ for various types of effect. Factors such as the route of exposure, the

type and quality of the effects, the biological plausibility of findings, the consistency of findings

across studies, and the potential for bioaccumulation all contribute to the strength of the hazard

identification statement.

There are many sources of information that can be brought to bear in the hazard

identification. Exhibit 5-2 summarizes important sources of information for hazard

identification. 
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EXHIBIT 5-2

SOURCES OF INFORMATION FOR HAZARD IDENTIFICATION

< Epidemiologic Data. Epidemiologic studies of human populations exposed to HAP in occupational

settings or in the general environment can provide valuable information on the effects of HAP. These

studies have advantages over other sources of information in that they directly assess the effects of

exposure to humans and, in the case of studies of the general population, address exposures that

actually occur in the environment. In addition, recent work with biomarkers (chemicals in the body

which allow for better quantification of exposure) promises to boost the utility of epidemiology in the

future. Shortcomings include concerns about the relevance of high exposure levels often seen in

occupational studies to lower levels of environmental contamination, concerns over the control of

confounding variables (such as tobacco use) that may obscure true causal relationships (or imply false

ones), difficulties in adequately characterizing exposure, and the difficulty most epidemiologic studies

have in discerning subtle effects.

< Human Data from Case Reports or Controlled Exposure Studies. Where available, human health

effects data from case reports or controlled exposure studies can be extremely valuable, although such

data generally have shortcomings. Case reports often involve one or a small number of people,

limiting the ability to generalize from them, and they may involve exposures very different than

typical environmental exposures. For most HAP and effect types of interest, controlled human

exposure studies are unlikely to be available.

< Animal Toxicology Data. High quality studies of human populations exposed to HAP are rare, due

to both expense and the inherent limitations of epidemiology. As a result, EPA and others commonly

rely on animal studies to infer potential risk to humans. Animal toxicologic data are typically much

easier to obtain than good epidemiologic data, and effects can be explicitly linked with exposure to

the HAP(s) being tested with little fear of confounding. However, issues of high-to-low dose

relevance are compounded by the need to extrapolate the effects seen in animals to those anticipated

in humans. Although there have been considerable advances in understanding the relevance of

specific results in animal studies to human biology, such extrapolations remain a considerable source

of uncertainty. The EPA has operated under the conservative public health policy that assumes that

adverse effects seen in animal studies indicate potential effects in humans.

< Short-term in Vitro Assays. In vitro (“test tube”) tests can be carried out quickly and at relatively

low cost, and they can provide valuable information on specific aspects of a pollutant’s toxicity, such

as a particular mechanism of mutagenicity that may be an initiating event for cancer. However, such

tests typically provide only supporting information about a pollutant’s effects, as few tests have been

developed that are specific to a particular effect or disease. 

< Structure-activity Relationships (SARs). By comparing the molecular structure of a pollutant with

that of others of known toxicity, toxic effects can sometimes be inferred, particularly if there is

knowledge about the mechanism of action. This approach is often useful when examining the hazards

associated with individual compounds within a class of related compounds (e.g., dioxins) or when

identifying compounds for future study. Although structure-activity analyses are rarely a substitute

for existing experimental or epidemiologic data, and represent a relatively uncertain basis for hazard

identification, they are useful when experimental data are absent.
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Noncancer Effects – Chronic and Acute. Due to the wide variety of endpoints, hazard

identification procedures for noncancer effects are less formally described in EPA guidance than

are procedures for the identification of carcinogens. The EPA has published guidelines for

assessing several specific types of noncancer effects, including mutagenicity (U.S. EPA, 1986a);

developmental toxicity (U.S. EPA, 1991); neurotoxicity (U.S. EPA, 1998a); and reproductive

toxicity (U.S. EPA, 1996a). 

For identification of long-term (chronic) hazards other than cancer, we review the health

effects literature and characterize its strengths and weaknesses, using a narrative approach rather

than a formal classification scheme. Available data on different endpoints are arrayed and

discussed, and the effects (and their attendant dose/exposure levels) are described. Particular

attention is given to effects that occur at relatively low doses or that may have particular

relevance to human populations. Information is presented in a narrative description that

discusses factors such as the methodological strengths and weaknesses of individual studies (as

well as the overall database), the length of time over which the studies were conducted, routes of

exposure, and possible biological mechanisms. We consider the severity of effects, which may

range from severe frank effects that can cause incapacitation or death to subtle effects that may

occur at the cellular level but are early indicators of toxic effects. Not all effects observed in

laboratory studies are judged to be adverse. The distinction between adverse and non-adverse

effects is not always clear-cut, and considerable professional judgment is required in applying

criteria to identify adverse effects. All of these observations are integrated into a presentation

that gives a concise profile of the toxicological properties of the pollutant. 

In addition to toxicity related to chronic exposures, many HAP also can cause toxic

effects after acute (short-term) exposures lasting from minutes to several hours. Indeed, for some

pollutants, acute exposures are of greater concern than chronic exposures. The hazard

identification step for acute effects is comparable to that for chronic effects, with the primary

difference being the duration of exposure. As with chronic exposures, the severity of effects

from acute exposures may vary widely. While several EPA offices have addressed acute

exposures across a variety of regulatory programs, we have only recently drafted Agencywide

guidance on how to assess toxic effects from short-term exposures. This guidance for acute

reference exposure (ARE) levels, when completed, will assist Agency acute risk assessment

activities (U.S. EPA, 1998b).

Cancer. The EPA’s 1986 Guidelines for Carcinogen Risk Assessment (U.S. EPA,

1986b) provide guidance on hazard identification for carcinogens. The approach recognizes

three broad categories of data: (1) human data (primarily epidemiological); (2) results of longterm experimental animal bioassays; and (3) supporting data, including a variety of short-term

tests for genotoxicity and other relevant properties, pharmacokinetic and metabolic studies,

physio-chemical properties, and SARs. In hazard identification of carcinogens under the 1986

guidelines, the human data, animal data, and "other" evidence are combined to characterize the

weight of evidence regarding the agent’s potential as a human carcinogen into one of several

hierarchic categories:
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C Group A ! Carcinogenic to Humans: Applies when there are adequate human data to

demonstrate the causal association of the agent with human cancer (typically

epidemiologic data).

C Group B ! Probably Carcinogenic to Humans: Agents with sufficient evidence (i.e.,

indicative of a causal relationship) from animal bioassay data, but either limited (i.e.,

indicative of a possible causal relationship, but not exclusive of alternative explanations)

human evidence (Group B1), or with little or no human data (Group B2).

C Group C ! Possibly Carcinogenic to Humans: Agents with limited animal evidence

and little or no human data.

C Group D ! Not Classifiable as to Human Carcinogenicity: Agents without adequate

data either to suggest or refute the suggestion of the human carcinogenicity.

C Group E ! Evidence of Noncarcinogenicity for Humans: Agents that show no

evidence for carcinogenicity in at least two adequate animal tests in different species or in

both adequate epidemiologic and animal studies (U.S. EPA, 1986b).

In 1996, we proposed major revisions of the carcinogen hazard identification scheme. 

The proposed revision to the cancer risk assessment guidelines (U.S. EPA, 1996b), currently

under public review prior to finalization, focuses on narrative statements describing the main

lines of evidence and their interpretation, replacing the current pre-defined hierarchical categories

with alphabetic designations. The proposed guidelines also replace the system of stepwise

consideration of different types of data with a single comprehensive evaluation process that

stresses the coherence of various data elements. The result is a single scientific interpretation

that evaluates, to the extent possible, how well the commonality of mode of carcinogenic action

between human beings and the various test systems has been established. Emphasis is also

placed on defining the qualitative conditions under which carcinogenic hazards might be

expected. If warranted, limitations to the finding of carcinogenic hazard can be drawn based on

route of exposure, existence of other factors needed for tumorigenesis, and doses below which

elevation of cancer risk is not expected. 

Human Health Dose-Response

Human health dose-response assessment is the characterization of the relationship

between the concentration, exposure, or dose of a pollutant and the resultant health effects. The

nature of quantitative dose-response assessment varies among pollutants. Sufficient data often

exist for criteria air pollutants, such as ozone or carbon monoxide, so that relatively complete

dose-response relationships can be characterized. In such cases, there is no need for

extrapolation to lower doses because adequate health effects data are available, often in humans,

at environmental levels. However, such is not the case for most air toxics. Most epidemiologic

and toxicologic data on HAP typically result from exposure levels that are high relative to

environmental levels.
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In summary, dose-response assessment methods for HAP generally consist of two parts. 

First is the evaluation of data in the observable range, and second is the extrapolation from the

observable range to low doses/risks. Recent terminology refers to the result of analysis in the

observable range as the “point of departure” from which extrapolation begins. The approaches

used for evaluation in the observable range are similar for all types of effects, while the Agency’s

current extrapolation methods differ considerably for cancer and noncancer effects. The 1996

draft cancer guidelines bring a greater degree of consistency to the extrapolations.

Noncancer Effects ! Chronic. The inhalation RfC and oral RfD are the primary Agency

consensus quantitative toxicity values for use in noncancer risk assessment. The RfC or RfD is

defined as an estimate, with uncertainty spanning perhaps an order of magnitude, of an inhalation

exposure/oral dose to the human population (including sensitive subgroups) that is likely to be

without appreciable risks of deleterious effects during a lifetime. The RfC or RfD is derived

after a thorough review of the health effects database for an individual chemical and

identification of the most sensitive and relevant endpoint and the principal study(ies)

demonstrating that endpoint. Inhalation RfCs are derived according to the Agency’s Methods for

Derivation of Inhalation Reference Concentrations and Application of Inhalation Dosimetry

(U.S. EPA, 1994a). The RfC or RfD should represent a synthesis of the entire data array. The

evaluation of and choice of data on which to base the RfC or RfD derivation are critical aspects

of the assessment and require scientific judgment.

Derivation of the RfC or RfD begins with identification of the critical adverse effect from

the available valid human and animal study data, followed by identification of a lowest-observedadverse-effect level (LOAEL) or, preferably, a no-observed-adverse-effect level (NOAEL). The

LOAELs or NOAELs from animal studies are converted to human equivalent concentrations

(HECs) using dosimetric methods (described in U.S. EPA, 1994a). The NOAEL[HEC] or

LOAEL[HEC] from one or a few studies that is representative of the threshold region of

observable effects is the key value gleaned from evaluation of the dose-response data. The RfC

or RfD is then derived by consistent application of uncertainty factors (UFs) to account for

recognized uncertainties in the extrapolation from the experimental data and exposure conditions

to an estimate (the RfC or RfD) appropriate to the assumed human lifetime exposure scenario

(U.S. EPA, 1994a).

The standard UFs are applied as appropriate for the following extrapolations or areas of

uncertainty:

C Laboratory animal data to humans;

C Average healthy humans to sensitive humans;

C Subchronic to chronic exposure duration;

C LOAEL to NOAEL; and

C Incomplete database.

The composite UF will depend on the number of extrapolations required. The RfCs have

been derived using composite UFs that range from 10 to 3,000, with most RfCs using factors of
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100 to 1,000. The use of order-of-magnitude uncertainty factors for RfCs and RfDs and the

definition of the RfC or RfD as having “uncertainty spanning perhaps an order of magnitude” are

indications of the general lack of precision in the estimates. 

It should be noted that exposures above an RfD or RfC do not necessarily imply

unacceptable risk or that adverse health effects are expected. Because of the inherent

conservatism of the RfC/RfD methodology, the significance of exceedances must be evaluated

on a case-by-case basis, considering such factors as the confidence level of the assessment, the

size of UFs used, the slope of the dose-response curve, the magnitude of the exceedance, and the

number or types of people exposed at various levels above the RfD or RfC.

Typically, screening assessments will identify HAP for which exposures may exceed the

RfC or RfD, and therefore have some potential to cause adverse effects. Because risk for

noncarcinogens is dependent on total exposure to a particular pollutant (as opposed to

incremental exposures as for carcinogens), it will be important for assessments to consider all

sources of exposure. These screening assessments may identify for further study sources that

exceed a default percentage (e.g., 20%) of a HAP exposure above an RfD or RfC. Sources that

appear to contribute to RfD or RfC exceedances for HAP at the screening level may be

prioritized for further analysis using more refined and localized assessment methods. In contrast

to screening assessments, refined assessments developed in support of regulatory standards may

include consideration of total uncertainty in the RfC or RfD, evidence of nonadditive interactions

with other HAP, and actual percentage of contribution to total exposures. 

The EPA is currently developing a risk management framework for the residual risk

program. This framework is being developed to facilitate decisionmaking to protect public

health with an "ample margin of safety." As part of the ample margin of safety framework, one

must first determine the "acceptability" of risks based on health considerations alone. The

framework will also include guidelines for appropriate consideration of factors other than risk in

regulatory decisionmaking, e.g., cost, economic impacts and feasibility. The framework, which

will be completed in time for the first residual risk standard, will address evaluating the

significance of exposures above the RfC or RfD on a case-by-case basis considering the factors

identified above.

Noncancer Effects ! Acute. Methods for dose-response assessment of acute exposures

are substantially similar to the approach for chronic exposure. Risk assessment for acute

inhalation exposure is complicated by the steep concentration-response curves that are often

observed, and because small differences in exposure duration (in some cases, a few minutes)

need to be taken into account. Because increased exposure duration increases the incidence and

severity of response, acute toxicity criteria or exposure guideline values are developed for a

specified duration (e.g., one hour). Although many acute toxicity studies only report incidence of

death, it is preferred to base criteria on studies that evaluate additional endpoints, including

clinical signs, clinical chemistry, and histopathology. For an inhalation criterion, the exposure

duration of the study should ideally be the same as the one of interest (e.g., one hour). If

significant interpolation across exposure durations is required, multiple studies are preferred to
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improve the quality of the interpolation. We are currently developing a new Agency method for

acute dose-response assessment, the resultant value of which is an ARE (U.S. EPA, 1998b).

Cancer. Our cancer risk assessment guidelines of 1986 adopted a default assumption

that chemical carcinogens would exhibit risks at any dose (U.S. EPA, 1986b). Extrapolation of

cancer risk using the linearized multistage model, which results in a linear extrapolation of risk in

the low dose region, was proposed as a reasonable upper-bound on risk, and this approach has

been used for most chemicals with adequate data since then. However, as stressed in the

Proposed Guidelines for Carcinogen Risk Assessment (U.S. EPA, 1996b), when there are

adequate mechanistic data to suggest that other models would be more appropriate to estimate

low exposure risk, they may be used on a case-by-case basis. In the absence of such data, the

assumption of response linearity is maintained although the modeling scheme has been

simplified.

