EPA420-R-00-023

December 2000

Technical Support Document:

Control of Emissions of Hazardous

Air Pollutants from Motor Vehicles

and Motor Vehicle Fuels

Assessment and Standards Division

Office of Transportation and Air Quality

U.S. Environmental Protection Agency
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Executive Summary

Today’s action addresses emissions of hazardous air pollutants from mobile sources and

their fuels. In this action, we identify those compounds that should be considered Mobile Source

Air Toxics (MSATs), and examine the mobile source contribution to national inventories of

these compounds and the impacts of existing and newly promulgated mobile source control

programs. We also evaluate whether additional mobile source air toxics controls are

technologically feasible at this time, and set new gasoline toxic emission performance standards

which require refiners to maintain current levels of overcompliance with RFG and anti-dumping

toxic emission performance requirements. Because the technology-forcing standards found in

our Tier 2 motor vehicle emissions standards and gasoline sulfur control requirements (Tier 2)

and our proposed heavy-duty engine and vehicle standards and on-highway diesel fuel sulfur

control requirements (HD2007) would represent the greatest degree of toxics control achievable

for vehicles and engines at this time, we do not set additional vehicle-based air toxics controls. 

Finally, because of our concern about potential health impacts of public exposure to air toxics,

today’s action establishes a process to continue to conduct research and analysis on mobile

source air toxics. Based on the information developed through this research, we will conduct a

future rulemaking, to be completed no later than July 1, 2004, in which we will revisit the

feasibility and need for additional controls under 202(l)(2).

This Technical Support Document (TSD) describes in greater detail the technical

reasoning behind each of the components of today’s program. We begin with background

information in support of the regulatory decisions for control of mobile source air toxics under

Section 202(l)(2) of the Clean Air Act, including a description of air toxics and a review of

Agency mobile source emission control programs that relate to mobile source air toxics control. 

This is followed by a discussion of how we identified our list of Mobile Source Air Toxics. Our

selection approach, as described in Chapter 2, is based on identifying those compounds that we

know are emitted by motor vehicles and comparing this list to EPA’s Integrated Risk Information

System (IRIS) database. IRIS is a database of compounds that presents EPA’s consensus

scientific judgment on the characterization of the potential adverse health effects that may result

from exposure to various substances. This process resulted in a list of 21 compounds, including

various volatile organic compounds (VOCs) and metals as well as diesel particulate matter and

diesel exhaust gases (collectively DPM+DEOG). Chapter 3 contains important health and

environmental information for each of those MSATs.

Chapter 4 examines the effectiveness of current and proposed controls in reducing onhighway emissions of these MSATs. Our analysis shows that the programs we currently have in

place, including our reformulated gasoline (RFG) program, national low emission vehicle

(NLEV) program, Tier 2, and our recently proposed HD2007 rule, are expected to yield

significant reductions of mobile source air toxics. Between 1990 and 2020, these programs are

expected to reduce on-highway emissions of benzene, formaldehyde, 1,3-butadiene, and

acetaldehyde by 67 percent or more. In addition, we expect to see on-highway diesel PM
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emission reductions of over 90 percent.

Chapter 5 reviews what we know about ambient concentrations and exposures associated

with emissions of mobile source air toxics. We look at monitoring and modeled data on ambient

concentrations of five of the 21 mobile source air toxics. These compounds are benzene, 1,3-

butadiene, formaldehyde, acetaldehyde, and diesel PM. We also review results of on-highway

vehicle inhalation exposure assessment prepared by EPA. The exposure estimates for gaseous

air toxics are compared to estimates of the highway vehicle contribution to modeled ambient

concentrations. We also discuss what we know about inhalation exposures from microenvironmental sources. 

Chapters 6 and 7 contain our analysis regarding additional toxics controls for vehicles and

fuels. The analysis in Chapter 6, which focuses on vehicle-based controls, leads us to conclude

that it is not appropriate at this time to propose more stringent standards than the technology

forcing standards found in our Tier 2 rule and our proposed HD2007 rule. Chapter 7 provides

our analysis for fuel-based controls. Our new toxic emissions performance requirement directs

refiners to maintain the current levels of over-compliance with RFG and anti-dumping toxic

emissions performance requirements. Because the proposed standards for each refiner are the

same as the 1998-2000 toxics emission performance level for that refiner, the proposed standards

are expected to impose only negligible costs. 

Finally, in Chapter 8 we describe our current nonroad engine emission control programs

and present our estimates of the impacts of these programs on future air toxics inventories. In

this chapter, we also highlight the significant uncertainty and several of the data gaps that exist

with respect to toxics emissions from nonroad engines. 
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List of Acronyms

μg/m3 micrograms per cubic meter

AIRS Aerometric Information Retrieval System

API American Petroleum Institute

ASPEN Assessment System for Population Exposure Nationwide

ATSDR Agency for Toxic Substances and Disease Registry

CAA or the Act Clean Air Act

CalEPA California Environmental Protection Agency

CARB California Air Resources Board

CASAC Clean Air Scientific Advisory Committee

CEP Cumulative Exposure Project

CG conventional gasoline

CHAD Consolidated Human Activity Database

CMB chemical mass balance

CO carbon monoxide

CPIEM California Population Indoor Exposure Model

DHHS Department of Health and Human Services

DOC diesel oxidation catalyst

EPA or the Agency U.S. Environmental Protection Agency

FAA Federal Aviation Administration

FTP federal test procedure

g/bhp-hr grams per brake-horsepower-hour

GVWR gross vehicle weight rating

HAP hazardous air pollutant

HAPEM Hazardous Air Pollutant Exposure Model

HAPEM-MS Hazardous Air Pollutant Exposure Model for Mobile Sources

HC hydrocarbon

HD2007 heavy-duty engine and vehicle standards and diesel sulfur controls

HD-FTP heavy-duty federal test procedure

HDE heavy-duty engine

HDV heavy-duty vehicle

HLDT heavy light-duty truck

I/M inspection/maintenance
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IARC International Agency for Research on Cancer

ICAO International Civil Aviation Organization

IRIS Integrated Risk Information System

IUATS Integrated Urban Strategy (also called Urban Air Toxics Strategy)

LDT light-duty truck

LDV light-duty vehicle

LEV low emission vehicle

LLDT light light-duty truck

MARPOL International Convention on the Prevention of Pollution from Ships

MDPV medium-duty passenger vehicle

MRL minimum risk level

MSAT mobile source air toxic

MTBE methyl tert butyl ether

NAAQS National Ambient Air Quality Standards

NATA National Air Toxic Assessment

NESCAUM Northeast States for Coordinated Air Use Management

NIPER National Institute for Petroleum and Energy Research

NLEV national low emission vehicle

NMHC non-methane hydrocarbons

NMOG non-methane organic gases

NOx oxides of nitrogen

NPC National Petroleum Council

NPRA National Petrochemical & Refiners Association

NPRM Notice of Proposed Rulemaking

NTE not-to-exceed

NTI national toxics inventory

OAQPS Office of Air Quality Planning and Standards

OBD on-board diagnostics

OMB Office of Management and Budget

ORD Office of Research and Development

ORVR on-board refueling vapor recovery

OTAQ Office of Transportation and Air Quality

PADD Petroleum Administrative Districts for Defense

PAH polycyclic aromatic hydrocarbon compounds
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PCM powertrain control module

PM particulate matter

POM polycyclic organic matter

PTD product transfer document

R&D research and development

REL reference exposure level

RFA Regulatory Flexibility Act

RfC reference concentration for noncancer effects

RfD reference dose for noncancer health effects

RFG reformulated gasoline

RVP Reid vapor pressure

SAB Scientific Advisory Board

SBA U.S. Small Business Administration

SBARP or the Panel Small Business Advocacy Review Panel

SBREFA Small Business Regulatory Enforcement Fairness Act

SCAQMD South Coast Air Quality Management District (California)

SFTP supplemental federal test procedure

SI spark ignited 

SIC Standard Industrial Classification

SIGMA Society of Independent Gasoline Marketers of America

SIP State Implementation Plan

SOF soluble organic fraction

SRP scientific review panel

TAC toxic air contaminant

TAP Technical Analysis Plan

TEAM Total Exposure Assessment Methodology study

THC total hydrocarbons

Tier 2 tier 2 motor vehicle emission standards and gasoline sulfur controls

TOG total organic gases

TSCA Toxic Substances Control Act

TSD technical support document

TWC three-way catalyst

ULEV ultra-low emission vehicles

VMT vehicle miles traveled

VOC volatile organic compound
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List of Tables

Table I.B-1: Hydrocarbon (HC) Exhaust Emission Standards for Light-Duty

Vehicles (gpm) 

Table I.B-2: Heavy-Duty Standards for Diesel and Gasoline Engines (g/bhp-hr)

Table I.B-3: Heavy-Duty Gasoline Vehicle Standards Proposed for 2004

Table I.B-4: New Urban Bus Standards (g/bhp-hr)

Table I.B-5: Current Light Duty Vehicles, Light Duty Truck, and Heavy-Duty

Gasoline Vehicle Evaporative Hydrocarbon and Refueling Spitback

Standards 

Table I.B-6: On-Board Vapor Recovery for Gasoline Vehicles Phase-In Periods

and Standard

Table II.B-1: List of Mobile Source Air Toxics (MSATs)

Table IV.A-1: 1996 On-Highway and Nonroad Emission Inventories of MSATs from

the 1996 National Toxics Inventory (short tons)

Table IV.B-1: Metropolitan Areas and Regions Included in Toxic Emissions

Modeling

Table IV.B-2: Example of Data File Format for Toxic Adjustment Factors

Table IV.B-3: Annual Emissions Inventory for Selected Toxics for the Total U.S.

On-Highway Vehicles Only

Table IV.B-4: Estimated Percent Reduction for Selected Toxics for the Total U.S.

On-Highway Vehicles Only

Table IV.B-5: Annual VOC Emissions Summary for the Total U.S. On-Highway

Vehicles Only

Table IV.B-6: Annual Diesel PM Emissions Summary for the Total U.S. OnHighway Vehicles Only

Table V.A-1: Monitored 1996 ambient concentration estimates nationwide from

AIRS

Table V.A-2: Monitored average ambient concentration estimates (μg/m3

), and
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estimated highway and nonroad contributions, in the South Coast Air

Basin and in Minnesota.

Table V.A-3: Ambient Diesel Particulate Matter Concentrations from Receptor

Modeling and Elemental Carbon Measurements

Table V.A-4: Average estimated nationwide concentrations of selected air toxics in

1990 from the Cumulative Exposure Project (μg/m3)

Table V.A-5: Draft average estimates of mobile source contributions to nationwide

concentrations of selected air toxics in 1996 from the NATA national

scale assessment

Table V.A-6: Agreement of modeled ambient concentrations from the NATA

national scale assessment and monitored ambient concentrations on a

point by point basis 

Table V.A-7: Annual average diesel particulate matter concentrations

predictedfrom dispersion modeling

Table V.B-1: California annual average diesel PM exposure estimates for all mobile

sources from the California Population Indoor Exposure Model

Table V.B-2: Comparison of 1990 average exposure attributable to on-highway

vehicle emissions (HAPEM-MS3) to 1990 ambient concentration

estimates attributable to on-highway vehicle emissions (CEP)

Table V.B-3: Comparison of 1996 annual average exposures attributable to onhighway vehicles (HAPEM-MS3) and the on-highway vehicle portion

of 1996 modeled ambient concentrations (National Scale Assessment)

Table V.B-4: Highway vehicle portion of nationwide average inhalation exposures

to benzene, 1,3-butadiene, formaldehyde, acetaldehyde, and diesel PM

for three demographic groups in 1996, based on HAPEM-MS3

Table V.B-5: On-Highway vehicle portion of 1996 benzene exposure estimates for

10 urban areas, and urban and rural areas nationwide, based on

HAPEM-MS3 exposure modeling

Table V.B-6: Annual Average Ambient CO Levels as a Function of Population

Density, 14 Cities

Table V.B-7: Seasonal Average Nationwide Exposures (μg/m3

) Attributable to OnHighway Vehicle Emissions, for the General Population, 1996
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Table V.C-1: Micro-environmental concentrations of benzene (μg/m3

)

Table V.C-2: Micro-environmental exposure to formaldehyde (μg/m3)

Table VI.A-1: Gaseous MSATs

Table VI.A-2: Gaseous MSATs in Typical Gasoline-Fueled Vehicle Exhaust

Table VI.A-3: Gaseous MSATs in Typical Gasoline-Fueled Evaporative Emissions

Table VII.A-1: Refinery Count and 1998 Gasoline Volumes by PADD

Table VII.A-2: 1998 Imported Gasoline

Table VII.A-3: Annual Average Refinery Fuel Benzene Content (vol%)

Table VII.A-4: Toxics Anti-backsliding Default Baseline

Table VII.A-5: Typical Refinery Benzene Supply Pattern

Table VII.B-1: Average fuel properties from 1998 annual reports

Table VII.B-2: Representative 2007 Fuel Properties

Table VII.B-3: Baseline Toxics Emission Estimates From the Complex Model

Table VII.B-4: Total Toxics Emissions With and Without Overcompliance

Table VII.B-5: Annual Emissions Inventory for Complex Model Toxics for the Total

U.S. Gasoline On-Highway Vehicles Only

Table VII.B-6: Annual Emissions Inventory for Complex Model Toxics for the Total

U.S. Gasoline Nonroad Vehicles Only

Table VII.B-7: Total Tons Reduced Due to Overcompliance

Table VII.C-1: Comparison of Average Emission Reductions Standards of RFG

Phase I and RFG Phase II

Table VII.C-2: Average Volume Weighted Benzene Levels for 2nd Quarter RFG

Table VII.C-3: Baseline (1999) conventional gasoline (summer & winter) fuel quality

parameters and volume fraction in PADDs I, II and III.
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Table VII.C-4: Projected (2005) conventional gasoline (summer & winter) fuel

quality parameters and volume fraction accounting for Phase II RFG,

Tier 2 Sulfur Gasoline and Ultra-Low Sulfur Diesel in PADDs I, II

and III

Table VII.C-5: Projected (2005) RFG (summer & winter) fuel quality parameters

and volume fraction accounting for Phase II RFG, Tier 2 Sulfur

Gasoline and Ultra-Low Sulfur Diesel in PADDs I, II and III

Table VII.C-6: Conventional gasoline (CG) exhaust toxic emissions performance for

the 1999 base case and projected year 2005 case on a PADD basis

Table VII.C-7: RFG exhaust toxic emissions performance for the 1999 base case and

projected year 2005 case on a PADD basis

Table VII.C-8: Annual Aggregate Cost Increase and Cent per Gallon Cost of a

Benzene Anti-backsliding Program for PADDs I, II and III and

Nationally

Table VII.E-1: Compliance Margins for Selected Refineries

Table VII.F-1: Select California Phase 2 and Phase 3 Gasoline Standards

Table VIII.B-1: Annual Emissions for Benzene, Acetaldehyde, Formaldehyde, and

1,3-Butadiene from Nonroad Sources (thousand short tons per year)

Table VIII.B-2: Emission Reductions for Benzene, Acetaldehyde, Formaldehyde, and

1,3-Butadiene from Nonroad Sources

Table VIII.B-3: Annual VOC Emissions from Nonroad Sources

Table VIII.B-4: Diesel PM Emissions from Nonroad Sources
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List of Figures

Figure IV.B-1: Example Plot of Target Fuel Benzene Versus Baseline Fuel TOG

under FTP Conditions

Figure V.A.-1: National trend in annual average benzene concentrations in

metropolitan areas, 1993–1998 (Source:1998 Air Quality Trends

Report)

Figure V.B-1: Average and 95th percentile benzene exposures (attributable to onhighway vehicles) in New York City, 1996

Figure V.B-2: Exposure levels for four gaseous toxics and diesel PM under

currentlyplanned controls and with 2007 Standards for Heavy Duty

Engines (ug/m3)

Figure VII.A-1: Location of PADDs in the Contiguous U.S.

Figure VII.A-2: Chemical Benzene Demand in the U.S. (Honeywell Hi-Spec Solutions forecast)

Figure VII.D-1: Effect of Incremental Volumes on Benzene for Reformulated Gasoline

Figure VII.D-2: Effect of Incremental Volumes on Benzene for Conventional Gasoline
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Table of Contents

Executive Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

List of Acronyms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4

List of Tables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7

List of Figures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

Chapter 1: Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

A. Roadmap of This Document . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

B. Brief Overview of Air Toxics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

C. Other Air Toxics Activities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

1. Motor Vehicle Air Toxics Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

2. Integrated Urban Air Toxics Strategy . . . . . . . . . . . . . . . . . . . . . . . . . . . 24

3. National Air Toxics Assessment Activities . . . . . . . . . . . . . . . . . . . . . . . 25

4. Urban Air Toxics Reports to Congress . . . . . . . . . . . . . . . . . . . . . . . . . . 27

5. Air Toxics Research Strategy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28

D. Description of Motor Vehicle Air Pollution Control Programs . . . . . . . . . . . . . . 28

1. Mobile Source Control Programs and the Clean Air Act . . . . . . . . . . . . 28

2. Passenger Car Tailpipe Emission Controls . . . . . . . . . . . . . . . . . . . . . . . 29

3. Heavy-Duty Truck Tailpipe Emission Controls . . . . . . . . . . . . . . . . . . . 30

4. Emission Control Programs for Buses . . . . . . . . . . . . . . . . . . . . . . . . . . . 32

5. Evaporative Emission Controls . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32

6. Fuel Control Programs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34

A. The Methodology Used to Identify Our List of Mobile Source Air Toxics . . . . . 35

B. How we Applied the Methodology to Identify our List of Mobile Sources Air

Toxics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36

1. Identifying Pollutants Emitted from Mobile Source . . . . . . . . . . . . . . . . 36

2. Using IRIS to Identify Pollutants with Potential Serious Adverse Health

Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

3. List of Mobile Source Air Toxics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39

Chapter 3: Health Effects of Mobile Source Air Toxics . . . . . . . . . . . . . . . . . . . . . . . . . . . . 50

A . Acetaldehyde . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53

B. Acrolein . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54

C. Arsenic Compounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55

D. Benzene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56

E. 1,3-Butadiene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58

F. Chromium Compounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 60

G. Dioxin/Furans . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61

H. Diesel Exhaust: Diesel Particulate Matter and Diesel Exhaust Organic Gases

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62
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1. Cancer Effects of Diesel Exhaust . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63

2. Noncancer Effects of Diesel Exhaust . . . . . . . . . . . . . . . . . . . . . . . . . . . . 64

I. Ethylbenzene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 64

J. Formaldehyde . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65

K. n-Hexane . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 68

L. Lead Compounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69

M. Manganese Compounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70

N. Mercury Compounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72

O. Methanol . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73

O. MTBE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75

P. Naphthalene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77

Q. Nickel Compounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78

R. POM (Polycyclic Organic Matter) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79

S. Styrene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80

T. Toluene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81

U. Xylene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82

Chapter 4: Impacts of Motor Vehicle Emission Control Programs on MSAT Emissions . . 84

A. Previous EPA Studies of Toxics Emissions Inventories . . . . . . . . . . . . . . . . . . . 85

1. The 1999 EPA Motor Vehicle Air Toxics Study . . . . . . . . . . . . . . . . . . . 85

2. The 1996 National Toxics Inventory . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85

B. Impacts of Motor Vehicle Emission Controls on Emission Inventories . . . . . . . 88

1. Overview of Inventory Methodologies . . . . . . . . . . . . . . . . . . . . . . . . . . 89

2. 1999 EPA Motor Vehicle Air Toxics Study . . . . . . . . . . . . . . . . . . . . . . 91

3. VOC Emissions Inventory . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 100

4. Diesel PM Inventory . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101

Chapter 5: Mobile Source Air Toxic Ambient Concentrations and Exposures . . . . . . . . . . 104

A. Survey of Data Ambient Concentrations of Mobile Source Air Toxics. . . . . . . 104

1. Ambient Monitoring . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 104

2. Modeled Ambient Concentrations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109

B. Modeled Inhalation Exposures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 114

1. Methodology for Modeling Inhalation Exposures to Benzene,

Formaldehyde, Acetaldehyde, 1,3-Butadiene and Diesel PM: HAPEMMS3 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115

2. Comparison of Exposure Modeling Results to Modeled Ambient

Concentrations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119

3. Variance in Exposures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 122

4. Impact of Current On-Highway Vehicle Control Programs on Toxics

Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127

5. Sensitivity Analyses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127

C. Exposures in Micro-environments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129

1. Diesel PM . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129

2. Benzene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130
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3. Acetaldehyde . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133

4. Formaldehyde . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133

5. 1,3-Butadiene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133

Chapter 6: Motor Vehicle-Based Controls of Mobile Source Air Toxics . . . . . . . . . . . . . . . . 143

A. Vehicle-Based Technologies that Control Air Toxics . . . . . . . . . . . . . . . . . . . . 143

1. Gaseous Organic Toxics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 143

2. Diesel Particulate Matter and Diesel Exhaust Organic Gases . . . . . . . . 149

3. Metals . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151

B. Emission Control Requirements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 152

1. Tier 2 Standards for Light-Duty Vehicles . . . . . . . . . . . . . . . . . . . . . . . 152

2. Heavy-Duty Engines and Vehicles . . . . . . . . . . . . . . . . . . . . . . . . . . . . 152

C. Potential for Further Reductions from New Vehicle Standards . . . . . . . . . . . . 153

D. Potential for Further Reductions from In-Use Vehicles . . . . . . . . . . . . . . . . . . 154

Chapter 7: Fuel Controls . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 156

A. Industry and product characterization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 156

1. Description of entities subject to the toxics anti-backsliding requirements

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 156

2. Toxics emissions variations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 158

3. Refinery Production of Benzene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 160

B. Toxics inventory and overcompliance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163

C. Costs and Benefits of the Program . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 170

D. Treatment of Incremental Volumes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181

E. Compliance Margins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 186

F. Exclusion of California gasoline . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 188

Chapter 8: Nonroad Mobile Source Air Toxics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 190

A. Overview of Current Nonroad Engine Emission Control Programs . . . . . . . . . 190

1. Land-Based Nonroad Diesel Engines . . . . . . . . . . . . . . . . . . . . . . . . . . 192

2. Small Land-Based SI Engines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 193

3. Large Land-Based Spark-Ignition Engines . . . . . . . . . . . . . . . . . . . . . . 193

4. Marine Engines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 193

5. Locomotives . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 195

6. Aircraft . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 196

7. Recreational Vehicles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 197

8. Fuels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 197

B. Impacts of Nonroad Control Programs on Air Toxics . . . . . . . . . . . . . . . . . . . . 197

1. Nonroad MSAT Baseline Inventories . . . . . . . . . . . . . . . . . . . . . . . . . . 198

2. Emission Reductions from Current Programs . . . . . . . . . . . . . . . . . . . . 198

C. Data Gaps and Uncertainties . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 202
15

Chapter 1: Introduction

The purpose of this Technical Support Document (TSD) is to provide background

information in support of the regulatory decisions for control of mobile source air toxics under

Section 202(l)(2) of the Clean Air Act. Chapter 1 begins with a “roadmap” of the organization of

this document. This is followed by a brief overview of air toxics (what they are, their general

health and environmental effects, and their sources) and a summary of some of the Agency’s air

toxics studies. The remainder of Chapter 1 reviews our mobile source emission control programs

that relate to mobile source air toxics control. 

A. Roadmap of This Document

Unlike the provisions for the control of toxic air pollutants from stationary sources found

in Section 112 of the Act, Section 202(l)(2) does not specify which compounds should be

controlled. Chapter 2 of this TSD describes the approach we took to identify a list of 21 mobile

source air toxics (MSATs). Chapter 3 provides background information about the potential

health impacts of these compounds, including how they enter the environment and how they can

affect human health. 

Chapter 4 provides estimates of highway motor vehicle emissions (“emission

inventories”) of these compounds. We present baseline inventory information for 1996 that

compares motor vehicle inventories to overall national inventories of emissions from both

mobile and stationary sources. This chapter also contains our estimates of the reductions in

emissions we can expect when our current and proposed on-highway emission control programs

are fully phased-in. We estimate that by 2020 highway inventories of certain key MSATs will

decrease by as much as 67 percent from 1990 levels. This chapter also describes the methods we

used to estimate these emission inventories and reductions. 

In Chapter 5 we review existing information on ambient concentrations of toxic

compounds from both monitoring and modeling efforts. We also present estimates of the human

exposure to highway motor vehicle emissions of these compounds. This chapter also describes

the methods we used to estimate the ambient concentrations and exposure, along with associated

limitations and uncertainties.

The next two chapters of this TSD contain our analysis of MSAT controls beyond those

mobile source emission controls that are already in place. Chapter 6 addresses vehicle-based

controls and concludes that our Tier 2 light-duty vehicle and our recently promulgated heavyduty engine standards represent the most stringent controls feasible for motor vehicle emissions

of air toxics at this time. Chapter 7 contains our analysis of fuel-based controls. In it we present

our rationale for our gasoline toxic emission performance requirement. We also discuss the

challenges to other types of fuel-based air toxics controls.

Finally, in Chapter 8 we describe our current nonroad engine emission control programs

and present our estimates of the impacts of these programs on future air toxics inventories. In
1

 Under §112(a)(1) of the Act, major stationary sources are sources that emit, or have the

potential to emit, 10 tons per year or more of any one HAP or 25 tons per year or more of a

combination of HAPs.

2

Area sources are those stationary sources that are not major sources. 

16

this chapter, we also highlight the significant uncertainty and several of the data gaps that exist

with respect to our estimates of toxics emissions from nonroad engines. 

B. Brief Overview of Air Toxics

This section contains a brief overview of what air toxics are, their health and

environmental effects, and their sources. This summary will help ensure that the remaining

discussion is based on a common understanding of the nature of the air toxics problem.

& What are air toxics?

Air toxics, which are also known as “hazardous air pollutants” or HAPs, are those

pollutants known or suspected to cause cancer or other serious health or environmental effects.

They include pollutants like benzene, perchloroethylene, methylene chloride, heavy metals like

mercury and lead, polychlorinated biphenyls (PCBs) and dioxins. While the harmful effects of

air toxics are of particular concern in areas closest to where they are emitted, they can also be

transported and affect other geographic areas. Some can persist for considerable time in the

environment and/or bioaccumulate in the food chain.

& What are the sources of air toxics?

There are literally millions of sources of air toxics, including: major stationary sources1

such as large industrial complexes like chemical plants, oil refineries and steel mills; small (area)

stationary sources2 such as dry cleaners, gas stations, and small manufacturers; and mobile

sources such as cars, trucks, buses, and nonroad vehicles such as construction and farm

equipment.

& What health and environmental effects do air toxics cause?

Hazardous air pollutants can cause many adverse health effects. Many of these

substances are known or suspected to be human carcinogens. Some of these chemicals are

known to have negative effects on people’s respiratory, neurological, immune, or reproductive

systems. Some chemicals pose particular hazards to people with preexisting illnesses, or those of

a certain age or stage in life, such as children or the elderly.

& What are the Urban HAPs? 
17

The urban HAPs are the 33 compounds that have been identified by the Agency in the

Integrated Urban Air Toxics Strategy (IUATS), published July 19, 1999 (64 FR 137, 38706), as

those HAPs posing the greatest threat to human health in the largest number of urban areas. 

These compounds are a subset of the 188 compounds listed in Section 112(b) of the Clean Air

Act. The 33 urban HAPs are listed in Table I-1. The IUATS is described in greater detail in

Section C.2., below.

Table I-1

List of Urban HAPs for the Urban Air Toxics Strategy

Acetaldehyde1 Coke oven emissions Mercury compounds1

Acrolein1 1,2-dibromomethane Methylene chloride

(dichloromethane)

Acrylonitrile 1,2-dichloropropane (propylene

dichloride)

Nickel compounds1

Arsenic compounds1 1,3-dichloropropene Polychlorinated biphenyls

(PCBs)

Benzene1 Ethyl dichloride (1,2-

dichloroethane)

Polycyclic organic matter

(POM)1

Beryllium compounds Ethylene oxide Quinoline

1,3-Butadiene1 Formaldehyde1 2,3,7,8-tetrachlorodibenzo-pdioxine (and cogeners and

TCDF cogeners)1

Cadmium compounds Hexachlorobenzene 1,1,2,2-tetrachloroethane

Carbon tetrachloride Hydrazine Tetrachloroethylene

(perchloroethylene)

Chloroform Lead compounds1 Trichloroethylene

Chromium compounds1 Manganese compounds1 Vinyl chloride

1

 Included in our Mobile Source Air Toxics List (see Chapter 2)

& What are mobile source air toxics?