In cancer dose-response assessments relying on ingestion animal studies for which

chemical-specific data are not available to guide the scaling of results to human equivalents, a

default scaling factor based on the body mass raised to the 3/4 power of the test animals relative

to humans is generally used to calculate a human equivalent dose. For inhalation exposure

studies, dosimetric methods such as those used in developing RfCs are generally used to

calculate a HEC from animal data. Dose-response models such as the multistage model have

historically been used to calculate upper-bound unit risk estimates. Typically, EPA has relied on

the unit risk estimate as a quantitative measure of potential cancer hazard. A unit risk estimate

represents an estimate of the increased cancer risk from a lifetime (assumed 70 year) exposure to

a concentration of one unit of exposure. The unit risk estimate for inhalation exposures is

typically expressed as risk per microgram per cubic meter for air contaminants. The unit risk

estimate is a plausible upper-bound estimate of the risk (i.e., the risk is not likely to be higher but

may be lower and may be zero).

Since the publication of the our original cancer guidelines (U.S. EPA, 1986b),

considerable new knowledge has been developed regarding the processes of chemical

carcinogenesis and the evaluation of human cancer risk. Currently, a revision of the cancer

guidelines is in process (U.S. EPA, 1996b) that represents a considerable departure from the

original guidelines (see Exhibit 5-3 for key differences in the dose-response assessment step

between the two sets of guidelines). As mentioned above, a fundamental and important advance

in the proposed revision is the distinction between linear and nonlinear modes of action. The

cancer data in the observable range are analyzed using a dose-response model similar to the

models used for noncancer effects. The method of extrapolation to lower doses from the point of

departure differs depending on whether the assessment of the available data on the mode of

action of the chemical indicates a linear or nonlinear mode of action.
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EXHIBIT 5-3

SUMMARY OF MAJOR DIFFERENCES BETWEEN

EPA’S 1986 GUIDELINES (U.S. EPA, 1986b) AND 1996 PROPOSED GUIDELINES FOR

CARCINOGEN RISK ASSESSMENT (U.S. EPA, 1996b)

1986 Guidelines 1996 Proposed Guidelines

Default model used for linear dose-response

relationships is the “linearized multistage”

procedure.

Biologically based dose-response models are

used whenever data are sufficient. 

Recommended default approaches include the

margin of exposure approach (comparison of

exposure level and point of departure) and

linear extrapolation to zero dose, zero response.

Dose-response evaluation is limited to

carcinogenicity data.

If appropriate, data on noncarcinogens effects

may be used to help characterize the

carcinogenicity dose-response relationship.

A linear extrapolation is generally appropriate when the evidence supports a mode of

action of gene mutation due to direct deoxyribonucleic acid (DNA) reactivity or another mode of

action that is thought to be linear in the low dose region. For linear extrapolation, a straight line

is drawn from the point of departure to the origin, and the risk at any concentration is determined

by interpolation along that line. A linear mode of action also will serve as a default when

available evidence is not sufficient to support a nonlinear extrapolation procedure, even if there

is no evidence for DNA reactivity.

Nonlinear methods are used when there is sufficient evidence to support a nonlinear

mode of action. A nonlinear mode of action could involve a dose-response pattern in which the

response falls much more quickly than linearly with dose, but still indicating risk at low doses. 

Alternatively, the mode of action may theoretically have a threshold if, for example, the cancer

response is a secondary effect of toxicity or an induced physiological change which is a threshold

phenomenon. In most cases, we will not try to distinguish between modes of action with a “true

threshold” and those that are nonlinear through the origin, because data are rarely sufficient to

make this determination. As a default science policy, nonlinear extrapolation to low doses will

not be performed because there is no current basis to choose a model or determine the shape of

the dose-response function. However, as more specific information on a HAP’s mechanism of

action becomes available and where the data are sufficient to support the use of alternative

models, we will use them.

5.2.3 Risk Characterization

The final product in the risk assessment process is the risk characterization, in which the

information from the previous steps is integrated and an overall conclusion about risk is

synthesized that is complete, informative, and useful for decisionmakers. The nature of the risk

characterization will depend on the information available, the regulatory application of the risk
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information, and the resources (including time) available. In all cases, however, major issues

associated with determining the nature and extent of the risk should be identified and discussed. 

Further, the EPA Administrator’s March 1995 Policy for Risk Characterization (U.S. EPA,

1995a) specifies that a risk characterization “be prepared in a manner that is clear, transparent,

reasonable, and consistent with other risk characterizations of similar scope prepared across

programs in the Agency.” The 1995 Guidance for Risk Characterization (U.S. EPA, 1995b) lists

several guiding principles for defining risk characterization in the context of risk assessment. 

The three principles with respect to the information content and uncertainty aspects of risk

characterization are as follows:

(1) The risk characterization integrates the information from the exposure and dose-response

assessments, using a combination of qualitative information, quantitative information,

and information regarding uncertainties. A good characterization should include different

kinds of information from all portions of the foregoing assessment, carefully selected for

reliability and relevance.

(2) The risk characterization includes a discussion of uncertainty and variability. The risk

assessor must distinguish between variability (arising from true heterogeneity) and

uncertainty (resulting from a lack of knowledge).

(3) Well-balanced risk characterizations present risk conclusions and information regarding

the strengths and limitations of the assessment for other risk assessors, EPA

decisionmakers, and the public. “Truth in advertising” is an integral part of the

characterization, discussing all noteworthy limitations while taking care not to become

mired in analyzing factors that are not significant. 

The 1995 Guidance for Risk Characterization (U.S. EPA, 1995b) identifies several

guiding principles, shown in Exhibit 5-4, with respect to descriptions of risk.

Risk assessments are intended to address or provide descriptions of risk to: (1)

individuals exposed at average levels and those in the high-end portions of the risk distribution;

(2) the exposed population as a whole; and (3) important subgroups of the population such as

highly susceptible groups or individuals (e.g., children), if known. Because cancer and

noncancer dose-response assessment methods are currently quite different, risk characterizations

also differ and are discussed separately.

Noncancer Effects. Unlike cancer risk characterization, noncancer risks typically are not

expressed as a probability of an individual suffering an adverse effect. Instead, “risk” for

noncancer effects typically is quantified by comparing the exposure to the reference level as a

ratio. The resultant HQ can be expressed as an equation, where HQ equals the exposure/

reference level. Exposures or doses below the reference level (HQ<1) are not likely to be

associated with adverse health effects. With exposures increasingly greater than the reference

level (i.e., HQs increasingly greater than 1), the potential for adverse effects increases. The HQ,

however, should not be interpreted as a probability of adverse effects. 
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EXHIBIT 5-4

GUIDING PRINCIPLES WITH RESPECT TO RISK DESCRIPTORS

< Information about the distribution of individual exposures is important to

communicating the results of a risk assessment. Both high-end and central tendency

descriptors are used to convey the variability in risk levels experienced throughout the

population. 

< Information about population exposure leads to another important way to describe

risk. Both a probabilistic number of cases (or environmental impacts) and an expected

percentage of the exposed population (or ecological resource) with risk greater than a certain

level are valuable ways to present information.

< Information about the distribution of exposure and risk for different subgroups of the

population are important components of a risk assessment. Highly susceptible

individuals or areas should be identified as well as those highly exposed, when possible. 

< Situation-specific information adds perspective on possible future events or regulatory

options. Consideration of alternative scenarios when conducting risk assessment can aid in

risk management decisions.

< An evaluation of the uncertainty in the risk descriptors is an important component of

the uncertainty discussion in the assessment. Both quantitative and qualitative

evaluations of uncertainty can be useful to users of the assessment.

While some potential environmental hazards may involve significant exposure to only a

single compound, exposure to a mixture of compounds that may produce similar or dissimilar

noncancer health effects is more common. In a few cases, reference levels may be available for a

chemical mixture of concern or for a similar mixture. In such cases, risk characterization can be

conducted on the mixture using the same procedures used for a single compound. However,

noncancer health effects data are usually available only for individual compounds within a

mixture. In screening-level assessments for such cases, a conservative HI approach, in which all

the HQs for individual contaminants are summed, is sometimes used. 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. This

assumption of dose additivity is most appropriate to compounds that induce the same effect by

similar modes of action (U.S. EPA, 1986c). As with the HQ, the HI should not be interpreted as

a probability of adverse effects, nor as strict delineation of “safe” and “unsafe” levels (U.S. EPA,

1986c; U.S. EPA, 1989). Rather the HI is a rough measure of potential for risk and needs to be

interpreted carefully.

Although the HI approach encompassing all chemicals in a mixture may be appropriate

for a screening-level study (U.S. EPA, 1989), it is important to note that application of the HI

equation to compounds that may produce different effects, or that act by different mechanisms,
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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 only

mechanisms of action are known to be similar (U.S. EPA, 1986c). 

Cancer. Risks for cancer are generally expressed as either individual risks or population

risks. The distribution of exposures and individual risks within a given population can also be

presented, providing an estimate of the number of people exposed to various predicted levels of

risk. The Agency’s risk characterization guidelines recommend that risk assessments describe

individual risk, population risk, and risk to important subgroups of the population such as highly

exposed or highly susceptible groups (U.S. EPA, 1995b). For air toxics emissions, cancer risks

can be estimated by multiplying the corresponding exposure by the unit risk estimate. Our doseresponse assessments for carcinogens are based on mathematical models and assumptions that

support extrapolation from high to low doses and from nonhuman test species to humans. As a

matter of science policy, many of these assumptions are protective to avoid underestimating

cancer risks where data are incomplete. The most important of these assumptions for most

carcinogenic chemicals is that risk is proportional to dose, with no threshold dose below which

there is no risk. Our dose-response assessments for inhalation of carcinogens are expressed as a

“unit risk,” that is, risk per microgram per cubic meter of daily exposure during a lifetime. The

unit risk is defined as a conservative estimate of an individual’s excess probability of contracting

cancer at the end of 70 years exposure to a continuous level of one microgram per cubic meter. 

Risks from exposures to concentrations other than one microgram per cubic meter are modeled

as proportional, with half the concentration producing half the estimated risk, and so on.

Each word in the above definition of unit risk carries significant meaning. First, the unit

risk is a conservative rather than a “best” estimate. This means that the actual unit risk is

unknown and is very likely to be lower than estimated and very unlikely to be higher. Second, as

already described, risks are estimated rather than measured. Third, the unit risk applies to an

individual, although cancer incidence in a population can be estimated across a group by

aggregating the risk of each person. Fourth, unit risk estimates focus only on the route of

exposure being analyzed. Fifth, unit risks are expressed in terms of probability. For example, we

may determine the unit risk of a particular HAP to be one in ten thousand per microgram per

cubic meter. This means that, of ten thousand people who continuously inhale an average of one

microgram per cubic meter of this particular HAP for 70 years, no more than one would be

expected to contract cancer from the exposure. Sixth, risks are generally expressed in terms of

contracting cancer, not dying from it. Finally, exposures are averaged over a 70-year lifetime to

account for long-term exposures to low levels of carcinogens. 

Cancer risk is defined as the upper-bound probability of contracting cancer following

exposure to a pollutant at the estimated concentration over a 70-year period (assumed human

lifespan). This predicted risk focuses on the additional risk of cancer predicted from the

exposure being analyzed, beyond that due to any other factors. Estimates of risk are usually

expressed as a probability represented in scientific notation as a negative exponent of 10. For

example, an additional risk of contracting cancer of 1 chance in 10,000 (or one additional person
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in 10,000) is written as 1x10-4. Because unit risk estimates are typically upper-bound estimates,

actual risks may be lower than predicted.

Population risk is an aggregated estimate of individual risks, integrated across the entire

population within the given area of analysis. The estimated level of individual risk for each

population group (separated geographically, demographically, or both) is multiplied by the

number of people in that group, producing an estimate of the incidence of cancer cases in the

group during a lifetime of exposure. As with individual risk estimates, EPA has typically

calculated these cancer incidence estimates based on upper-bound unit risk values. Therefore, 

they provide a high-end estimate of future cancer risk. The population risk estimates for each

population group are then summed to provide a prediction of excess cancer incidence in the

entire exposed population. These lifetime incidence estimates are sometimes divided by 70 to

obtain an upper-bound prediction of the number of cancer cases per year.

People are often exposed to multiple chemicals rather than a single chemical. In those

few cases where weight of evidence classifications and unit risk estimates are available for the

chemical mixture of concern or for a similar mixture, risk characterization can be conducted on

the mixture using the same procedures used for a single compound. However, cancer doseresponse assessments and unit risk estimates are usually available only for individual compounds

within a mixture. Consequently, 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 total risk.

For carcinogens being assessed based on the assumption of nonlinear dose-response, the 

margin-of-exposure approach (MOE, analogous to the HQ approach for noncarcinogens) may be

considered, consistent with the proposed revision of EPA’s cancer guidelines (U.S. EPA, 1996b). 

The MOE approach leaves the decision about the appropriate reduction in exposure compared to

the point of departure (i.e., the observable toxicity data) up to the risk manager. 

In the risk characterization step of final assessments, estimates of health risk will be

presented in the context of uncertainties and limitations in the data and methodology. 

Uncertainties and limitations related to the hazard identification and dose-response assessment

may also be discussed. The degree to which all types of uncertainty need to be quantified and the

amount of uncertainty that is acceptable varies. For a screening-level analysis, a high degree of

uncertainty is often acceptable, provided that conservative assumptions are used to bias potential

error toward protecting human health. Similarly, a regionwide or nationwide study will be more

uncertain than a site-specific one. In general, the more detailed or accurate the risk

characterization, the more carefully uncertainty needs to be considered.
National Air Toxics Program: The Integrated Urban Strategy

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2RBCs for cancer are ambient concentrations associated with specific levels of cancer risk, assuming 70 years

of continuous exposure. RBCs for noncancer effects are ambient concentrations that pose no appreciable risk to

humans, assuming continuous exposure. The use of RBCs does not imply a judgment that the concentrations are either

acceptable or unacceptable, only that they have been derived in the same way for all HAP.

3Peer-reviewed examples of this approach include the EPA/Office of Pollution Prevention and Toxic

Substances’ Risk-Based Environmental Indicators (Science Advisory Board, 1998), the EPA/Office of Solid Waste’s

WMPT (U.S. EPA, 1998c), and the EPA/Office of Air Quality Planning and Standards’ ranking analysis for urban HAP

(Smith et al., 1999).

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5.3 Methods, Tools, and Data to Estimate Risk

5.3.1 Assessing Exposures and Characterizing Risks

In general, the choice of appropriate risk characterization approaches will be influenced

by both the availability of data to support exposure assessment, and the level of detail and

resolution needed to support the purpose of the assessment. Possible approaches range from

simple weighting adjustments of emissions data or ambient concentrations to detailed

multipathway risk assessments. We’ve identified four basic approaches that we plan to use for

various assessments to evaluate the progress of the Strategy in reducing estimated risk. Each of

these approaches uses the same dose-response information described above, but relies on

different types of data to represent exposures. The four basic approaches we intend to use are:

(1) emissions or ambient concentration weighting, (2) comparisons between ambient

concentrations and RBCs2, (3) comparisons between estimated exposures and RBCs that may

yield quantitative estimates of risk, and (4) quantitative estimates of carcinogenic risk for

individuals and populations.

Approaches (1) and (2) are considered hazard-based approaches because they lack the

dispersion and/or human exposure modeling steps of an exposure assessment and, therefore,

cannot provide quantitative estimates of risk. However, they can provide valuable information,

subject to substantial uncertainty, that may be useful in evaluating progress toward risk reduction

goals. In contrast, approaches (3) and (4) are considered risk-based approaches because they do

incorporate exposure assessments and thereby can provide quantitative risk estimates, although

these too are usually subject to substantial uncertainty. Below, we will compare the differences

in these approaches.

(1) Weighted emissions or ambient concentrations. Weighting of emissions or

ambient concentrations is the least resource-intensive approach of the four in terms of data needs

and computational requirements3. This hazard-based approach combines HAP emissions or

monitored HAP concentrations (acting as surrogates for exposure) with weighting factors

(developed from unit risks and reference concentrations) that account for differences in relative

toxicity among HAP. Other weighting factors could also potentially be developed to account for

differences in dispersion characteristics or variations in population density or behavior.
National Air Toxics Program: The Integrated Urban Strategy

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4Peer-reviewed examples of the use of this approach include the concentration-toxicity screen used by EPA’s

Superfund program to select contaminants and exposures for detailed risk assessment (U.S. EPA, 1989) and EPA’s

CEP, which compared modeled ambient air concentration estimates with RBCs (termed “health benchmarks” by the

authors) for 148 HAP nationwide (Woodruff et al., 1998).

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The toxicity adjustment is intended to account for differences in toxic potency among

substances, placing all emissions data on the same scale of hazard potential. For example,

acrylamide is approximately 160 times more potent a carcinogen than benzene, such that

weighting by potency would consider one ton of acrylamide emissions equivalent to 160 tons of

benzene. In a cumulative analysis, emissions or concentrations of each HAP would be weighted

by its relative potency to allow for direct comparison and aggregation across HAP (with

carcinogenic and noncarcinogenic estimates aggregated separately). This type of analysis permits

comparisons of relative hazard between pollutants with large mass emissions and low toxicity

(e.g., many non-chlorinated volatile compounds) against pollutants with small mass emissions

but high toxicity (e.g., dioxin).

As discussed above, the weighted emissions- or concentration-based approach lacks the

last two steps of an exposure assessment, and therefore doesn’t provide a quantitative estimate of

risks. Also, because of the absence of these important exposure assessment steps, it isn’t

possible to say how closely changes in weighted emissions or concentrations will be related to

changes in health risks. Nevertheless, emissions and ambient concentrations clearly have a

strong influence over exposure and risk, and we anticipate that the toxicity-weighting approach

will provide useful information to estimate progress where appropriate data for more refined

assessment approaches aren’t available.

(2) Ratios of ambient concentrations to RBCs. A second type of hazard-based

approach is the comparison of ambient HAP concentrations with RBCs4. Ambient

concentrations may be measured or modeled. Appropriate modeling approaches for estimating

ambient concentrations at different spatial scales using emissions data include national-scale and

urban- to neighborhood-scale air quality models, as well as multimedia models for urban- to

neighborhood-scale analyses.

The RBCs used for comparison are derived from unit risks or reference concentrations. 

Specifically, cancer RBCs can be defined in terms of a fixed risk level (e.g., HAP concentrations

conservatively estimated to result in a 1 in 10,000 or a 1 in 1,000,000 upper-bound risk of

contracting cancer from a lifetime exposure at the RBC). Noncancer RBCs can be defined in

terms of estimates of continuous exposure levels at which even sensitive subgroups are likely to

be without any appreciable risk of adverse effects during a lifetime.

Because it is more complex than emissions-weighting, this type of analysis brings two

significant advantages. First, it supports a more complete treatment of ambient HAP

concentrations that are already below noncancer RBCs, for which further reductions may not

carry significant health benefits. Second, the use of dispersion models to predict ambient

concentrations can potentially account for variations in factors such as location of exposed
National Air Toxics Program: The Integrated Urban Strategy

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5Peer-reviewed analyses of this type of analysis include many single-substance risk assessments. Several

examples concern the fuel additives MMT (Davis et al., 1998; U.S. EPA, 1994b) and MTBE (U.S. EPA, 1993).

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populations relative to sources of HAP, differences in meteorological conditions, and differences

in fate and transport characteristics among HAP.

Nevertheless, this approach still lacks the third, human behavior-related step in an

exposure assessment. Therefore, it doesn’t provide a quantitative estimate of risk, and its use in

estimating progress is subject to greater uncertainty than approaches (3) and (4), below. Changes

in health risks may not precisely track changes in concentration/RBC ratios. However, because

ambient concentrations are important determinants of exposure and risk, we anticipate that the

concentration/RBC approach will provide useful information to estimate progress where

exposure assessment is not possible.

(3) Ratios of exposures to RBCs. A third type of approach begins with measured or

modeled ambient HAP concentrations and adds further refinement by overlaying estimates or

measurements of population exposures. Thus, this risk-based approach is qualitatively different

from the first two hazard-based approaches, because it incorporates all three steps of an exposure

assessment.

While human exposures are directly affected by ambient concentrations, they’re also

influenced by behavioral factors such as time spent outdoors, periodic movements (such as

commuting) within an urban area, and activity levels. Exposures may be estimated with

exposure models that simulate the behavioral factors that determine exposure. Human exposure

may also be directly measured by personal monitoring, in which subjects wear small air samplers

and record their daily activities.

These estimated or measured exposures are then compared to RBCs5 (as described above

for approach (2)). Analogous to the comparisons in approach (2), hazard potential would

typically be presented in terms of ratios of the exposure concentrations divided by RBCs. The

additional complexity of estimating exposure provides three significant advantages over

considering ambient concentrations alone. First, it provides a more realistic comparison with

RBCs, which are based on unit risks and reference concentrations usually derived from doses

actually received by test organisms. Second, exposure estimates can take into account behavioral

differences between populations in different cities, or between different demographic groups. 

Third, exposure estimates support combining effects of multiple HAP, considering non-additivity

and similarities or differences in toxic mechanisms. Comparison of exposures with reference

concentrations for noncancer effects (surrogates for RBCs) is currently the most advanced

approach used for assessing noncarcinogenic HAP, although this may change in the future for

some substances.

(4) Risk estimation. A fourth type of approach that can be used to estimate cancer

incidence (but typically not for noncancer assessments) is comprehensive risk estimation,
National Air Toxics Program: The Integrated Urban Strategy

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6Examples of such multichemical, multipathway risk assessments include many performed by EPA’s Superfund

program under the Risk Assessment Guidelines for Superfund (U.S. EPA, 1989).

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focusing on the most exposed individual or on entire populations or subgroups6. We’ll derive

risk estimates by combining exposure estimates with dose-response assessment results in terms

of unit cancer risk estimates. Risk estimates will also consider nonstandard dose-response

models and complex interactions among different HAP, if information is available. Such risk

estimates represent the most refined analysis of the four approaches considered. Comprehensive

assessments may contain modeling to account for environmental fate and transport of released

pollutants, estimation of exposures to different subpopulations, detailed dose-response

assessments for each HAP, and information on complex, nonadditive interactions among HAP. 

Results are expressed in terms of probabilities of developing cancer during a lifetime. Cancer

risks are usually aggregated across HAP by addition, but nonadditive interactions are included if

data permit.

In its most complete form, risk estimation produces results in probabilistic form (that is,

with calculations considering a range of cancer risks and the likelihood of each), expressed in

terms of a frequency distribution rather than as a single deterministic estimate. Of currently

available approaches, risk estimation, presented probabilistically, provides the most complete,

best-supported, and most accurate presentation of both risk and the variability and uncertainty

surrounding it. However, this risk-based approach is much more resource- and calculationintensive than are simpler approaches, and is often not possible to conduct due to data

limitations.

5.3.2 Summary

We anticipate tracking progress in reducing estimated cumulative risks from air toxics in

urban areas by relying on estimates of health risk rather than by directly observing reductions in

adverse health impacts in human populations. We consider these health risk estimates to be

reasonable and appropriate indicators of progress toward meeting the goals of the Strategy. Their

use is made necessary by the long latency period for cancer, the high background rate of many

health effects (including cancer), and complexities involved in attributing various noncancer

health effects to specific environmental causes. Our assessments will use a variety of

approaches, including some that do not include all exposure assessment steps. In some cases the

information may be too uncertain to support conclusions. We intend to evaluate these

approaches against each other, in terms of their ability to estimate risk and their resource and data

requirements, when supporting data become available during 2000. These results will assist us in

determining the scope, refinement, and precision of future assessments developed to reflect

different purposes under the Strategy.
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5.4 The Overall Risk Assessment Approach for the Strategy

In previous sections, we discussed the key role that assessing air quality, exposure, and

estimated risks will play in assessing progress toward meeting the goals of the Strategy. In

addition, these assessment activities will, over time, also serve the following broader purposes:

C Improve the definition of the goal for “substantial” reduction in noncancer risk;

C Support development of national area and mobile source standards;

C Support decisions on how to conduct future risk assessments;

C Evaluate the effectiveness of each of the four approaches to characterizing risk

reductions, described above;

C Provide guidance for State, local and Tribal agency efforts in conducting local

assessments and developing risk reduction programs at the State, local, and Tribal levels;

and

• Guide us in determining significant research needs to better inform future assessments. 

Our assessment approach will be generally iterative in nature so as to take advantage of

emerging science, new data, and improved tools that become available as future assessments are

performed. Consistent with this approach, beginning in mid-2000, we’ll conduct an initial set of

assessments that will be based on final, updated emissions data. Future assessments will reflect

the best available data, methods, and tools.

Our national database of air toxics emissions from major, area, and mobile sources, the

NTI, will be a fundamental component of our risk assessments. We are now completing a

baseline NTI representing the 1990 to 1993 period, and obtaining State review of a draft 1996

NTI suitable for dispersion and exposure model inputs (scheduled for completion in 1999). We

plan to update the NTI every three years and to conduct future risk assessments to coincide with

these revisions. Monitored air toxics concentrations will also be an important component of our

assessment activities, in part to help us evaluate and refine our air quality models. We are now

working with the States to design and implement a national air toxics monitoring network that

will provide important information for future assessment activities. 

5.4.1 Designing the Assessments

We’ll tailor each assessment to the purpose(s) it is to serve (e.g., measuring progress

against the 75 percent estimated cancer incidence reduction goal). Accordingly, assessments will

vary in scope, level of refinement, and, thus, data and resource requirements. The scope of each

assessment will generally be defined by the following characteristics:
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C The number of HAP to be evaluated (all 188 or some subset);

C The types of sources included (area, major, mobile);

C The spatial resolution (e.g., aggregation of results on the national, State, urban, or

neighborhood scale); and

C The pathways/media to be evaluated (inhalation/air only or multipathway/

multimedia).

Further, for each assessment, we need to specify an appropriate approach to use in

estimating progress toward our risk reduction goals, since, as discussed above, it will not be

possible to directly measure reduction in cancer incidence or noncancer risks attributable to

hazardous air pollutant emissions. Alternative approaches range from rough approximations to

more precise risk estimates, with data and resource requirements increasing for more precise

assessments that require greater refinement.

5.4.2 Addressing Disproportionate Risks

Disparities in risks from air toxics in the urban environment may exist between different

cities, between neighborhoods or demographic groups within a city, or within a similarlyexposed population that includes sensitive groups. In our assessments, we intend to pay

particular attention to areas, populations, and sensitive groups with substantially higher-thanaverage risks.

While differences in risk between different urban areas may be discernible from national

screening-level modeling, more refined modeling will generally be needed to evaluate localized

disparities within any one urban area. This is because highly localized disparities may be

obscured by the simplifying assumptions that are necessarily inherent in national screening-level

assessments. For this reason, the ability of EPA or State and local authorities to assess localized

risk disparities will depend on the availability of detailed data on emissions and population

distribution, local-scale models, and sufficient resources.

5.5 Designing Future Assessments

We’ll conduct a series of assessments starting in mid-2000 and periodically thereafter at

appropriate times during the implementation of the Strategy. The assessments will include both

national-scale and urban-scale analyses. All assessments will incorporate the most current data,

information, and assessment tools available. As the Strategy progresses, we may eventually use

risk assessment tools that are now only in early development, or perhaps have not yet been

envisioned. For this reason, we can’t describe in detail the assessments that will be conducted

several years from now.
National Air Toxics Program: The Integrated Urban Strategy

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7As part of our CEP, the ASPEN model, used to estimate HAP ambient concentrations nationwide, was

developed and tested using a 1990 emissions inventory based on the limited HAP information that was available in the

mid-1990s (prior to the substantial improvements now reflected in the 1993 NTI). While that first national-scale

modeling exercise provided the screening-level information that we’ve used in conjunction with other information in

creating the urban HAP list, we believe that the uncertainties in the CEP’s 1990 emission inventory are too large to

support a meaningful comparison with modeled concentrations for future years that will result from the application of

the ASPEN model using updated emissions inventories. These updated inventories, starting with the 1996 NTI, are

specifically designed to include sufficient source-specific information to support air quality modeling.

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5.5.1 Initial Assessments – National

We’ll conduct an initial national assessment in mid-2000 to serve several purposes. First,

we'll develop an estimate of progress that has already been made toward the goals of the strategy. 

Consistent with section 112(k) of the CAA, which focuses on reducing ambient concentrations of

HAP to levels “below those currently experienced,” we've established 1990 as the base year for

assessing progress. To estimate progress since the base year, we'll compare the base year

emissions inventory to the inventory for 1996, due to be completed in 1999, using a weighted

emissions analysis. This assessment will be limited to the weighted-emissions approach because

the 1990 base year inventory, although a comprehensive county-level inventory, will lack the

source-specific information necessary to support air quality modeling. Subsequent assessments,

however, will not be limited in this way because emission inventory data, beginning in 1996, will

include information needed for modeling7.