We use the term “mobile source air toxics,” or “MSATs,” to signify those air toxics

emitted by nonroad engines and on-highway motor vehicles. Section 202(l) of the Act, which

addresses controls for hazardous air pollutants from motor vehicles and motor vehicle fuels, does

not specify which pollutants are to be evaluated as air toxics, other than benzene, formaldehyde,

and 1,3-butadiene. As a result, we must develop a list of compounds to be addressed. Using the

methodology described in Chapter 2, we identified 21 MSATs. These are listed in Table I-2

below. 

Of our 21 MSATs, thirteen are also included on the list of urban HAPs for the Integrated

Urban Air Toxics Strategy (see above). Of the remainder, all but one are specifically identified
18

in the CAA Section 112(b) HAP list. Diesel particulate matter and diesel exhaust organic gases

(DPM+DEOG) is not included in these other two lists because this pollutant was not included by

Congress in the Section 112(b) HAP list and, consequently, was not included in the group of

pollutants that were considered for inclusion in the urban HAP list. Although not specifically

listed in the CAA Section 112(b) list, and consequently with the Urban HAPs, DPM+DEOG is a

particular type of emission which is composed of many listed HAPs, including chemicals that fall

into the group of POM chemicals, as well as some HAP metals and volatile organic compounds. 

In the IUATS, we specifically recognized it as a pollutant of concern in urban areas.

Table I-2

List of Mobile Source Air Toxics (MSATs)

Acetaldehyde4 Ethylbenzene Naphthalene

Acrolein4 Formaldehyde4 Nickel Compounds1,4

Arsenic Compounds1,4 n–Hexane POM3

Benzene4 Lead Compounds1,4 Styrene

1,3-Butadiene4 Manganese Compounds1,4 Toluene

Chromium Compounds1,4 Mercury Compounds4 Xylene

Dioxin/Furans2,4

Diesel Particulate Matter &

Diesel Exhaust Organic Gases

MTBE

1

 Although the different metal compounds differ in their toxicity, the on-road mobile source

inventory contains emissions estimates for total metal compounds (i.e., the sum of all forms).

2

 This entry refers to two large groups of chlorinated compounds. In assessing their cancer risks,

their quantitative potencies are usually derived from that of the most toxic, 2,3,7,8-

tetrachlorodibenzodioxin.

3

 Polycyclic Organic Matter includes organic compounds with more than one benzene ring, and

which have a boiling point greater than or equal to 100 degrees centigrade. A group of seven

polynuclear aromatic hydrocarbons, which have been identified by EPA as probable human

carcinogens (benz(a)anthracene, benzo(b)fluoranthene, benzo(k)fluoranthene, benzo(a)pyrene,

chrysene, 7,12-dimethylbenz(a)anthracene, and indeno(1,2,3-cd)pyrene) are sometimes used as

surrogates for the larger group of POM compounds.

4

 Although the different metal compounds differ in their toxicity, the on-road mobile source inventory

contains emissions estimates for total metal compounds (i.e., the sum of all forms).

& How are air toxics from mobile sources formed?

Mobile source air toxics come from four sources. First, some air toxics are present in fuel

and are emitted to the air when the fuel evaporates or passes through the engine unburned. 

Benzene, for example, is a component of gasoline. Cars emit small quantities of benzene in

unburned fuel, or as vapor when gasoline evaporates. Second, mobile source air toxics are

formed through engine combustion processes. A significant amount of automotive benzene

comes from the incomplete combustion of compounds in gasoline such as toluene and xylene
3

EPA, 1993. Motor Vehicle-Related Air Toxics Study. Report No. EPA 420-R-93-005. 

This report can be accessed at http://www.epa.gov/otaq/toxics.htm.

19

that are chemically very similar to benzene. Like benzene itself, these compounds occur

naturally in petroleum and become more concentrated when petroleum is refined to produce high

octane gasoline. DPM+DEOG emissions, as well as formaldehyde, acetaldehyde, and

1,3-butadiene, are also by-products of incomplete combustion. Third, some compounds, like

formaldehyde and acetaldehyde, are also formed through a secondary process when other mobile

source pollutants undergo chemical reactions in the atmosphere. Finally, metal air toxics result

from engine wear or from impurities in oil or gasoline. They can also be present in fuel

additives.

C. Other Air Toxics Activities

This section describes the most important of these research and regulatory programs. The

first of these is the study required pursuant to Section 202(l) of the Act. That section calls on

EPA to study the need for and feasibility of controlling toxic air pollutants associated with motor

vehicles and motor vehicle fuels. The study is to focus on those categories of emissions that pose

the greatest risk to human health or about which significant uncertainties remain. The Act

specifies that, at a minimum, the study focus on emissions of benzene, formaldehyde, and 1,3-

butadiene. This study was completed in 1993, and is summarized below. An update of the

inventory and exposure data was completed in 1999, and is also summarized below.

In addition, as we developed and prepared this mobile source air toxics rule, we worked

in the context of two other important activities that are ongoing at the Agency. These are EPA’s

Integrated Urban Air Toxics Strategy (IUATS) development and the National Air Toxics

Assessment (NATA) activities. Because these two programs are also important parts of our

efforts to reduce toxics emissions from all sources, this section contains a brief summary of their

key components as well as a description of the Report to Congress that was prepared pursuant to

Section 112(k) of the Act. Interested readers are encouraged to visit EPA’s Toxics website for

more information about these programs (www.epa.gov/otaq/toxics.htm). Finally, EPA’s Office

of Research and Development has developed a draft Air Toxics Research Strategy (ATRS) to

assist in improving our understanding of air toxics and to provide a framework to help manage

air toxics research objectives and priorities. The ATRS is described briefly below.

1. Motor Vehicle Air Toxics Studies

In 1993, EPA released a study of motor vehicle-related air toxics in compliance with

Section 202(l)(1) of the Clean Air Act.3

 The study provided estimates of motor vehicle

emissions of several pollutants believed to pose the greatest risk to public health, including

benzene, formaldehyde, and 1,3-butadiene, as required by the Act, as well as acetaldehyde, diesel

particulate matter, gasoline particulate matter, and gasoline vapors. Exposure and risk were

evaluated for four different years: 1990, 1995, 2000, and 2010. A total of three scenarios were
4

Peer review comments on the 1993 study can be accessed at

http://www.epa.gov/otaq/toxics.htm

5

EPA 1998. Environmental Protection Agency, Carcinogenic Effects of Benzene: An

Update, National Center for Environmental Assessment, Washington, DC. 1998. This report

can be accessed at http://www.epa.gov/ncea/benzene.htm.

6

EPA 1998. Environmental Protection Agency, Health Risk Assessment of 1,3-Butadiene.

EPA/600/P-98/001A, February 1998. This report can be accessed at

http://www.epa.gov/ncea/butadiene.htm

7

EPA. 1999. Health Assessment Document for Diesel Emissions: SAB Review Draft.

EPA/600/8-90/057D Office of Research and Development, Washington, D.C. The document is

available electronically at www.epa.gov/ncea/diesel.htm.

8

Analysis of the Impacts of Control Programs on Motor Vehicles Toxics Emissions and

Exposure in Urban Areas and Nationwide (Volumes 1 and 2), November 1999. EPA420-R-99-

029/030

20

modeled to explore the exposure and risk attributable to motor vehicle emissions: a baseline case

reflecting motor vehicle related Clean Air Act requirements, expanded use of reformulated

gasoline, and expanded adoption of the California LEV standards. The study also explored air

toxics emissions from alternative fuel vehicles and nonroad engines, but for the baseline cases

only and not for control scenarios. It should be noted that this study did not address whether to

promulgate air toxics standards or suggest what those standards should be. That discussion was

deferred to a future rulemaking under Section 202(l)(2). An evaluation of the costs or benefits of

the control scenarios examined for on-highway engines and vehicles was also deferred to a future

Section 202(l)(2) rulemaking. 

We sought peer review of this study in 1994.4

 The comments from the peer review

included suggestions for improving EPA’s exposure modeling and risk assessment methodology. 

In response to these comments, EPA updated its exposure model for motor vehicle-related air

toxics. Also, since 1993, significant new information on vehicle emission rates has been

developed as part of the Auto/Oil program, the development of the Complex Model for

reformulated gasoline, CARB test programs, and other sources, and much more is known about

the impact of fuel properties on toxic emissions. Furthermore, EPA has developed new

programs, such as the National Low Emission Vehicle (NLEV) program and Tier 2 standards,

which have significant effects on projections of toxic emissions and exposure. Finally, EPA has

released an updated cancer risk assessment for benzene, a draft reassessment for 1,3-butadiene,

and an assessment for diesel exhaust emissions.5, 6, 7

In light of this new information, and in response to peer review comments, EPA updated

the estimates of emissions and exposure contained in the 1993 study.8

 A slightly different list of

compounds was studied, and a different set of scenarios. Specifically, the updated study
21

considers exposure and risk for six air toxics (acetaldehyde, benzene, 1,3-butadiene,

formaldehyde, MTBE, and diesel PM) for four years (1990, 1996, 2007, and 2020). Different

control scenarios were modeled to reflect the regulatory controls under consideration at that time. 

Instead of the baseline and expanded use of reformulated gasoline, and expanded adoption of the

California LEV standards, scenarios were chosen to reflect some of the options under

consideration for both EPA’s Tier 2 motor vehicle emission standards and gasoline sulfur

controls rule, and the mobile source air toxics rule and the 2004 heavy-duty engine controls. 

Like the 1993 study, however, the 1999 update considered only on-highway vehicle emissions

and not nonroad emissions. Finally, while the 1993 study evaluated only nationwide exposure

and risk, the 1999 update examined exposure at the national level as well as for ten urban areas

and 12 geographic regions. Providing even more detail, results were also reported by

demographic group. As of the date of this Technical Support Document, EPA is still working on

an update of the 1993 risk study. This update will be submitted for peer review and finalized in

the next twelve to eighteen months and will also reflect comment received during the peer review

process of the original 1993 study.

In the above air toxics studies, there are limitations in how ranges of exposures are

modeled or characterized. For instance, the screening models the Agency has used do not

consider ‘hotspots’ for elevated air toxics concentrations. For this reason, EPA has not been able

to conduct a complete exposure assessment. Additional discussion of the limitations of these

studies are included in Chapter 5 of this Technical Support Document. The Agency also needs to

do more work on considering the costs and performance levels of pollution controls on air toxics.

These activities will be included in the proposed Technical Analysis Plan discussed later in this

TSD. Finally, the peer review comments of the 1999 emissions and exposure study contained

many suggestions on how to improve the methodology and modeling techniques. These

comments will also be taken into account as part of the Technical Analysis Plan.

2. Integrated Urban Air Toxics Strategy

EPA’s Integrated Urban Air Toxics Strategy (IUATS), published July 19, 1999 (64 FR

137, 38706), focuses on reducing the human health threats of air toxics in urban areas. In urban

areas, toxic air pollutants raise special concerns because sources of emissions and people are

concentrated in the same geographic areas, leading to large numbers of people being exposed to

the emissions of many HAPs from many sources. In the IUATS, EPA outlined future actions

that we plan to take to reduce emissions of air toxics and improve our understanding of the health

threats posed by air toxics in urban areas. The over-arching goal for the IUATS is to reduce

cancer and noncancer risks associated with air toxics in urban areas. Also, because air toxics in

urban areas may threaten the health of some people more than others, depending on factors such

as where they live in relation to toxic sources, 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 low-income communities). 

The goals of the Strategy reflect both the statutory requirements stated in section 112(k)
22

of the Act and the goals of EPA’s overall air toxics program. These goals consist of the

following:

& Attain a 75 percent reduction from 1990 incidence of cancer attributable to

exposure to HAPs emitted by stationary sources. This is relevant to all HAPs

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.

& Attain a substantial reduction from 1990 levels in public health risks posed by

HAP emissions from area sources. This includes health effects other than cancer

posed by all HAPs (e.g., birth defects and reproductive effects). Reductions can

be the result of actions by Federal, State, local and/or Tribal governments,

achieved by any regulations or voluntary actions.

& Address disproportionate impacts of air toxics hazards across urban areas. This

will necessarily involve consideration of both stationary and mobile source

emissions of all HAPs, as well as sources of HAPs in indoor air. EPA intends 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 low-income communities)

As a first step in the IUATS, EPA identified 33 of the 188 Section 112(b) toxic air

pollutants that EPA concluded pose the greatest threat to public health in the largest number of

urban areas (see Table I-1, above). It should be noted that while diesel exhaust emissions are not

included as a specific pollutant in the list of 33 urban HAPs, many of the hazardous constituents

of diesel exhaust emissions are included among the list of 33, and it is a pollutant that we

identified in the IUATS as a concern in urban areas.

 The IUATS outlines several steps that EPA will take to reduce urban air toxics and

address risks, and as part of the IUATS, EPA has prepared an Action Plan. The key components

of the Action Plan are as follows.

& Achieve reductions through regulatory actions and related projects. The strategy

presents a framework for reducing air toxics emissions from all types of sources

found in urban areas, including mobile sources, major industrial sources, and

smaller stationary sources. Today’s action contains mobile source-specific toxics

regulations. We are also developing programs to reduce emissions from several

area source categories (i.e., smaller commercial and industrial operations), and

plan to complete regulations to address the new 13 area sources identified in the

IUATS by 2004. Regulations are already under development or exist for the 16

other area source categories listed in the IUATS.
9

It should be noted that NATA will estimate only exposure to diesel particulate matter,

and not risk.

23

& Collaborate with interested parties. We are working with state, local, and tribal

agencies, environmental groups, environmental justice communities, and affected

industries, including small businesses, to assure that any actions under the IUATS

are responsive to health concerns while promoting fairness, encouraging urban

redevelopment, and minimizing regulatory burdens.

& Education and outreach efforts. We will make an effort to inform stakeholders

about the IUATS and obtain their input on designing programs to implement it.

3. National Air Toxics Assessment Activities

National Air Toxics Assessment (NATA) activities are an important component of the

IUATS and EPA's overall goal of reducing exposure to air toxics. These assessment activities

include air toxics monitoring, emissions inventory development, exposure modeling, research

activities, and risk assessment. Over time, these activities will help us set program priorities,

characterize risks, and track progress toward reducing exposure to air toxics. Specifically, our

current NATA activities include expanding air toxics monitoring, improving and periodically

updating emissions inventories, periodically conducting national- and local-scale air quality,

multimedia and exposure modeling, characterizing risks associated with air toxics exposures, and

continued research on health and environmental effects and exposures to both ambient and

indoor sources of air toxics.

As part of these NATA activities, EPA is now conducting an initial national-scale

assessment to demonstrate our approach to characterizing air toxics risks nationwide. This initial

screening-level assessment will help to characterize the potential health risks associated with

inhalation exposures to the 33 urban HAPs and diesel particulate matter.9

 While such a

broad-scale assessment is necessarily limited in the scope of the risks that it can assess

quantitatively, and by the uncertainties inherent in the various types of data and methods

currently available, it represents an important step in characterizing air toxics risks nationwide.

Our initial national-scale assessment includes four major steps:

& Compile a national emissions inventory of 1996 air toxics emissions from outdoor

sources of air toxics emissions. 

& Estimate 1996 air toxics ambient concentrations across the continental United

States (and Puerto Rico and the Virgin Islands) for the 33 urban HAPs and diesel

PM; compare modeled ambient concentrations with monitor values.

& Estimate 1996 population exposures across the continental United States (and

Puerto Rico and the Virgin Islands) to the 33 urban HAPs and diesel PM.
24

& Characterize potential public health risks due to inhalation of the 33 urban HAPs. 

In describing what national-scale assessment will include, it is also important to note the

potentially important sources and pathways of risks to public health that are beyond the scope of

this quantitative assessment. For example, while we recognize that indoor sources of air toxics

emissions likely contribute substantially to the total exposures that people experience for a

number of these HAPs, assessing these indoor sources of exposure cannot be done on a national

scale at this time. Further, for a subset of these HAPs (i.e., those that persist and bioaccumulate

in the environment), dietary exposures (e.g., eating contaminated fish) likely contribute much

more to the total risk associated with exposure to these pollutants than do the inhalation

exposures that will be addressed in this assessment. These and other important aspects of total

population exposures to air toxics will be addressed more fully over time as part of our NATA

activities as more comprehensive data and assessment tools become available.

Additionally, NATA activities include other key activities that will support further risk

characterizations on the local and national level in the future. These include:

& Developing and implementing a plan to characterize the concentrations of ambient

air toxics through an expanded monitoring network. Data from existing state and

local air monitoring programs will be compiled to summarize our current

knowledge about ambient concentrations of air toxics. Existing ambient air toxics

monitoring data will be compiled and summarized and then used as a "reality

check" on model output. 

& Improving existing monitoring networks, guided by data analysis and model

predictions, to improve the collection of ambient concentration data for future

model evaluations. As the monitoring program matures, trend sites will be

established to assess the effectiveness of all of our air toxics control programs. 

& Evaluating air toxics on a more local scale (e.g., an urban area) using more refined

air quality modeling tools that factor in specific local information such as terrain

(e.g., mountainous or flat) and local weather patterns. The results of national and

local-scale modeling can be compared to provide a more complete context for the

evaluation of air toxics. 

& Comparing air toxics inventories from 1990, 1996, and 1999 on a

toxicity-weighted basis to help inform assessments of progress toward meeting the

IUATS risk reduction goals. 

& Recommending tools to state, local and tribal regulatory agencies for evaluating

air toxics concentrations, exposures and risk. This will include a comparison of

the results from national-scale models to those from more local-scale models. 

While there continue to be significant uncertainties and gaps in methods, models, and
25

data that limit our ability to assess risks to public health and the environment associated with

exposures to air toxics, continued research will enable future assessment activities, both at the

national screening-level and at more local refined levels, to yield improved assessments of

cumulative air toxics risks.

4. Urban Air Toxics Reports to Congress

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

Reports to Congress on actions taken under the Act that reduce the risk to public health posed by

the release of hazardous air pollutants from area sources. The first of these two reports was

issued on September 15, 2000 (EPA-453/R-99-007, July 2000). That report expands on much of

the information provided in IUATS, such as the methodology for developing the emissions

inventory, identifying the 33 urban hazardous air pollutants (urban HAPs), and identifying the

area source categories that will be subject to regulation. The report also 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, the

Report also provides a very detailed discussion of 13 research needs to address in achieving the

goals of the IUATS. These needs were identified in the following areas: exposure assessment,

health effects, dose-response assessment, risk assessment, risk characterization and risk

management. The research needs identified in the Report provide a valuable platform for

development of the Air Toxics Research Strategy described below. The Report also provides a

summary of ongoing EPA activities to address those needs. 

5. Air Toxics Research Strategy

EPA’s Office of Research and Development is developing an Air Toxics Research

Strategy (ATRS) to provide information to guide the development of the Agency’s air toxics

research program over the next five to ten years. In particular, it provides an air toxics risk

framework, a list of key overarching research questions within that framework, a set of summary

research needs associated with each research question, the rationale for the strategy and guiding

principles and four groups of air toxics that would be the focus of research for the next 10 years. 

The Mobile Source Air Toxics identified in today’s action are included among the four groups of

air toxics identified in the ATRS (e.g., aldehydes, halides, metals, and hydrocarbons/POM). The

hydrocarbon/POM category includes benzene and diesel exhaust as well as several other gaseous

air toxics. The ATRS will undergo SAB review in 2001.

D. Description of Motor Vehicle Air Pollution Control Programs

In this section, we present a short history of some of EPA’s key programs addressing car,

truck, and bus tail pipe emission controls, evaporative emission controls, and fuel controls. 

1. Mobile Source Control Programs and the Clean Air Act
26

Our national mobile source emission control program began in the early 1970s, when we

issued the first sets of motor vehicle standards to reduce air pollution. These early standards

focused on emissions of hydrocarbons (HC), nitrogen oxides (NOx), and carbon monoxide (CO). 

While they were not designed to address toxics emissions specifically, these standards

nevertheless helped to reduce the emission of toxics. Catalytic converters designed to reduce HC

and CO emissions also reduce gaseous air toxics, and the removal of lead from gasoline to permit

the use of catalytic converters (used to meet the HC and NOx standards) led to a significant

reduction in the inventory of toxic lead emissions.

More recently, the 1990 Clean Air Act Amendments added new elements to our mobile

source emission control programs. Like the earlier versions of the Act, the primary focus of the

mobile source provisions, contained in Title II of the Act, continues to be directed at attainment

of the National Ambient Air Quality Standards (NAAQS), primarily for ozone, CO, nitrogen

dioxide, and particulate matter (PM). The CAA Amendments led to a set of EPA programs that

focus on highway motor vehicles (passenger cars, light-duty trucks, and heavy duty trucks and

truck engines), nonroad engines, and their fuels. Section 202(l), by contrast, calls on us to focus

specifically on controls for hazardous air pollutants emitted from motor vehicles and their fuels. 

Our mobile source emission control programs can take several forms. In some cases, the

instructions in the Clean Air Act are very specific and prescribe specific levels of control. In

these cases, our role is to promulgate these controls within fairly precise boundaries. For

example, §202(g) of the Act sets out specific emission limits for Tier 1 controls for motor

vehicles; these requirements went into effect beginning in 1994. Similarly, §211(k) of the Act

also sets out specific requirements for gasoline fuel reformulation for certain areas of the country. 

In other cases, the requirements of the Act are broader and direct us to consider controls

in certain areas but give us discretion in determining the appropriate level. For example,

§202(a)(1) of the Act directs us to “prescribe (and from time to time revise) ... standards

applicable to the emission of any air pollutant from any class or classes of new motor vehicles or

new motor vehicle engines, which ... cause, or contribute to, air pollution which may reasonably

be anticipated to endanger public health or welfare.” Section 202(a)(3)(A)(i) specifies that those

regulations “shall contain standards which reflect the greatest degree of emission reduction

achievable through the application of technology which ... will be available for the model year to

which such standards apply, giving appropriate consideration to cost, energy, and safety factors

associated with the application of such technology.” This type of broad language is echoed in

other sections of Title II, notably those concerning fuels (§211(c)(1)), nonroad engines (§213)

and toxics (§202(l)).

In addition to developing traditional regulatory programs, we have also engaged in

collaborative efforts with industry, states, and other outside parties using our authorities under

the Clean Air Act. An example is the national low-emission vehicle (NLEV) program, in which

we worked with the auto industry and the Northeast states to develop an innovative, voluntary

program to put cleaner cars on the road before they could be mandated by programs developed
10 Our programs achieve VOC reductions through standards that limit HC, NMHC, or NMOG. For

gasoline vehicles, the slight technical distinctions among these ways of expressing emissions can generally be

ignored.

27

under the Clean Air Act. Another example is our reformulated gasoline program, where an early

part of the regulatory process consisted of a broad “regulatory negotiation” during which many

stakeholders participated in crafting the basic elements of the ultimate program.

The remainder of this chapter briefly describes our key mobile source emission control

programs and their relationship to air toxics emission control.

2. Passenger Car Tailpipe Emission Controls 

Since 1970, emission limits for hydrocarbons (HC), oxides of nitrogen (NOx), and carbon

monoxide (CO) from cars have been steadily declining. The history of HC control is particularly

important to today’s rule because many of the gaseous toxics from motor vehicles and their fuels

are hydrocarbons and are thus controlled through controls of HC. (HC emissions are a large

component of volatile organic compounds (VOC) emissions; the two terms are generally used

interchangeably in the context of motor vehicle emissions.)

Before our regulations, cars emitted 9 grams per mile (gpm) HC, or more. Our HC

emission standards in the 1970s and 1980s cut these levels by more than an order of magnitude,

to a level of 0.41 gpm in 1980. In 1991, we finalized Tier 1 controls for light-duty vehicles and

light-duty trucks to be phased in from 1994 to 1996 (56 FR 25724). In 1998, we developed an

innovative, voluntary nationwide program to make new cars, called National Low Emission

Vehicles (NLEV), significantly cleaner than Tier 1 cars (63 FR 926). The NLEV program went

into effect in the Northeast states in 1999 and will go into effect in the rest of the country in

2001. We recently finalized the Tier 2/Gasoline Sulfur control program with stringent NOx and

non-methane organic gas (NMOG) standards for all passenger vehicles (see Chapter 6 of this

TSD for a more detailed discussion of the Tier 2/Sulfur control program). Table I.B-1 illustrates

the declining standards through the NLEV program that have resulted in VOC and air toxic

reductions from car exhaust in the 1970s through the 1990s.10

Table I.B-1 

Hydrocarbon (HC) Exhaust Emission Standards for Light-Duty Vehicles (gpm) 

Year 1972 1975 1980 1994 1999

HC 3.4 1.5 0.41 0.311 0.092

1 The 1994 standard is a NMHC standard. 

2 The 1999 standard is a NMOG standard.

We also control HC emissions from cars, and thus emissions of gaseous toxics, through a

number of other standards and programs. For example, our requirements controlling carbon
28

monoxide emissions at cold temperatures also have an important effect in reducing HC emissions

at cold temperatures, since strategies that reduce cold CO also reduce cold HC (through such

strategies as better control of the air/fuel ratio and quicker catalyst “light-off”). Another example

is the Supplemental Federal Test Procedure and standards, finalized in 1996, which better

capture actual driving conditions in the test procedures for our control programs (61 FR 54852). 

We also have programs that track how cars are performing in use. One program is the “on-board

diagnostics” (OBD) program, which is required for all cars and light-duty trucks beginning in

1994 (58 FR 9468). Another such program is our state-run inspection and maintenance (I/M)

program, in which the individual state programs check whether the emission control system on a

vehicle is working correctly. I/M programs are currently in place in over 150 areas (57 FR

52950).

3. Heavy-Duty Truck Tailpipe Emission Controls

We have controlled emissions from heavy-duty engines and vehicles since 1984. These

standards are expressed in terms of grams of pollutant emitted for horsepower-hour of work done

by the engine (g/bhp-hr). As of 1998, new heavy-duty truck engines must meet standards of 4

g/bhp-hr NOx, 1.3 g/bhp-hr HC, and 0.10 g/bhp-hr PM. In a 1997 rulemaking, we finalized

more stringent standards for diesel trucks only. These standards will become effective in 2004

(62 FR 54695). We recently issued a final rule to reaffirm these standards for diesel trucks for

2004, and to adopt separate standards for gasoline trucks (65 FR 59896; see below, Table I.B-3). 

Table I.B-2 illustrates the declining standards for NOx, PM and HC for heavy-duty trucks since

1984. 

Table I.B-2

Heavy-Duty Standards for Diesel and Gasoline1

 Engines (g/bhp-hr)

Year 1984 1988 1990 1991 1993 1994 1996 1998 2004 2005

NOX 10.7 –> 6.0 5.0 –> 4.0 2.42 1.03

PM N/A 0.60 –> 0.25 –> 0.10 –>

HC 1.3 –> 2.42 1.03

1. Standards for Gasoline Engines are the same as for diesel, until 2004. See Table I.B-3 for gasoline vehicle

standards that will be applicable to complete HD gasoline vehicles beginning in 2005

2. This is a combined NMHC + NOx standard for heavy-duty diesel engines only. Typically, HC emissions for HD

diesel engines are in the 0.3 g/bhp-hr range or lower. 

2. This is a combined NMHC + NOx standard for heavy-duty gasoline engines only. HC emissions for HD

gasoline engines are expected to be in the 0.3-0.4 g/bhp-hr range. 
29

Table I.B-3

Heavy-Duty GasolineVehicle Standards for 2005

Gross Vehicle Weight NOX HC1

8,000-10,000 lbs 0.9 gpm 0.28 gpm

10,001-14,000 lbs 1.0 gpm 0.33 gpm

14,001 lbs and above See Table I.B.2

1. The standards for HC is in the form of NMOG standards. Manufacturers have the option to submit test

data in the form of NMHC emissions.

In our recent final rule for 2004 and later heavy-duty engines and vehicles, we also made

improvements to the test procedure for heavy-duty diesel engines, including a “not-to-exceed”

(NTE) test and a steady-state certification test to ensure that emissions are met under a wide

range of operating conditions. This program also extended the on-board refueling vapor recovery

(ORVR) program (see discussion, Section 1.B.5, below) to heavy-duty gasoline engines

weighing between 8,500 and 10,000 lbs (gross vehicle weight). Also, we extended requirements

for on-board diagnostic (OBD) systems to more diesel and gasoline fueled vehicles to help

identify any possible failure of components of the emission control system.

 Our proposed Heavy-Duty Engine/Diesel Sulfur (2007) program, published June 2, 2000

(65 FR 35430), would set stringent exhaust emission standards for heavy-duty engines and

vehicles beyond the 2004 levels starting in 2007, and require reductions in sulfur levels from onroad diesel fuel starting in 2006. We describe this proposed program in greater detail in Chapter

6 of this TSD. In general, we project that the proposed standards would cut HC emission by

about one-third, and diesel PM emissions by 90 percent. 