Second, the initial national assessment will provide basic information to assist us in

prioritizing HAP and source categories for regulatory development, based on their relative

importance as contributors of risk. Third, the assessment will provide the clearest and most

current picture of inter-urban and demographic disparities in risk and will provide insight on

more refined analyses that may be appropriate to identify types of sources associated with

particularly high risk levels. Fourth, we intend to use information from the initial assessment to

develop a more complete and quantitative goal for a “substantial” reduction in noncancer risk. 

Finally, we’ll use the initial assessment to compare different hazard- and risk-based approaches. 

In particular, we intend to correlate results of assessment approaches (1) and (2) (which lack

exposure assessments) with exposure assessment-based approaches to determine their relative

accuracy and to quantify uncertainties. These comparisons, in combination with data and

resource availability, will help us to scope the details of future assessments and finalize our

estimates of progress from 1990 to 1996.

We’ll use all four types of approaches (emissions weighting, comparisons between

ambient concentrations and exposure estimates, RBCs, and modeled estimates of risk) in the

initial national assessments, to the extent possible. We plan to use the ASPEN model to estimate

national air quality concentrations in conjunction with the use of the Hazardous Air Pollutant

Exposure Model (HAPEM) to estimate national exposures. We’ll conduct screening level

analyses before progressing to more refined analyses to ensure that we’re allocating appropriate

amounts of resources to each assessment, given our information needs. The assessment will
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focus on inhalation exposures, with the expectation of including multipathway exposures, as

appropriate, in subsequent assessments. The initial assessment will include all urban areas in the

United States, and we anticipate presenting results with county- and/or urban-scale resolution. 

The assessment will address as many HAP as the data support, but will include at least the 33

HAP considered in the initial national scale assessment.

5.5.2 Initial Assessments – Urban

We plan to conduct urban-scale assessments for a few selected cities over the next few

years to serve as case studies that may be particularly useful as guidance for State, local and

Tribal program assessments. We’ll also provide technical support and risk assessment tools for

authorities that wish to conduct their own local assessments to analyze area-specific progress and

intra-urban disparities. The experience we gain through these analyses will also help us refine

future assessments.

We’ll develop these initial urban assessments using the specific approaches that are

appropriate for the quality of data available. Each assessment will describe a single urban area,

and we anticipate presenting the results with high spatial resolution (e.g., a one kilometer grid). 

The scope of each assessment will address a subset of HAP that we identify as being priority

HAP for the particular urban area being assessed. We plan to consider both inhalation and

multipathway exposures as appropriate and as available data permit.

5.5.3 Periodic Assessments

In the years following the initial national assessment, we’ll conduct new analyses at

appropriate intervals as new data become available. These periodic assessments will serve two

principal purposes. First, they’ll measure progress toward the goals of the Strategy, considering

all actions taken that reduce HAP emissions for any purpose. These include Federal, State, local

and Tribal actions, as well as voluntary initiatives by local communities and industry. Second,

the new analyses will assist us in prioritizing which future regulatory actions would be most

effective in making further progress. We’ll develop the periodic assessments using the specific

approaches that have proved most efficient (that is, the least resource-intensive approach that

accomplishes the purpose of the assessment). Assessments will include all urban areas in the

U.S., with results presented on county- and urban-scale level resolution. Assessments will

address the full list of 188 HAP, to the extent to which emissions, monitoring, and health data are

available. If appropriate tools become available, periodic assessments for bioaccumulative HAP

will include multimedia exposures.

By measuring ongoing progress, periodic assessments will also inform us when we have

met our goals, and will help us to measure the degree to which we have reduced disparities in

risk. The approaches used for such goal-specific comparisons will be determined by the results

of earlier assessments and will be developed to fit the Strategy’s purposes.
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5.6 References

Davis, J.M., Jarabek, A.M., Mage, D.T., and J.A. Graham. 1998. The EPA health risk

assessment of methylcyclopentadienyl manganese tricarbonyl (MMT). Risk Analysis 18:

57-70.

Science Advisory Board. 1998. Review of the Toxics Release Inventory (TRI) relative riskbased environmental indicators methodology. SAB Report No. EPA-SAB-EEC-98-007. 

Available on-line at http://www.epa.gov:80/science1/eec9807.pdf.

Smith, R.L., French, C.L. and R. Thompson. 1999. Ranking and selection of hazardous air 

pollutants for listing under section 112(k) of the Clean Air Act Amendments of 1990. 

Technical Support Document. EPA Docket A-97-44.

U.S. EPA. 1986a. Guidelines for mutagenicity risk assessment. Federal Register 51:34006-

34012. September 24.

U.S. EPA. 1986b. Guidelines for carcinogen risk assessment. Federal Register 51:33992-

34003. September 24.

U.S. EPA. 1986c. Guidelines for the health risk assessment of chemical mixtures. Federal 

Register 51:34014-34025. September 24. 

U.S. EPA. 1989. Risk assessment guidance for Superfund, volume I: human health evaluation 

manual. Office of Emergency and Remedial Response. EPA/540/1-89/002.

U.S. EPA. 1991. Guidelines for developmental toxicity risk assessment. Federal Register 

56:63798-63826.

U.S. EPA. 1992. Guidelines for exposure assessment. Federal Register 57:22888-22938. May 

29.

U.S. EPA. 1993. Assessment of potential health risks of gasoline oxygenated with methyl 

tertiary butyl ether (MTBE). Office of Research and Development. EPA/600/R-93/206.

U.S. EPA. 1994a. Methods for derivation of inhalation reference concentrations and application

of inhalation dosimetry. Washington, DC.

U.S. EPA. 1994b. Reevaluation of inhalation health risks associated with

methylcyclopentadienyl manganese tricarbonyl (MMT) in gasoline. Office of Research

and Development. EPA/600/R-94/062.

U.S. EPA. 1995a. Policy for risk characterization (“Browner Memorandum”). Office of the 

Administrator, Washington, DC. March.
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U.S. EPA. 1995b. Guidance for risk characterization. Science Policy Council, Washington, 

DC. February.

U.S. EPA. 1996a. Guidelines for reproductive toxicity risk assessment. EPA/630/R-96/009. 

September.

U.S. EPA. 1996b. Proposed guidelines for carcinogen risk assessment. Office of Research and 

Development, Washington, DC. EPA/600/P-92/003C.

U.S. EPA. 1998a. Guidelines for neurotoxicity risk assessment. Federal Register 63:26926. May

14.

U.S. EPA. 1998b. Methods for exposure-response analysis for acute inhalation exposure to 

chemicals: development of the acute reference exposure. Review draft. Office of

Research and Development, Washington, DC. EPA/600/R-98/051.

U.S. EPA. 1998c. Waste Minimization Prioritization Tool spreadsheet document for the RCRA 

waste minimization PBT chemical list docket (#F-98-MMLP-FFFFF). Available on-line

at http://www.epa.gov/epaoswer/hazwaste/minimize/chemlist/intro.pdf.

Woodruff, T.J., Axelrad, D.A., Caldwell, J., Morello-Frosh, R., and A. Rosenbaum. 1998. 

Public health implications of 1990 air toxics concentrations across the United States.

Environmental Health Perspectives 106(5): 245-251.
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1

EPA research and assessment activities are performed by various EPA offices and laboratories including

the Office of Research and Development, the Office of Air Quality Planning and Standards, the Office of

Transportation and Air Quality , the Office of Prevention, Pesticides, and Toxic Substances, and Regional Offices.

6-1

6. Research Needed to Address Knowledge Gaps

The purpose of this chapter is to summarize the types of scientific information (and

related research) needed to better inform future risk assessment and risk management judgments

that will be made in carrying out the Strategy. To provide some perspective, we are also

providing a summary of planned and/or ongoing EPA research activities1. Also, while we have

not undertaken a complete inventory of State and local research activities, we mention them in

the chapter where we are aware of them. State and local activities are especially important since

the Strategy recognizes that the responsibility for reducing health risks from exposure to urban

HAP is shared by all levels of government.

This chapter details the development of EPA research strategies and research plans which

reflect Agency commitments to specific actions within specified time periods. To aid this

process, research needs presented in this chapter are categorized into both short-term (less than

five years) and long-term needs (greater than five years). We are now developing, with this

chapter as a starting point, an Air Toxics Research Strategy that will identify key questions that

need to be answered and the research that needs to be conducted by EPA and others to answer

them. 

The scientific needs presented in this chapter are organized around the risk

assessment/risk management approach described previously, which links the elements of risk

assessment (i.e., the description of a health problem, including whether one exists) with risk

management (i.e., actions to address the risk). Consistent with this approach, research needs are

presented below in four areas:

1. Exposure assessment information needs, which include research into the areas of

emission sources, environmental concentrations, and human exposure factors;

2. Health effects information needs, including hazard determinations and doseresponse assessments, which include toxicity and mode of action research, as well

as development of methods and models for producing probabilistic doseresponses assessments with reduced uncertainty;

3. Risk assessment/characterization information needs, which include development

of assessment methods for chemical mixtures and techniques for risk

communication; and 
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4. Risk management information needs, which include emission control assessments

and pollution prevention alternatives with a focus on categories of area sources.

6.1 Exposure Assessment

An exposure assessment provides estimates of exposures that are occurring or are

anticipated to occur under specified conditions. Exposure assessments include: 

• An emissions source assessment;

• An evaluation of transformation and fate;

• A determination of environmental concentrations;

• A characterization of pathways that may lead to exposure; and

• An understanding of population characteristics and activity profiles influencing contact

between a person and a contaminant, and aggregation of exposure across pathways and

chemicals.

In order to assess human exposures to urban HAP, information is needed on emissions

(from area, major, and mobile sources), on atmospheric transport and fate, on actual exposures to

populations of interest, and on methods to measure the HAP at the places of interest (e.g., at

sources, in different media). Also, because it is impossible to measure all the events of interest,

models of these events are needed. To be fully effective, the models should encompass the

source-to-exposure relationship. Thus, models of contaminant distribution, apportionment, and

population activity profiles are needed to assess and predict microenvironmental exposures,

preferably on a probabilistic basis. These models should be founded on scientific principles and

evaluated using a variety of data. Developing such models is an iterative process, with the

scientific foundation improving at each iteration. It is important that the models explicitly

address uncertainty and that they be sufficiently detailed so that they can identify the most

effective risk reduction approach, should that be necessary. For example, knowledge of which

sources and pathways result in the highest exposures can form the basis for optimal risk

management. Descriptions of the wide range of exposure-related research needs follow.

Need 1: Improved ambient monitoring methods, characterization, and network

design to support a national ambient air toxics monitoring network

Description: The current lack of a national ambient air toxics monitoring network

hampers efforts to characterize ambient levels of HAP. Such a network is needed in the Strategy

to support efforts to provide information that will assist in: 

• Evaluating models;

• Characterizing risk;

• Tracking progress with respect to the risk goals over time; and

• Targeting areas of concern.
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Monitoring methods should be developed for those urban HAP for which no methods are

currently available. Field (ambient) studies of macro and micro environments require methods

that are sensitive to ambient concentrations of HAP. The spatial extent to which such point

measurements are valid needs to be determined to allow the assignment of an air quality

measurement to a representative area rather than to just a point location in space. These efforts

can build on the previous work performed to support the monitoring for the criteria pollutants. 

Research is needed to evaluate the uncertainties and limitations of current ambient monitoring

methods and to improve methods where appropriate. This work should include, for example, an

evaluation of current minimum detection limits with respect to expected ambient levels,

background concentrations, and health reference levels. Evaluation of “natural background

levels” of HAP through ambient monitoring needs to be completed. This should build on

existing work and would help define levels of HAP which cannot be reduced through traditional

control programs. Research is needed to evaluate the amount of monitoring data (and

measurements) needed to develop estimates of annual average concentrations with an appropriate

level of confidence. The usefulness of emerging ambient measurement methods for national

application (e.g., Light Detecting and Ranging (LIDAR), other optical methods, mobile sampling

methods, etc.) need to be evaluated and refined as appropriate.

EPA Activities: We are developing a plan for a national air toxics monitoring network

that will build directly on existing monitoring efforts managed by individual State and local air

pollution agencies. The network will foster scientific consistency across those existing networks

with respect to pollutants measured, methodologies used, and quality assurance techniques

employed. Also, it will expand the measurement of air toxics to new areas across the country

with the aim of providing a more comprehensive assessment of ambient air toxics levels

nationwide, with a particular emphasis on higher population areas. This monitoring network will

be designed (in collaboration with the States) to site monitors that will assist in the evaluation of

national scale modeling assessments and to facilitate tracking progress with respect to

emissions/risks reductions. Other monitors will be sited to support localized assessment

activities.

Need 2: Improved area source emissions estimation methodologies and spatial

allocation methods

Description: Area source categories present special challenges for estimating emissions. 

For example, they include stationary emissions sources that are individually too small, too

numerous, or too dispersed to be inventoried as individual sources (e.g., landfills, and residential

fuel combustion).

We often estimate area source emissions using “top-down” approaches that require a

combination of emission factors and source activity data. The available activity data may exist

only for large areas, such as the Nation as a whole, or at the State level. Once emissions are

estimated at this top level, they must then be spatially allocated down to smaller areas in order to

support control strategy development, dispersion and exposure modeling studies, or simply to
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permit comparisons of emissions in different geographic areas. A “bottom-up” approach, on the

other hand, would involve collection of actual measured emissions from individual sources. This

approach more accurately estimates emissions, but often is not practical because of the cost of

collecting such data for a large number of area sources and source categories. Emission factors

for area sources come from various source tests or other industry specific data (e.g., mass

balance). Sometimes emission factors are supported by data from several facilities, but often

there are only one or two tests to support them. Therefore, area source emission factors should

be improved as new data are collected.