4. Emission Control Programs for Buses

In 1993, we finalized the Urban Bus Retrofit/Rebuild Program which is intended to

reduce the ambient levels of PM in urban areas (58 FR 21359). The program is limited to buses

operating in metropolitan areas with 1980 populations of 750,000 or more, and applies only to

1993 and earlier model year buses whose engines are rebuilt or replaced after January 1, 1995. It

requires that these urban buses be retrofitted with improved PM emission controls. 

Approximately 40 urban areas are affected. In addition, in 1993, we finalized more stringent PM

standards that apply to new urban buses (58 FR 15781) as indicated in Table I.B-4. 

Table I.B-4

New Urban Bus Standards (g/bhp-hr)

Year 1993 1994 1996

PM 0.10 0.07 0.05
30

5. Evaporative Emission Controls

Evaporative and refueling emissions are a significant portion of the HC emissions

inventory for gasoline-fueled vehicles and trucks (in 1990 more than half of the VOC emissions

from light-duty vehicles were evaporative emissions). In 1971, we began testing motor vehicles

for evaporative emissions by subjecting test vehicles to typical drive and park conditions. The

test procedure measures emissions from fuel evaporation during a simulated parking experience

(diurnal emissions) and immediately following a drive (hot soak emissions). Currently, we

measure diurnal emissions over a three-day test and also a supplemental two-day test. In 1993,

we finalized revised evaporative emission test procedures which apply to light-duty and heavyduty gasoline vehicles. These procedures were fully phased-in as of 1999 (58 FR 16002). We

expect the test procedure to ensure that properly functioning vehicles will effectively control

evaporative emissions for most in-use events. The 1993 rule also addressed fuel spitback during

refueling with a vehicle test to ensure that no spillage occurs when a vehicle is refueled at a rate

of up to 10 gallons (37.9 liters) per minute.

Our current evaporative emission and refueling spitback standards are shown in Table

I.B-5 (the Tier 2/Gasoline Sulfur rule further reduced evaporative emission standards, and our

new requirements for heavy-duty engines will also reduce evaporative emissions standards for

heavy-duty gasoline trucks, as described in Chapter 6 of the TSD).

Table I.B-5

Current Light Duty Vehicles, Light Duty Truck, and Heavy-Duty Gasoline Vehicle

Evaporative Hydrocarbon and Refueling Spitback Standards 

Evaporative Hydrocarbons Refueling

Spitback

Category 3 Diurnal + Hot (grams/test)

Soak (grams/test)

2 Diurnal + Hot

Soak (grams/test)

Running Loss

(grams/mile)

Light-Duty1 2 2.5 0.05 1.0 

Heavy-Duty to

14,000 lbs GVW

3.0 3.5 0.05 1.0

Heavy-Duty

above 14,000 lbs

GVW

4.0 4.5 0.05 ---

1. Note that we have different standards for light-duty trucks with fuel tanks over 30 gallons.

We have also finalized on-board refueling vapor recovery (ORVR) requirements for

light-duty gasoline vehicles (59 FR 16262), and recently extended them to heavy-duty gasoline

vehicles between 8,500 and 10,000 lbs (gross vehicle weight) (65 FR 59896). ORVR is a

nationwide program for capturing refueling emissions by collecting vapors from the vehicle gas

tank during refueling and storing them in the vehicle. The gas tank and fill pipe are designed so

that when refueling the vehicle, fuel vapors in the gas tank travel to an activated carbon packed
31

canister, which adsorbs the vapor. When the engine is in operation, it draws the gasoline vapors

into the engine intake manifold to be used as fuel. Table I.B-6 indicates the phase-in periods for

ORVR for different size gasoline vehicles.

Table I.B-6

On-Board Vapor Recovery for Gasoline Vehicles Phase-In Periods and Standard

Category Phase-In Standard

Light-Duty Vehicles 1998-2000

0.2 g/gallon Light Light-Duty Trucks (to 6,000 lbs

 gross vehicle weight)

2001-2003

Heavy Light-Duty Trucks (6,000 to 8,500 lbs

gross vehicle weight)

2004-2006

Heavy-Duty Gasoline Vehicles (to 10,000 lbs

gross vehicle weight)

2005-2006

6. Fuel Control Programs

The emissions that come out of a vehicle depend greatly on the fuel that goes into it. Fuel

composition and type are critical factors in the clean vehicle equation. Since 1990, the Clean Air

Act explicitly recognizes that changes in fuels as well as in vehicle technology must play a role in

reducing air pollution from motor vehicles. 

One of the first and most successful programs to control harmful motor vehicle emissions

by changing fuel composition was the removal of lead from gasoline. The lead phase-out began

in the mid-1970s in order to enable the use of catalytic converters on cars to meet early HC

standards. This resulted in dramatic reductions in ambient lead levels and alleviated many

serious environmental and human health concerns associated with lead pollution. The Clean Air

Act prohibited the introduction of gasoline containing lead or lead additives into commerce for

use as a motor vehicle fuel after December 31, 1995. In February 1996, we finalized an action to

implement the ban on leaded gasoline (61 FR 3832). The removal of lead from gasoline has

essentially eliminated motor vehicle emissions of this highly toxic substance. The reduction and

virtual elimination of lead from gasoline has resulted in significant risk reduction to the public

and environment.

In 1990 and 1991, we promulgated regulations to reduce the volatility of gasoline (the

basic regulations were promulgated at 55 FR 23658). Like the vehicle-based evaporative and

refueling emission control programs discussed above, our gasoline volatility program has

reduced VOC emissions by reducing evaporation of gasoline.
11The list of databases and recent studies we used is provided at the end of this chapter in

Appendix I.

32

The reformulated gasoline (RFG) program (59 FR 7716) resulted from the mandate in the

1990 Clean Air Act Amendments requiring areas of the country with the worst ozone problems

to use gasoline that is reformulated to help improve air quality. The RFG program, which began

January 1, 1995, contains two phases. On an average basis under the Complex Model, Phase I 

required emissions reductions from 1990 conventional gasoline baseline gasoline of 16.5 percent

for air toxics, 36.6 or 17.1 percent for VOC (depending on the region of the country), and 1.5

percent for NOx (40 CFR 80.41). RFG must also contain a minimum oxygen content of 2

percent by weight, a maximum benzene content of 1 percent by volume, and no lead, manganese,

or other heavy metals. At its inception, RFG was required in the nine worst ozone areas, with the

provision that other ozone nonattainment areas could voluntarily opt in to the program. 

Currently 17 states and the District of Columbia participate in the program, with RFG

representing about 30 percent of the gasoline sold in the United States. Phase II of the program

began January 1, 2000, and contains more stringent emissions reduction requirements. On an

average basis, air toxics must be reduced by 21.5 percent, VOC by 27.4 or 29.0 percent

(depending on the region of the country), and NOx by 6.8 percent (summertime) and 1.5 percent

(wintertime) from the 1990 conventional gasoline baseline (40 CFR 80.41).

Chapter 2: Identification of Mobile Source Air Toxics 

(MSATs)

Introduction

There are hundreds of compounds and elements known to be emitted from passenger

cars, on-highway trucks, and various types of nonroad equipment, several of which may have

serious effects on human health and welfare. In recognition of this fact, Congress instructed

EPA, in Section 202(l)(2) of the Act, to set standards for hazardous air pollutants from motor

vehicles and their fuels. Except for benzene and formaldehyde which are specifically mentioned

in 202(l)(2), the Act does not specify the compounds that should be considered for control. 

Therefore, the first step in developing a mobile source air toxics control program is to identify

the compounds that should be evaluated for possible control measures.

This chapter describes the methodology we used to identify our list of 21 mobile source

air toxics (MSATs). A more detailed description of the health effects information for these

compounds is provided in Chapter 3.

A. The Methodology Used to Identify Our List of Mobile Source Air Toxics

 

EPA developed the list of MSATs by first searching for lists of compounds in all

available databases and recent (i.e., ten years old or less) studies11 that speciated the emissions
12A further discussion of the potential cancer and noncancer risks, and other doseresponse information for each MSAT can be found in Chapter 3 of the TSD.

33

from motor vehicles and their fuels. Data for vehicles and engines more than ten years old are

considered to be outdated and thus are judged not to be representative of current emissions. We

then compared the lists of compounds to the list of toxic compounds in EPA’s Integrated Risk

Information System (IRIS) database. IRIS is a database of compounds that identifies EPA’s

consensus scientific judgment on the characterization of the potential serious adverse health

effects that may result from a lifetime exposure to the listed compounds. Where feasible, IRIS

classifies the carcinogenic potential of the compounds and provides the noncancer reference

concentrations or doses, RfC, or RfD, respectively. IRIS also lists compounds for which the

Agency has reviewed currently available information and concluded that 1) there are insufficient

data to calculate an RfC or RfD for the noncancer hazard potentially posed by the compound(s),

and/or 2) there is an absence of sufficient information to identify a cancer hazard. 

In our original analysis, we compared the lists of compounds identified in the motor

vehicle emission databases and studies with the toxic compounds listed in IRIS and we identified 

21 compounds, each of which have the potential to cause serious adverse health effects as

reflected in IRIS (e.g., these compounds are known, probable, or possible human carcinogens

and/or pollutants for which the Agency has calculated an RfC or RfD).12 We therefore consider

each of these compounds to be MSATs. EPA data suggests that nonroad engines and on-road

vehicles emit the same pollutants as motor vehicles and their fuels, so we characterize this list as

a list of toxic compounds from mobile sources.

We also compared the lists of compounds emitted from motor vehicles and their sources

with other lists or sources of information on toxic substances, and identified two additional

substances (propionaldehyde and 2,2,4-trimethylpentane) for which we requested comment. A

summary of the public comments received on our MSAT list and our responses is provided

below.

B. How we Applied the Methodology to Identify our List of Mobile Sources Air

Toxics

In the sections that follow, we describe in more detail our methodology for identifying the

list of MSATs and how we applied this methodology.

1. Identifying Pollutants Emitted from Mobile Source 

In identifying a list of MSATs, EPA compiled all available databases and recent studies

(i.e., ten years old or less) that contain information on the various species of compounds emitted

from motor vehicles and their fuels. There are several limitations to these speciation studies that

should be noted. To identify the species of compounds emitted from motor vehicles, vehicles

and engines are tested on a dynamometer, which is basically a mechanical treadmill for the

vehicle/engine. The test vehicle/engine is run through a set pattern of starts, stops, idle, and
13 The majority of PM emitted by mobile sources is less than 1 micrometer in diameter. 

14Ethanol is not currently listed in EPA’s Integrated Risk Information System database.

34

acceleration, over a standard quantity of miles. The studies generally follow the U.S. Federal

Test Procedure (FTP), though other test cycles may be used. The tailpipe and evaporative

emissions are collected under a strict set of guidelines and then taken to a laboratory for analysis. 

Metal and particulate emissions are collected on particulate filters and analyzed. Analysis of

metals usually doesn’t specify the actual individual chemical form of the metal, but instead

reports the total amount of the identified metal emitted. Particulate samples have routinely been

collected for PM10 (all particles less than ten micrometers in diameter) which captures all PM

emitted by mobile sources.13 Once the chemical, metal, and/or particle analysis of the collected

material is complete, the results are routinely presented as mass (grams or milligrams) of

chemical “x” per mile driven (g/mi) or mass per unit of work accomplished (e.g., g/brake-horse

power hour).

Many toxic air pollutants are hydrocarbons (HCs). To identify specific compounds in the

complex exhaust mixture, the hydrocarbon component of exhaust is chemically separated

(speciated). In addition, the compounds that comprise the particulate phase of mobile source

emissions are also chemically speciated. Most test programs that characterize vehicle emissions

identify only total hydrocarbons and particulate matter without separating the individual species

of hydrocarbons and other elements. As a result, motor vehicle emissions may contain other

toxic compounds that are not currently included on our MSAT list because studies have not yet

specifically identified these compounds.

In addition, there are limited speciation data for certain vehicle classes. Databases and

recent studies reporting emissions from light-duty gasoline vehicles (LDGV), heavy-duty diesel

vehicles (HDDV), heavy-duty gasoline vehicles (HDGV), and gasoline nonroad engines are

listed Appendix I at the end of this chapter. Data for other vehicle and engine types (e.g., lightduty diesel engines and nonroad diesel engines) either do not exist or are outdated (more than ten

years old) and thus are judged not to be representative of current emissions. However, it is

unlikely that the lack of recent data for these particular vehicle and engine types would lead us to

overlook compounds that should be included on our list of MSATs, because the combustion

processes for these missing vehicle and engine types are similar to those for the vehicle and

engine types for which we do have data.

This compilation did not include speciation of emissions from alternative-fueled vehicles,

which are currently few in number. It should be noted that, depending on the fuel used, these

vehicles may also emit unburned ethanol14 and methanol. Low level ethanol mixtures (10%

ethanol and 90% gasoline) are widely used in the United States. Higher level ethanol mixtures

(e.g., 85% ethanol) are used as alternative fuel sources in a small number of flexible fuel

vehicles. 

The speciation studies listed in Appendix I at the end of this chapter provide speciation
15 EPA IRIS Database, http://www.epa.gov/iris/intro.htm

35

profiles for the gaseous and/or particulate phase of mobile source emissions or fuels. Each study

identifies the types of vehicles or engines from which data was collected (e.g., light-duty gas

vehicles, heavy-duty diesel engines, nonroad engines, or a mix of various types). The vehicles

tested represent a mix of older and newer models, with varying mileage. The type of fuel used

was also specified.

In the next section we describe the health effects information that is used to determine

which compounds emitted from mobile sources and their fuels may be considered MSATs.

2. Using IRIS to Identify Pollutants with Potential Serious Adverse Health

Effects

IRIS is an EPA database of scientific information that contains the Agency consensus

scientific positions on potential serious adverse health effects that may result from a lifetime

exposure to substances found in the environment. IRIS was initially developed for EPA staff in

response to a growing demand for consistent information on chemical substances for use in risk

assessments, decision-making and regulatory activities. IRIS currently provides health effects

information on over 500 specific chemical compounds.15

IRIS contains chemical-specific

summaries of qualitative and quantitative

health information. IRIS information

includes the reference concentration for

noncancer health effects resulting from

inhalation exposure (RfC), the reference dose

for noncancer health effects resulting from

oral exposure (RfD) and the carcinogen

assessment for both inhalation and oral

exposure.

The RfC or RfD is an estimate (with

uncertainty spanning perhaps an order of

magnitude) of a daily exposure to the human

population (including sensitive subgroups)

that is likely to be without appreciable risk of

deleterious effects during a lifetime. RfCs

and RfDs are based on an assumption of

lifetime exposure and may not be

appropriately applied to less-than-lifetime

exposure situations. RfCs and RfDs may be

derived for the noncarcinogenic effects of

How Chemicals Are Added to the IRIS

Database

 Our Office of Research and Development

(ORD) maintains IRIS through a scientific

consensus and review process that precedes

entry of a pollutant into the IRIS database. 

This process consists of:

• An annual Federal Register announcement

of the IRIS agenda and a call for scientific

information from the public on the selected

chemical substances;

• A search of the current literature;

• Development of health assessment and draft

IRIS summaries;

• Internal EPA peer review;

• External peer review;

• Agency consensus review and management

approval within EPA;

• Preparation of final IRIS summaries and

supporting documents; and

• Entry of summaries and supporting

documents into the IRIS database.
36

chemicals whether or not they are also carcinogenic. 

The carcinogenicity assessments in IRIS begin with a qualitative weight-of-evidence

judgment as to the likelihood that a chemical may be a carcinogen for humans (hazard

identification). Using the EPA 1986 Risk Assessment Guidelines, a carcinogen can be classified

as a known, probable, or possible human carcinogen (Group A, B or C, respectively). A

quantitative assessment is performed depending on the weight-of-evidence and the suitability of

the available information regarding a relationship between the dose of a compound and the effect

it causes (dose-response data). If suitable dose-response data are available, a quantitative

assessment is calculated which can be presented in one or m ore of three ways. If the agent is

active upon ingestion, then the slope of a dose-response curve generated from orally exposed

animals or humans is calculated. This is referred to as the oral slope factor and is presented as

risk per milligram of agent ingested per kilogram of body weight per day. Alternatively, the

carcinogenic activity of an agent might be assessed in terms of the concentration in drinking

water or air, yielding unit risk estimates of risk per microgram agent per liter of drinking water or

risk per microgram agent per cubic meter of air, respectively. The oral slope factor and the unit

risk factors are generally characterized as upper-bound estimates of the human cancer risk; the

true risk could be higher, but is likely to be lower.

IRIS also lists compounds for which the Agency has reviewed currently available

information and concluded that 1) there are insufficient data to calculate an RfC or RfD for the

noncancer hazard potentially posed by the compound(s), and/or 2) there is an absence of

sufficient information to identify a cancer hazard. 

Each reference dose/concentration and carcinogenicity assessment is reviewed by a group

of EPA health scientists using consistent chemical hazard identification and dose-response

assessment methods. These methods are discussed or referenced in the IRIS Background

Documents which are specific to, and referenced in, each individual chemical profile on IRIS. It

is important to note that the information in IRIS may be revised by EPA, as appropriate, when

additional health effects data become available and new developments in assessment methods are

adopted.

It is also important to note that IRIS does not provide situational information on

individual instances of exposure. In order to evaluate potential public health risks, the summary

health hazard and dose-response information in IRIS must be combined with data on specific

exposure situations.

3. List of Mobile Source Air Toxics

In our notice of proposed rulemaking we compared the lists of compounds identified in

the motor vehicle emission databases and studies with the toxic compounds listed in IRIS. We

identified 21 compounds, each of which have the potential to cause serious adverse health effects

as reflected in IRIS (e.g., these compounds are known, probable, or possible human carcinogens

and/or pollutants for which the Agency has calculated an RfC or RfD) and in the ongoing agency
16A further discussion of the potential cancer and noncancer risks, and other doseresponse information for each MSAT can be found in Chapter 3 of the TSD.

17Note, however, that Congress has expressly directed EPA to adopt controls in

accordance with 202(l)(2) for benzene and formaldehyde.

37

scientific assessments.16 We therefore consider each of these compounds to be MSATs. We

received comments on ten proposed MSATs (arsenic compounds, chromium compounds,

dioxin/furans, diesel exhaust, n-hexane, lead compounds, manganese compounds, mercury

compounds, nickel compounds, and styrene) as well as other compounds (methanol, methyl

nitrite, ethanol, propionaldehyde, 2,2,4-trimethylpentane). We have changed the listing for diesel

exhaust to diesel particulate matter and diesel exhaust organic gases. A discussion of the

comments received on the proposed MSAT list is provided below and the MSAT list is provided

in Table II.B-1. 

It is important to note that inclusion on the list is not itself a determination by EPA that

emissions of the compound in fact present a risk to public health or welfare, or that it is

appropriate to adopt controls to limit the emissions of such a compound from motor vehicles or

their fuels.17 The purpose of the list is to provide a screening tool that identifies those

compounds emitted from motor vehicles or their fuels for which further evaluation of emissions

controls is appropriate. In conducting any such further evaluation, pursuant to sections 202(a) or

211(c) of the Act, EPA would consider whether emissions of the compound cause or contribute

to air pollution which may reasonably be anticipated to endanger public health or welfare. Such

an evaluation would also consider the appropriate level of any controls, based on the criteria

established in section 202(l)(2). Inclusion of a compound on the MSAT list does not decide

these issues, but instead identifies those compounds for which such an evaluation would appear

to be warranted.
38

Table II.B-1

List of Mobile Source Air Toxics (MSATs)

Acetaldehyde Ethylbenzene Naphthalene

Acrolein Formaldehyde Nickel Compoundsa

Arsenic Compoundsa n–Hexane POMc

Benzene Lead Compoundsa Styrene

1,3-Butadiene Manganese Compoundsa Toluene

Chromium Compoundsa Mercury Compoundsa Xylene

Dioxin/Furansb

Diesel Particulate Matter +

Diesel Exhaust Organic Gases

(DPM + DEOG)

MTBE

a

 Although the different metal compounds generally differ in their toxicity, the on-road mobile

source inventory contains emissions estimates for total metal compounds (i.e., the sum of all

forms).

b

 This entry refers to two large groups of chlorinated compounds. In assessing their cancer risks,

their quantitative potencies are usually derived from that of the most toxic, 2,3,7,8-

tetrachlorodibenzodioxin.

c

 Polycyclic Organic Matter includes organic compounds with more than one benzene ring, and

which have a boiling point greater than or equal to 100 degrees centigrade. A group of seven

polynuclear aromatic hydrocarbons, which have been identified by EPA as probable human

carcinogens, (benz(a)anthracene, benzo(b)fluoranthene, benzo(k)fluoranthene, benzo(a)pyrene,

chrysene, 7,12-dimethylbenz(a)anthracene, and indeno(1,2,3-cd)pyrene) are used here as

surrogates for the larger group of POM compounds.

In response to public comments we are changing the way we list toxics in diesel exhaust

as an MSAT. We believe a better approach is to list diesel particulate matter and diesel exhaust

organic gases (DPM + DEOG) as the MSAT. This listing approach is more precise about the

components of diesel exhaust expected to contribute to the observed cancer and noncancer health

effects and provides a framework for developing regulatory control strategies. Currently

available science, while suggesting an important role for the particulate phase component of

diesel exhaust, does not attribute the likely cancer and noncancer health effects independently to

diesel particulate matter as distinct from the gas phase components. Because the studies cannot

separate the health effects of the particulate and gaseous components of diesel exhaust we are

listing them together as a single MSAT.

While this listing departs slightly from the approach described above, we believe this is

reasonable because 1) there are several nontoxic components of diesel exhaust (e.g., water vapor,

nitrogen, oxygen) that we are excluding from the listing, 2) this listing includes the components

of diesel exhaust that are likely to contribute to the cancer and noncancer hazard (with the
39

exception of the gaseous phase criteria pollutants, such as NOx, SO2 and CO which are subject to

National Ambient Air Quality Standards), 3) the more precise listing provides Federal and State

government, industry, and public interest groups an ability to focus on the components of diesel

exhaust that pose a potential concern for public health, and 4) this focus provides specific targets

for emissions reductions should future analysis indicate that additional controls are necessary.

Throughout the TSD we are using diesel PM as the surrogate for the particulate matter

and exhaust gas components of diesel exhaust. Data regarding exposure assessment and

inventory analysis for specific constituents in the diesel exhaust organic gas phase are available

for some compounds (e.g., benzene, 1,3-butadiene, formaldehyde, acetaldehyde, and acrolein)

and are presented in Chapters 4 and 5 of the TSD. 

We received comments regarding the proposed listing of diesel exhaust that were either

strongly supportive of the proposed listing or requested that diesel exhaust be removed from the

list of MSATs. Among the supporting comments, one commenter specifically requested that the

proposed diesel exhaust listing not be changed to diesel particulate matter, stating that future

developments, while controlling particulate matter, could lead to increased risks from the

gaseous diesel emissions. Among the comments requesting that diesel exhaust be removed from

the MSAT list, recommendations for alternative listing approaches included diesel particulate

matter, ambient particulate matter, or the specific components of diesel exhaust for which health

effects have been determined. 

The IRIS listing and the summary of cancer and noncancer health effects described in the

draft Health Assessment Document for Diesel Exhaust are based on studies linking serious

adverse health effects to whole diesel exhaust exposure, using diesel particulate matter as the

measure of dose. Available science, while suggesting an important role in toxicity for the

particle phase component of diesel exhaust, cannot rule out a role for the gas phase components

such as semi-volatile organics that are partly in both the gas and particle phases. Accordingly,

we are listing the MSAT diesel exhaust as diesel particulate matter and diesel exhaust organic

gases (DPM + DEOG). This listing addresses commenters’ concerns that diesel exhaust is an

imprecise and overly-inclusive designation that does not focus attention properly on the toxic

fractions of concern. In addition, the listing of DPM + DEOG provides industry with more

specific targets for making improvements by reducing the toxic portions of the exhaust stream. 

We are not listing ambient PM as an MSAT because it does not conform to the approach

described above for listing an MSAT. The Agency has specific information regarding the cancer

and noncancer hazard posed by diesel exhaust and we are acting on this basis. Listing the only

specific compounds in of diesel exhaust for which health effects have been determined would be

under-inclusive, because the cancer and noncancer health effects observed with exposure to

diesel exhaust cannot currently be attributed to individual compounds.

We received comments questioning the listing of several other MSATs. One commenter

questioned the listing of n-hexane. This commenter suggested that since the levels of n-hexane

required to cause adverse health effects are significantly higher than those found in motor vehicle
18This commenter is correct that in the NPRM we mistakenly listed styrene as a

component in gasoline. Styrene is a product of combustion of gasoline.

19Ball, James C. (1997) Emission Rates and Elemental Composition of Particles

Collected from 1995 Ford Vehicles Using the Urban Dynamometer Driving Schedule, the

Highway Fuel Economy Test, an the US06 Driving Cycle. Society of Automotive Engineers,

SAW paper No. 97Fl-376.

20EPA (1993) Volatile Organic Compound (VOC) / Particulate Matter (PM) Speciation

Data System (SPECIATE), Version 1.5. http://www.epa.gov/ttn/chief/software.html#speciate.

40

exhaust, this compound should not be on the MSAT list. As explained above, our approach for

listing a compound as an MSAT is based on the presence of the compound in the emissions from

motor vehicles or their fuels and an Agency consensus view, as expressed on IRIS, that the

compound has the potential to cause serious adverse health effects. In keeping with this

approach, we will maintain n-hexane on our list of MSATs. It should be noted that inclusion of

these compounds on the MSAT list is not itself a determination by EPA that environmental

exposures to emissions of the compound in fact present a risk to public health or welfare, or that

it is appropriate to adopt controls to limit the emissions of such a compound from motor vehicles

or their fuels. The purpose of the list is to provide a screening tool that identifies those

compounds emitted from motor vehicles or their fuels for which further evaluation of emissions

controls is appropriate.

This same commenter suggested that EPA provide information regarding the source of

chlorine in the formation of dioxin during combustion. Another commenter indicated that dioxin

is not being emitted in significant quantities. Sources of chlorine include fuel, motor oil and

intake air and while the emission rates measured for dioxin are low, the levels are above

detection limits in several studies. As explained above, inclusion on the MSAT list does not

imply that emissions are sufficiently high to pose actual risk levels needing immediate control. 

Rather, listing only identifies those toxics for which controls should be evaluated.

One commenter suggested that the decision to list styrene among the MSATs be deferred

to a future rulemaking as the Agency is currently re-assessing the cancer and noncancer health

effects of this compound and because the compound, while admittedly found in vehicle exhaust,

is not routinely found in gasoline.18 The Agency re-assessment of styrene is being conducted to

incorporate new information regarding potential noncancer and cancer health effects resulting

from exposure to this compound and will not result in the removal of styrene from the IRIS

database.

One commenter provided evidence that in one speciation study,19 arsenic was not found

in motor vehicle exhaust at levels above the method detection limit and therefore, arsenic should

not be included on the list as an MSAT being emitted from motor vehicles. We include arsenic

on the motor vehicle list of MSATs due to the presence of this element in the SPECIATE

database for motor vehicle emissions.20 Updates to the SPECIATE database are planned for the
Arsenic is found in profiles 32102 and 32103, for light duty diesel vehicles. These data were

originally from the PM10 Source Composition Library for the South Coast Air Basin, Prepared

by NEA, Inc., July 15, 1987.

41

future which may change the listing of some compounds, including arsenic. Any changes to the

SPECIATE database will be used to revise the MSAT list as required.

Regarding the listing of metals, we have chosen to list the entire group of metal

compounds if any compound of the metal has been detected in mobile source exhaust and any

compound of the metal is listed in IRIS as potentially causing adverse human health effects. 

Literature values report only the total amount of the metal compound identified and not the

specific form of the metal being emitted in mobile source exhaust. For example, chromium (Cr)

can be emitted from combustion sources in different forms, the most toxic of which is Cr+6. In

the literature, the form of Cr emissions from mobile sources is unidentified. In our list of MSAT,

we therefore list chromium compounds generally, and do not attempt to list specific forms of

these metals because we lack metal speciation information. When we assess the range of

potential health impacts associated with exposure to chromium compounds, we consider the

health effects associated with all forms of the compound for which we have health effects

information. For chromium, the most toxic form in IRIS is Cr+6; hence the health impacts

described for chromium compounds refer to these most serious effects even though it is highly

unlikely that all motor vehicle emissions of Cr are Cr+6. EPA believes this listing approach is a

reasonable, health-protective way to handle the uncertainty surrounding motor vehicle emissions

of metals. Moreover, it is consistent with Congress’ list of HAPs for stationary sources in

Section 112(b) of the Act. At the same time we recognize that to accurately assess the actual

health risks associated with exposure to metal emissions from mobile sources, identification of

the specific forms of the metals emitted would be important.

In the NPRM, we requested comment on whether methanol and ethanol, by virtue of their

use in alternative fuel vehicles, should be included on the MSAT list. We did not include

methanol on our proposed list of MSATs because it was not identified in our analysis of

speciated emissions from motor vehicles.

During the comment period, one commenter directed EPA to studies that identify

methanol as an emissions product of motor vehicles burning reformulated gasoline. This

commenter suggested that further research needed to be conducted to determine whether

methanol should be added to the list of MSAT. Recently submitted comments echoed the need

to conduct further research and requested more time to consider the addition of methanol to the

MSAT list.

In order to provide a full opportunity for public comment and to respond to these

comments in more detail, we will address the addition of methanol to the MSAT list in a separate

rulemaking. We believe it is reasonable to defer making a decision on listing methanol until

after today’s rulemaking, because listing in today’s rulemaking would not result in additional

controls. The existing motor vehicle VOC controls will reduce emissions of methanol along with
42

other gaseous toxics and fuel controls will need to be considered in subsequent rulemakings. As

part of the future notice addressing addition of methanol to our list of MSATs, we will also

evaluate possible controls in accordance with section 202(l)(2) as appropriate. 

 One commenter responded to our request for commenton the addition of ethanol to the

list of MSATs based on the presence of ethanol in alternative fuels and stated that ethanol should

not be listed as an MSAT. At this time, EPA is not including ethanol in the list of MSATs

because we do not have an Agency consensus view as expressed on IRIS regarding the potential

adverse health effects associated with exposure to ethanol. The Agency is continuing toxicity

testing and risk assessment of potential adverse health effects resulting from exposure to this

compound. We will reassess available information regarding potential health effects of exposure

to ethanol when we evaluate whether additional controls are appropriate in 2003. 

As a final step, we compared our lists of emitted compounds to four lists of toxic air

pollutants to confirm that our MSAT list was reasonable. The four lists of toxic air pollutants we

used were: the Clean Air Act (CAA) Section 112(b) list of hazardous air pollutants; California

EPA (CalEPA) list of toxic air contaminants (TAC); U.S. Department of Health and Human

Service Agency for Toxic Substances and Disease Registry (ATSDR) list of Minimal Risk

Levels (MRLs); and International Agency for Research on Cancer (IARC) monographs on

cancer. Comparing these four lists against the emissions speciation studies and databases, we

identified two additional compounds not included on our list of MSATs – propionaldehyde and

2,2,4-trimethylpentane. We received comments on both of these compounds. Some commenters

suggested that further study was needed to determine the potential for adverse health effects,

while others asserted the position that both compounds should be added to the list of MSATs

based on their presence in the CAA section 112(b) HAP list or due to the presence of these

compounds on the emissions lists.

After consideration of these comments, we are not including propionaldehyde or 2,2,4-

trimethylpentane in the list of MSATs at this time. We believe that because we do not have an

Agency consensus view as expressed on IRIS regarding the potential serious adverse health

effects associated with exposure to these pollutants it is inappropriate to include them. EPA

assessments of these compounds have been proposed and we will reassess the possible inclusion

of these compounds in the list of MSATs when we evaluate whether additional controls are

appropriate in 2003.

Appendix I

Toxics Inventory/Speciation References

1. Auto/Oil Air Quality Improvement Research Program, 1990. Phase 1 Working Data Set

(published in electronic form). Prepared by Systems Applications International, San

Rafael, CA.
43

2. Ball, James C. Emission Rates and Elemental Composition of Particles Collected from

1995 Ford Vehicles Using the Urban Dynamometer Driving Schedule, the Highway Fuel

Economy Test, and the US06 Driving Cycle. Society of Automotive Engineers, SAE

paper No. 97FL-376. 1997.

3. Bass, E. A., and M. S. Newkirk, 1995. Reactivity Comparison of Exhaust Emissions

from Heavy-Duty Engines Operating on Gasoline, Diesel, and Alternative Fuels. 

Southwest Research Institute, Report No. SwRI 9856, December, 1995.

4. Billings, R., T. Kraus, B. Hunt, and J. Mangino, R. Cook, L. Driver, 1998. Development

and Comparison of 1990 and 1996 Mobile Source Hazardous Air Pollutant Emissions

Estimates. Presented at AWMA Conference “Emissions Inventory: Living in a Global

Environment,” New Orleans, LA, December 8-10, 1998.

5. Boekhaus, K. L., J. M. DeJovine, D. A. Paulsen, L. A. Rapp, J.S. Segal and D. J.

Townsend, 1991. Clean Fuels Report 91-03: Fleet Test Emissions Data -- EC-Premium

Emission Control Gasoline. Arco Products Co., Anaheim, California.

6. CARB, 1991. Butadiene Emission Factors. memo from K. D. Drachand to Terry

McGuire and Peter Venturini, July 17, 1991.

7. Carroll, J. N., 1991. Emission Tests of In-use Small Utility Engines: Task III Report,

Non-road Source Emission Factors Improvement. Prepared for U.S. EPA by Southwest

Research Institute. Report No. SwRI 3426-006.

8. Censullo, A. C., 1991. Development of Species Profiles for Selected Organic Emission

Sources. California Polytechnic University, report prepared for California Air Resources

Board.

9. College of Engineering - Center for Environmental Research and Technology, University

of California, 1998. Evaluation of Factor that Affect Diesel Exhaust Toxicity. Submitted

to California Air Resources Board, Contract No. 94-312.

10. Eastern Research Group, 1999. Documentation for the 1996 Base year National Toxics

Inventory for Commercial Marine Vessel and Locomotive Sources. Draft Report

prepared for Emission Factor and Inventory Group, Office of Air Quality Planning and

Standards, U. S. EPA, November 1, 1999.

11. Eastern Research Group, 1999. Documentation for the 1996 Base year National Toxics

Inventory for Aircraft Sources. Draft Report prepared for Emission Factor and Inventory

Group, Office of Air Quality Planning and Standards, U. S. EPA, November 1, 1999.

12. Eastern Research Group, 1999. Documentation for the 1996 Base year National Toxics

Inventory for Nonroad Sources. Draft Report prepared for Emission Factor and Inventory

Group, Office of Air Quality Planning and Standards, U. S. EPA, November 1, 1999.

13. Eastern Research Group, 1999. Documentation for the 1996 Base year National Toxics

Inventory for On-road Sources. Draft Report prepared for Emission Factor and Inventory

Group, Office of Air Quality Planning and Standards, U. S. EPA, November 1, 1999.

14. EPA,1999. Estimation of Motor Vehicle Toxic Emissions and Exposure in Selected

Urban Areas. Prepared by Sierra Research, Inc., Radian International Corp., and Energy

& Environmental Analysis, Inc. for U. S. EPA, Office of Mobile Sources, Assessment

and Modeling Division, Ann Arbor, MI, Report No. EPA420-D-99-002, March 1999.

15. EPA, 1996. "Determining POM/PAH Emission Factors for Mobile Sources." 

Memorandum from Pam Brodowicz, Office of Mobile Sources, to Eric Ginsburg and
44

David Mobley, Office of Air Quality Planning and Standards, December 19, 1996.

16. EPA, 1999. 1990 Emissions Inventory of Forty Potential Section 112(k) Pollutants:

Supporting Data for EPA’s Section 112(k) Regulatory Strategy. Distributed by Office of

Air Quality Planning and Standards, U. S. EPA, May 21, 1999.

17. EPA, 1997. Memo from Rich Cook, Rich, Office of Mobile Sources, to Anne Pope,

Office of Air Quality Planning and Standards, Source Identification and Base Year 1990

Emission Inventory Guidance for Mobile Source HAPs on the OAQPS List of 40 Priority

HAPs. June 11, 1997.

18. EPA, 1998. Memo from Rich Cook, Office of Mobile Sources, to Laurel Driver and

Anne Pope, Office of Air Quality Planning and Standards, Guidance on Mobile Source

Emission Estimates in the 1996 National Toxics Inventory. June 9, 1998. 

19. EPA, 1993. Final Regulatory Impact Analysis for Reformulated Gasoline. U. S.

Environmental Protection Agency, December 13, 1993.

20. EPA,1992. Speciation for SAI Runs. April 14, 1992 memo by Chris Lindhjem, Penny

Carey, and Joe Somers.

21. EPA, 1992. 11% MTBE Exhaust Speciation. August 14, 1992 memo by Rich Cook. 

22. EA, 1992. Exhaust, Evaporative, and Running Loss Speciation. July 10, 1992 memo by

Chris Lindhjem, Penny Carey, and Joe Somers.

23. EPA, 1993. Motor Vehicle-Related Air Toxics Study. Office of Mobile Sources,

Emission Planning and Strategies Division, Ann Arbor, MI. Report No. EPA 420-R-93-

005. 

24. EPA, 1993. Volatile Organic Compound (VOC)/ Particulate Matter (PM) Speciation

Data System (SPECIATE), Version 1.5.

25. Cook, Rich, and Pam Brodowicz. 1998. Derivation of Mobile Source Toxic Fractions

Applied to the Gridded Houston VOC Inventory. Appendix III.C. in “Air Dispersion

Modeling of Toxic Air Pollutants in Urban Areas. Emissions, Monitoring and Analysis

Division, Office of Air Quality Planning and Standards, July, 1998.

26. EPA, 1997. "Revisions to Nonroad Toxic Emission Estimates for Five Candidate Title

III Section 112(k) Hazardous Air Pollutants: Benzene, 1,3-Butadiene, Formaldehyde,

Hexavalent Chromium, and Polycyclic Organic Matter." Memorandum from Richard

Cook, Office of Mobile Sources, to Anne Pope, Office of Air Quality Planning and

Standards, February 20, 1997.

27. EPA, 1994. Estimating Exposure to Dioxin-Like Compounds -- Volume II: Properties,

Sources, Occurrence and Background Exposures. Office of Research and Development,

Washington, DC. June, 1994 External Review Draft, Report No. EPA/600/6-88/005Cb.

28. EPA, 1993. “Piston Engine Particulate Matter Emission Factors, Toxic Emission

Fractions, and VOC to TOG Correction Factor for Aircraft.” Memorandum from Richard

Cook, Office of Mobile Sources, to Patricia Morris, Region 5, February 17, 1993.

29. Gabele, P., 1997. Exhaust Emissions from Four-Stroke Lawn Mower Engines. J. Air &

Waste. Manage. Assoc. 47:945-952.

30. Hare, C. T., and J. J. White, 1991. Toward the Environmentally Friendly Small Engine:

Fuel, Lubricant, and Emission Measurement Issues. SAE Paper No. 911222.

31. Hare, C. T., and J. N. Carroll, 1993. Speciation of Organic Emissions to Study Fuel

Dependence of Small Engine Exhaust Photochemical Reactivity. Report for Advisory
45

Committee for Research, Southwest Research Institute, July, 1993.

32. Sierra Research, Inc., 1998. On-Road Motor Vehicle National Toxics Exposure

Estimates. Memorandum from Philip Heirigs to Rich Cook, U.S. EPA. October 15, 1998.

33. Sierra Research, Inc., 1999. Methodologies Used to Generate Emission Estimates for

Five Motor Vehicle HAPs in the 1996 National Toxics Inventory. Memorandum from

Philip Heirigs to Rich Cook, July 23, 1999.

34. Sigsby, J. E., S. Tejeda, W. Ray, J. M. Lang, and J. W. Duncan, 1987. Volatile organic

compound emissions from 46 in-use passenger cars. Environ. Sci. Technol. 21:466-475.

35. Spicer, C. W., M. W. Holdren, D. L. Smith, D. P. Hughes, and M. D. Smith, 1992. 

Chemical composition of exhaust from aircraft turbine engines. Journal of Engineering

for Gas Turbines and Power 114: 111-117.

36. Spicer, C. W., M. W. Holdren, R. M. Riggin, and T. F. Lyon, 1994. Chemical

combustion and photochemical reactivity of exhaust from aircraft turbine engines. Ann.

Geophysicae 12:944-955.

37. Stump, F. D., 1997. Sun Fuels Alaska II Study. Unpublished data.

38. Stump, F. D., S. Tejada, W. Ray, D. Dropkin, F. Black, R. Snow, W. Crews, P. Siudak,

C. O. Davis, L. Baker and N. Perry, 1989. The influence of ambient temperature on

tailpipe emissions from 1984 to 1987 model year light-duty gasoline vehicles. 

Atmospheric Environment 23: 307-320.

39. Stump, F. D., K. T. Knapp, and W. D. Ray, 1996. Influence of ethanol-blended fuels on

the emissions from three pre-1985 light-duty passenger vehicles. J. Air & Waste Manage.

Assoc. 46: 1149-1161.

40. Stump, F. D., S. Tejeda, W. Ray, D. Dropkin, F. Black, R. Snow, W. Crews, P. Siudak,

C. O. Davis and P. Carter, 1990. The influence of ambient temperature on tailpipe

emissions from 1985-1987 model year light-duty gasoline vehicles -- II. Atmospheric

Environment 24A: 2105-2112.

41. Stump, F. D., K. T. Knapp, W. D. Ray, P. D. Siudak, and R. F. Snow, 1994. Influence of

oxygenated fuels on the emissions from three pre-1985 light-duty passenger vehicles. J.

Air & Waste Manage. Assoc. 44:781-786.

42. Warner-Selph, M. A. and J. DeVita, 1989. Measurements of Toxic Exhaust Emissions

from Gasoline-Powered Light-Duty Vehicles. SAE Technical Paper No. 892075.

43. Warner-Selph, M. A., and L. R. Smith, 1991. Assessment of Unregulated Emissions

from Gasoline Oxygenated Blends. Ann Arbor, Michigan: U.S. Environmental

Protection Agency, Office of Mobile Sources.

44. Wyborny, L. Methyl Tertiary Butyl Ether (MTBE) Emissions from Passenger Cars. Draft

Technical Report. U. S. Environmental Protection Agency, Office of Mobile Sources,

April, 1998.
21 National Academy of Science. 1983. Risk Assessment in the Federal Government: Managing the

Process. Committee on the Institutional Means for Assessment of Risks to Public Health, National Research

Council.

22 EPA. 1986. . Guidelines for carcinogen risk assessment. Federal Register 51:33992-

34003. September 24.

46

Chapter 3: Health Effects of Mobile Source Air Toxics

Chapter 2 of this Technical Support Document describes how we identified the list of

mobile source air toxics (MSATs). This chapter begins with a description of some of the key

components of risk assessment and then provides specific information on the 21 MSATs,

including their physical properties, uses, sources of potential exposure, and health hazards.

Since most cancer and noncancer health impacts of air toxics cannot be directly isolated

and measured, risk assessment methods and tools have been developed to assist in evaluating

them. The EPA framework for assessing and managing risks reflects the risk assessment and risk

management paradigm set forth by the National Academy of Sciences in 198321 and incorporated

into the 1986 EPA risk guidance.22 The paradigm 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, involves evaluation of information provided by the risk assessment to the

environmental manager who makes a risk management decision. 

An exposure assessment is the quantitative or qualitative evaluation of contact to a

specific pollutant and includes such characteristics as intensity, frequency, and duration of

contact. The numerical output of an exposure assessment may be either exposure or dose,

depending on the purpose of the evaluation and available data.

The dose-response assessment produces two sequential analyses. The first analysis is the

hazard identification, which identifies contaminants that are suspected to pose health hazards,

describes the specific forms of toxicity (e.g., neurotoxicity, carcinogenicity, etc.) that they may

cause, and evaluates 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 second analysis is the human health dose-response assessment, which generally

describes 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
23 EPA. 1986. Guidelines for mutagenicity risk assessment. Federal Register 51:34006-34012. Sept. 24.

24 EPA. 1991. Guidelines for developmental toxicity risk assessment. Federal Register 56:63798-63826.

25 EPA. 1998. Guidelines for neurotoxicity risk assessment. Federal Register 63:26926. May 14. 

http://www.epa.gov/ncea/nurotox.htm

26 EPA. 1996. Guidelines for reproductive toxicity risk assessment. EPA/630/R-96/009. Federal Register

56274-56322, 31 October 1996. http://www.epa.gov/ORD/WebPubs/repro/

27 EPA. 1994. Methods for derivation of inhalation reference concentrations and application of inhalation

dosimetry. Washington D.C. EPA/600/8-90/066F.

47

air toxics. Most, if not all, epidemiologic and toxicologic data on air toxics typically result from

exposure levels that are high when compared to environmental levels. Dose-response assessment

methods for air toxics 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.

Chronic noncancer dose response assessment

Chronic noncancer effects include a wide range of effects in all organ systems, e.g.,

cardiovascular, immune, kidney. Hazard identification procedures for chronic 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,23 developmental toxicity,24 neurotoxicity25; and reproductive

toxicity.26 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, as with cancer, a formal classification scheme. Available data on different endpoints

are ordered 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. The inhalation reference concentration (RfC)

and oral reference dose (RfD) are the primary Agency consensus quantitative toxicity values for

use in chronic 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 1994 guidance.27

Acute noncancer dose-response assessment

Acute effects can result from short-term exposures to chemicals. At present, no peer

reviewed metrics exist for evaluating short-term exposure to hazardous air pollutants. EPA’s

Office of Research and Development has proposed an Acute Reference Exposure (ARE)
28 EPA. 1998. 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,

D.C. EPA/600/R-98/051.

29 EPA. 1986. . Guidelines for carcinogen risk assessment. Federal Register 51:33992-

34003. September 24.

48

approach28 which is adaptable to any duration of exposure up to 24 hours.

Cancer dose response assessment

“Cancer” describes a group of related diseases that affect a variety of organs and tissues. 

Cancer results from a combination of genetic damage and nongenetic factors that favor the

growth of damaged cells. The EPA’s 1986 Guidelines for Carcinogen Risk Assessment29 provide

guidance on hazard identification for carcinogens. The approach recognizes three broad

categories of data: (1) human data (primarily epidemiological); (2) results of long-term

experimental animal bioassays; and (3) supporting data, including a variety of short-term tests for

genotoxicity and other relevant properties. 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:

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).

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).

Group C - Possibly Carcinogenic to Humans: Agents with limited animal

evidence and little or no human data.

Group D - Not Classifiable as to Human Carcinogenicity: Agents without

adequate data either to suggest or refute the suggestion of the human

carcinogenicity.

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.

Dose-response models such as the linear multistage model, which assumes a default

assumption that chemical carcinogens would exhibit risks at any dose, have historically been

used to calculate upper-bound unit risk estimates (URE). 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
30 EPA. 1996. Proposed Guidelines for Carcinogen Risk Assessment. Office of Research and

Development, Washington, DC. EPA/600/P-92/003C. http://www.epa.gov/ORD/WebPubs/carcinogen/

31 EPA. 1987. Health Assessment Document for Acetaldehyde. EPA/600/8-86-015A. Environmental

Criteria and Assessment Office, Office of Health and Environmental Assessment, Office of Research and

Development, Research Triangle Park, NC. 1987.

32 EPA 1993. Motor Vehicle-Related Air Toxics Study, U.S. Environmental Protection Agency, Office of

Mobile Sources, Ann Arbor, MI, EPA Report No. EPA 420-R-93-005, April 1993.

49

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).

In 1996, EPA/ORD proposed major revisions of the carcinogen hazard identification

scheme. The proposed revision to the cancer risk assessment guidelines,30 currently under public

review prior to finalization represents a considerable departure from the original guidelines.

Considerable new knowledge has been developed regarding the processes of chemical

carcinogenesis and the evaluation of human cancer risk. Please consult the guidelines for a

complete explanation.

A . Acetaldehyde

Acetaldehyde is ubiquitous in the ambient environment. It is an intermediate product of

higher plant respiration and is formed as a product of incomplete wood combustion in fireplaces

and wood stoves, coffee roasting, burning of tobacco, vehicle exhaust fumes, and coal refining

and waste processing. Hence, many individuals are exposed to acetaldehyde by breathing

ambient air. It should be noted that residential fireplaces and wood stoves are the two highest

sources of emissions, followed by various industrial emissions. Exposure may also occur in

individuals occupationally exposed to acetaldehyde during its manufacture and use. In addition,

acetaldehyde is formed in the body from the breakdown of ethanol; this would be a source of

acetaldehyde among those who consume alcoholic beverages.31

Acetaldehyde is a saturated aldehyde that is found in vehicle exhaust and is formed as a

result of incomplete combustion of both gasoline and diesel fuel. It is not a component of

evaporative emissions. Acetaldehyde comprises 0.4 to 1.0 percent of exhaust total organic gases

(TOG), depending on control technology and fuel composition.32 Primary acetaldehyde

emissions from mobile sources account for approximately 66 percent of the emissions in the

1996 National Toxics Inventory.

The atmospheric chemistry of acetaldehyde is similar in many respects to that of
33 Ligocki, M.P., and G.Z. Whitten, Atmospheric transformation of air toxics: acetaldehyde and polycyclic

organic matter, Systems Applications International, San Rafael, CA, (SYSAPP-91/113), 1991.

34 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH, 1999.

35 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH, 1999.

36 A RfC is defined as is an estimate (with uncertainty spanning perhaps an order of magnitude) of a daily

inhalation exposure to the human population (including sensitive subgroups) that is likely to be without appreciable

risk of deleterious effects during a lifetime. RfCs are based on an assumption of lifetime inhalation exposure and

may not be appropriately applied to less-than-lifetime exposure situations. RfCs are derived for the noncarcinogenic

effects of chemicals that are carcinogenic. 

37 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH, 1999.

38 EPA. 1987. Health Assessment Document for Acetaldehyde. EPA/600/8-86-015A. Environmental

Criteria and Assessment Office, Office of Health and Environmental Assessment, Office of Research and

Development, Research Triangle Park, NC. 1987.

50

formaldehyde.33 Like formaldehyde, it can be both produced and destroyed by atmospheric

chemical transformation. Mobile sources contribute to ambient acetaldehyde levels both through

direct emissions of acetaldehyde and as a result of secondary formation of acetaldehyde from

VOC emissions.

Although human data on the carcinogenic potential of acetaldehyde are extremely limited,

acetaldehyde is classified as a probable human carcinogen.34 This classification is based on a

formal risk characterization using sufficient database of animal carcinogenicity studies.35

Specifically, increased incidences of nasal tumors in male and female rats and laryngeal tumors

in male and female hamsters have been documented after inhalation exposure. Updated

noncancer and cancer potencies for acetaldehyde, addressing the issue of animal to human

extrapolation, will be developed in a similar fashion to that for formaldehyde, as discussed later.

The primary acute effects associated with exposure to acetaldehyde include irritation of

the eyes, skin, and respiratory tract. Effects on the respiratory system have been reported from

studies of animals exposed to long-term lower concentrations. The data from these studies was

found to be sufficient for EPA to develop a RfC36 (inhalation reference concentration) for

acetaldehyde exposure. Although no information is available on the reproductive or

developmental effects of acetaldehyde in humans, data from animal studies suggest that

acetaldehyde may be a potential developmental toxicant.37,38

B. Acrolein

Acrolein is an aldehyde primarily used as an intermediate in the manufacture of acrylic
39 ATSDR. 1990. Toxicological Profile for Acrolein. USDHHS, PHS, ATSDR. TP-90-01.

40 EPA 1991. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH.

41 ATSDR. 1992. Toxicological Profile for Arsenic. USDHHS, PHS, ATSDR. TP-92/02.

51

acid. It can be formed from the breakdown of certain pollutants in outdoor air or from burning

tobacco or gasoline.39 Acrolein is found in vehicle exhaust and is formed as a result of

incomplete combustion of both gasoline and diesel fuel. It is not a component of evaporative

emissions. Acrolein comprises 0.05 to 0.4 percent of exhaust total organic gases (TOG),

depending on control technology and fuel composition. Primary acrolein emissions from mobile

sources account for approximately 38 percent of the emissions in the 1996 National Toxics

Inventory. The atmospheric chemistry of acrolein is expected to be similar in many respects to

that of acetaldehyde and formaldehyde.

Although no information on the carcinogenic effects of acrolein in humans is available,

limited laboratory data for animals exposed by drinking water ingestion indicated an increased

incidence of adrenal cortical adenomas (non-malignant tumors of the adrenal glands adjacent to

the kidney). EPA has classified acrolein as a Group C, possible human carcinogen, based on

limited animal and mutagenticity data. A formal risk characterization has not conducted due to

this limited data set.

The respiratory system is the primary target in humans and animals for acrolein toxicity

resulting from inhalation exposure. Acute exposure results in upper respiratory tract irritation

and congestion, whereas chronic exposures in animals indicated an increase in cell proliferation

and in the numbers of white blood cells in the tissues lining the nasal passages. The data from

these studies was found to be sufficient for EPA to develop a RfC (inhalation reference

concentration) for acrolein exposure. No information is available on the reproductive or

developmental effects of acrolein in humans.40

C. Arsenic Compounds

Arsenic, a naturally occurring element, is found throughout the environment. It is

released into the air by volcanoes, the weathering of arsenic-containing minerals and ores, and by

commercial or industrial processes. For most people, food is the largest source of arsenic

exposure (about 25 to 50 μg/d), with lower amounts coming from drinking water and air. 

Among foods, some of the highest levels are in fish and shellfish; however, this arsenic exists

primarily as organic compounds, which are essentially nontoxic. Elevated levels of inorganic

arsenic may be present in soil, either from natural mineral deposits or contamination from human

activities, which may lead to dermal or ingestion exposure. Workers in metal smelters and

nearby residents may be exposed to above-average inorganic arsenic levels from arsenic released

into the air. Other sources of inorganic arsenic exposure include burning plywood treated with

an arsenic wood preservative or dermal contact with wood treated with arsenic.41
42 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH, 1999.

43 EPA 1999. Environmental Protection Agency, National Air Toxics Program: The Integrated Urban

Strategy Report to Congress, Office of Air Quality Planning and Standards, RTP, NC. EPA 453/R-99-007.

44 A RfD is defined as is an estimate (with uncertainty spanning perhaps an order of magnitude) of a daily

oral exposure to the human population (including sensitive subgroups) that is likely to be without appreciable risk of

deleterious effects during a lifetime. RfDs are based on an assumption of lifetime oral exposure and may not be

appropriately applied to less-than-lifetime exposure situations. RfDs are derived for the noncarcinogenic effects of

chemicals that are carcinogenic. 

52

Arsenic emissions from mobile sources are minimal, accounting for less than 1 percent of

the emissions in the 1996 National Toxics Inventory. It is thought that the arsenic found in the

emissions is due to impurities in either fuel additives or the fuel itself.

Inhalation exposure to inorganic arsenic has been shown to be strongly associated with

lung cancer in humans, while ingestion of inorganic arsenic in humans has been linked to a form

of skin cancer and also to bladder, liver, and lung cancer. There is sufficient data in humans for

EPA to classify inorganic arsenic as a Group A, human carcinogen42 and a full risk

characterization has been conducted by EPA.

Acute (short-term) high-level inhalation exposure to arsenic dust or fumes has resulted in

gastrointestinal effects (nausea, diarrhea, abdominal pain); central and peripheral nervous system

disorders have occurred in workers acutely exposed to inorganic arsenic. Chronic (long-term)

inhalation exposure to inorganic arsenic in humans is associated with irritation of the skin and

mucous membranes. Human data suggest a relationship between inhalation exposure of women

working at or living near metal smelters and an increased risk of reproductive effects, such as

spontaneous abortions. However, as these studies evaluated smelter pollutants in general,

arsenic's role is not clear. Chronic oral exposure has resulted in gastrointestinal effects, anemia,

peripheral neuropathy, skin lesions, hyperpigmentation, and liver or kidney damage.43 The data

from these studies was found to be sufficient for EPA to develop a RfD44 (oral reference dose)

for oral arsenic exposure.

D. Benzene

Benzene is an aromatic hydrocarbon which is present as a gas in both exhaust and

evaporative emissions from motor vehicles as well as from the burning of coal and oil. Benzene

comprises 3.0 to 5.0 percent of mobile source exhaust total organic gases (TOG ), which varies

depending on control technology (e.g., type of catalyst) and the levels of benzene and aromatics

in the fuel. The benzene fraction of evaporative TOG emissions is generally about one percent,

but depends on control technology and fuel composition (e.g., benzene level and Reid Vapor
45 EPA 1993. Motor Vehicle-Related Air Toxics Study, U.S. Environmental Protection Agency, Office of

Mobile Sources, Ann Arbor, MI, EPA Report No. EPA 420-R-93-005, April 1993.

46 Wallace, L.A. 1995. Human exposure to environmental pollutants: a decade of experience. Clinical

and Experimental Allergy 25:4-9.

47 ATSDR. 1997. Toxicological Profile for Benzene (update). USDHHS, PHS, ATSDR. Atlanta , GA.

48 EPA 1998. Environmental Protection Agency, Carcinogenic Effects of Benzene: An Update, National

Center for Environmental Assessment, Washington, DC. 1998.

49 Leukemia is a blood disease in which the white blood cells are abnormal in type or number. Leukemia

may be divided into nonlymphocytic (granulocytic) leukemias and lymphocytic leukemias. Nonlymphocytic

leukemia generally involves the types of white blood cells (leukocytes) that are involved in engulfing, killing, and

digesting bacteria and other parasites (phagocytosis) as well as releasing chemicals involved in allergic and immune

responses.