The availability, geographic level of specificity, and overall quality of the activity data for

area sources vary from one category to another. Most often, the activity data are obtained from

published business and manufacturing sources, governmental statistics publications, and

background information from EPA regulatory programs. Examples of sources of activity data

are industrial trade associations, the Department of Commerce’s Bureau of the Census, the

Department of Transportation, the Department of Energy’s Energy Information Administration,

and various State and local government planning and regulatory agencies. Emissions are

allocated geographically by a number of methods. For major sources, the emissions for each

facility may be assigned to counties or more specific geographic locations based the address of

the facility or its latitude and longitude. Highway passenger vehicle emissions can be assigned to

counties based on total county VMT data, which are normally available from State Departments

of Transportation (DOTs). Sub-county allocation of these emissions may be based on VMT

estimates for specific major roadway links and travel demand model outputs produced by local

Metropolitan Planning Organizations (MPOs). Area source emissions are typically more difficult

to allocate to counties and sub-county areas. Most often, where facility specific data are not

available, emissions are assigned to individual counties or other areas using a surrogate factor for

area source activity. Some examples of surrogate approaches include apportioning national

emissions to counties based on population, and apportioning emissions from specific industrial

sectors to counties based on Standard Industrial Classification (SIC) code-based employment

statistics.

These area source estimation methods have several weak points, particularly when the

estimates are to be used in dispersion models to predict ambient pollutant concentrations for very

small geographic areas, like census tracts. Actual measures of area source activity for small areas

are normally not available. Existing methods are thought to produce results with a high degree of

uncertainty, but the actual activity data needed to establish credible uncertainty measures are not

readily available. New and improved methods for area source emissions estimation and spatial

allocation of area source emissions are needed to avoid inaccuracies resulting from the

“smearing” effect of the methods described above. Development of such methods requires the

completion of rigorous and demanding survey activities to establish credible databases that can

be used to develop improved area source methods. While area source needs have been

determined to have the higher priority, there is still a need to improve emissions data for major

sources over the longer term.
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EPA Activities: We have developed a baseline NTI representative of the 1990 - 1993

period, and are now updating these data to a 1996 base year. The objective of the NTI is to

provide a compilation of emissions estimates for all CAA listed HAP for point, area, and mobile

sources. The NTI therefore will serve as the most comprehensive emissions inventory of air

toxics. The NTI incorporates available information from the TRI, State and local inventory data,

data from various regulatory programs, and data from other special studies. Also, we have been

conducting research to develop an improved method for estimating area source emissions.

Need 3: Methodologies that allow for identification and speciation of important HAP

and their combustion and transformation products

Description: Some chemicals are inventoried as compound classes like “mercury

compounds” or “chromium compounds.” In addition, VOCs include many individual organic

species, some of which have been listed as HAP. Some chemical species included in these

composite chemical groups are likely to contribute to public health impacts while others may be

relatively harmless. There is currently a shortage of data available to characterize individual

species, particularly at the source category emissions level.

EPA Activities: We have begun studies to characterize the emissions of mercury and

mercury compounds from chlor-alkali manufacturing facilities, believed to be the largest noncombustion source of mercury and speciated mercury compounds (i.e., elemental mercury,

mercuric chloride, and mercuric oxide). We also maintain facilities for characterizing HAP

emissions from combustion sources, such as boilers, rotary kilns, and municipal waste

combustors (MWC). The MWC program performs basic research on MWC pollutant formation

and on control mechanisms for acid gas, trace organic, and trace metal emissions. We also have

conducted analyses of the products of incomplete combustion of agricultural plastic, and of

emissions from the open burning of household waste in barrels.

For mobile sources, we perform in-house vehicle testing programs for determining the

effects on emissions of a variety of vehicle operating conditions, including various temperatures,

malfunctioning emissions control systems, driving schedules, and fuels. We emphasize such air

toxics as benzene and total aromatics, 1,3-butadiene, formaldehyde, acetaldehyde, other

aldehydes, MTBE, and primary particles.

Need 4: A more accurate nonroad mobile source emissions characterization

Description: Nonroad mobile sources include a wide variety of mostly gasoline and

diesel-powered equipment used for nonroad transportation purposes, industrial and construction

activities, agricultural operations, recreational, and other purposes. Examples include aircraft,

farm tractors, lawn and garden tractors, snowmobiles, and recreational marine vessels. As is the

case for area sources, emissions from nonroad mobile sources are estimated using emission

factors and estimates of source activity. As for highway mobile sources, emissions result from

the incomplete combustion of motor fuels and evaporation of motor fuel components. In general,
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the data needed to estimate emissions include an estimate of the population that exists for a

particular class of equipment, an estimate of the average number of hours of use in a year, the

average load factor and power requirement for the equipment while in use, and information to

spatially and temporally allocate the equipment use. Emission factors for nonroad equipment are

based on emissions tests for specific equipment, and may be adjusted to consider deterioration of

equipment with age and to account for any applicable emissions controls on the equipment. 

Emission standards for most nonroad categories have only recently been adopted so that many of

the engines in use today were placed in service before controls were applied.

 We are currently developing an emissions model for nonroad equipment. This model,

NONROAD, estimates VOC and other criteria pollutant emissions using methods like those

described above. Draft versions of this model have been released for review. The model does

not include methods for aircraft and rail locomotives, or commercial marine vessels. To extend

the capabilities of NONROAD to cover air toxics, more research is needed to characterize toxic

emission rates (either in absolute terms or as fractions of total VOC emissions). The nonroad

mobile source category includes a wide variety of subcategories, each of which may have

different emission characteristics because engine sizes and designs, duty cycles, fuel

consumption, and approaches to engine cooling and fuel management vary.

Considerable uncertainty is inherent in the methodologies that are used to estimate

nonroad engine activity for the temporal and spatial scales needed to support air quality or

exposure modeling for urban areas. Typically, there are no State or Federal equipment

registration databases that can be used to determine equipment populations. Also, there is no

system to measure equipment utilization at either the national or local levels. The national

estimates of equipment populations, lifetimes, and utilization are based on limited survey data. 

To improve the methods for estimating nonroad engine activity in urban areas, more complete

information for both national and local equipment population and utilization is needed. Field

survey data to better establish nonroad equipment activity levels in urban areas are needed to

improve the databases that are needed to develop improved activity level estimation methods, to

correlate nonroad equipment activity with other available surrogate parameters that may be better

indicators of equipment activity, and to better define the uncertainty bounds of existing methods.

EPA Activities: As discussed above, we are developing a comprehensive nonroad

emissions model, called NONROAD, which estimates emissions for criteria pollutants. In

addition, our National Exposure Research Laboratory (NERL) is conducting some limited testing

to better characterize toxics emissions from some categories of nonroad equipment (e.g.,

lawnmowers and other lawn and garden equipment, and marine engines).

Need 5: Improved characterization of air toxics from trucks and improvement of

modal emissions modeling capabilities for all vehicle classes

Description: The highway vehicle category includes emissions from the operation of all

classes of motor vehicles (e.g., light duty gasoline vehicles, light duty gasoline trucks, heavy duty
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diesel trucks) on the Nation’s highways and streets. Emissions are usually estimated using an

emission factor model, such as the EPA MOBILE model or the California EMFAC model, in

combination with estimates of VMT, which are developed by State or local transportation

planning departments. The EPA’s MOBILE5 model calculates fleet average emission factors for

specific calendar years, expressed as grams of pollutant emitted per mile of travel. Built into the

model are computational methods that will adjust the calculated emission factors to reflect how

the age distribution of the vehicle fleet, average vehicle travel speeds, ambient temperatures, the

effects of local vehicle Inspection and Maintenance (I/M) programs, and other modal variables,

such as movement up a grade, affect emission rates.

For carbon monoxide, VOCs, and nitrogen oxides, basic vehicle emission rates are

derived from standard EPA laboratory tests, the Federal Test Procedure (FTP) for highway

vehicles. For estimation of air toxic emissions, data to develop emission factors are more

limited. However, it is generally accepted that implemented control standards for reduction of

VOC emissions can achieve proportional reductions. Some additional research to verify that

VOC controls are achieving the expected effects in controlling toxics, especially in unusual

driving and ambient conditions, may be appropriate. Relative to other vehicle classes, however,

the toxic emissions from light duty gasoline fueled cars and trucks are reasonably well

characterized. Not as much information exists to characterize toxic emissions from heavy-duty

trucks, which are primarily diesel-fueled vehicles.

The following three research components describe various aspects of work that would be

useful to improve the characterization of air toxics from medium and heavy duty trucks. First, a

significant research need exists for the development of improved toxics emission factors activity

data. In the past, most of our efforts for improving highway vehicle emission models have been

focused on passenger vehicles. However, medium and heavy duty truck emissions, most notably

PM emissions, may add significantly to the human health risks posed by exposure to motor

vehicle emissions. Diesel exhaust is thought to be a likely human carcinogen at ambient levels of

exposure. The EPA has prepared a draft health assessment document that was reviewed by

CASAC in December 1999. The document is currently being revised to address the review

panel’s comments and will be reviewed again in late 2000. The temporal and spatial operating

patterns for diesel vehicles are significantly different than for personal passenger vehicles. 

Highway-vehicle-travel-demand forecasting models concentrate on predicting passenger vehicle

trips, not truck trips. Thus, there is a need for better characterizations of real world truck activity

and emissions rates on current and emerging technologies in urban areas. Second, in addition to

research designed to improve emissions characterization (in terms of g/mile and g/min emission

factors), work is also needed to construct models that will predict population exposure levels

using existing emission factors. This type of work is needed for all air toxics but especially

diesel exhaust where questions have been raised about the usefulness of models (such as the

HAPEM as developed for mobile sources) which use vehicle carbon monoxide emissions to

estimate exposure to diesel exhaust. Third, additional work is needed on size distribution and

chemical composition of diesel particulate emissions from new technology engines. While there
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is extensive work under way on size distribution of diesel particulates from new technology

engines, it is too early to make any conclusions.

The MOBILE5 and total VMT approach is best suited for estimating emissions for county

or comparable political subdivision-size areas. Due to the complexity of factors that affect

highway vehicle emissions, this approach may yield very uncertain emissions estimates, when

used for smaller areas, such as the grid cells needed for atmospheric modeling, or for individual

road links. A more sophisticated modeling approach is needed to obtain highway vehicle

emission estimates that are accurately resolved in space and time for small areas. Highway

vehicle emissions vary considerably based on the operating mode of the engine. For example,

following a cold start, hydrocarbon emissions are significantly higher than during hot stabilized

operation. This is due primarily to the lower emission control effectiveness of the vehicles’s

catalytic converter and the need for increased fuel enrichment to promote proper vehicle

operation while the engine is cold. Variations in highway vehicle emission rates result from fuel

enrichment events caused by “real world” engine loads imposed on vehicles traveling up

roadway grades, carrying heavy loads, or hard accelerations by drivers. An alternate modeling

approach that employs engine operation mode-based emission factors and uses Geographic

Information System (GIS) technology for managing the increased detail of spatial data is capable

of producing more accurate estimates of highway vehicle emissions for the detailed temporal and

spatial scales that are needed to support air quality dispersion modeling and population exposure

studies.

EPA Activities: Pursuant to section 202(l) of the CAA, in 1993 we released the Motor

Vehicle-Related Air Toxics Study (U.S. EPA, 1993). This study summarized information on

emissions of toxic air pollutants associated with motor vehicles and motor vehicle fuels, as well

as estimated exposures and potential risks. The study also provided cancer risk estimates for

several air toxics for different years under various control scenarios. We’ve recently updated the

emissions and exposure analyses done for this study to account for new information (U.S. EPA,

1999a). 

 The MOBILE6 emission factor model, when released, will incorporate additional and

improved algorithms for estimation of criteria pollutants. 

Also, we have been working with the Georgia Institute of Technology to develop a GISbased modal emissions model for ozone precursor pollutants for highway vehicles (the Mobile

Emissions Assessment System for Urban and Regional Evaluation or MEASURE). By the end

of 1999, MEASURE will also include some simple capabilities for estimation of air toxics and

PM emissions. 

 In addition, we have conducted a limited number of on-road emissions measurements for

heavy duty diesel trucks, primarily aimed at identifying modal emissions rates and correction

factors for nitrogen oxide and PM. This work is being extended to provide for collection of data

for PAH and other toxic species. 
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Additional motor vehicle research focuses on in-house vehicle testing, “real-world”

vehicle testing, and human exposure to vehicle emissions in cabin air.

Need 6: Development of source-based urban-scale air quality models for the urban

HAP

Description: As mentioned previously, it is necessary to understand the relationship

between source emissions and the concentrations of chemicals in the media that may come in

contact with humans. Adequate modeling is very important, since measuring all potential

exposure scenarios is not feasible. While existing models may be applied to urban areas, no air

dispersion model has currently been developed that is tailored specifically to the urban

environment. Ultimately, the most effective model (which will actually be a combination of

models) should estimate the relationships among the source, the ambient air, and the exposure

dose. In this section, we describe the first component of this relationship, from source to the

ambient air. A separate Need 7 describes research that will estimate concentrations in

microenvironments for use in exposure studies, the second component of the relationship. It is

important to recognize that while Need 6 and Need 7 outline needs for exposure assessment in a

modeling framework, measurement methods and data collection studies are equally important for

the development, evaluation, and use of any model.

In order to develop and operate a numerical simulation model for the fate and transport 

of any HAP, a scientific understanding of key chemical and physical properties for that pollutant

under typical atmospheric conditions is needed. Additionally, some HAP will be transported 

and dispersed without undergoing any significant chemical transformations (i.e., they are nonreactive). Other HAP undergo significant chemical transformations or are formed in the air as a

result of atmospheric transformation of their precursors. For example, formaldehyde is directly

emitted from some sources and is created as a result of the atmospheric transformation of other

pollutants present. Particle-gas phase partitioning in the atmosphere may also be important for

certain HAP. Some HAP are semi-volatile and can exist simultaneously in both gaseous and

aerosol forms. The fraction of the total HAP air concentration in each form is a function of the

chemical and physical properties of the HAP, the atmospheric conditions, the concentrations of

precursors, and the availability of condensate nuclei. Thus, a simulation model for semi-volatile

HAP should simulate the behavior of key interacting aerosol materials, not just the gaseous and

aerosol fraction of the HAP in question–likewise for HAP that are totally in particulate form with

no significant gaseous fraction. These HAP, as particles, may coagulate to form larger particles

which deposit through settling out and washout to the earth’s surface differently than smaller

particles. Therefore, to provide accurate representations of the atmospheric behavior of these

HAP, a numerical simulation model should include both chemical and physical behavior of the

HAP being considered as well as the surrounding HAP constituents. These processes, together

with terrestrial and aquatic fate and transport processes, can be important for assessing noninhalation pathways of exposure (e.g., ingestion or absorption) that are associated with deposition

of these pollutants in soil, water, and various media.
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For urban-scale modeling, a comprehensive atmospheric model should also simulate the

fate and transport of the pollutant on a local scale. To predict maximum impacts and

concentration gradients required to assess human exposure, horizontal simulation may have to

have a resolution on the order of hundreds of meters. The vertical resolution of existing

simulation models for photochemical oxidants and acidic deposition are expected to be sufficient

for urban HAP studies. Further, the model domain size for a typical urban study is on the order

of 100 kilometers (km). No such modeling capability currently exists at these resolutions to

simulate the necessary physical and chemical processes to predict urban HAP fate and transport. 