50 EPA 1998. Environmental Protection Agency, Carcinogenic Effects of Benzene: An Update, National

Center for Environmental Assessment, Washington, DC. 1998

53

Pressure (RVP)).45 Benzene emissions from mobile sources account for approximately 76

percent of the outdoor emissions in the 1996 National Toxics Inventory. Tobacco smoke

contains benzene and accounts for nearly half the national exposure to benzene.46

Benzene is also used as a solvent for fats, waxes, resins, oils, inks, paints, plastics, and

rubber; in the extraction of oils from seeds and nuts; and in photogravure printing. It is also used

as a chemical intermediate. Benzene is also used in the manufacture of detergents, explosives,

pharmaceuticals, and dyestuffs.47

The EPA has recently reconfirmed that benzene is a known (Group A) human carcinogen

by all routes of exposure and a full risk characterization has been conducted by EPA.48

Respiration is the major source of human exposure and at least half of the respiratory exposure is

by way of gasoline vapors and automotive emissions. Long-term exposure to high levels of

benzene in air has been shown to cause cancer of the tissues that form white blood cells. 

Specifically, benzene has been linked to acute (rapid and fatal) nonlymphocytic49 leukemia,

chronic (lingering, lasting) lymphocytic leukemia and possibly multiple myeloma (primary

malignant tumors in the bone marrow), although the evidence for the latter has decreased with

more recent studies. Leukemias, lymphomas, and other tumor types have been observed in

experimental animals that have been exposed to benzene by inhalation or oral administration. 

Exposure to benzene and/or its metabolites has also been linked with genetic changes in humans

and animals and increased proliferation of mouse bone marrow cells. The occurrence of certain

chromosomal changes in individuals with known exposure to benzene may serve as a marker for

those at risk for contracting leukemia.

A number of adverse noncancer health effects, blood disorders such as preleukemia and

aplastic anemia, have also been associated with low-dose, long-term exposure to benzene.50
51 Pancytopenia is the reduction in the number of all three major types of blood cells (erythrocytes, or red

blood cells, thrombocytes, or platelets, and leukocytes, or white blood cells). 

52 Aksoy, M. 1991. Hematotoxicity, leukemogenicity and carcinogenicity of chronic exposure to benzene. 

In: Arinc, E.; Schenkman, J.B.; Hodgson, E., Eds. Molecular Aspects of Monooxygenases and Bioactivation of

Toxic Compounds. New York: Plenum Press, pp. 415-434.

53 Goldstein, B.D. 1988. Benzene toxicity. Occupational medicine. State of the Art Reviews. 3: 541-

554.

54 Rothman, N., G.L. Li, M. Dosemeci, W.E. Bechtold, G.E. Marti, Y.Z. Wang, M. Linet, L.Q. Xi, W. Lu,

M.T. Smith, N. Titenko-Holland, L.P. Zhang, W. Blot, S.N. Yin, and R.B. Hayes. 1996. Hematotoxicity among

Chinese workers heavily exposed to benzene. Am. J. Ind. Med. 29: 236-246.

55 EPA 1993. Motor Vehicle-Related Air Toxics Study, U.S. Environmental Protection Agency, Office of

Mobile Sources, Ann Arbor, MI, EPA Report No. EPA 420-R-93-005, April 1993.

56 ATSDR. 1992. Toxicological Profile for 1,3-Butadiene. USDHHS, PHS, ATSDR. TP-91/07. 

54

People with long-term exposure to benzene may experience harmful effects on the blood-forming

tissues, especially the bone marrow. These effects can disrupt normal blood production and

cause a decrease in important blood components. Chronic inhalation exposure to benzene in

humans and animals can result in pancytopenia,51 a condition characterized by decreased

numbers of circulating erythrocytes (red blood cells), leukocytes (white blood cells), and

thrombocytes (blood platelets).52,53 Some individuals that develop pancytopenia and continue to

be exposed to benzene may develop aplastic anemia, a more severe blood disease that occurs

when the bone marrow ceases to function. The aplastic anemia can progress to AML (acute

mylogenous leukemia). The most sensitive noncancer effect observed in humans is the

depression of absolute

 lymphocyte counts in the circulating blood.54 EPA is currently reassessing the noncancer health

impacts of benzene.

E. 1,3-Butadiene

1,3-Butadiene is formed in vehicle exhaust by the incomplete combustion of gasoline and

diesel fuel. It is not present in vehicle evaporative and refueling emissions, because it is not

present in any appreciable amount in gasoline. 1,3-Butadiene accounts for 0.4 to 1.0 percent of

total exhaust TOG, depending on control technology and fuel composition.55 1,3-Butadiene

emissions from mobile sources account for approximately 60 percent of the emissions in the

1996 National Toxics Inventory.

Sources of 1,3-butadiene released into the air also include manufacturing and processing

facilities, especially oil refineries, chemical manufacturing plants, and plastic and rubber

factories. Other sources are forest fires or other combustion, and cigarette smoke.56

1,3-Butadiene was classified by EPA as a Group B2 (probable human) carcinogen in
57 EPA, 1985. Mutagenicity and carcinogenicity assessment of 1,3-butadiene. EPA/600/8-85/004F. U.S. 

Environmental Protection Agency, Office of Health and Environmental Assessment. Washington, DC. 

58 EPA 1998c. Environmental Protection Agency, Health Risk Assessment of 1,3-Butadiene. EPA/600/P98/001A, February 1998.

59 Scientific Advisory Board. 1998. An SAB Report: Review of the Health Risk Assessment of 1,3-

Butadiene. EPA-SAB-EHC-98, August, 1998.

60EPA 1996. Proposed guidelines for carcinogen risk assessment. Federal Register 61(79):17960-18011.

61 Delzell, E., N. Sathiakumar, M. Macaluso, M. Hovinga, R. Larson, F. Barbone, C. Beall, and P. Cole,

1995. A follow-up study of synthetic rubber workers. Final report prepared under contract to International Institute

of Synthetic Rubber Producers, October 2, 1995.

55

198557. This classification was based on evidence from two species of rodents and epidemiologic

data. EPA recently prepared a draft risk assessment that proposes that sufficient evidence exists

to characterize 1,3-butadiene be a known human carcinogen.58 This designation is based on a

combination of epidemiologic evidence as well as experimental evidence demonstrating

causality. The Environmental Health Committee of EPA’s Scientific Advisory Board (SAB),

reviewed the draft document in August 1998 and recommended that designation of 1,3-butadiene

as a known human carcinogen be based on observational studies in humans, without regard to

mechanistic or other information.59 In applying the 1996 proposed Guidelines for Carcinogen

Risk Assessment, the Agency relies on both observational studies in humans as well as

experimental evidence demonstrating causality and therefore the designation of 1,3-butadiene as

a known human carcinogen remains applicable.60 The SAB panel also recommended that EPA

calculate the lifetime cancer risk estimates based on the human data from Delzell et al. 199561

and account for the highest exposure of “360 ppm-year” for 70 years. Further input

recommended that EPA take into account additional data on health effects observed in female

laboratory animals, hence indicating that females may be a sensitive subpopulation.

1,3-Butadiene also causes a variety of reproductive and developmental effects in mice

and rats exposed to long-term, low doses of butadiene (EPA 1998c). The most sensitive effect

was reduced litter size at birth and at weaning. These effects were observed in studies in which

male mice exposed to 1,3-butadiene were mated with unexposed females. In humans, such an

effect might manifest itself as an increased risk of spontaneous abortions, miscarriages, still

births, or very early deaths. The data from these studies was found to be sufficient for EPA to

develop a draft chronic, subchronic, and acute RfC for 1,3-butadiene exposure as part of the draft

risk characterization mentioned above. The RfC values will be reported on IRIS.

F. Chromium Compounds

Chromium is a naturally occurring element in rocks, animals, plants, soil, and volcanic

dust and gases. Chromium occurs in the environment predominantly in one of two valence

states: trivalent chromium (Cr III), which occurs naturally and is an essential nutrient, and
62 EPA. 1998. Toxicological Review of Trivalent Chromium (CAS No. 16065-83-1). In Support of

Summary Information on the Integrated Risk Information System (IRIS). U.S. EPA, Washington D.C..

63 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH, 1999.

64 EPA 1999. Environmental Protection Agency, National Air Toxics Program: The Integrated Urban

Strategy Report to Congress, Office of Air Quality Planning and Standards, RTP, NC.

56

hexavalent chromium (Cr VI), which, along with the less common metallic chromium (Cr 0), is

most commonly produced by industrial processes. Chromium (III) is essential to normal glucose,

protein, and fat metabolism and is thus an essential dietary element with a daily intake of 50 to

200 μg/d recommended for an adult. The body has several systems for reducing chromium (VI)

to chromium (III). This chromium (VI) detoxification leads to increased levels of chromium

(III).

Air emissions of chromium are predominantly of trivalent chromium, and in the form of

small particles or aerosols. The most important industrial sources of chromium in the

atmosphere are those related to ferrochrome production. Ore refining, chemical and refractory

processing, cement-producing plants, automobile brake lining and catalytic converters for

automobiles, leather tanneries, and chrome pigments also contribute to the atmospheric burden of

chromium.62 Total chromium emissions from mobile sources account for approximately 4

percent of the emissions in the 1996 National Toxics Inventory.

Human studies have clearly established that inhaled chromium (VI) is a human

carcinogen, resulting in an increased risk of lung cancer. Animal studies have shown chromium

(VI) to cause lung tumors via inhalation exposure. There is sufficient data in humans for EPA to 

classify chromium (VI) as a Group A, human carcinogen and a full risk characterization has been

conducted by EPA.63

The respiratory tract is the major target organ for acute (short-term) and chronic

(long-term) inhalation exposures to chromium (VI). Shortness of breath, coughing, and

wheezing were reported from a case of acute exposure to chromium (VI), while perforations and

ulcerations of the septum, bronchitis, decreased pulmonary function, pneumonia, and other

respiratory effects have been noted from chronic exposure. Limited human studies suggest that

chromium (VI) inhalation exposure may be associated with complications during pregnancy and

childbirth, while animal studies have not reported reproductive effects from inhalation exposure

to chromium (VI).64 The data from these studies was found to be sufficient for EPA to develop a

RfC for chromium (VI) exposure. Additional data from oral exposure studies was found to be

sufficient for EPA to develop a RfD for chromium (VI) oral exposure.

Chromium (III) is much less toxic than chromium (VI). The respiratory tract is also the

major target organ for chromium (III) toxicity, similar to chromium (VI) but data from animal

studies do not demonstrate that the effects observed following inhalation of chromium (VI)
65 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH, 1999.

66 U.S. EPA (2000). Sources of Dioxin-Like Compounds in the United States; In: Exposure and Human

Health Reassessment of 2,3,7,8-TCDD and Related compounds. Part 1: Estimating Exposure to Dioxin-like

Compounds; Volume 2. National Center for Environmental Assessment, Office of Research and Development,

U.S. Environmental Protection Agency, Washington, DC. March 2000 draft final. EPA/600/P-00/001Ab.

67 Draft Final Report Exposure and Human Health Reassessment of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin

(TCDD) and Related Compounds, Part I: Estimating Exposure to Dioxin-Like Compounds, Volume 2: Sources of

Dioxin-Like Compounds in the United States. U.S. Environmental Protection Agency, Office of Research and

Development, National Center for Environmental Assessment - Washington Office, Exposure Assessment and Risk

Characterization Group. EPA/600/P-00/001Bb, September 2000.

57

particulates. Chromium (III) is most appropriately designated a Group D carcinogen (not

classified as to its human carcinogenicity) because there are inadequate data to conduct a full risk

characterization and determine its potential carcinogenicity.65

G. Dioxin/Furans

Dioxin comes from both natural and industrial sources, such as medical and municipal

waste incineration and paper-pulp production. Recent studies have confirmed that dioxins are

formed by and emitted from heavy-duty diesel trucks and are estimated to account for one

percent of total dioxin emissions in the dioxin inventory for the year 1995.66 The actual process

of dioxin and furan formation in the combustion of organic materials is discussed in detail in the

EPA report, Exposure and Human Health Reassessment of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin

(TCDD) and Related Compounds.67

In general, dioxin exposures of concern have primarily been noninhalation exposures

associated with human ingestion of certain foods (e.g., beef, pork, poultry, fish, eggs and dairy

products) contaminated by dioxin. The two primary pathways for dioxin to enter the human diet 

are: air-to-plant-to-animal and water/sediment-to-fish. Vegetation receives these compound via

atmospheric transport and deposition. The compounds are retained on plant surfaces and

bioaccumulate in fatty tissues of animals that feed on the vegetation. In the aquatic food chain, 

dioxins enter water systems via direct discharge or deposition and runoff from watersheds. Fish

accumulate dioxin through their direct contact with water, suspended particles, bottom sediments

and through the consumption of aquatic organisms. Exposure to dioxin occurs over a lifetime,

and the exposure is cumulative over a lifetime.

Based on recent human epidemiological studies from Europe and the United States,

dioxin has been linked to several cancers, including lymphomas and lung cancer, by the

International Agency For Research on Cancer (IARC). The IARC classifies the most potent form

of dioxin, 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD), as a "Group 1" carcinogen, meaning it is
68 IARC (1997). Polychlorinated dibenzo-para-dioxins and Polychlorinated Dibenzofurans. Volume 69,

IARC Monogram on the Evaluation of Carcinogenic Risks to Humans, International Agency for Research on

Cancer, Work Health Organization, Lyon France.

69 U.S. EPA (1994) Health Assessment Document for 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and

Related Compounds: Volume III Summary Draft Document. EPA/600/BP-92/001c.

58

carcinogenic to humans.68

Low-grade exposure to dioxin/furans have also been linked to a wide array of other health

problems, including changes in hormone levels and developmental defects in babies and

children.69 EPA classified dioxins as probable human carcinogens in 1985. Recently EPA has

proposed, and the Scientific Advisory Board has concurred, to classify TCDD as a human

carcinogen and the complex mixtures of dioxin-like compounds as likely to be carcinogenic to

humans using the draft 1996 carcinogen risk assessment guidelines.1 Using the 1986 cancer risk

assessment guidelines, the hazard characterization for 2,3,7,8-tetrachlorodibenzo-p-dioxin is

‘known’ human carcinogen and the hazard characterization for complex mixtures of dioxin-like

compounds is ‘probable’ human carcinogens.

H. Diesel Exhaust: Diesel Particulate Matter and Diesel Exhaust Organic Gases

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,

acrolein). The health effects of these and other gaseous compounds in diesel exhaust are

discussed elsewhere in this chapter. Three classes of compounds associated with particle-phase

diesel exhaust (e.g., polycyclic organic matter, metals, and dioxins) are also discussed here in

relation to diesel exhaust particulate matter and are also discussed under separate sections in this

chapter. Diesel exhaust is a complex mixture of carbon particles and associated organics and

inorganics, and it is not known what fraction or combination of fractions cause the health effects

(discussed below) that have been observed with exposure to diesel exhaust. While we are listing

diesel exhaust as diesel particulate matter and diesel exhaust organic gases (DPM + DEOG) to

provide specific targets for emission reduction and therefore a framework for developing

regulatory control strategies, the available science cannot separate the health effects of the

particulate and gaseous components of diesel exhaust. This listing includes the components of

diesel exhaust that are likely to contribute to the cancer and noncancer hazard (with the exception

of the gaseous phase criteria pollutants, such as NOx, SO2 and CO which are subject to National

Ambient Air Quality Standards); however, currently available science, as summarized in the draft

Health Assessment for Diesel Exhaust, while suggesting an important role for the particulate

phase component of diesel exhaust, does not attribute the serious likely cancer and noncancer

health effects independently to diesel particulate matter separate as distinct from the gas phase

components. Accordingly, we discuss the health effects attributed to whole diesel exhaust in this

section.
70 EPA. 2000. Health Assessment Document for Diesel Exhaust: SAB Review Draft. EPA/600/8-

90/057E Office of Research and Development, Washington, D.C. The document is available electronically at

www.epa.gov/ncea/dieslexh.htm.

71Bhatia, R., Lopipero, P., Smith, A. (1998) Diesel Exhaust Exposure and Lung Cancer.

Epidemiol. 9:84-91.

72Lipsett, M., Campleman, S. (1999) Occupational Exposure to Diesel Exhaust and Lung

Cancer: A Meta-analysis. Am J Public Health 80:1009-1017.

59

1. Cancer Effects of Diesel Exhaust

The EPA has concluded that diesel exhaust is likely to be carcinogenic to humans by

inhalation at occupational and environmental levels of exposure.70 The draft Health Assessment

Document for Diesel Exhaust (draft Assessment), was reviewed in public session by the Clean

Air Scientific Advisory Committee (CASAC) on October 12-13, 2000. The CASAC found that

the Agency’s conclusion that diesel exhaust is likely to be carcinogenic to humans is

scientifically sound. CASAC concurred with the draft Assessment’s findings with the proviso

that EPA provide modifications and clarifications on certain topics. The Agency expects to

produce the finalized Assessment in early 2001. Information presented here is consistent with

that to be provided in the final Assessment.

In its review of the published literature, EPA found that about 30 individual

epidemiologic studies show increased lung cancer risk associated with diesel emissions. In the

draft Assessment EPA evaluated 22 studies that were relevant for risk assessment, 16 of which

reported significant increased lung cancer risks, ranging from 20 to 167 percent, associated with

diesel exhaust exposure. Published analytical results of pooling many of the 30 studies showed

that on average, the risks were increased by 33 to 47 percent.71 72 Questions remain about the

influence of other factors (e.g., effect of smoking, other particulate sources), the quality of the

individual epidemiologic studies, exposure levels, and consequently the precise magnitude of the

increased risk of lung cancer. From a weight of evidence perspective, EPA concludes that the

epidemiologic evidence, as well as supporting data from certain animal and mode of action

studies, support the Agency’s conclusion that exposure to diesel exhaust is likely to pose a

human lung cancer hazard to occupationally exposed individuals as well as to the general public

exposed to typically lower environmental levels of diesel exhaust.

While available evidence supports EPA's conclusion that diesel exhaust is likely to be a

human lung carcinogen, and thus is likely to pose a cancer hazard to humans, EPA has concluded

that the available data is not sufficient to develop a confident estimate of cancer unit risk. The

absence of a cancer unit risk for diesel exhaust limits our ability to quantify, with confidence, the

potential impact of the hazard (magnitude of risk) on exposed populations. In the draft

Assessment, EPA acknowledged this limitation and provided a discussion of the possible

environmental cancer risk consistent with the majority of the occupational epidemiological

findings of increased lung cancer risk and the exposure differences between the occupational and
73 See Chapter 8.4 and 9.5.2 of the U.S. EPA (2000) Health Assessment Document for Diesel Emissions:

SAB Review Draft. EPA/600/8-90/057E Office of Research and Development, Washington, D.C. The document is

available electronically at www.epa.gov/ncea/dieselexh.htm.

74 ATSDR. 1999. Toxicological Profile for Ethylbenzene (update). USDHHS, PHS, ATSDR. 

60

environmental settings.73 

2. Noncancer Effects of Diesel Exhaust

The acute and chronic exposure-related noncancer effects of diesel exhaust emissions are

also of concern to the Agency. Acute exposure to diesel exhaust can result in physiologic

symptoms consistent with irritation and inflammation, and evidence of immunological effects

including increased reaction to allergens and some symptoms associated with asthma. The acute

effects data, however, lack sufficient detail to permit the calculation of protective levels for

human exposure.

For chronic diesel exhaust exposure, EPA is completing the development of an inhalation

reference concentration (RfC) for diesel exhaust exposure. The RfC is an estimate of the

continuous human inhalation exposure (including sensitive subgroups) that is likely to be without

an appreciable risk of deleterious non-cancer effects during a lifetime. While the limited amount

of human data is suggestive of respiratory distress, animal test data is quite definitive in

providing a basis to anticipate a hazard to the human lung based on the irritant and inflammatory

reactions in test animals. Thus, EPA believes that chronic diesel exhaust exposure, at sufficient

exposure levels, increases the hazard and risk of an adverse health effect.

In addition, it is also instructive to recognize that diesel exhaust particulate matter is part

of ambient fine PM. A qualitative comparison of adverse effects of exposure to ambient fine PM

and diesel exhaust particulate matter shows that the respiratory system is adversely affected in

both cases, though a wider spectrum of adverse effects has been identified for ambient fine PM. 

Relative to the diesel PM database, there is a wealth of human data for fine PM noncancer

effects. Since diesel exhaust PM is a component of ambient fine PM, the fine PM health effects

data base can be informative. The final Assessment will discuss the fine PM health effects data

and its relation to evaluating health effects associated with diesel exhaust. 

I. Ethylbenzene

Ethylbenzene is a colorless, aromatic hydrocarbon, that smells like gasoline. It is used

primarily in the production of styrene. It is also used as a solvent, as a constituent of asphalt and

naphtha. It is present as a gas in both gasoline and diesel exhaust and evaporative emissions

from gasoline powered vehicles.74 Ethylbenzene emissions from mobile sources account for

approximately 84 percent of the emissions in the 1996 National Toxics Inventory.

Ethylbenzene exposure also occurs from the use of consumer products, pesticides,
75 ATSDR. 1999. Toxicological Profile for Ethylbenzene (update). USDHHS, PHS, ATSDR.

76 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH, 1999.

77 Ligocki, M.P., G.Z. Whitten, R.R. Schulhof, M.C. Causley, and G.M. Smylie, Atmospheric

transformation of air toxics: benzene, 1,3-butadiene, and formaldehyde, Systems Applications International, San

61

solvents, carpet glues, varnishes, paints, and tobacco smoke. Indoor air usually has a higher

average concentration of ethylbenzene (about 1 ppb) than ambient air, due to the use of

household cleaning products or paints.75

Limited information is available on the carcinogenic effects of ethylbenzene in humans

and animals. Based on inadequate data from animal bioassays and human studies, EPA has

classified ethylbenzene as a Group D carcinogen, meaning it is not classifiable as to human

carcinogenicity and a full risk characterization has not been conducted by EPA due to this limited

data.76

 Acute (short-term) exposure to ethylbenzene in humans results in noncancer respiratory

effects, such as throat irritation and chest constriction, irritation of the eyes, and neurological

effects such as dizziness. Chronic (long-term) exposure to ethylbenzene by inhalation in humans

may result in effects on the blood. Animal studies have reported effects on the blood, liver, and

kidneys from chronic inhalation exposure to ethylbenzene. The data from these studies was

found to be sufficient for EPA to develop a RfC for ethylbenzene exposure. No information is

available on the developmental or reproductive effects of ethylbenzene in humans, although

animal studies have reported developmental effects, including birth defects in animals exposed

via inhalation.

J. Formaldehyde

Formaldehyde is used mainly to produce resins used in particle board products and as an

intermediate in the synthesis of other chemicals. It also has minor uses in agriculture, as an

analytical reagent, in concrete and plaster additives, cosmetics, disinfectants, fumigants,

photography, and wood preservation. The highest levels of airborne formaldehyde have been

detected in indoor air, where it is released from various consumer products such as building

materials and home furnishings.

Formaldehyde is the most prevalent aldehyde in vehicle exhaust. It is formed from

incomplete combustion of both gasoline and diesel fuel and accounts for one to four percent of

total exhaust TOG emissions, depending on control technology and fuel composition. It is not

found in evaporative emissions. Primary formaldehyde emissions from mobile sources account

for approximately 41 percent of the emissions in the 1996 National Toxics Inventory.

Formaldehyde exhibits extremely complex atmospheric behavior.77 It is present in
Rafael, CA (SYSAPP-91/106), 1991.

78 EPA 1987. Environmental Protection Agency, Assessment of health risks to garment workers and

certain home residents from exposure to formaldehyde, Office of Pesticides and Toxic Substances, April 1987.

79Chemical Industry Institute of Toxicology, Hazard Characterization and Dose-Response Assessment for

Carcinogencity by the Route of Inhalation, September 28, 1999.

62

emissions and is also formed by the atmospheric oxidation of virtually all organic species,

including biogenic (produced by a living organism) hydrocarbons. Mobile sources contribute

both primary formaldehyde (emitted directly from motor vehicles) and secondary formaldehyde

(formed from photooxidation of other VOCs emitted from vehicles). 

By conducting a formal risk characterization, EPA has classified formaldehyde as a

Group B1, probable human carcinogen, based on limited evidence for carcinogenicity in humans

and sufficient evidence of carcinogenicity in animal studies78. Epidemiological studies in

occupationally exposed workers suggest that long-term inhalation of formaldehyde may be

associated with tumors of the nasopharyngeal cavity (generally the area at the back of the mouth

near the nose), nasal cavity, and sinus. Studies in experimental animals provide sufficient

evidence that long-term inhalation exposure to formaldehyde causes an increase in the incidence

of squamous (epithelial) cell carcinomas (tumors) of the nasal cavity. The distribution of nasal

tumors in rats suggests that not only regional exposure but also local tissue susceptibility may be

important for the distribution of formaldehyde-induced tumors. Research has demonstrated that

formaldehyde produces mutagenic activity in cell cultures.

Since completion of the current IRIS cancer assessment several years ago, research has

been published regarding formaldehyde and the occurrence of respiratory tract tumors in rats

whose breathing patterns are different than those of humans. Due to new work done in

partnership with the Chemical Industry Institute of Toxicology (CIIT), a biologically-based doseresponse (BBDR) model79 has been developed to address these issues. The CIIT model is

composed of a computational fluid dynamics (CFD) model and a clonal growth model (CGM). 

The CFD model of airflow in rats and humans more accurately accounts for differences in

geometry of respiratory system and delivery of formaldehyde to the tissue. The CGM accounts

for mutations and tumor development. The models developed by CIIT will be used to describe

nose, throat, and lung tumor development and also revise the current cancer potency estimate. 

The draft reassessment is expected to be ready for SAB review in spring 2001.

Formaldehyde exposure also causes a range of noncancer health effects. At low

concentrations (0.05-2.0 ppm), irritation of the eyes (tearing of the eyes and increased blinking)

and mucous membranes are the principal effects observed in humans. At exposures of 1 to 11

ppm, other human upper respiratory effects associated with acute formaldehyde exposure include

a dry or sore throat, and a tingling sensation of the nose. Sensitive individuals may experience

these effects at lower concentrations. Forty percent of workers at formaldehyde-producing

factories reported nasal symptoms such as rhinitis (inflammation of the nasal membrane), nasal
80 Wilhelmsson, B. and M. Holmstrom. 1987. Positive formaldehyde PAST after prolonged formaldehyde

exposure by inhalation. The Lancet:164.

81 Burge, P.S., M.G. Harries, W.K. Lam, I.M. O'Brien, and P.A. Patchett. 1985. Occupational asthma due

to formaldehyde. Thorax 40:225-260.

82 Hendrick, D.J., R.J. Rando, D.J. Lane, and M.J. Morris. 1982. Formaldehyde asthma: Challenge

exposure levels and fate after five years. J. Occup. Med. 893-897.

83 Nordman, H., H. Keskinen, and M. Tuppurainen. 1985. Formaldehyde asthma - rare or overlooked? J.

Allergy Clin. Immunol. 75:91-99.

84 EPA 1991. Environmental Protection Agency. Formaldehyde risk assessment update. June 11, 1991.

Office of Toxic Substances, U.S. Environmental Protection Agency, Washington, DC. External review draft, June

11, 1991.

85 U.S. Environmental Protection Agency. Health and Environmental Effects Profile for Formaldehyde.

EPA/600/x-85/362. Environmental Criteria and Assessment Office, Office of Health and Environmental

Assessment, Office of Research and Development, Cincinnati, OH. 1988. 

86 World Health Organization. Environmental Health Criteria for Formaldehyde. Volume 89. World

Health Organization, Geneva, Switzerland. 1989. 

87 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH, 1999.

http://www.epa.gov/ngispgm3/iris/index.html

63

obstruction, and nasal discharge following chronic exposure.80 In persons with bronchial asthma,

the upper respiratory irritation caused by formaldehyde can precipitate an acute asthmatic attack,

sometimes at concentrations below 5 ppm.81 Formaldehyde exposure may also cause bronchial

asthma-like symptoms in nonasthmatics.82,83 It is unclear whether asthmatics are more sensitive

than nonasthmatics to formaldehyde's effects.84

An increased incidence of menstrual disorders and pregnancy problems were observed in

women workers using urea-formaldehyde resins. However, possible confounding factors were

not evaluated in this study. In another study of hospital equipment sterilizing workers there was

no reported association between formaldehyde exposure and increased spontaneous abortions. 

Developmental effects, such as birth defects, have not been observed in animal studies with

formaldehyde.85,86

Though EPA has not completed the calculation of an RfC for formaldehyde inhalation

exposure, additional data from oral exposure studies was found to be sufficient for EPA to

develop a RfD for formaldehyde oral exposure.87

K. n-Hexane
88 ATSDR. 1999. Toxicological Profile for Hezane. USDHHS, PHS, ATSDR. 

89 ATSDR. 1999. Toxicological Profile for Hexane. USDHHS, PHS, ATSDR.

90 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH, 1999.

91 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH, 1999.

http://www.epa.gov/ngispgm3/iris/index.html

64

n-Hexane is a colorless volatile liquid that is insoluble in water and is highly flammable. 

Commercial grades of n-hexane are used as solvents for glues, varnishes, cements, and inks. It is

also used as a solvent in the extraction of edible fats and oils. n-Hexane is also a component of

gasoline and it is also found in the exhaust and evaporative emissions from motor vehicles.88 nHexane emissions from mobile sources account for approximately 43 percent of the emissions in

the 1996 National Toxics Inventory.

The most probable route of human exposure to n-hexane is by inhalation. Individuals are

most likely to be exposed to n-hexane in the workplace. Monitoring data indicate that n-hexane

is a widely occurring atmospheric pollutant as well.89

No information is available on the carcinogenic effects of n-hexane in humans or animals.

EPA has made no determination as to the human carcinogenicity of n-hexane.90

Acute (short-term) inhalation exposure of humans to high levels of n-hexane causes mild

central nervous system (CNS) depression and irritation of the skin and mucous membranes. 

Nervous system effects include dizziness, giddiness, slight nausea, and headache in humans. 

Chronic (long-term) exposure to n-hexane in air is associated with polyneuropathy in humans,

with numbness in the extremities, muscular weakness, blurred vision, headache, and fatigue

observed. Neurotoxic effects have also been exhibited in rats. Mild inflammatory and

degenerative lesions in the nasal cavity have been observed in rodents chronically exposed by

inhalation. Limited information is available on the reproductive or developmental effects of nhexane; one study reported testicular damage in rats exposed to n-hexane through inhalation. 

Birth defects have not been observed in the offspring of rats chronically exposed via inhalation in

several studies. The data from these studies was found to be sufficient for EPA to develop a RfC

for n-hexane exposure.91 

L. Lead Compounds

The largest source of lead in the atmosphere has been from leaded gasoline combustion. 

With the phase down of lead in gasoline, however, air lead levels have decreased considerably,

though lead is still a component of racing and aviation fuels. In the 1996 National Toxics

Inventory, mobile sources account for approximately 24 percent of the total inventory. This
92 ATSDR. 1999. Toxicological Profile for Lead (Update). USDHHS, PHS, ATSDR.

93 ATSDR. 1999. Toxicological Profile for Lead (Update). USDHHS, PHS, ATSDR.

94 EPA. 1997. Deposition of Air Pollutants to the Great Waters-Second Report to Congress, Office of Air

Quality Planning and Standards, June 1997, EPA-453/R-97-011.

95 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH, 1999.

96 EPA. 1989. Evaluation of the potential carcinogenicity of lead and lead compounds: In support of

reportable quantity adjustments pursuant to CERCLA Section 102. Prepared by the Office of Health and

Environmental Assessment, Washington, DC. EPA/600/8-89/045A. (External Review Draft). 

65

declining trend should continue since there was a total lead phase-out from highway gasoline and

its additives that went into effect in January 1996. Other airborne sources include combustion of

solid waste, coal, and oils, emissions from iron and steel production, lead smelters, and tobacco

smoke.92

Exposure to lead can also occur from food and soil. Children are at particular risk to lead

exposure since they commonly put hands, toys, and other items, that may come in contact with

lead-containing dust and dirt in their mouths. Lead-based paints were commonly used for many

years and flaking paint, paint chips, and weathered paint powder may be a major source of lead

exposure, particularly for children. Lead in drinking water is due primarily to the presence of

lead in certain pipes, solder, and fixtures. Exposure to lead may also occur in the workplace,

such as lead smelting and refining industries, steel and iron factories, gasoline stations, and

battery manufacturing plants.93 Lead has been listed as a pollutant of concern in EPA's Great

Waters Program due to its persistence in the environment, potential to bioaccumulate, and

toxicity to humans and the environment.94

Human studies are inconclusive regarding lead exposure and cancer, while animal studies

have reported an increase in kidney cancer from lead exposure by the oral route. The EPA

considers lead to be a Group B2, probable human carcinogen based on sufficient data in

animals.95,96

Lead is a very toxic element, causing a variety of effects at low dose levels. Brain

damage, kidney damage, and gastrointestinal distress are seen in humans receiving acute

(short-term) exposure to high levels of lead. Chronic (long-term) exposure to lead affects the

blood, central nervous system (CNS), blood pressure, kidneys, and Vitamin D metabolism in

humans. Children are particularly sensitive to the chronic effects of lead, with slowed cognitive

development, reduced growth and other effects reported. Reproductive effects, such as decreased

sperm count in men and spontaneous abortions in women, have been associated with lead

exposure. The developing fetus is at particular risk from maternal lead exposure, with low birth
97 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH, 1999.

98 EPA. 1986. Air Quality Criteria Document for Lead. Prepared by the Office of Health and

Environmental Assessment, Environmental Criteria and Assessment Office, Research Triangle Park, NC, for the

Office of Air Quality Planning and Standards. EPA-600/8-83/028dF. 

99 EPA 1994. EPA Health Effects Notebook for Hazardous Air Pollutants-Draft, EPA-452/D-95-00,

December 1994, Office of Air Quality Planning and Standards, RTP, NC. 

http://www.epa.gov/ttn/uatw/hapindex.html

100 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH, 1999.

66

weight and slowed postnatal neurobehavioral development noted.97 EPA has found the

noncancer health effects sufficient to warrant the establishment of a National Ambient Air

Quality Standard (NAAQS) for Lead.98

M. Manganese Compounds

Manganese is a naturally occurring substance found in many types of rock and soil; it is

ubiquitous in the environment and found in low levels in water, air, soil and food. Manganese

can also be released into the air by iron and steel production plants, power plants, and coke

ovens. The average manganese levels in various media are as follows: levels in drinking water

are approximately 0.004 ppm; average air levels are approximately 0.02 μg/m3

; levels in soil

range from 40 to 900 ppm; the average daily intake from food ranges from 1 to 5 mg/d. People

who work in factories where manganese metal is produced from manganese ore or where

manganese compounds are used to make steel or other products are most likely to be exposed

through inhalation to higher than normal levels of manganese.99 Manganese compounds from

mobile sources comprise less than 2 percent of the 1996 National Toxics Inventory.

No studies are available regarding the carcinogenic effects of manganese in humans, and

animal studies are inadequate. Based on this information, EPA has classified manganese as a

Group D carcinogen (not classifiable as to carcinogenicity in humans).100

Key health effects concerns in humans have been associated with neurotoxic and perhaps

developmental effects. Chronic exposure to high levels of manganese by inhalation in humans

results primarily in central nervous system (CNS) effects. Visual reaction time, hand steadiness,

and eye-hand coordination were affected in chronically-exposed workers. A syndrome named

manganism may result from chronic exposure to higher levels; manganism is characterized by

feelings of weakness and lethargy, tremors, a mask-like face, and psychological disturbances.

Respiratory effects have also been noted in workers chronically exposed by inhalation. Based on

these occupational studies, EPA has found the data to be sufficient to develop a RfC for

manganese oxides and salts exposure. Impotence and loss of libido have been noted in male

workers afflicted with manganism attributed to high-level inhalation exposures to manganese. 
101 ATSDR. 1990. Toxicological Profile for Manganese (Draft). U.S. Public Health Service, U.S.

Department of Health and Human Services, Altanta, GA.

102 EPA. 1994. ORD’s “Re-evaluation of Inhalation Health Risks Associated with MMT in Gasoline,

July 1, 1994". Office of Research and Development, Washington, D.C.

103 The fuels and fuel additives testing program regulations are codified at 40 CFR part 79, subpart F. The

Alternative Tier 2 provisions appear at 40 C.F.R. § 79.58(c).

67

Animal studies have reported reproductive effects such as sterility and developmental effects

such as decreased activity levels in the offspring of animals exposed to manganese.101,102

In December, 1995, the fuel additive methylcyclopentadienyl manganese tricarbonyl

(MMT), an octane enhancer commercially labeled as HiTEC 3000, became legal to blend into

unleaded gasoline in the U.S. The approved fuel waiver for MMT allows up to 0.03125 (1/32)

gram per gallon manganese (60 FR 36414, July 17, 1995). Ethyl Corporation is still required to

perform health research but is able to do the research while the product is marketed. On May 19

2000, the Agency notified Ethyl Corporation of the final test program requiring emission and

health effects testing for the gasoline additive MMT, in accordance with the Alternative Tier 2

provision of the fuels and fuel additives health effects testing regulations.103 The Alternative Tier

2 health effects testing will give the general public a greater awareness of the comparative risks

associated with inhalation exposures to gasoline fuels containing MMT. The Alternative Tier 2

test requirements are within two general categories, pharmacokinetic testing of manganese

compounds and characterization of manganese emissions from vehicles utilizing fuels containing

MMT. These Alternative Tier 2 testing requirements are intended to be the first stage in a twostage Alternative Tier 2 test program. EPA intends to evaluate the results produced in the first

stage of testing, as well as any other information which may be submitted to or obtained by EPA

in the meantime, in determining the specific nature and scope of the second stage of Alternative

Tier 2 testing. Any additional Alternative Tier 2 tests proposed for fuel and additives containing

MMT in the future will be announced in a separate Federal Register notice. The docket number

for the MMT Alternative Tier 2 testing requirements is A-98-35. Section 211 allows for the

development of a Tier 3 set of tests, if necessary, to further answer questions related to these

fuels in the interest of protecting public health.

N. Mercury Compounds

Mercury exists in three forms: elemental mercury, inorganic mercury compounds

(primarily mercuric chloride), and organic mercury compounds (primarily methyl mercury). All

forms of mercury are quite toxic, and each form exhibits different health effects. Elemental

mercury is used in thermometers, barometers, and pressure-sensing devices. It is also used in

batteries, lamps, industrial processes, refining, lubrication oils, and dental amalgams. Inorganic

mercury was used in the past in laxatives, skin-lightening creams and soaps, and in latex paint. 

In 1990, EPA canceled registration for all interior paints that contained mercury. Mercury use in

exterior paint was discontinued after 1991. Methyl mercury has no industrial uses; it is formed in
104 ATSDR. 1999. Toxicological Profile for Mercury (update). USDHHS, PHS, ATSDR.

105 EPA. 1997. Mercury Study Report to Congress. Volume II: An Inventory of Anthropogenic Mercury

Emissions in the United States. EPA-452/R-97-004. http://www.epa.gov/oar/mercury.html

106 Ball, James C. Emission Rates and Elemental Composition of Particles Collected from 1995 Ford

Vehicles Using the Urban Dynamometer Driving Schedule, the Highway Fuel Economy Test, and the US06 Driving

Cycle. Society of Automotive Engineers, SAE paper No. 97FL-376. 1997.

107 Schroeder, W.H., Hamilton, M.C. and Stobart, S.R. (1985) The use of noble metals as collection media

for mercury and its compounds in the atmosphere. Revs. In Anal. Chem. 8:179-209.

108 Cooper. J.A. et al., NEA, INC. PM10 for the South Coast Air Basin, Volumes I and II. Prepared for

the South Coast Air Quality Management District, El Monte, CA. July 15, 1987

109 EPA. 1997. Mercury Study Report to Congress. Volume IV: An Assessment of Exposure to Mercury

in the United States. EPA-452/R-97-006. http://www.epa.gov/oar/mercury.html

110 EPA. 1997. Deposition of Air Pollutants to the Great Waters-Second Report to Congress, Office of

Air Quality Planning and Standards, June 1997, EPA-453/R-97-011.

68

the environment from the methylation of the inorganic mercurial ion.104, 105

The most recent data, for various varieties of gasoline vehicles and heavy duty diesel

vehicles, showed negligible emissions of elemental mercury and no indication that inorganic

mercury is emitted using laboratory test cycles.106 Analytical methods typically used to collect

and measure mercury from mobile sources are not sensitive enough to measure trace level

emissions. Thus, if data were developed using appropriate collection media and sensitive

analytical methods, such as cold-vapor atomic fluorescence, mercury may be detected in mobile

source emissions.107 Current inventory estimates of mobile source mercury emissions rely on an

older database that speciates PM emissions from mobile sources.108 For one category of vehicle,

light duty diesel vehicles, no recently developed emissions factors were available, so we used

factors developed in the 1987 South Coast Air Quality Management District study. The mobile

source emissions estimate, therefore has zero emissions from gasoline powered vehicles and

 heavy duty diesels, but there were emission estimates for light duty diesels. 

There is no reason to believe that light duty vehicles are uniquely emitters of mercury among all

mobile sources; the more likely explanation is a measurement artifact. Mercury emissions from

mobile sources are traditionally not speciated and are presented as total elemental mercury

emissions. Mercury compounds from mobile sources comprise less than 4 percent of the 1996

National Toxics Inventory.

A major source of exposure for elemental mercury is through inhalation in occupational

settings.109 Mercury has been listed as a pollutant of concern in EPA's Great Waters Program due

to its persistence in the environment, potential to bioaccumulate, and toxicity to humans and the

environment.110
111 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH, 1999. 

112 EPA. 1997. Mercury Study Report to Congress. Volume V: Health Effects of Mercury and Mercury

compounds. EPA-452/R-97-007. http://www.epa.gov/oar/mercury.html

113 EPA 1993. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. 

http://www.epa.gov/ngispgm3/iris/index.html

114 Bird, M. G.; Burleigh-Flayer, H. D.; Chun, J. S.; Douglas, J. F.; Kneiss, J. J.; Andrews, L. S. (1997)

Oncogenicity studies of inhaled methyl tertiary-butyl ether (MTBE) in CD-1 mice and F-344 rats. J. Appl. Toxicol.

69

Human and animal studies are inconclusive regarding the carcinogenicity of elemental

mercury. Based on this data, the EPA has classified elemental mercury as a Group D, not

classifiable as to human carcinogenicity.111 Mercuric chloride is categorized as a Group C,

possible human carcinogen.

Acute (short-term) exposure to high levels of elemental mercury in humans results in

central nervous system (CNS) effects such as tremors, mood changes, and slowed sensory and

motor nerve function. High inhalation exposures can also cause kidney damage. Acute

inhalation exposure also has effects on the gastrointestinal tract and respiratory system in

humans. Chronic (long-term) inhalation exposure to elemental mercury in humans also affects

the CNS, with effects such as erethism (increased excitability), irritability, excessive shyness, and

tremors.112 The data from these studies was found to be sufficient for EPA to develop a RfC for

elemental mercury exposure. Additional data from oral exposure studies was found to be

sufficient for EPA to also develop a RfD for elemental mercury oral exposure.

O. MTBE

Methyl tert-butyl ether (MTBE) is a colorless liquid that has been used in the United

States since the late-1970's as an octane-enhancing replacement for lead. Currently, MTBE’s

main use is as a fuel oxygenate as part of the Wintertime Oxygenated Fuel and Federal

reformulated gasoline (RFG) programs. MTBE emissions from mobile sources account for

approximately 86 percent of the total MTBE inventory in the 1996 National Toxics Inventory.

Human exposure to MTBE may occur via inhalation, ingestion, or dermal contact.

The majority of the research on the health effects of MTBE to date has focused on the

effects of inhalation exposure. By the inhalation route, MTBE has been found to cause increases

in liver and kidney weights and increased severity of spontaneous kidney lesions, as well as

swelling around the eyes and increased prostration in laboratory rats113. These effects were cited

as the basis for EPA’s inhalation reference concentration (RfC) for MTBE. In addition to noncancer effects, long-term inhalation exposure to high concentrations of MTBE has been

associated with tumors in the kidneys and testes of male rats and in the liver of female mice.114
17(suppl. 1): S45-S55.

115 Belpoggi F., Soffritti M and Maltoni C. 1995. Methyl-tertiary-butyl ether (MTBE)- a gasoline additive

- causes testicular and haematopoietic cancers in rats. Toxicol Ind Health 11:119-149.

116 Belpoggi, F.; Soffritti, M.; Maltoni, C. (1998) Pathological characterization of testicular tumours and

lymphomas-leukaemias, and of their precursors observed in Sprague-Dawley rats exposed to methyl-tertiary-butylether (MTBE). Eur. J. Oncol. 3: 201-206. 

117 EPA. 1994. Health risk perspectives on fuel oxygenates. Washington, DC: Office of Research and

Development; report no. EPA 600/R-94/217.

118 Interagency Oxygenated Fuels Assessment Steering Committee. 1997. Interagency assessment of

oxygenated fuels. Washington, DC: National Science and Technology Council, Committee on Environment and

Natural Resources and Office of Science and Technology Policy. http://www.epa.gov/otaq/fuels.html.

119 International Agency for Research on Cancer. 1999. Methyl tert-butyl ether (group 3).

http://193.51.164.11/htdocs/Monographs/Vol73/73-13.html.

120 National Institute of Environmental Health Sciences, National Toxicology Program. 2000. Summary

of RG1, RG2, and NTP Board Subcommittee Recommendations for the Report on Carcinogens. Ninth Edition.

http://ehis.niehs.nih.gov/roc/toc9.html

70

However, there have been no human or animal health effects studies concerning the ingestion of

MTBE in drinking water. In one study, animals were given MTBE in olive oil by gavage for up

to 24 months.115,116 Lymphomas and leukemia were observed in the female rats and testicular

tumors in the male rats.

A report by EPA’s Office of Research and Development concluded that, under the 1986

EPA cancer risk assessment guidelines, inhalation cancer test results would support placing

MTBE in Group C as a "possible human carcinogen."117 An Interagency Assessment of

Oxygenated Fuels similarly concluded that “While there are no studies on the carcinogenicity of

MTBE in humans, there is sufficient evidence to indicate that MTBE is an animal carcinogen and

to regard MTBE as having a human hazard potential. However, estimates of human risk from

MTBE contain large uncertainties in both human exposure and cancer potency.”118 Other public

health bodies, such as the International Agency for Research on Cancer119 and the U.S.

Department of Health and Human Services120 have indicated that there is not enough information

to classify MTBE with regard to human carcinogenicity under their classification schemes. The

Agency will continue to reevaluate the potential carcinogenicity of MTBE as new information

becomes available. 

P. Naphthalene

Naphthalene occurs as a white solid or powder that is insoluble in water. It has a strong,

mothball odor. The primary use for naphthalene is in the production of phthalic anhydride. 

Other uses include carbamate insecticides, surface active agents and resins, dye intermediates,
121 EPA. 1998. Toxicological Review of Naphthalene, In support of Summary Information on the

Integrated Risk Information system. Washington, D.C. http://www.epa.gov/ngispgm3/iris/subst/0436.htm

122 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. 

http://www.epa.gov/ngispgm3/iris/index.html

123 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. 

http://www.epa.gov/ngispgm3/iris/index.html

71

synthetic tanning agents, and moth repellents. Naphthalene is found in small quantities in

gasoline and diesel fuels. Naphthalene emissions have been measured in larger quantities in both

gasoline and diesel exhaust and evaporative emissions from mobile sources. Individuals may be

exposed to naphthalene through the use of mothballs. Workers may be occupationally exposed

during its manufacture and use, especially in coal-tar production, wood preserving, tanning, or

ink and dye production. Coal tar production, wood preserving, and other industries release small

amounts. Naphthalene has also been detected in tobacco smoke.121

Workers occupationally exposed to vapors of naphthalene and coal tar developed

laryngeal carcinomas or neoplasms of the pylorus and cecum. Di-, tri-, and tetramethyl

naphthalene contaminants of coal tar were found to be carcinogenic when applied to the skin of

mice, but naphthalene alone was not. An increased number of lung adenomas were reported in

mice exposed by inhalation, but this was not dose-related. No carcinogenic responses were

reported in rats exposed to naphthalene in their diet and by injection. The human carcinogenic

potential of naphthalene via the oral or inhalation routes cannot be determined at this time based

on human and animal data; however, there is suggestive evidence. EPA has classified

naphthalene as a Group C, possible human carcinogen but no risk estimate can be derived due to

the weak data set.122

Acute (short-term) exposure of humans to naphthalene by inhalation, ingestion, and

dermal contact is associated with hemolytic anemia, damage to the kidneys, and, in infants, brain

damage. Symptoms of acute exposure include headache, nausea, vomiting, diarrhea, malaise,

confusion, anemia, jaundice, convulsions, and coma. Cataracts have also been reported in

workers acutely exposed to naphthalene by inhalation and ingestion. Chronic (long-term) results

from rodent studies, supported by other subchronic and acute studies, identify nasal and

respiratory lesions as critical effects from chronic inhalation exposure to naphthalene. The data

from these animal studies was found to be sufficient for EPA to develop a RfC for naphthalene

exposure. Additional data from rat oral exposure studies was found to be sufficient for EPA to

also develop a RfD for naphthalene oral exposure.123

Q. Nickel Compounds

Nickel is a natural element of the earth's crust; as a result, small amounts are found in

food, water, soil, and air. Food is the major source of nickel exposure, with an average intake for
124 ATSDR. 1997. Toxicological Profile for Nickel (Update). USDHHS, PHS, ATSDR

125 EPA. 1986. Health Assessment Document for Nickel and Nickel Compounds. Prepared by the Office

of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Research Triangle Park,

NC. EPA/600/8-83/012FF.

126 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. 

http://www.epa.gov/ngispgm3/iris/index.html

127 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. 

http://www.epa.gov/ngispgm3/iris/index.html

72

adults estimated to be approximately 100 to 300 μg/d. Individuals also may be exposed to nickel

in occupations involved in its production, processing, and use, or through contact with everyday

items such as nickel-containing jewelry and stainless steel cooking and eating utensils, and by

smoking tobacco. Nickel is found in ambient air at very low levels as a result of releases from

oil and coal combustion, nickel metal refining, sewage sludge incineration, manufacturing

facilities, and other sources. Nickel compounds have also been identified in trace quantities in

exhaust emissions from gasoline and diesel engines.124 Nickel compounds from mobile sources

comprise less that nine percent of the 1996 National Toxics Inventory.

The EPA has not evaluated soluble salts of nickel as a class of compounds for potential

human carcinogenicity. Human and animal studies have reported an increased risk of lung and

nasal cancers from exposure to nickel refinery dusts and nickel subsulfide. EPA has classified

nickel refinery dust and nickel subsulfide as Group A, human carcinogens and has completed a

formal risk characterization for nickel and nickel compounds.125 Sufficient data from animal

studies of soluble nickel compounds (i.e., nickel carbonyl) have reported lung tumors though the

human data is insufficient. EPA has classified nickel carbonyl as a Group B2, probable human

carcinogen, and given its high instability, nickel carbonyl exposure is extremely rare.126

Nickel dermatitis, causing itching of the fingers, hands, and forearms, is the most

common effect in humans from chronic (long-term) skin contact with nickel. Respiratory effects

have also been reported in humans from inhalation exposure to nickel. No information is

available regarding the reproductive or developmental effects of nickel in humans, but animal

studies have reported reproductive and developmental effects. The data from these studies was

found to be insufficient for EPA to develop a RfC for nickel exposure. Additional data from

animal oral exposure studies was found to be sufficient for EPA to also develop a RfD for nickel

soluble salts exposure.127

R. POM (Polycyclic Organic Matter)

Polycyclic organic matter, or POM, defines a broad class of compounds that includes the

polycyclic aromatic hydrocarbon compounds (PAHs), of which benzo[a]pyrene is a member. 
128 ATSDR. 1995. Toxicological Profile for Poylcyclic Aromatic Hydrocarbons (PAHs) (Update). 

USDHHS, PHS, ATSDR.

129 EPA. 1997. Deposition of Air Pollutants to the Great Waters-Second Report to Congress, Office of

Air Quality Planning and Standards, June 1997, EPA-453/R-97-011.

130 EPA. 1991. Dose-Response Analysis of Ingested Benzo[a]pyrene (CAS No. 50-32-8). Human

Health Assessment Group, Office of Health and Environmental Assessment, Washington, DC. EPA/600/R-92/045.

131 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH, 1999.

73

The primary source of POM is formation during combustion. A less significant formation

mechanism is the volatilization of light weight POM compounds, which occurs in the production

and use of naphthalene. Polycyclic organic compounds have been detected in ambient air from

sources including cigarette smoke, gasoline and diesel engine exhausts, asphalt road paving, coal

burning, application of coal tar, agricultural burning, residential wood burning, and hazardous

waste sites. The compounds present in POM and their relative amounts differ among different

sources (e.g, POM from diesel exhaust is chemically different than POM from wood burning).128

POM from mobile source particulate, as the sum of the seven PAHs that are probable human

carcinogens, accounts for approximately six percent of the 1996 National Toxics Inventory. 

PAHs have been found in some drinking water supplies. Cooking meat or other foods at

high temperatures increases the amount of PAHs in the food. Occupational exposure to PAHs

may occur in coal tar production plants, coking plants, coal-gasification sites, smokehouses,

municipal trash incinerators, and other facilities. POM has been listed as a pollutant of concern

in EPA's Great Waters Program due to its persistence in the environment, potential to

bioaccumulate, and toxicity to humans and the environment.129

Skin exposures to mixtures of carcinogenic PAHs cause skin disorders in humans and

animals. No information is available on the reproductive or developmental effects of POM in

humans, but animal studies have reported that oral exposures to benzo[a]pyrene causes

reproductive and developmental effects. Cancer is the major concern from exposure to POM.

Epidemiologic studies have reported an increase in lung cancer in humans exposed to coke oven

emissions, roofing tar emissions, and cigarette smoke; all of these mixtures contain POM

compounds. Animal studies have reported respiratory tract tumors from inhalation exposure to

benzo[a]pyrene and forestomach tumors, leukemia, and lung tumors from oral exposure to

benzo[a]pyrene.130 The EPA has classified seven PAHs (benzo[a]pyrene, benz[a]anthracene,

chrysene, benzo[b]fluoranthene, benzo[k]fluoranthene, dibenz[a,h]anthracene, and

indeno[1,2,3-cd]pyrene) as Group B2, probable human carcinogens based only on sufficient

animal data.131 No formal risk characterization has been conducted.

EPA has determined that the data set is insufficient for EPA to develop either a RfC or a

RfD for POM exposure.
132 ATSDR. 1992. Toxicological Profile for Styrene. USDHHS, PHS, ATSDR TP-91/25.

133 ATSDR. 1992. Toxicological Profile for Styrene. USDHHS, PHS, ATSDR TP-91/25.

134 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. 

http://www.epa.gov/ngispgm3/iris/index.html

74

S. Styrene

Styrene is a colorless liquid that has a sweet smell. It is used predominately in the

production of polystyrene and resins. Styrene is also used as an intermediate in the synthesis of

materials used for ion exchange resins and to produce copolymers. Styrene is also emitted in

significant quantities in the exhaust gases of both gasoline and diesel powered engines.132

Styrene from mobile sources accounts for approximately 40 percent of the 1996 National Toxics

Inventory.

 

 Indoor air is the principal route of styrene exposure for the general population, due to

building materials, consumer products, and tobacco smoke. Occupational exposure to styrene

occurs in the reinforced plastics industry and polystyrene factories.133

Several epidemiologic studies suggest there may be an association between styrene

exposure and an increased risk of leukemia and lymphoma. However, the evidence is

inconclusive due to confounding factors. Animal studies have produced both negative and

positive results. EPA is currently assessing the potential of styrene to cause cancer.

Acute (short-term) exposure to styrene results in mucous membrane and eye irritation,

and gastrointestinal effects in humans. Chronic (long-term) exposure of humans to styrene

results in effects on the central nervous system (CNS), such as headache, fatigue, weakness,

depression, peripheral neuropathy, minor effects on some kidney enzyme functions and on the

blood. Human studies are inconclusive on the reproductive and developmental effects of styrene;

several studies did not report an increase in developmental effects in women who worked in the

plastics industry, while an increased frequency of spontaneous abortions and decreased frequency

of births were reported in another study. respiratory lesions as critical effects from chronic

inhalation exposure to naphthalene. The data from human studies was found to be sufficient for

EPA to develop a RfC for styrene exposure. Additional data from animal oral exposure studies

was found to be sufficient for EPA to also develop a RfD for styrene oral exposure.134

T. Toluene

Toluene occurs as a colorless, flammable, refractive liquid that is slightly soluble in

water. It has a sweet, pungent odor. The major use of toluene is as a mixture added to gasoline

to improve octane ratings. Toluene is also used to produce benzene and as a solvent in paints,

coatings, adhesives, inks, and cleaning agents. It is used in the production of polymers used to
135 ATSDR 1995. Toxicological Profile for Toluene (Update). USDHHS, PHS, ATSDR.