If the HAP in question can be transported long distances (i.e., beyond the 100-km range), then

nesting of a larger-scale grid model (or regional-scale model) within the urban study area will be

required. Regional-scale models for some HAP do exist, but their usefulness on a local scale is

still very much in doubt due to model approximations about small-scale air flows and

atmospheric reactions of the HAP in question. Further, model evaluation is difficult because of

the lack of any monitoring techniques capable of measuring ambient air concentrations of the

HAP in question at temporal and spatial scales of the study. 

EPA Activities: We previously developed and applied regional-scale Lagrangian-type

models for certain HAP (i.e., mercury, dioxins and furans) with very simple or chemical specific

treatments for chemical and physical processes. These Lagrangian models are currently used to

model HAP that are transported over long distances, but cannot accurately model many HAP at

the spacial scale that need to be considered. Generally, they provide 40-km or larger horizontal

resolution, which may be inadequate or inappropriate for some urban assessments. 

We have also previously developed and applied a more local-scale, emissions-based

Eulerian-type model, the Industrial Source Complex 3 (ISC3) model, for some HAP in candidate

urban areas. As mentioned above, while this may have been appropriate for some HAP, there are

still many questions associated with the spatial and temporal uncertainties of modeling HAP with

this method.

We are now developing a new comprehensive air model of acid deposition, tropospheric

oxidants, and aerosols with available horizontal resolutions down to 4 kilometers. This model,

the Community Multi-scale Air Quality (CMAQ) model (Byun et al., 1998), is designed to

operate within the Models-3 system. Models-3 is a flexible, software system designed to

simplify the development and use of environmental assessment and decision support tools for a

wide range of applications from regulatory and policy analysis to understanding the interactions

of atmospheric chemistry and physics. This effort could serve as a basis for the development of

urban-scale HAP models with nesting capabilities within larger-scale models. Current chemical

mechanisms of tropospheric chemistry within the CMAQ model are available as a starting point

for this work. These mechanisms could probably be expanded to include the many additional

reaction pathways and species necessary to describe the detailed transformations of HAP, as well

as significant pathways for the production of HAP from non-HAP precursors.
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We have developed a set of integrated models, the Integrated Exposure Methodology

(IEM), that permits estimation of concentrations of stack-emitted pollutants in various media and

associated exposures. This methodology was used in the Mercury Study Report to Congress

(U.S. EPA, 1997) and in the Study of Hazardous Air Pollutant Emissions from Electric

Utility/Steam Generating Units (U.S. EPA, 1998), mandated by the 1990 CAA Amendments.

We are developing a modeling system called the Total Risk Integrated Methodology

(TRIM), which is intended to provide a framework that is scientifically defensible, flexible, and

user-friendly, for assessing human health and ecological risks resulting from multimedia (air,

water, soil and food), multipathway (via inhalation, ingestion, and absorption exposure routes)

exposure to air toxics and to criteria pollutants. The modeling system will consist of multiple

modeling tools from which to select, depending on the level of analysis, data availability, and

needed outputs. TRIM will track the movement of pollutant mass through a comprehensive

system of compartments. Over time and with additional research, the compartments will attempt

to represent all possible locations of the pollutant in the physical and biological environments of

a defined study area or species. Also, the modeling system should make use of mass conserving

relationships, fugacity, and biokinetics to determine the movement of HAP, and, thus, will be

able to provide an inventory of a pollutant throughout the entire system. Also, the modeling

system will reflect an integration of uncertainty and variability analysis capabilities.

Need 7: An understanding of the distribution of human exposures (including

susceptible subpopulations) and the pathways by which HAP reach humans

Description: Human exposure to HAP occurs at the point of contact between the

environmental concentration and the personal receptor. If addressed, previous research needs

(see Need 6) would enable improved estimation of air quality. However, further refinement in

scale may be needed to estimate the population distribution of exposures in an urban

environment. For example, a HAP at a 4-km distance may undergo transport and transformation

processes in the ambient air during and after penetration into indoor environments before

contacting a human. Also, many additional sources could be present within this “4-km grid” and

contribute to overall exposure. To account for these possibilities, models developed around

sound scientific principles, evaluated with measurements from targeted studies, and capable of

providing probabilistic estimates of the number of persons exposed to different concentrations of

HAP of interest, should be developed.

Exposure to HAP can more accurately be evaluated in a microenvironmental modeling

framework which considers the human as a receptor passing through a series of

microenvironments in which exposure occurs. Clearly, there are two critical factors in this

approach: (1) characterizing the range and variability of HAP concentrations in each

microenvironment, and (2) characterizing the nature of the human exposure in each

microenvironment (i.e., when, how long, how often, and with what intensity do people come in

contact with the HAP in each microenvironment). Both elements are involved in characterizing

susceptible subpopulations. For example, people with low incomes may live closer to sources; 
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children spend different times in different microenvironments compared to adults; and people

with pre-existing diseases (e.g., asthma) also have different activity patterns. 

Estimating exposure to HAP is complicated by the range of temporal and spatial scales of

emissions that may significantly contribute to personal exposures. Significant HAP emissions

may come from a few point sources with high emissions or a collection of sources with relatively

low emissions. Exposures of interest may be for an hour or a lifetime. The longer the duration

of exposure, the more complicated the assessment, given the variability in the exposure and in

personal activities. Although daily exposure may best be evaluated by a model that considers the

human receptor as passing through a series of microenvironments of exposure, long-term

exposure estimates require development of reliable simplified modeling methods because it is

not practical to follow every individual through a daily series of activities.

Research to bridge the gap between available regional-scale models of air pollution

transport and stochastic and probabilistic models of personal exposure, include: a) the

development of models and data that consider key human exposure microenvironments, b)

studies of concentration measurements and activity patterns to support modeling evaluation on

selected urban HAP, c) measurements of HAP in various media to which susceptible

populations may be exposed to ensure that models adequately capture those populations likely to

receive high-end exposures or be more biologically sensitive, and d) development of databases

and integration of all data. The data on demography, geography, meteorology, human activity

patterns, source emissions, and regional/urban/microenvironmental scale concentrations would

need to be integrated. These data support the application of a HAP population-based

probabilistic modeling system of personal exposures. It is important that both the inherent

variability and the uncertainty of all significant factors for connecting emission sources,

environmental concentrations and the magnitude, duration, and frequency of human exposures be

understood, and models be developed so that risks may be assessed and managed.

In the context of activity patterns and microenvironments, an existing gap is the need for

personal monitoring (e.g., personal monitoring exposure to VOCs and other air toxics through

use of gasoline fueled lawn and garden equipment, including commercial equipment which is

typically used for many hours per day). The development of biological markers of exposure such

as breath, hair, or tissue samples would also help characterize personal exposure of VOCs and

other air toxics. An adjunct to the need to determine personal exposure is the long-term need to

identify indoor air exposures. In the short-term, this need may be satisfied by knowing the

indoor/outdoor ratios of the urban HAP, but in the long-term, more specific data are needed on

the movement of HAP between indoors and outdoors. Toxics can absorb onto other items in the

indoor environment and then be re-released later as the concentration of the toxic is reduced. 

Therefore, information on the potential sinks and reservoirs of HAP would add useful

information to the indoor characterizations of exposures.

EPA Activities: We have completed some studies, the National Human Activity Pattern

Survey (NHAPS) and Total Exposure Assessment Methodology (TEAM), that can contribute
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limited human activity and personal exposure data in support of this need. The NHAPS did not

evaluate susceptible subpopulations, and TEAM measured only a small number of HAP. Even

so, these studies provide valuable direction for the design of necessary follow-up studies. We

have developed databases for supporting human exposure modeling [e.g., Consolidated Human

Activity Database (CHAD) and Total Human Exposure database and Advanced Simulation

Environment (THERdbASE)]. We also have a small ongoing project to develop

microenvironmental exposure measurements and models for mobile-source related emissions. 

These studies will contribute both measurements and models toward developing air pathway,

human exposure estimates along and near highways (including urban street canyons). We have

sponsored the development of receptor models for source apportionment. Chemical Mass

Balance models, and models like UNMIX, have been developed and tested on particulate and

other pollutants. Their application to microenvironmental and personal exposure measurements

is both feasible and reasonable. These past and present projects are helpful in providing some of

the needed data and models.

 We are currently using models to estimate ambient levels of air toxics which will

subsequently be used as inputs to an exposure model, HAPEM. This exposure model will

provide national exposure estimates to air toxics based on the 1996 NTI. This work will be

completed in the spring of 2000. We have a small project that develops breath analysis methods

for VOCs. Though we currently have no projects on source test methods or ambient methods for

the urban HAP, we have recently developed a prototype real-time monitor for formaldehyde. 

While HAPEM is currently being applied, there are many areas where additional information

developed through research is needed to improve the model. 

Recently, we sponsored the National Human Exposure Assessment Survey (NHEXAS)

which is a multiroute exposure study focusing on metals, pesticides, PAHs, and VOCs. In

addition, we recently funded two research centers (New Jersey Medical School and University of

California at Berkeley) to develop comprehensive exposure models for a large spectrum of air

pollutants, including HAP. Coordination between this particulate matter initiative and the urban

air toxics initiative will be beneficial to the urban air toxics program.

6.2 Health Effects and Dose-Response Assessment

Various types of toxicity, mode of action, and interactive (mixture) information are 

needed to reduce uncertainty in our estimates of risks from exposure to urban air toxics. The

needed information includes cancer and noncancer (acute and chronic) toxicity information for

HAP and risk assessment techniques that can combine data, produce statistical likelihood of risk

from HAP exposure, and reduce uncertainty through the application of better extrapolation

models (e.g., animal to human, low dose to high dose).
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Need 8: Use alternative sources of human health effects data (chronic and acute) for

urban HAP to develop and update dose-response assessments

Description: As described in Chapter 3, a variety of sources of dose-response

information was relied upon in identifying the urban HAP.

Additional health effects assessments, including the development of inhalation reference

concentrations and oral reference doses for chronic noncancer effects and acute reference

exposures for acute effects are needed for a number of the urban HAP. Although enough

information exists to raise our concern level and to select urban HAP presenting the greatest

threat to public health, more information is needed to complete the knowledge base necessary for

quantitative risk assessment, especially for the assessments of mixtures. The EPA’s Integrated

Risk Information System (IRIS) lacks cancer unit risk estimates for 13, and RfCs and RfDs for

24 and 21, respectively, of the 33 urban HAP identified in the July 19, 1999 Federal Register

Notice of the Integrated Urban Air Toxics Strategy (U.S. EPA, 1999b). Consequently, unless

peer-reviewed, dose-response assessments can be obtained from other sources, significant

uncertainty will be present in any risk assessments performed for these pollutants. An important

short-term activity is estimation of cancer unit risk and RfCs/RfDs for the HAP that currently

lack this information. Our preference is to obtain inhalation and oral data for these assessments

through the use of EPA’s test rule authority (described below).

When no chronic inhalation dose-response assessments have been available for particular

HAP from any source, we have sometimes adapted oral data to inhalation exposure as a shortterm solution. Such conversions are not optimal for deriving inhalation dose-response and risk

assessments because they involve important uncertainties. For example, confounding features

such as portal-of-entry effects and first-pass metabolic effects may play a significant role in

altering the concentration of the dose delivered to the target organ and, thereby, attenuating

expected responses. Because of the relatively large amount of oral data, the development of

validated route-to-route methods and models to extrapolate from oral exposures would expand

our ability to perform risk assessments for urban HAP in the near future.

There is a need to develop acute reference exposure values for the short term using

methods such as EPA’s proposed Acute Reference Exposure (U.S. EPA, 1994a) approach, which

is adaptable to any duration of exposure up to 24 hours. These values should be externally peer

reviewed, Agency consensus reviewed, and then listed on IRIS for use in developing risk

assessments under the Strategy. The methods used to generate the values should be evaluated so

that there will be a clearer understanding of the uncertainties associated with each method. 

Models and software to facilitate acute dose-response assessments should also be developed over

the long term whereas developing the methods and data are short-term needs.

Another research need is for information to reduce uncertainty associated with the doseresponse assessments now on IRIS. Four HAP (acetaldehyde, acrolein, acrylonitrile, and

ethylene dibromide) have RfCs with relatively high associated uncertainty, i.e., with uncertainty
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factors greater than or equal to 1000. (The RfC methodology involves the application of

uncertainty factors to information in health studies so as to account for chronic noncancer effects

on humans, including sensitive subpopulations. For example, a 10-fold uncertainty factor may be

needed to account for a lack of understanding of human effects when only subchronic animal

studies are available.) Those urban HAP having dose-response assessments on IRIS but that

have not been externally peer reviewed should be updated based on current literature and

reanalyzed to include external peer review and Agency consensus review. Those pollutants

having high uncertainty should be reassessed when test rule data are made available over the

longer term. While awaiting test rule data, evaluation of dose-response information developed

by States could be useful in deriving interim values for use in the short term.

Where multipathway exposures are deemed relevant to exposures to urban HAP (e.g.,

mercury, dioxins), RfDs should be developed, as should route-to-route extrapolation methods,

that allow their use in assessing inhalation risks. No AREs are available for any of the HAP

because the method to calculate them is still being developed. The ARE method currently under

development has been reviewed by the EPA Science Advisory Board (SAB) which recognized

that large amounts of data are required to support ARE derivation by categorical regression.

Finally, the quantitative structure-toxicity relationship (QSTR) approach is another

method for gathering data on the toxicity of urban HAP. By knowing various structural attributes

and functions and how these attributes relate to toxicity, QSTR models can predict relative

toxicities of urban HAP. Thus far, QSTR model outputs have provided the probability of a

compound being carcinogenic and are most appropriate for use in ranking toxicity but not in

developing quantitative health assessments themselves (i.e., RfCs or cancer unit risks). 

Therefore, a short-term research need is to develop the QSTR for the urban HAP and the other

HAP on the list in order to expand our knowledge database. A longer-term research need is to be

able to use the QSTR to actually predict cancer unit risks or noncancer reference values. 