136 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. 

http://www.epa.gov/ngispgm3/iris/index.html

137 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. 

http://www.epa.gov/ngispgm3/iris/index.html

75

make nylon, plastic soda bottles, and polyurethanes, and for pharmaceuticals, dyes, cosmetic nail

products, and the synthesis of organic chemicals. The highest concentrations of toluene usually

occur in indoor air from the use of common household products (paints, paint thinners, and

adhesives) and cigarette smoke. The deliberate inhalation of paint or glue by solvent abusers

may produce high levels of exposure to toluene, as well as to other chemicals. Toluene exposure

may also occur in the workplace, especially in occupations such as printing or painting, where

toluene is frequently used as a solvent.135

Mobile sources are the principal source of toluene to the ambient air. Toluene is found in

both gasoline and diesel fuel as well as the exhaust emissions of both types of engines. Toluene

from mobile sources accounts for approximately 74 percent of the 1996 National Toxics

Inventory. Toluene can also be released to the ambient air during the production, use, and

disposal of industrial and consumer products that contain toluene.

None of the data suggest that toluene is carcinogenic. Two epidemiological studies did

not detect a statistically significant increased risk of cancer due to inhalation exposure to toluene.

However, these studies had many confounding factors. Animal studies have been negative for

carcinogenicity. Considering no human data and inadequate animal data, and the lack of positive

results in the majority of genotoxic assays, EPA has classified toluene as a Group D compound

(not classifiable as to human carcinogenicity).136

The central nervous system (CNS) is the primary target for toluene toxicity in both

humans and animals for acute (short-term) and chronic (long-term) exposures. CNS dysfunction

(which is often reversible) and narcosis have been frequently observed in humans acutely

exposed to low or moderate levels of toluene by inhalation; symptoms include fatigue,

sleepiness, headaches, and nausea. Cardiac arrhythmia has also been reported in humans acutely

exposed to toluene. CNS depression has been reported to occur in chronic abusers exposed to

high levels of toluene. Symptoms include ataxia, tremors, cerebral atrophy, nystagmus

(involuntary eye movements), and impaired speech, hearing, and vision. Chronic inhalation

exposure of humans to toluene also causes irritation of the upper respiratory tract, eye irritation,

sore throats, nausea, skin conditions, dizziness, headaches, and difficulty with sleep.137

Human studies have also reported developmental effects, such as CNS dysfunction,

attention deficits, and minor craniofacial and limb anomalies, in the children of pregnant women

exposed to toluene or mixed solvents by inhalation. Reproductive effects, including an
138 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. 

http://www.epa.gov/ngispgm3/iris/index.html

139 ATSDR. 1995. Toxicological Profile for Xylenes (Update). USDHHS, PHS, ATSDR.

140 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. 

http://www.epa.gov/ngispgm3/iris/index.html

76

association between paternal exposure to toluene and an increased odds ratio for spontaneous

abortions but not birth defects, have also been noted. However, these studies are not conclusive

due to many confounding variables. Animal studies have shown toluene to have developmental,

but not reproductive, effects from inhalation exposure. The data from human and animal studies

was found to be sufficient for EPA to develop a RfC for toluene exposure. Additional data from

animal oral exposure studies was found to be sufficient for EPA to also develop a RfD for

toluene oral exposure.138

U. Xylene

Mixed xylenes are colorless liquids with a sweet odor. They are used in the production of

ethylbenzene, in solvents, and for paints and coatings. They are also blended into gasoline and

are also present in diesel fuel. Xylenes are emitted in the exhaust emissions of both gasoline and

diesel powered engines accounting for 78 percent of the 1996 National Toxics Inventory. 

Xylenes are distributed throughout the environment; they have been detected in air, rainwater,

soils, surface water, sediments, drinking water, and aquatic organisms. Xylenes have also been

detected in indoor air; xylenes have been widely used in home use products such as paints. 

Occupational exposure to mixed xylenes may occur at workplaces where mixed xylenes are

produced and used as industrial solvents.139

No information is available on the carcinogenic effects of mixed xylenes in humans, and

animal studies have reported negative results from exposure via gavage (experimentally placing

the chemical in the stomach). Considering there is no human data and the animal data is 

negative, EPA has classified mixed xylenes as a Group D compound (not classifiable as to

human carcinogenicity).140

Acute (short-term) inhalation exposure to mixed xylenes in humans results in irritation of

the nose and throat, gastrointestinal effects such as nausea, vomiting, and gastric irritation, mild

transient eye irritation, and neurological effects. Chronic (long-term) inhalation exposure of

humans to mixed xylenes results primarily in central nervous system (CNS) effects, such as

headache, dizziness, fatigue, tremors and uncoordination. Other effects noted include labored

breathing and impaired pulmonary function, increased heart palpitation, severe chest pain and an

abnormal EKG, and possible effects on the blood and kidney. This data has been determined by

EPA to be insufficient to calculate a RfC. Insufficient data are available on the developmental or

reproductive effects of mixed xylenes in humans. Animal studies have reported developmental
141 EPA 1999. Environmental Protection Agency, Integrated Risk Information System (IRIS), Office of

Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. 

http://www.epa.gov/ngispgm3/iris/index.html

77

effects, such as an increased incidence of skeletal variations in fetuses, and fetal resorptions via

inhalation. Additional data from animal oral exposure studies was found to be sufficient for EPA

to develop a RfD for oral xylene exposure.141
78

Chapter 4: Impacts of Motor Vehicle Emission Control

Programs on MSAT Emissions

In Chapter 2 of the TSD we identified the 21 MSATs. We now turn to an evaluation of

the impact of existing and proposed controls on inventories of those air toxics by examining the

emissions inventories and estimated reductions expected to be achieved by our various mobile

source control programs. 

The data and information available on emissions of these 21 MSATs vary considerably.

While we have 1996 inventory data for all of the MSATs except naphthalene, we do not have

inventory projections for all of them. Therefore, we are examining the projected impacts of our

current mobile source control program by groupings of air toxics. More specifically, we have

projections of future emissions for five gaseous toxics (benzene, formaldehyde, 1,3-butadiene,

acetaldehyde, MTBE) and for diesel PM (as the surrogate for diesel PM and diesel exhaust

organic gases) and we present these in this section. We do not have emissions projections for the

remaining gaseous toxics (acrolein, POM, styrene, toluene, xylene, ethylbenzene, naphthalene,

and n-hexane) but, because these compounds are part of VOCs, we believe it is reasonable to

utilize VOC emissions inventory projections to estimate the expected impact of our control

programs on these other gaseous MSATs. Finally, we also do not have emissions inventory

projections for the metals on the MSAT list (arsenic compounds, chromium compounds, mercury

compounds, nickel compounds, manganese compounds, and lead compounds) or for

dioxins/furans. While metal emissions and dioxin/furans emissions are associated with particles

and it is possible that some of these compounds track PM emissions to some extent, we do not

have good data on these relationships. Therefore, we are not presenting emission projections for

these compounds in this analysis. We believe this is reasonable because the mobile source

contribution to metals inventories is small and comes primarily from engine wear and impurities

in engine oil, or from fuel additives.

As we describe in the following discussion, there have been and will continue to be

significant reductions in MSATs as a result of on-highway emission control regulations. By

2020, we project on-highway emission control programs (up to and including our Tier 2 control

program and our recently proposed 2007 heavy-duty engine rule) will reduce benzene emissions

by 73 percent, formaldehyde emissions by 76 percent, 1,3-butadiene emissions by 72 percent,

and acetaldehyde emissions by 67 percent from 1990 levels. Under these controls we project onhighway diesel PM emissions will be reduced by 94 percent by 2020, as compared with 1990

levels.

This chapter consists of two parts. First, we describe two previous EPA studies that have

estimated inventories of MSAT emissions. Second, we describe the methodologies used for this

rulemaking to develop our toxics emissions inventories, including our estimates of how our

current and proposed on-highway emission control programs will reduce MSAT emissions in the

future.
142 EPA. 1999. Analysis of the Impacts of Control Programs on Motor Vehicle Toxics Emissions and

Exposure in Urban Areas and Nationwide. Prepared for U. S. EPA, Office of Transportation and Air Quality, by

Sierra Research, Inc., and Radian International Corporation/Eastern Research Group. Report No. EPA 420 –R-99-

029/030.

143 Naphthalene emissions are not reported in the 1996 NTI separately from 16-PAH. 

79

A. Previous EPA Studies of Toxics Emissions Inventories

The following section presents a discussion of two previous EPA studies that have

estimated toxics emissions inventories from mobile sources.

1. The 1999 EPA Motor Vehicle Air Toxics Study

We developed inventory estimates for several gaseous MSATs (acetaldehyde, benzene,

1,3-butadiene, formaldehyde, MTBE) and also for diesel PM as part of the 1999 EPA Motor

Vehicle Air Toxics Study, “Analysis of the Impacts of Control Programs on Motor Vehicle Toxic

Emissions and Exposure in Urban Areas and Nationwide,”142 (hereafter referred to as the 1999

EPA Motor Vehicle Air Toxics Study, or the 1999 Study). The six pollutants examined in the

1999 Study were chosen becuase we had adequate data to perform a rigorous modeling analysis

for those pollutants (examining the impact of fuel properties, emission control technologies, and

type of in-use operation on the emission inventories for these six pollutants). The modeling

performed for the 1999 Study form the basis of the inventories presented in Section B. of this

chapter.

The 1999 EPA Motor Vehicle Air Toxics Study provided estimates of toxics emission

inventories for these compounds for 1990, 1996, 2007, and 2020. The 1990 inventories reflected

toxics emissions before any of the programs added by the 1990 Clean Air Act Amendment were

implemented. The 1996 inventories reflected the impact of some of the new Clean Air Act

programs, such as Phase 1 of the RFG program. The 2007 and 2020 inventories were intended to

reflect the impact of all of our mobile source regulations under development at the time the study

was completed (including the Tier 2 standards for light-duty and the proposed 2007 standards for

heavy-duty engines).

As noted above, the inventory estimates presented in Section B. of this chapter are based

on the inventories presented in the 1999 Study. A number of updates, as described in Section B.

of this chapter, have been made to account for updated information for heavy-duty engines.

2. The 1996 National Toxics Inventory

The 1996 National Toxics Inventory (NTI) prepared in connection with the Agency’s

National Air Toxic Assessment (NATA), contains 1996 emission estimates for all 21 MSATs,

except naphthalene.143 The 1996 NTI contains 1996 emissions estimates for both on-highway
144 The nonroad inventory in the 1996 NTI includes emissions data for a number of nonroad categories

including aircraft. Under the Clean Air Act definition, nonroad vehicles do not include aircraft. For convenience,

in this document the term “nonroad” will generally include aircraft. It should be noted that the nonroad emissions

estimates contained in the 1996 NTI are based on the draft NONROAD model, and, therefore, are subject to

change.

80

and nonroad sources.144 (Because diesel exhaust is not included on the list of 112(b) hazardous

pollutants that are the focus of the 1996 NTI, diesel PM estimates were not compiled in the 1996

NTI.) Table IV.A-1 presents the MSAT inventories from the 1996 NTI and indicates the onhighway and nonroad percentages of the national inventories for each of the MSATs. The

percentages are based on the total national inventories which include on-highway and nonroad

mobile sources, major and area stationary sources, and other sources such as forest fires.
145Mass given in tons of TEQ (toxic equivalency quotient). EPA’s Office of Research and Development

(ORD) has recently developed an inventory for dioxin and dioxin-like compounds using different methods than

those used in the NTI. For 1995, the EPA-ORD estimate of on-highway emissions of dioxin compounds is 0.00005

tons TEQ, comprising 1.5 percent of the national inventory in that year. (The TEQ rates the toxicity of each dioxin

and furan relative to that of 2,3,7,8-TCDD, which is assigned a TEQ of 1.0.)

81

Table IV.A-1

1996 On-Highway and Nonroad Emission Inventories of Some MSATs

from the 1996 National Toxics Inventory (short tons)

Compound

On-Highway Nonroad Mobile Sources

Tons

Percent of

Total

National

Emissions Tons

Percent of

Total

National

Emissions Tons

Percent of

Total

National

Emissions

1,3-Butadiene* 23,500 42% 9,900 18% 33,400 60%

Acetaldehyde* 28,700 29% 40,800 41% 69,500 70%

Acrolein* 5,000 16% 7,400 23% 12,400 39%

Arsenic Compounds* 0.25 0.06% 2.01 0.51% 2.26 0.57%

Benzene* 168,200 48% 98,700 28% 266,900 76%

Chromium Compounds* 14 1.2% 35 3% 49 4.2%

Dioxins/Furans*145 0.0001 0.2% N.A. N.A. 0.0001 0.2%

Ethylbenzene 80,800 47% 62,200 37% 143,000 84%

Formaldehyde* 83,000 24% 86,400 25% 169,400 49%

Lead Compounds* 19 0.8% 546 21.8% 565 22.6%

Manganese Compounds* 5.8 0.2% 35.5 1.3% 41.3 1.5%

Mercury Compounds* 0.2 0.1% 6.6 4.1% 6.8 4.2%

MTBE 65,100 47% 53,900 39% 119,000 86%

n-Hexane 63,300 26% 43,600 18% 106,600 44%

Naphthalene N.A. N.A. N.A. N.A. N.A. N.A.

Nickel Compounds* 10.7 0.9% 92.8 7.6% 103.5 8.5%

POM (as sum of 7 PAH)* 42.0 4% 19.3 2% 61.3 6%

Styrene 16,300 33% 3,500 7% 19,800 40%

Toluene 549,900 51% 252,200 23% 802,100 74%

Xylene 311,000 43% 258,400 36% 569,400 79%

* Also on the urban HAPs list for the Integrated Urban Air Toxics Strategy (64 FR 38706, July 19,1999).
146 This list can be found in the National Air Toxics Programs: The Integrated Urban Strategy; Notice. 

July 19, 1999, 64 Federal Register 38706-38740.

147 Aviation gasoline is used by a relatively small number of aircraft, those with piston engines, which are

generally used for personal transportation, sightseeing, crop dusting, and similar activities. 

82

The NTI data reflect certain interesting characteristics of mobile source air toxics

emissions. First, mobile sources account for the majority of the 1996 national inventory of three

of the gaseous MSATs that are included on the urban HAP list.146 These three are 1,3-butadiene

(60 percent), acetaldehyde (70 percent), and benzene (76 percent). Mobile sources account for

39 percent of the national inventory of acrolein and 49 percent of the national inventory of

formaldehyde, two other gaseous urban HAPs. All of these MSATs are formed as part of the

combustion process. In addition, benzene is also released through evaporative emissions from

gasoline.

Second, with regard to the other MSATs that are included on the urban HAP list, the

mobile source contribution generally is small (arsenic compounds, chromium compounds,

manganese compounds, nickel compounds, POM, and dioxins/furans). The sole exception is

lead compounds. Mobile sources contribute 23 percent of the national inventories of lead

compound emissions due primarily to nonroad sources and, more specifically, to the use of a

lead-additive package which boosts the octane of aviation gasoline.147 The mobile source

contribution to the other metals on the urban HAP list comes primarily from engine wear, from

some fuel additives, or from impurities in engine oil.

With regard to the gaseous MSATs that are not included on the urban HAP list, mobile

source contributions are high due to the presence of some of these compounds in gasoline (e.g.,

ethylbenzene, MTBE, n–hexane, toluene, and xylene). 

In addition, mobile sources account for almost all diesel PM emissions. (A limited

number of stationary sources, such as large generators, do operate on diesel fuel. Because there

are relatively few stationary sources that operate on diesel fuel, we believe that diesel PM from

stationary sources is relatively small compared to diesel PM from mobile sources. However, for

this analysis we have not generated an estimate of diesel PM from stationary sources.) As shown

later in this chapter, we estimate that 1996 on-highway diesel PM emissions are approximately

180,000 tons. We estimate that 1996 nonroad diesel PM emissions are approximately 346,000

tons, as discussed in Chapter 8 of this Technical Support Document.

B. Impacts of Motor Vehicle Emission Controls on Emission Inventories

Many of the programs that we have put in place since the passage of the 1990 Clean Air

Act Amendments to achieve attainment of the National Ambient Air Quality Standards

(NAAQS) for ozone, PM and CO have also reduced MSAT emissions. For example, measures

to control hydrocarbons from motor vehicles are also effective in controlling gaseous toxics. In
83

addition, certain programs address air toxics directly, such as the RFG program and the phase-out

of leaded gasoline. We describe some of our key mobile source control programs in Chapter 1 of

this Technical Support Document. 

This section presents the inventories of MSATs and describes how we derived these

inventories. To provide a framework for understanding our results, we first present an overview

of our various inventory methodologies. We then present the emissions estimates for the five

gaseous toxics addressed in the 1999 EPA Motor Vehicle Air Toxics Study. Next, we discuss

our VOC emission trends as a surrogate to reflect the emission trends of other gaseous toxics for

which we do not have specific inventory projections, including acrolein, POM, styrene, xylene,

toluene, ethylbenzene, naphthalene, and n-hexane. We conclude by discussing the trend for

diesel PM emissions.

We are not reporting inventory trends for the metals on our list of MSATs (arsenic

compounds, chromium compounds, mercury compounds, nickel compounds, manganese 

compounds, and lead compounds) or for dioxins/furans. Metals in mobile source exhaust can

come from fuel, fuel additives, engine oil, engine oil additives, or engine wear. Formation of

dioxin and furans requires a source of chlorine. Thus, while metal emissions and dioxin/furan

emissions are associated with particles, there are a number of other factors that contribute to

emission levels. While it is possible that these compounds track PM emissions to some extent,

we do not have good data on these relationships.

1. Overview of Inventory Methodologies

We analyzed emissions trends for gaseous air toxics addressed in the 1999 EPA Motor

Vehicle Air Toxics Study (benzene, 1,3-butadiene, formaldehyde, acetaldehyde, and MTBE), for

VOC as a surrogate for the emissions trends for other gaseous air toxics, and for diesel PM. We

estimated emissions for each of these classes of air toxics for four separate years (1990, 1996,

2007, and 2020). The methods used to estimate these emissions are summarized below and

described in more detail in the following pages.

In the 1999 Study, we produced inventory estimates for various years and control

scenarios that account for the effects of fuel and vehicle technology changes for five gaseous

toxics. The inventories were calculated for different vehicles, including light-duty vehicles and

trucks, and heavy-duty gasoline and diesel vehicles. For this rulemaking analysis, we used the

light-duty vehicle and truck toxics emissions inventories from the 1999 Study directly to estimate

emissions for all four years of interest. (The light-duty inventories used in this analysis include

the effect of the Tier 2 program recently adopted by EPA). To calculate toxics emissions

inventories for heavy-duty gasoline and diesel vehicles, we relied on inventories contained in the

1999 Study that included the impacts of all heavy-duty engine programs up until the 2004 model

year standards, and adjusted the inventories to account for the impact of the recently proposed

2007 heavy-duty engine standards, including updated modeling information for heavy-duty

engines. A description of the methodology used to project the heavy-duty gasoline and diesel

vehicle toxic emissions inventories (assuming the proposed 2007 heavy-duty engine standards
148 The analysis methodology is described in a memorandum from Meredith Weatherby, Eastern Research

Group, to Rich Cook, EPA, entitled “Estimating of 1990 VOC and TOG Emissions” in EPA Air Docket A-2000-

12. 

149 EPA. 2000. National Air Pollution Emission Trends, 1900-1998 (March 2000). Office of Air Quality

Planning and Standards, Research Triangle Park, NC. Report No. 454/R-00-002. 

84

take effect) is contained in section B.2.a. of this chapter.

We did not evaluate other gaseous air toxics in our 1999 Study. However, since all of

these compounds are VOCs, we expect their emissions trends to follow the VOC emissions

trend. For 1996 and later years, we developed VOC inventories assuming all of the on-highway

control program, including the recent 2007 heavy-duty engine proposal, have taken effect. These

VOC inventory estimates are based on our most up-to-date information on both light-duty

vehicle and heavy-duty engine emissions factors and VMT developed for MOBILE6, and also

reflect county-by-county information on VMT distribution by vehicle class, roadway type, and

speed.

For 1990, we modified the modeling methods applied in the 1999 Study to produce direct

estimates of VOC emissions that account for the effects of fuel and vehicle technology changes

as well as the information that will be used in EPA’s MOBILE6 emissions model.148 We could

not use the inventories presented in the 2007 heavy-duty engine proposal, because they do not

extend back as far as 1990. Our other alternative was to use the 1990 VOC estimates from

EPA’s Trends Report. However, such estimates would not be comparable to the 1996 and later

estimates, since EPA’s 1990 Trends estimates have not been updated to reflect the data and

analyses that will be used in MOBILE6. 

Diesel PM inventories for 1996 and later years were developed assuming all of the onhighway control programs, including the recent 2007 heavy-duty engine proposal, have taken

effect and included a number of modeling updates. The light-duty diesel PM emission estimates

reflect the effects of the Tier 2 program for light-duty vehicles and trucks. The heavy-duty diesel

PM emissions estimates incorporate recent findings on heavy-duty diesel engine PM emissions

that were not reflected in the 1999 Study including updated emission factors and VMT. The

modeling also considered county-by-county information on VMT distribution by vehicle class,

roadway type, and speed.

The modeling performed for the 2007 heavy-duty engine proposal did not produce heavyduty diesel PM estimates for 1990, so we chose to use the heavy-duty diesel PM inventory

estimates for 1990 from EPA’s Trends Report.149 We believe this approach is reasonable, since

we have not substantially changed our estimates of emissions from 1990 and earlier engines since

the Trends Report estimates were developed. We also used data from the EPA’s Trends Report

for light-duty diesel PM estimates for 1990. The 1990 diesel PM inventories from EPA’s Trends

Report (presented in this analysis) and the diesel PM inventory from the 1999 Study are roughly

comparable; the Trends Report inventory is 235,000 tons while the 1999 Study inventory is
150 EPA. 1993. Motor Vehicle-Related Air Toxics Study. Report No. EPA 420-R-93-005. 

151 Peer review comments on the 1993 study can be accessed at http://www.epa.gov/otaq/toxics.htm

152 EPA. 1999. Analysis of the Impacts of Control Programs on Motor Vehicle Toxics Emissions and

Exposure in Urban Areas and Nationwide. Prepared for U. S. EPA, Office of Transportation and Air Quality, by

Sierra Research, Inc., and Radian International Corporation/Eastern Research Group. Report No. EPA 420 –R-99-

029/030.

85

202,000 tons. The 1999 Study results do not explicitly account for county-specific inputs, unlike

Trends and the heavy-duty engine inventory presented in this analysis; furthermore, we consider

it likely that the 1999 Study underestimates nationwide diesel PM emissions due to the way it

extrapolates urban emissions to broader regions. 

2. 1999 EPA Motor Vehicle Air Toxics Study

Section 202(l)(1) of the Clean Air Act calls on EPA to study the need for and feasibility

of controlling toxic air pollutants associated with motor vehicles and motor vehicle fuels. We

completed the study required under Section 202(l)(1) in April 1993. The report, entitled “Motor

Vehicle-Related Air Toxics Study,” is available on our website

(www.epa.gov/otaq/toxics.htm).150 Specific pollutants or pollutant categories which are

discussed in this report include benzene, formaldehyde, 1,3-butadiene, acetaldehyde, diesel

particulate, gasoline particulate, gasoline vapors as well as selected metals. The study focuses on

carcinogenic risk although discussions of non-cancer effects for these and other pollutants are

also included. The study provided estimates of emissions, exposure, and risk, with projections to

the year 2010. Peer review comments on this study were received in 1994.151 Peer review

comments suggested improvements to EPA’s exposure modeling and risk assessment

methodology.

In response to these comments, EPA updated its exposure model for motor vehiclerelated air toxics. Also, since 1993, significant new information on vehicle emission rates has

been developed, and much more is known about the impact of fuel properties on toxic emissions. 

Moreover, EPA has updated its cancer risk assessment for benzene, and has released draft risk

assessments for 1,3-butadiene and diesel exhaust emissions. Furthermore, EPA has developed

new programs, such as the NLEV and Tier 2 standards, which significantly impact projections of

toxic emissions, exposure, and risk. 

In light of new information that was developed after 1993, and in response to peer review

comments, EPA has updated estimates of emissions and exposure. The updated final emissions

and exposure assessment, “Analysis of the Impacts of Control Programs on Motor Vehicle

Toxics Emissions and Exposure in Urban Areas and Nationwide,” (the 1999 EPA Motor Vehicle

Air Toxics Study) was released in November, 1999.152

The remainder of this subsection provides additional information on how we developed

the inventories contained in the 1999 Study. We also present the updated toxic emissions
153 Note that 1996 NTI estimates for the Northeast States were developed using VMT data supplied by

those states, rather than estimates in the Emission Trends Database.

86

inventory results developed for this analysis assuming all currently promulgated mobile source

control programs are in effect (including the Tier 2 program) as well as the proposed 2007 heavyduty engine standards. While we addressed diesel PM emissions in the 1999 Study, we discuss

the diesel PM emissions inventory projections in a later section, to reflect recent updates to the

heavy-duty engine inventory modeling.

a. Methodology for Estimating Gaseous Mobile Source Air Toxic Emission

Inventories

In the 1999 Study we estimated emissions of benzene, formaldehyde, acetaldehyde, 1,3-

butadiene, and MTBE using a toxic emission factor model, MOBTOX5b. This model is based

on a modified version of MOBILE5b, which estimates emissions of regulated pollutants, and

essentially applies toxic fractions to total organic gas (TOG) estimates. The model accounted for

differences in toxic fractions between technology groups, driving cycles, and normal versus high

emitting vehicles and engines (“high emitters”). Impacts of fuel formulations were also

addressed in the modeling. The TOG basic emission rates used in this modeling incorporated

available elements from MOBILE6 used to develop the VOC inventory for the Tier 2 final rule. 

(The modeling did not incorporate impacts of evaporative emission standards in the Tier 2 rule

which are expected to result in further reductions in evaporative emissions from light-duty

vehicles and trucks. Therefore, for those toxics emissions which have an evaporative emissions

component (i.e., benzene and MTBE), the 2007 and 2020 inventories presented in this chapter

are slightly overestimated, and the reductions are slightly underestimated.)

We modeled toxic emissions for 10 urban areas and 16 geographic regions. These urban

areas and geographic regions are listed in Table IV.B-1. They were selected to encompass a

broad range of I/M programs, fuel parameters, and temperature regimes. The intent of the

selection process was to best characterize the different combinations needed to perform accurate

nationwide toxic emissions estimates. Every U. S. county in the country was then “mapped” to

one of these modeled areas or regions (i.e., the emission factor for the modeled area was also

used for the area “mapped” to it). Mapping was done based on a combination of geographic

proximity, I/M program, and fuel control programs. Details of this process are provided in the

1999 Study. We then multiplied the resulting county-level emission factors by the county-level

VMT estimates from EPA’s Emission Trends Database and summed the results across all

counties to come up with nationwide emissions in tons. This approach was also used to develop

the inventory estimates in the 1996 NTI.153

Table IV.B-1

Metropolitan Areas and Regions Included in Toxic Emissions Modeling

Chicago, IL Atlanta, GA Florida
154 Costs for Meeting 40 ppm Sulfur Content Standard for Gasoline in PADDs 1-3, via MOBILE and CD

TECH Desulfurization Processes. A Study performed for the American Petroleum Institute by Mathpro, Inc.,

February 26, 1999. EPA Air Docket A-97-10, Document Number IV-G-122.

155 EPA. 1994. Regulatory Impact Analysis for the Final Rule on Reformulated and Conventional

Gasoline, February, 1994.

87

Denver, CO Western WA/OR Northeast States – non-I/M and nonRFG

Houston, TX Northern CA Northeast States - I/M and non-RFG

Minneapolis, MN Southern CA Northeast States - non-I/M and RFG

New York, NY ID/MT/WY Ohio Valley – non-I/M and non-RFG

Philadelphia, PA UT/NM/NV Ohio Valley – I/M and non-RFG

Phoenix, AZ West TX Ohio Valley – I/M and RFG

Spokane, WA ND/SD/NB/IA/KS/Western MO Northern MI/WI

St. Louis, MO AR/MS/AL/SC/Northern LA

Modeling for these areas was done on a seasonal basis. Information on fuel properties for

1990 and 1996 was obtained from surveys conducted by the National Institute for Petroleum and

Energy Research (NIPER) and the American Automobile Manufacturers Association (AAMA). 

Fuel parameters for 2007 and 2020 were projected from 1996 baseline values using information

from a February 26, 1999 report from Mathpro to the American Petroleum Institute.154 Data from

the EPA Emission Trends Database and other agency sources were used to develop appropriate

local modeling parameters for I/M programs, Stage II refueling controls, fuel RVP, average

ambient temperature, and other inputs. 