EPA Activities: EPA’s authority for acquiring toxicological testing data is found in 

section 112(b)(4) of the CAA. We have proposed to use the test rule authority under the Toxic

Substance Control Act (TSCA) section 4(a) which will require testing of 21 HAP. We noted

deficiencies in testing guidelines previously used under TSCA section 4(a) and promulgated

eleven harmonized test guidelines. Pharmacokinetic studies and other mechanistic studies were

also requested in the test rule protocols to support route-to-route extrapolation and to inform

EPA of toxicity by routes other than inhalation. The only urban HAP included in that initial test

rule is ethylene dichloride. Additional toxicological testing needs to be conducted, and an

amalgamated test rule considered by EPA and ATSDR for the Children’s Risk Initiative, Urban

HAP, ATSDR VOC, and the metals rule. Testing needs for the urban HAP are candidates for the

amalgamated test rule. 

Some of the completed assessments and some of the planned assessments have high

uncertainty associated with their conclusions based on the underlying toxicological data. In order

to significantly reduce the uncertainty of dose-response assessments, future test rule data will be
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used for dose-response reanalyses. In addition, only a few of the cancer unit risks on IRIS were

developed using the approach described in the Proposed Guidelines for Carcinogen Risk

Assessment (U.S. EPA, 1996). An updating of present IRIS cancer unit risk values consistent

with the proposed guidelines should be accomplished in the longer term. Exhibit 6-1 presents

the current status of activities to update IRIS.

EXHIBIT 6-1

STATUS OF FY00 IRIS ACTIVITIES FOR URBAN HAP

Completed In Progress Scheduled New Starts

Arsenic Compounds Acetaldehyde Acrolein

Beryllium Compounds Benzene Arsenic (inorganic)

Chromium Compounds 1,3-Butadiene 1,2-Dibromoethane

Methylene Diphenyl

Diisocyanate (MDI)

Cadmium Compounds Methylene Chloride

Chloroform Methyl Mercury

1,3-Dichloropropene

Dioxin

Ethylene Oxide

Formaldehyde

Nickel Compounds

POM

Quinoline

Styrene

Tetrachloroethylene

Trichloroethylene

Vinyl Chloride

The IRIS program has recently been altered to provide improved Agency consensus

review and external peer review of dose-response assessments. We have ensured that external

peer review has been conducted or is planned for the assessments listed in Exhibit 6-1. Although

all of the assessment activities for the chemicals in Exhibit 6-1 do not include the development of

an RfC, as data are made available (e.g., through test rules), including those relevant to
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noncancer dose-response assessments, more RfCs will be derived. Pollutants with high

uncertainty factors (>1000) will be reassessed as data become available. No ARE values are

available for any HAP, but a framework for their incorporation into IRIS is being considered. 

The MRLs, acute exposure guidance levels (AEGLs), and levels of concern (LOCs) may be

developed as they are necessary to estimate hazard. Work has progressed on using QTSR models

to rank 250 disinfection byproducts for the Water Program. This method holds potential for any

further ranking of HAP by toxicity as well.

Section 202(l) of the Clean Air Act requires EPA to identify the need for and consider

regulation for control of HAP from motor vehicles and motor vehicle fuels. These regulations

are at a minimum to apply to emissions of benzene and formaldehyde. The following three

ongoing mobile source pollutant health assessment efforts will inform us as we continue our

work as part of the Strategy:

• Benzene health assessment. Benzene is a carcinogen found in baseline gasoline and

reformulated fuels. Calculating the cancer unit risk for benzene will serve to estimate a

risk associated with use of fuels containing this hazardous air pollutant. The benzene

RfC and RfD are being completed.

• 1,3-Butadiene health assessment. 1,3-Butadiene is a common emission product and

carcinogen resulting from combustion of gasoline and reformulated fuels. The health

assessment of 1,3-butadiene was reviewed by the SAB in 1998, and the final assessment

document is expected in late 2000.

• Fuel additive risk assessments. The health risk assessments of fuel additives, such as

methylcyclopentadienyl manganese tricarbonyl MMT (Davis et al., 1998; U.S. EPA,

1994b), are being conducted in support of various EPA mobile source programs. MMT is

an organic manganese compound that can be used as an octane enhancer. Questions have

been raised about whether there may be inhalation risks associated with exposure to

manganese emissions from MMT-fueled vehicles.

Need 9: Development of statistical and mode of action methods for developing acute

and chronic dose-response assessments

Description: The lack of toxicity data or the availability of seemingly disparate data

often forces the application of uncertainty factors and default assumptions when developing

dose-response assessments. Certain cases may arise where multiple toxicity studies are available

for developing dose-response assessments. Methods of combining data for cancer and noncancer

dose-response assessments that include confidence profiles (Bayesian statistics) or meta-analysis,

for example, need to be developed, codified, and incorporated into software packages for easy

use. The development of many of these methods can be completed over the shorter term.
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The current methodology for developing RfCs divides gases into three classes based on

their reactivity and solubility. Developing dose-response assessments on the basis of these

classes offers increased certainty and reduces the number of mode of action parameters necessary

to define gas behavior. The current RfC methodology utilizes a paradigm which describes gas

solubility using mass transfer coefficients. Gas models that can predict the dosimetry of reactive

and nonreactive gases and water soluble and insoluble gases are needed. Thus, over the shorter

term, mass transfer coefficients are needed for the three categories of gases: Category 1, which

are highly water soluble, rapidly reactive, and do not penetrate to blood; Category 2, which are

water soluble and show accumulation in the blood; and Category 3, which are water insoluble

and perfusion limited. This physical process of mass transfer should also be coupled with

chemical reactions in the system.

Estimating risks associated with human exposure to priority urban air toxics under the

Strategy will best be done on the basis of probability. The determination of cancer unit risk

factors for HAP readily permits such determinations of risk or probability for cancer endpoints. 

However, for noncancer endpoints, EPA has no definitive methodology for determining risk

above reference levels such as the RfC. The RfC is useful in that it indicates a reference

concentration below which it can be reasonably expected that no adverse effects will occur, even

in the most sensitive subpopulations. The basis of the RfC, which includes the application of

either a single point no-observed-adverse-effect level (NOAEL) or a statistical approach such as

the benchmark dose (BMD) (U.S. EPA, 1995), does not permit it to be used in probabilistic risk

assessments where knowing the probability of the occurrence of a health effect in a population is

desired. Though the BMD method utilizes data over a range of doses, the data are normalized to

a single effect. If higher exposure/doses are encountered, other endpoints would likely be

manifested making the basis of the BMD (dose-response for a single sentinel effect) no longer

relevant. It is important to understand that any dose-response method that utilizes a single doseresponse function, where response is a single endpoint, cannot provide a probabilistic risk

assessment by simply assuming higher doses will produce higher probabilities based on the doseresponse function originally chosen. Thus, both the NOAEL and BMD approaches provide

deterministic dose-response assessments, but not probabilistic ones. Categorical regression and

Bayesian statistics may be useful in developing methods for probabilistic risk assessments, but

these methodologies need to be developed on large adequate databases. Probabilistic approaches

to dose-response assessments are a longer-term need. Developing noncancer risk as a probability

also avoids the problem of having to combine probabilistic exposure assessments with

deterministic dose-response assessments. Guidance on the biological motivation and statistical

limitations of combining data involving different endpoints would be of added value.

The BMD method and related software are being developed as other tools for developing

both acute and chronic noncancer dose-response assessments. This methodology has many

similarities to the cancer dose-response method which utilizes curvilinear data fitting. Currently,

BMD methods are being used for the development of dose-response assessments entered on

IRIS. New software is being readied that will serve to facilitate the selection of models, provide

statistical comparisons, and present results in a graphical manner. A finite set of models for
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dichotomous data (incidence) are now available, but over the longer term additional models for

continuous data (quantitative increases or decreases in a metric) will be needed to develop

additional risk assessments. Guidelines for censoring data to develop more relevant doseresponse curves and adjusting for poor fit of models are also needed.

The ARE method is a process for developing acute dose response assessments that

includes the single point NOAEL approach, the BMD approach, and categorical regression

depending on the data availability. The ARE is defined as the exposure (concentration and

duration) with an uncertainty spanning an order of magnitude that is not likely to cause adverse

effects in a human population, including sensitive subgroups, when exposed on an acute and

intermittent basis. Adverse-effect levels are those at which there are increases in frequency,

magnitude, or severity of effects due to exposure, which are considered to be adverse. 

Intermittent implies sufficient time between exposures such that there is no effect of one

exposure on the effect of the next, and acute exposure is defined as one of less than 24 hours. 

Standard methods using the NOAEL and the BMD approaches as used in derivation of RfCs, and

RfDs are invoked for ARE derivation with limited amounts of data. When more complete data

sets are available encompassing sufficient concentration and duration information, then a

categorical regression approach is used to combine the data from different studies and derive the

ARE. The ARE methodology uses categorical regression data from many studies. Data are

grouped into categories such as no-observed-adverse effects, adverse effects, or frank effects. 

No-observed-adverse effects and adverse effects have been defined previously. Frank effects are

those effects occurring at levels that produce frankly apparent and very severe effects, such as

irreversible functional impairment or mortality. Effects data from different experiments,

different animals, and different endpoints may be plotted and regressed by category across

exposure duration. All the ARE methods sacrifice some certainty. The categorical regression

procedure holds the most promise to determine dose-response across various durations of

exposure. As a longer-term need, an adaptation of this method or other methods should be

developed to reduce uncertainty while still allowing development of dose-response assessments

across a duration of exposure.

The magnitude of response to a toxic chemical exposure is often dependent on both the

concentration and the duration of the exposure. The response has been related to their product

with an assumption that their product is a constant (a linear assumption). A significant number

of RfCs, which are assessments of chronic noncancer effects, are based on subchronic studies in

animals with no knowledge of whether a linear relationship exists between the toxic response at

greater exposure (considering concentration and duration) and that at lower exposure. 

Operationally, this lack of understanding is usually accounted for by use of a 10-fold uncertainty

factor. Over the longer term, an understanding is needed of the appropriate response metrics

(e.g., peak height, area under the curve, peak duration, and frequency of response) to help guide

the use of data in developing dose-response assessments of less than chronic exposure durations.

Advances in cancer research leading to proposed changes in EPA’s guidelines for cancer

risk assessment (U.S. EPA, 1996) have necessitated an improved knowledge of mode of action. 
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To develop cancer unit risk estimates under the new guidelines, we will have to understand the

binding and repair of exogenous agents to DNA on (1) cancer induction, receptor-mediated

mechanisms of action, and (2) mechanisms of toxicant interference with critical cellular

pathways such as signal transduction and receptors involved in cell growth. Gaps in our

knowledge of mode of action as it relates to human susceptibility also present significant

uncertainty in cancer and noncancer dose-response assessments. The National Research Council

has recognized that with respect to cancer, EPA does not account for person-to-person variations

in susceptibility. Factors such as carcinogen metabolism, DNA-adduct formation, DNA-repair

rate, synergistic effects of carcinogens, and age may contribute to different modes of action that 

influence susceptibility to cancer. Research is needed over the longer term to understand the

effects of receptor mediation on dose response of toxic chemicals and to model the interaction of

environmental chemicals with receptors. In addition, the susceptibility of humans should be

compared to human epidemiological and animal toxicological data to validate the assumption of

similar susceptibility. Modes of action responsible for increased susceptibility of certain

subpopulations (e.g., children, elderly, asthmatics) should be identified and described over the

longer term in order to reduce uncertainty in dose-response assessments.

EPA Activities: Some work is ongoing to develop methods for combining data. We are

using a meta analysis technique to combine data for health assessments when the available data

are directed toward the same endpoint. We have conducted some preliminary research on the use

of Bayesian statistics as a way of combining studies to develop a confidence profile around

parameters such as a NOAEL. Such a synthesis of data incorporates the uncertainty of parameter

estimates and provides visual display of distribution about a central point. Uncertainties in doseresponse assessments are also being reduced by research which incorporates mechanistic data. 

We are also studying a class of chemicals with a common mode of action, endocrine disruptors,

which bind to androgenic receptors for reproductive or developmental endpoints in order to

determine cumulative risk for multiple chemicals within the same mode-of-action class.

We have several activities which are integral to reducing uncertainty in RfCs and cancer

unit risk estimates. Physiologically based pharmacokinetic (PBPK) models for priority HAP

(e.g., trichloroethylene and MTBE as shorter-term examples) which permit improved estimation

of target tissue concentrations of compounds needed for derivation of RfCs are being developed. 

A long-term research activity is the development of improved pulmonary dosimetry models for

gases and particles. Uptake efficiency data in the upper and lower respiratory tract of nonhuman

primates and rodents, which will permit calculation of mass transfer coefficients for certain types

of gases, are being gathered. We are compiling a guidance document for use in interspecies

adjustments and incorporation of mode of action data that would facilitate development of oral

and inhalation cancer and noncancer dose-response assessments. Use of this guide is expected to

result in improved risk assessments. We are also developing a more precise model of the

regional deposited dose ratio (RDDR) for particles of large and small mass medium aerodynamic

diameters. The original model is being altered such that deposition estimates from the existing

RDDR model will be based on the ICRP66 model structure with modifications of rate and

parameter values as necessary after evaluation and application of new data. This new lung
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dosimetry model is being developed to improve precision of dose-response assessments of

particles and will soon be available as a software product. We are also upgrading the RDDR

model to contain a module for human ventilation activity patterns. Ventilation rates as a function

of oro-nasal switching patterns and activity patterns in children are being compared to the

patterns in adults to determine susceptibility of children to particle deposition. This work is

being conducted in cooperation with the University of North Carolina. New information on

particle emission, transport, exposure assessment, and biological mechanisms will be of great

value to the urban air toxics research program.

We are conducting some preliminary explorations into statistical methods to develop

probabilistic dose-response assessments. Categorical regression is a mathematical tool that can

be used to estimate health risk from chemical exposures. Ordered categories of toxics severity or

pathological staging can be regressed on exposure-dose to estimate the likelihood of observing

any of the categories of severity at any dose level. These estimates can be in the form of

incidence. Preliminary work on the toxicity of aldicarb has invoked such a procedure and

determined a 0.1 percent probability (risk level) of adverse effects at a dose 10-fold higher than

the aldicarb RfD. We have also undertaken a small amount of initial work regarding the

application of Bayesian statistics to determining risk above a reference level. Building upon

limited Bayesian approaches for estimating dose-response assessments for a single effect,

Bayesian statistics have been used to estimate the probability of adverse effects for aldicarb and

toluene. The Bayesian approach was used to develop distributions of effects from different

sources and then combine these distributions into a single distribution that could be used to

provide probability of a given severity of effect at various exposure-doses. Probabilistic doseresponse assessments will likely require longer-term research.

Current research in the area of dose-response assessments for acute exposures includes

the determination of the effects of the categorical regression model on derived dose-response

assessment estimation versus the role of the data. It is important that the available data drive the

shape of the regression line and not the mathematical model itself. Idealized data sets are being

used to further understand this uncertain aspect of categorical regression of toxicological data. In

vivo uptake experiments in animals and humans and generic PBPK models for central nervous

system (CNS) effects are being studied to determine the magnitude and appropriateness of

performing an interspecies dosimetric adjustment for high exposure concentrations at short

durations. An additional activity is the development of a framework for utilizing data from a

standard acute database previously developed to derive ARE values, bring them to external peer

review followed by Agency consensus review, and finally incorporate them in IRIS. Categorical

regression software that facilitates ARE value development is also being developed. Usable

forms of the ARE methodology will be realized over the shorter term.

We are also conducting research to determine the most appropriate metric for quantifying

toxicity from acute exposures. Given that concentration multiplied by time is often not linear,

other relationships defining toxicity are being sought. Using endpoints of neurotoxicity and

reproductive/developmental toxicity, we are exploring the relevancy of metrics such as peak
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height, area under the curve, peak duration, and frequency of response as better predictors of

dose-response relationships.

6.3 Risk Assessment/Characterization

After an exposure assessment and a dose-response assessment are completed, it is

necessary to combine them into a clear and useful characterization of risk. This section addresses

the need to improve risk assessments of chemical mixtures and also the need for better risk

communication.

Need 10: Improved risk assessment methods for mixtures

Description: It is possible that the combined exposures to multiple pollutants may

produce synergistic or antagonistic effects; effects either more detrimental or less detrimental

than exposure to each pollutant individually. Recent epidemiological evidence indicates

associations between air pollution and increased illness and death in humans are unlikely to be

the result of exposure to a single compound. Rather, exposure to a mixture of pollutants

including tropospheric ozone, PM, and other constituents such as HAP, seems to be correlated

with adverse effects. There are, however, significant gaps in methods, models, and data that

influence the evaluation of the risk to public health from air pollution mixtures. Research is

needed on methods of extrapolation from toxicity information about one or more complex

mixtures of air pollutants to others. Determination of toxic equivalency factors (TEF) is one

approach to gaining information about the toxicity of several compounds within a mixture. More

TEF information on mixture components such as polyorganic matter is needed for urban

assessments. Short-term toxicity tests of actual mixtures, if performed systematically, would

provide information that could be used for priority-setting and risk management.

Other longer-term work that would aid the risk assessment of mixtures is atmospheric

fate and dose-response information on mixtures. This should include basic work on chemical

characteristics and transformation factors which may affect urban HAP transformation and

dispersion in air and other media (e.g., chemical half-life, transformation rates, chemical partition

information). Longer-term information is needed concerning the antagonistic, synergistic, or

additive nature of risks associated with the components of various mixtures. This kind of

information will be useful to EPA as it moves toward enhancing its ability to evaluate cumulative

risks. The needs of the urban air toxics program should influence the priority selection of

chemicals for which binary and higher order interaction data are developed.

EPA Activities: We are presently developing a strategy to conduct laboratory and

clinical studies to identify and quantify the effects associated with exposures to typical mixtures

of pollutants in urban areas of the U.S. Particulate matter, ozone and HAP are the primary
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pollutants of interest, and the endpoints of interest include both carcinogenicity and noncancer

effects, particularly respiratory and immune system responses.

Though resources committed to mixtures research are comparatively small, EPA

maintains a mixtures database to help in the development of risk assessments involving more

than one chemical. A pilot upgrade of the MIXTOX database is under way. This database is an

interaction-based hazard index which can be used to incorporate chemical interactions into risk

assessments for mixtures. The MIXTOX database on interactions is available as an easily-used

computer program. The current version is years out of date, and the revision project is to

establish a priority list of chemical pairs based on their potential interaction and toxicity. 

Detailed interaction profiles on these priority pairs are being developed. After the revision is

complete, a new set of 20 priority chemicals or pairs will be selected and binary mixture

interactions data will be gathered, evaluated for binary weight-of-evidence determinations, and

entered into the database. Finally, we will update the profiles for 50 more chemicals to be

included in the database.

In addition, our original Mixtures Guidelines (U.S. EPA, 1986) are being revised and

provide a good first step toward the evaluation and assessment of mixtures. This mixtures risk

guidance document includes several methods for addressing different types of data, from whole

mixture dose-response data to in vitro toxicity data on individual component chemicals. The risk

methods include mathematical models for well-understood interactions as well as decision

frameworks for handling sparse and qualitative data.

We are studying mode of action for cancer to include receptor-mediated toxicity in

humans and model laboratory animals. Research will include studies of polycyclic aromatic

hydrocarbons present in urban environments to assess application of the structure-activity-based

TEF approach as has been applied to dioxin-like compounds (U.S. EPA, 1989). Future

comparative potency research will examine utility of TEF methods to predict biochemical and

toxicological responses in animal models to assess potential human health risks.

Need 11: Development of better information for more effective techniques for

communicating the results of health risk assessments for urban HAP

Description: The results of health risk assessments for urban HAP should be

communicated effectively to those participating in the policy-making process and to various

members of the public who may not have technical or scientific backgrounds. For example, the

general public needs to be provided with information and the tools to protect their families and

communities from exposure to air toxics. Unless a common understanding on the meaning of the

assessments is reached between scientists preparing the assessments and persons using the

assessments to affect policy, the overall process of risk assessment/risk management may be

defeated, sometimes with costly consequences. There are many ideas that can be explored. For

example, near real-time measurement, reporting, and access to air toxics ambient air

concentrations, together with the actual monitored or modeled data, the estimated risk of health
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effects, and the tools for interpreting this information, could be provided to communities

throughout the Nation by use of the Internet. Communication of the science to these audiences,

however, can pose challenges requiring the development of new scientific information.

 Various approaches can be investigated, including: 1) adaption and refinement of stateof-the-art techniques for visualizing air toxics information and evaluating the utility of these

techniques for communicating the information to various stakeholders, including the scientific

community, regulators, and the public; and 2) development of mechanisms to deliver air toxics

information in a timely and easily accessible format (e.g., through the Internet, over radio and

television, in the newspaper). Local or regional maps could be provided through the Internet

with color-coded air toxics concentrations to match predetermined indices of hazard. In keeping

with the Environmental Monitoring for Public Access and Community Tracking (EMPACT)

initiative, these risk communication activities should begin over the shorter term.

EPA Activities: We have developed a pollutant standard index (PSI) for ozone. Timerelevant air quality data are provided in an easily accessible and understandable format to the

general public for their use in decisionmaking. The approach uses existing air quality monitoring

and telemetry technology coupled with the latest Internet technology to provide time-relevant

data to the public. This project is intended to expand mapping capabilities for ozone, PM, and

air toxics to cover 85 cities across the U.S. Ongoing and completed work includes development

of a new ozone PSI format, development of more descriptive ozone health effects messages that

can be linked to a map on the Internet, and development of hard copy health effects pamphlets

for environmental protection offices (more technical) and doctors’ offices (less technical). We

may also conduct focus groups to determine whether the most effective process is being used on

the Internet and in print to communicate the risks of ozone exposure. Expansion of this approach

to air toxics would provide beneficial risk communications to the public and risk managers.

6.4 Risk Management

Engineering information is needed on emissions and emissions reductions over time to

support the application of regulatory strategies and compliance programs to achieve HAP

emissions reductions. The expanded focus on risk-based activities must be supported by the

development of improved risk management tools and information. In large measure, the needs

for improved emissions information to support risk management are the same as those discussed

under Needs 1 - 5 to support the risk assessment process.

Need 12: Identification of processes contributing to the HAP emissions from area

source categories, and listing of control options and pollution prevention (P2)

alternatives for these processes

Description: Area source categories considered for regulation under section 112(k) also

require technology-based controls, such as GACT standards. More detailed knowledge of the

area sources and their emission-producing processes is needed to identify appropriate control
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technologies and pollution prevention options. This is a short-term task. To identify applicable

control options, it is necessary to identify the processes that produce the HAP emissions. 

EPA Activities: Our ongoing pollution prevention (P2) research activities are centered

on the identification, evaluation, and demonstration of source reduction options for industrial and

commercial surface coating and cleaning operations. Planned activities for FY99 include

establishment of an in-house laboratory for testing of low-VOC, low-HAP coating alternatives,

demonstration of P2 techniques for autobody refinishing operations, and coating/cleaning

research for other metal and plastic substrates. We also maintain software tools showing

information on P2 techniques for use by industry, academia, and the regulatory community.

Pollution prevention research areas have included office equipment, aerosol consumer

products, textile products, engineered wood products, and conversion varnishes used on wood

products. In addition, we have focused on the application of P2 techniques for the improvement

of indoor air quality. For example, we have developed a model for analyzing the impact of

sources, sinks, ventilation, and air cleaners on indoor air quality. We have studied emissions

from various combustion sources, including hazardous waste incineration in boilers, rotary kilns,

and other combustors such as municipal waste combustion. The MWC) program supports the

development of revised rules for air pollutant emissions from the MWC source category and

performs basic research on MWC pollutant formation and control mechanisms for acid gas, trace

organic, and trace metal emissions. It also supports field tests, regulation development, and

laboratory research for medical waste incinerators (MWI). Much of the MWC regulatory support

effort has involved the development of good combustion practices and field evaluations of the

performance of air pollution control systems. Additional research has focused on the collection

of experimental data and a statistical approach to determine the effect of combustion- and

sorbent-injection-related parameters on the mechanism of polychlorinated dibenzo-p-dioxin and

polychlorinated dibenzofuran (PCDD and PCDF) formation and prevention in waste combustors. 

We have also conducted analyses of the products of incomplete combustion of agricultural

plastic, as well as the open burning of household waste in barrels.

In a broader perspective, many P2 research opportunities are cross-cutting. Multimedia

issues arise with common problems requiring a systems approach. This is why P2 research in the

development of tools and technologies for Life Cycle Analysis (LCA), process simulation, P2

measurement, P2 technology, systems integration, cost effectiveness, environmental impact,

cleaner production design, and generic decision-making tools for reducing risks fit within and cut

across all categories.

Need 13: Identification of pollution prevention alternatives for HAP emissions from

mobile sources

Description: Because P2 has been very broadly defined by the Federal Government,

many environmental quality and related transportation system management options fit within its

scope. Some areas may require an interdisciplinary approach, including emissions control
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experts, transportation system experts, economists and behavioral science specialists. Some P2

strategies relate to the actual reduction of emissions, including HAP emissions, from motor

vehicles, while others relate to changes in the transportation system infrastructure that will in

turn, effect emissions reductions. 

EPA Activities: We are involved in a number of activities addressing cleaner fuels and

vehicles:

• Partnership for a New Generation of Vehicles (PNGV) -- a joint industry-government

research and development agreement to develop a vehicle with three times the fuel

efficiency of today’s family sedan without sacrificing size, performance, cost, safety, or

emissions. As an active partner in PNGV, EPA’s interest in high-efficiency vehicles

includes efforts to ensure low criteria emissions as well as reduced fuel use and low

carbon dioxide..

• Development of technology for clean and efficient engines which operate on renewable

alcohol fuels and promotion of the use of advanced technology and emission control

equipment to improve air quality. 

• Development and evaluation of after-treatment technology to reduce emissions from

diesel engines (particularly to reduce PM [soot], NOx, and sulfur emissions). EPA also

plans to test different diesel fuel formulations to reduce emissions.

6.5 References

Byun, D.W., Ching, J.K.S., Novak, J., and Young, J. 1998. Development and Implementation of

the EPA’s Models-3 Initial Operating Version: Community Multi-scale Air Quality

(CMAQ) Model. In: Air Pollution Modeling and Its Application XII, ed. S.E. Gryning

and N. Chaumerliac, Plenum Publishing Corp.

Davis, J.M., Jarabek, A.M., Mage, D.T., and Graham, J.A. 1998. The EPA Health Risk

Assessment of Methylcyclopentadienyl Manganese Tricarbonyl (MMT), Risk Analysis

18: 57-70.

U.S. EPA. 1986. Guidelines for the Health Risk Assessment of Chemical Mixtures. Federal 

Register 51(185): 34014-34025.

U.S. EPA. 1989. Interim Procedures for Estimating Risks Associated with Exposures to

Mixtures of Chlorinated Dibenzo-p-dioxins and Dibenzofurans (CDDs and CDFs) and

1989 Update. Washington, DC: Risk Assessment Forum, Office of Research and

Development; EPA/625/3-89/016.
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U.S. EPA. 1993. Motor Vehicle-Related Air Toxics Study. Office of Mobile Sources. EPA420/R-93-005. Ann Arbor, MI. April.

U.S. EPA. 1994a. Methods for Exposure-Response Analysis and Health Assessment for Acute 

Inhalation Exposure to Chemicals: Development of the Acute Reference Exposure. 

Draft Working Paper. Research Triangle Park, NC: Office of Health and Environmental

Assessment.

U.S. EPA. 1994b. Reevaluation of Inhalation Health Risks Associated with Methylcyclopentadienyl Manganese Tricarbonyl (MMT) in Gasoline. Office of Research and

Development, EPA/600/R-94/062

U.S. EPA. 1995. The Use of the Benchmark Dose Approach in Health Risk Assessment. 

Washington, DC: Risk Assessment Forum, Office of Research and Development;

EPA/630/R-94/007.

U.S. EPA. 1996. Proposed Guidelines for Carcinogen Risk Assessment. Federal Register 

61(79): 17960-18011.

U.S. EPA. 1997. Mercury Study Report to Congress, Vols. I-VIII, EPA-452/R-97-003 through 

EPA-452/r-97-010, Washington, D.C.

U.S. EPA. 1998. Study of Hazardous Air Pollutant Emissions from Electric Utility/Steam 

Generating Units–Final Report to Congress, EPA-453/R-98-004a and b, Washington,

D.C.

U.S. EPA. 1999a. Estimation of Motor Vehicle Toxic Emissions and Exposure in Selected 

Urban Areas, Office of Mobile Sources, Ann Arbor, MI, Report No. EPA 420-D-99-002,

March 1999.

U.S. EPA. 1999b. National Air Toxics Program: The Integrated Urban Strategy; Notice. 

Federal Register 64(137): 38705-38740.
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