Exhaust Emissions

Analysis of speciation data from 1990 technology light-duty gasoline vehicles done for

the EPA Complex Model for Reformulated Gasoline showed that the fraction of toxic emissions

relative to TOG differs among the eight technology groups within the Complex Model as well as

between normal emitters and high emitters.155 This difference is especially significant for 1,3-

butadiene; its toxic/TOG fraction is about three times larger for high emitters than for normal

emitters. If this difference is not taken into account, the impact of I/M programs and fleet

turnover to vehicles with lower deterioration rates will be underestimated. Thus, the input format

for exhaust toxic adjustment factors in MOBTOX5b was structured to allow input of high and

normal emitter toxic emission rates for a given “target” fuel. The target fuel is simply the fuel of

concern in the modeling analysis. These toxic emission rates were then weighted to come up with

a composite toxic emission factor based on a distribution of normal and high emitters. This
88

distribution is not supplied directly by the MOBILE model. Instead, this distribution was

determined from the fleet average TOG emission rate on baseline fuel as determined by MOBILE

and average normal and high TOG emission rates on baseline fuel derived from the Complex

Model. Essentially, “toxic-TOG curves” were developed that plot the target fuel toxic emission

rate against the base fuel TOG emission rate.

To construct these curves, the distribution of normal and high emitters was determined in

the following manner for each model year. A TOG gram per mile emission rate for normal

emitters (TOG-N) and a TOG emission rate for high emitters (TOG-H) on baseline fuel were

input into MOBTOX5b. TOG-N from newer technology light-duty gasoline vehicles and trucks

were obtained from an unconsolidated version of the Complex Model, which provides output for

normal emitters in each of eight technology groups. The Complex Model provides estimates for

mass of exhaust VOC, which is TOG minus the mass of methane and ethane. TOG was

estimated by applying a conversion factor which accounts for the mass of these compounds. The

conversion factor was derived by analysis of weight percent emissions of methane and ethane

from available speciation data. Based on the distribution of technology groups in a given model

year, the individual TOG estimates were weighted appropriately to obtain a composite estimate

for all normal emitters. Since the unconsolidated model’s TOG-N emission rates are applicable

only to Tier 0 light duty vehicles, they had to be adjusted for Tier 1 and later vehicles. This

adjustment was performed by multiplying the unconsolidated model results by the ratio of the

emission standard for these later vehicles to the Tier 0 emission standard. TOG-H was also

obtained from the unconsolidated version of the Complex Model. TOG-H was assumed to be the

same for all Tier 0 and later high emitting vehicles.

For benzene, 1,3-butadiene, formaldehyde, and acetaldehyde, milligram per mile toxic

emission rates for normal and high emitters running on a given fuel formulation were also

entered into MOBTOX5b using output from the unconsolidated version of the Complex Model.

An example of the data file format is provided in Table IV.B-2. 

Table IV.B-2

Example of Data File Format for Toxic Adjustment Factors

IV MYA MYB TOG-N TOG-H BZ-N BZ-H AC-N AC-H FR-N FR-H BD-N BD-H

1 1965 1974 0.000 10.00 0.00 276.93 0.00 109.72 0.00 224.28 0.00 93.15

1 1975 1980 0.000 10.00 0.00 263.61 0.00 108.70 0.00 173.41 0.00 44.57

1 1981 1987 0.640 4.03 28.63 113.23 5.07 32.89 7.16 44.59 2.14 25.84

1 1988 1999 0.570 4.03 17.49 116.45 4.02 28.65 5.67 36.68 2.04 30.82

Notes: IV = vehicle class, MYA = initial model year, MYB = final model year, TOG-N = TOG for normal emitters

running on baseline fuel in g/mi, TOG-H = TOG for high emitters on baseline fuel in g/mi, BZ = benzene in mg/mi

for vehicles running on fuel A, AC = acetaldehyde in mg/mi on fuel A, FR = formaldehyde in mg/mi on fuel A, BD

= 1,3-butadiene in mg/mi on fuel A.

Using the information in the data file, an overall FTP (Federal test procedure) toxic
89

emission rate for each vehicle class in a given model year is calculated. This overall rate takes

into account the distribution of normal and high emitters by calculating the slope and intercept of

a straight line (the “toxic-TOG” curve), where the FTP toxic emission rates for a vehicle class in

a given model year are a linear function of the baseline fuel TOG emission rate:

TOXFlt, Fuel A, FTP = A + B*TOGBaseline fuel, FTP (1)

A and B are determined as follows:

A = (TOG-H*TOX-N - TOG-N*TOX-H)/(TOG-H - TOG-N) (2)

B = (TOX-H - TOX-N)/(TOG-H - TOG-N) (3)

where:

TOX-N = toxic emission rate for normal emitters derived from the Complex Model

TOX-H = toxic emission rate for high emitters derived from the Complex Model

TOG-N = total organic gas emission rate for normal emitters derived from the Complex

Model

TOG-H = total organic gas emission rate for high emitters derived from the Complex

Model

These relationships can be thought of graphically, as illustrated in Figure IV.B-1, below.
90

 Figure IV.B-1

Example Plot of Target Fuel Benzene Versus 

Baseline Fuel TOG under FTP Conditions

Hypothetical Benzene-TOG Curve

0

20

40

60

80

100

120

140

0 0.5 1 1.5 2 2.5

Baseline Fuel TOG (g/mi)

Target Fuel Benzene (mg/mi)

TOG

Normal

TOG

High

An issue related to the above methodology is whether the linear assumption is valid for baseline

TOG values above the high emitter point and below the normal emitter point. This is particularly

relevant in cases where A and B values are determined from Tier 0 vehicles (e.g., the Complex

model), but the results are applied to Tier 1 and LEV-category vehicles. For the simple example

presented above, negative benzene emissions are estimated for the target fuel when the baseline

fleet-average TOG emission rate falls below 0.295 g/mi. Thus, for fleet-average emission rates

below (and above) the normal (and high) emitter values, a different methodology was needed. In

those cases, it was assumed that the toxic emission rate was the same on a fractional basis (for

VOC emission rates below the Tier 0 normal emitter rate, for example, the toxic fraction stays

constant at the toxic fraction for Tier 0 normal emitters). In the example above, the benzene

emission rate for a baseline TOG value of 0.1 g/mi would be calculated as follows:

BZ(TOG=0.1 g/mi) = 0.1 g/mi * (16 mg/mi BZ / 0.5 g/mi TOG) = 3.2 mg/mi

This has the effect of forcing the toxic-TOG curve from the normal-emitter point back through

the origin and thus avoids negative toxic emission rate estimates for Tier 1 and LEV-category

vehicles. The same approach is used in cases where the fleet-average baseline TOG emission

rate is above the high emitter point. 

For non-light-duty vehicle classes and older technology light-duty vehicles, such as non-
156 These studies include: Auto/Oil Air Quality Improvement Research Program. “Technical Bulletin No.

19: Dynomometer Study of Off-Cycle Exhaust Emissions”; April, 1996; Black, F.; Tejada, S.; Gurevich, M. 

“Alternative Fuel Motor Vehicle Tailpipe and Evaporative Emissions Composition and Ozone Potential”, J. Air &

Waste Manage. Assoc. 1998, 48, 578-591; and CARB, 1998, Unpublished data.

157 1,3-Butadiene, formaldehyde, and acetaldehyde are not found in fuel and hence are not found in

nonexhaust emissions. Because their nonexhaust emissions are zero, they were not included in the portions of

MOBTOX5b used to estimate nonexhaust emissions.

91

catalyst and oxidation catalyst vehicles, adequate toxic emissions data were not available to

distinguish between emission rates of normal and high emitters. In such cases, the toxic fraction

was assumed to be constant regardless of the VOC emission level.

Next, aggressive driving corrections were applied to the FTP toxic emission rates for

light-duty vehicles. These corrections were provided in an external data file and were

multiplicative in form. Several recent studies suggest that toxic fractions of TOG differ between

FTP and aggressive driving conditions.156 Thus, another adjustment to the toxic emission rates

was applied to take into account this difference in toxic fractions. This adjustment took the form

of the ratio of the toxic mass fraction over the unified cycle (FTP and off-cycle) to the toxic mass

fraction over the FTP. The adjustment was obtained from an analysis of unpublished CARB data

as described in EPA (1999d). The toxic emission rate under the unified cycle (FTP and offcycle) was calculated in the model as follows:

TOXUC = TOXFTP * ADJAggressive Driving * ADJTOX UC/FTP (4)

where

TOXUC = Unified Cycle toxic emission rate

TOXFTP = FTP toxic emission rate

ADJAggressive Driving = Adjustment to TOG emissions for aggressive driving

ADJTOX UC/FTP = Adjustment for difference in toxic mass fraction over the UC versus FTP

 MOBTOX5b then applies temperature, speed, humidity and load corrections.

Evaporative, Refueling, Running Loss, and Resting Loss Emissions

MOBTOX5b estimated evaporative, refueling, running loss, and resting loss toxic

emissions for benzene.157 Benzene fractions of total hydrocarbons were entered in an external

data file. Separate fractions were entered for hot soak, diurnal, refueling, running loss, and

resting loss. Toxic fractions for evaporative, refueling and running loss emissions of benzene

from gasoline vehicles were obtained from the Complex Model (EPA 1994). The Complex

Model does not estimate resting loss emissions. EPA assumed that the benzene fractions of

diurnal and resting loss emissions were the same.

Calculating Gaseous Toxic Emissions Under the Proposed 2007 Heavy-Duty Engine

Standards
158 “VMT Estimates for the 2007 Heavy-Duty Final Rule Analyses,” EPA memorandum from Penny

Carey, ASD, May 9, 2000. EPA Air Docket A-2000-12, Document Number IV-B-03.

92

We expect the recently proposed 2007 heavy-duty engine standards to reduce gaseous

toxics emissions. To estimate the effect of the proposed 2007 and later model year heavy-duty

engine standards on toxics inventories, we started with the toxics inventories estimated in the

1999 Study assuming all heavy-duty engine programs up until the 2004 model year standards are

in effect. Using these “baseline” inventory estimates and the nationwide vehicle miles traveled

(VMT) estimates from the 1999 Study, we then estimated the “baseline” gram per mile emissions

for the five toxics (on a nationwide, average basis). Next, we estimated the percent reduction in

hydrocarbon emissions expected from the proposed 2007 heavy-duty engine standards for each of

the projection years (as described in more detail in the discussion of VOC inventories below). 

To obtain the estimated “control” emission factors, we applied the same percent reduction to the

“baseline” gram per mile toxic emission estimates. Finally, we then multiplied the gram per mile

estimates by updated nationwide vehicle mile traveled (VMT) estimates to obtain the heavy-duty

gasoline and diesel toxic inventories used in this analysis.158 (Because benzene and MTBE have

an exhaust and an evaporative component, we applied the percent reduction based on total

(exhaust and evaporative) NMHC benefits for these compounds. For formaldehyde,

acetaldehyde, and 1,3-butadiene, which do not have an evaporative component, we applied the

percent reduction based on exhaust NMHC only.)

b. Projected Emissions Inventories of Selected Gaseous Toxics

Tables IV.B-3 and IV.B-4 present the on-highway emission inventories for the five

gaseous MSATs addressed in 1999 EPA Motor Vehicle Air Toxics Study. The inventory

estimates reflect all of the on-highway control programs currently promulgated including the

Tier 2 program, plus the recently proposed 2007 heavy-duty engine standards.
93

 Table IV.B-3

Annual Emissions Inventory for Selected Toxics for the Total U.S.

On-Highway Vehicles Only*

(thousand short tons per year)

Compound 1990 Emissions 1996 Emissions 2007 Emissions 2020 Emissions

1,3-Butadiene 36 24 12 10

Acetaldehyde 41 31 17 13

Benzene 257 171 89 68

Formaldehyde 139 93 43 34

MTBE 55 67 26 18

* - Includes the impact of our current on-highway control programs and the proposed 2007 and

later model year heavy-duty engine standards.

Table IV.B-4

 Estimated Percent Reduction for Selected Toxics for the Total U.S.

On-Highway Vehicles Only*

Compound

Cumulative Percent Reduction from 1990

1996 2007 2020

1,3-Butadiene 35% 67% 72%

Acetaldehyde 23% 58% 67%

Benzene 33% 65% 73%

Formaldehyde 33% 69% 76%

MTBE -22% 52% 67%

* - Includes the impact of our current on-highway control programs and the proposed 2007 and

later model year heavy-duty engine standards.

3. VOC Emissions Inventory

With the exception of the five gaseous MSATs examined in the 1999 EPA Motor Vehicle

Air Toxics Study, we do not have detailed emissions data for the other gaseous MSATs (acrolein,

POM, styrene, xylene, toluene, ethylbenzene, naphthalene, and n-hexane). In this section, we

present the VOC emissions trend as a surrogate to understand the trend in emissions of the other

gaseous MSATs in order to estimate projected inventory impacts from our current and proposed
159 EH Pechan & Associates, Inc, “Procedures for Developing Base Year and Future Year Mass and

Modeling Inventories for the Heavy-Duty Diesel (HDD) Rulemaking,” Prepared for U.S. Environmental Protection

Agency, September 29, 2000. EPA Air Docket A-2000-12, included in Item IV-A-01.

160 EH Pechan & Associates, Inc, “Data Summaries of Base Year and Future Year Mass and Modeling

Inventories for the Heavy-Duty Diesel (HDD) Rulemaking–Detailed Report,” Prepared for U.S. Environmental

Protection Agency, September 29, 2000. EPA Air Docket A-2000-12, included in Item IV-A-01.

161 Memorandum from Michael Samulski and John Koupal to Docket A-99-06, “Heavy-Duty Vehicle

Emission Factors and Adjustment Factors for the Final 2007 Heavy-Duty Rule Inventory Analysis,” May 26, 2000. 

EPA Air Docket A-2000-12, Item IV-B-01.

162 Memorandum from Michael Samulski to Docket A-99-06, “Revisions to Heavy-Duty Vehicle

Emission Factors and Adjustment Factors for the Final 2007 Heavy-Duty Rule Inventory Analysis,” November 2,

2000. EPA Air Docket A-2000-12, Item IV-B-02.

163The analysis methodology is described in a memorandum from Meredith Weatherby, Eastern Research

Group, to Rich Cook, EPA, entitled “Estimating of 1990 VOC and TOG Emissions” in EPA Air Docket A-2000-

12, Document Number IV-D-04. 

94

mobile source emission control programs. First, we describe how we developed our VOC

inventory estimates, and then we present the results from these analyses.

a. VOC Inventory Methodology

As described in the methodology overview section, other gaseous air toxics were not

evaluated explicitly in our 1999 Study. However, since all of these compounds are VOCs, we

expect their emissions trends to follow the VOC emissions trend. For 1996 and later years, we

based our VOC inventories on modeling that reflects adoption of all current mobile source

program plus the proposed 2007 heavy-duty engine standards. We have also integrated our most

recent information on emissions factors with county-specific modeling inputs. (One recent

update with regard to emission factors is that we assume the technologies used by diesel engine

manufacturers to meet the proposed 2007 standards will result in only a small compliance

margin, instead of the larger margin we had assumed in the modeling used for the toxics

proposal.) A detailed description of the modeling used as the basis for this rule can be found in

the docket for this rulemaking.159159,

160,161,162162 We do not include crankcase VOC emissions in

our estimates of VOC emissions since these emissions are not a portion of the exhaust from the

engine, and toxics speciation data are based on tailpipe exhaust. 

In the modeling that was used as the basis for this rulemaking, we did not recalculate the

1990 VOC inventory. We could not use the 1990 VOC estimates from EPA’s Trends Report,

since such estimates would not be comparable to the 1996 and later estimates contained in this

analysis, because EPA’s 1990 Trends estimates have not been updated to reflect the data and

analyses that were used in this analysis (and will be used in MOBILE6). Therefore, for 1990 we

modified the modeling methods applied in the 1999 Study to produce direct estimates of VOC

emissions that account for the effects of fuel and vehicle technology changes as well as the

information that will be used in EPA’s MOBILE6 emissions model.163
164 EPA. 2000. National Air Pollution Emission Trends, 1900-1998 (March 2000). Office of Air Quality

Planning and Standards, Research Triangle Park, NC. Report No. 454/R-00-002. 

165 The 1999 Study’s approach is the more appropriate one when estimating emissions, ambient

concentrations, and exposures for urban areas, which were the focus of the study.

95

b. Projected VOC Emissions Inventory

The results of this analysis, presented in Table IV.B-5, show that on-highway VOC

inventories are projected to decrease by 72 percent between 1990 and 2020 with the currently

promulgated and proposed on-highway control programs. We assume that other gaseous toxics

will decrease by approximately 72 percent as well. Most of the emission decrease is expected to

occur before 2007.

Table IV.B-5

Annual VOC Emissions Summary for the Total U.S. 

On-Highway Vehicles Only*

1990 1996 2007 2020

Inventory (1,000 short tons/year) 7,585 4,933 3,028 2,153

Cumulative Annual Reductions

from 1990 (1,000 short tons)

--. 2,652 4,557 5,433

Cumulative Percent Reductions

from 1990 

-- 35% 60% 72%

* - Includes the impact of our current on-highway control programs and the proposed 2007 and

later model year heavy-duty engine standards.

4. Diesel PM Inventory 

This section describes how we derived diesel PM estimates for this rule, and then

presents those estimates. We do not have inventory data on all of the organic gas components of

diesel exhaust, and so we are using diesel PM as the surrogate for the particulate matter and

organic gas components of diesel exhaust. Where we have data regarding specific constituents in

the diesel exhaust organic gas phase we presented those above.

a. Diesel PM Inventory Methodology

As described in the methodology overview section, our diesel PM emissions estimates are

based on several sources. For 1990, we used the diesel PM emissions estimates from EPA’s

Emissions Inventory Trends Report.164 These estimates account for county-specific inputs in a

more reliable way than our 1999 Study.165
166 EPA. 2000. National Air Pollution Emission Trends, 1900-1998 (March 2000). Office of Air Quality

Planning and Standards, Research Triangle Park, NC. Report No. 454/R-00-002. 

96

For 1996 and later years, the diesel PM inventories have been updated for this final rule. 

(As referenced in the previous section on VOC inventories, a detailed description of the

modeling used as the basis for this rule can be found in the docket for this rulemaking.) The

light-duty diesel PM emissions are based on the PART5 model, which is similar in structure and

function to the MOBILE series of models. It calculates exhaust and non-exhaust (e.g., road dust)

particulate emissions for each vehicle class included in the MOBILE models. A particle size cutoff of 10 μm was specified in the model inputs since essentially all exhaust PM from diesel

engines is smaller than 10 μm. The light-duty PM inventory was developed from county-specific

modeling inputs. We believe this updated inventory is a more appropriate source for national

light-duty diesel PM emission estimates than the 1999 Study because it better accounts for

county-specific conditions. 

The heavy-duty engine diesel PM emission inventories for 1996 and later years have been

updated for this final rule. These estimates incorporate recent findings on heavy-duty diesel

engine PM emissions that were not reflected in the 1999 Study and are developed from countyspecific modeling inputs. (As referenced in the previous section on VOC inventories, a detailed

description of the modeling used as the basis for this rule can be found in the docket for this

rulemaking.) We did not include crankcase PM emissions in our estimates because these

emissions are not a portion of the exhaust emissions, and toxics speciation data are based on

tailpipe exhaust.

In the modeling used as the basis for this rulemaking, we did not recalculate the 1990

VOC inventory. Therefore, we chose to use the heavy-duty diesel PM inventory estimates for

1990 from EPA’s Trends Report.166 We believe this approach is reasonable, since we have not

substantially changed our estimates of emissions from 1990 and earlier engines since the Trends

Report estimates were developed. We also used data from the EPA’s Trends Report for lightduty diesel estimates for 1990.

b. Projected Diesel PM Emissions Inventory

Our diesel PM inventory estimates are presented in Table IV.B-6. Diesel PM emissions

are expected to decline by 63 percent in 2007, as compared with 1990 levels. These emissions

are expected to decline even more by 2020, by 94 percent as compared with 1990 levels.
97

Table IV.B-6

 Annual Diesel PM Emissions Summary for the Total U.S.

On-Highway Vehicles Only*

1990 1996 2007 2020

Inventory (1,000 short tons/year) 235 182 85 15

Cumulative Annual Reductions

from 1990 (1,000 short tons)

-- 53 150 220

Cumulative Percent Reductions

from 1990 

--. 23% 64% 94%

* - Includes the impact of our current on-highway control programs and the proposed 2007 and

later model year heavy-duty engine standards.
98

Chapter 5: Mobile Source Air Toxic Ambient

Concentrations and Exposures

The purpose of this chapter is to review what we know about ambient concentrations and

exposures associated with emissions of mobile source air toxics. First, we will review

monitoring and modeled data on ambient concentrations of five of the 21 mobile source air

toxics. These compounds are benzene, 1,3-butadiene, formaldehyde, acetaldehyde, and diesel

PM. We will then review results of an on-highway vehicle inhalation exposure assessment

prepared by EPA. The exposure estimates are compared to estimates of the on-highway vehicle

contribution to modeled ambient concentrations. As discussed in Chapter 4, we have the most

reliable inventory data for the five compounds listed above, and hence the most accurate modeled

mobile source estimates of ambient concentrations and exposure. As exposure estimates from

the NATA national scale assessment are not yet available for comparison, the national scale

assessment modeled ambient concentration estimates are used to evaluate the reasonableness of

the exposure estimates. We will also discuss what we know about inhalation exposures in

various micro-environments. Diesel PM is used as the dosimeter to assess exposure to whole

diesel exhaust (which includes diesel PM and diesel exhaust organic gases), which the Agency

has classified as a likely human carcinogen.

Because of uncertainties associated with assessing ambient concentrations and exposures,

particularly for micro-environments and mobile source “hotspots,” we have developed a

technical analysis plan to further investigate these issues. The plan is described in the preamble.

A. Survey of Data Ambient Concentrations of Mobile Source Air Toxics.

In this section, analyses of monitor data for benzene, 1,3-butadiene, formaldehyde,

acetaldehyde, and diesel PM from EPA and State and local programs are reviewed. They will

then be compared to modeled ambient concentrations. This comparison provides a check on

modeled concentrations that will be used to assess exposures to MSATs.

1. Ambient Monitoring

As discussed below, monitor data for air toxics are somewhat limited. However, they are

still very useful for evaluating the reasonableness of modeled ambient concentrations and

bounding exposure estimates. Monitor data can also be used to identify the locations where

concentrations are highest. It should be noted, however, that duration of exposure as well as

concentration level influence the potential for chronic health risks. Thus, if individuals spend

only a short period of time at a location where high monitored values of a pollutant have been

found, there may not be a big impact on overall exposure or risk.

EPA is working with State and local air agencies to develop a monitoring network that

will develop estimates of ambient concentrations that are representative of regional area
167 The AIRS Air Quality System contains measurements of ambient concentrations of air pollutants and

associated meteorological data. The data is collected by thousands of monitoring stations operated by EPA, national,

state and local agencies. EPA uses this data to assess the overall status of the nation's air quality and to prepare

reports to Congress as mandated by the Clean Air Act. EPA also uses the data to identify areas where

improvements in air quality are needed.

99

concentrations throughout the U.S. A National Air Toxics Monitoring Pilot Program has been

established to provide funds for State and local governments to conduct monitoring in four urban

areas and six small city and rural areas. The urban areas selected for this pilot program are

Providence, Rhode Island; Seattle, Washington; Tampa Bay, Florida; and Detroit, Michigan. 

Awards have been made or are imminent for the six small city and rural areas. Monitoring sites

are being selected to provide a better understanding of the sources and magnitudes of variability

associated with ambient air toxics concentrations within and between neighborhood scale areas

across the U.S. and to characterize annual average concentrations for geographic areas under

various environmental conditions. Sampling will take place in late 2000 and 2001.

a. EPA Monitoring Data

This section summarizes monitored air toxics concentration data from the EPA

Aerometric Information Retrieval System (AIRS), Air Quality System.167 Using data where yearround measurements were available, we calculated 1996 mean ambient concentrations

nationwide for benzene, acetaldehyde, formaldehyde, and 1,3-butadiene. These data are

presented in Table V.A-1. Also presented are the number of monitor sites, standard deviations

and the concentrations at monitor sites in the 95th percentile. The 95th percentile concentrations

for these compounds are about twice the level of the mean concentrations. Data are especially

limited for aldehydes, where only 26 sites have complete data in 1996. 

Because the monitored ambient concentration results have been compiled using data from

a number of different sources, often using different collection and chemical analysis methods,

there is a significant amount of variability in the numbers. In addition, differences in criteria

used to select the sites of monitors may make it difficult to use the data to draw conclusions

about implications for population exposures. For example, many monitors are placed at sites

where readings are expected to be high, often to monitor specific facilities. Conversely, other

monitors might be sited away from areas of highest concentration (for instance to measure

concentrations in residential areas). 

Air toxics trends were recently analyzed by EPA using ambient monitor data, and results

were summarized in the recently released 1998 Air Quality Trends Report.2

 Between 1993 and

1998, ambient concentrations of benzene decreased by 37% (Figure V.A-1). It is likely that this

decrease is largely attributable to penetration of new highway vehicles compliant with tighter

VOC standards into the existing fleet, and use of reformulated gasoline. Data for 1,3-Butadiene

were also analyzed, but a consistent downward trend was not observed. 
100

Table V.A-1

Monitored 1996 ambient concentration estimates nationwide from AIRS

Compound No. of

sites

Mean

Conc.

(μg/m3) 

Standard

deviation

95th percentile

conc. (μg/m3

) 

Benzene 119 1.90 0.91 3.7

1,3-Butadiene 51 0.79 2.5 1.6

Formaldehyde 26 2.90 1.2 5.4

Acetaldehyde 26 1.89 0.81 3.5
101

Figure V.A.-1 

National trend in annual average benzene concentrations in metropolitan areas, 1993–1998

(Source:1998 Air Quality Trends Report).

(Lines on box plots show highest value, 75th percentile value, average, 25th percentile value, and

lowest value)

b. State and Local Monitoring Data

Table V.A-2 presents ambient monitor concentration estimates from studies conducted in

the South Coast Air Basin and the State of Minnesota, with highway and nonroad concentrations

estimated using inventory apportionment.3, 4

 In other words, the relative contribution of each

source sector to overall ambient concentration was assumed to be proportional to the contribution

of each source sector to total direct emissions. It should be noted that there is considerable

uncertainty in apportioning concentrations of aldehydes in this way, because much of the ambient

concentration of aldehydes is formed secondarily from other precursors. The South Coast

represents an area with a toxic emissions inventory dominated by mobile sources. According to

American Association of Automobile Manufacturers’ fuel survey data, Minnesota has high levels
102

of benzene in gasoline (average 1.73% in 1996, compared to a nationwide average of 1.1% for

non-RFG areas). As a result, we might expect that ambient benzene concentrations are higher in

Minnesota than in other States, but the average monitor values for benzene in Minnesota are not

significantly higher than the nationwide average based on AIRS in Table V.A-1. 

Table V.A-2

Monitored average ambient concentration estimates (μg/m3), and estimated highway

and nonroad contributions, in the South Coast Air Basin and in Minnesota

South Coast Air District (1998-9) Minnesota (1996)

Compound All

Sources

Highway Nonroad All

Sources

Highway Nonroad

Benzene 3.53 2.46 0.73 1.69 0.48 0.78

1,3-Butadiene 0.79 0.53 0.21 N.A. N.A. N.A.

Formaldehyde 4.82 2.28 2.21 1.64 0.65 0.43

Acetaldehyde 3.17 1.52 1.57 N.A. N.A. N.A.

Sources: 1. South Coast Air Quality Management District. 1999. Multiple Air Toxics Exposure

Study in the South Coast Air Basin – MATES-II. 2. Minnesota Pollution Control Agency. 1999. 

MPCA Staff Paper on Air Toxics.

 

c. Diesel PM Monitoring

We do not have a way of actually measuring diesel PM. However, there are two indirect

methods of estimating diesel PM ambient concentrations based on monitor data. First,

monitoring data on elemental carbon concentrations can be used as a surrogate to determine

ambient diesel PM concentrations. Elemental carbon is a major component of diesel exhaust,

contributing to approximately 60%-80% of diesel particulate mass, depending on engine

technology, fuel type, duty cycle, lube oil consumption, and state of engine maintenance.5 6 7 8

 In

most areas, diesel engine emissions are major contributors to elemental carbon, with other

potential sources including gasoline exhaust, combustion of coal, oil, or wood, charbroiling,

cigarette smoke, and road dust. Because of the large portion of elemental carbon in diesel

particulate matter, and the fact that diesel exhaust is one of the major contributors to elemental

carbon in most areas, ambient diesel PM concentrations can be bounded using elemental carbon

measurements. The Agency’s draft Health Assessment Document for Diesel Exhaust9 presents

one approach for calculating ambient diesel particulate matter concentrations using elemental

carbon measurements. In the absence of a more sophisticated modeling analysis, using elemental

carbon as a surrogate for diesel PM is a useful approach where elemental carbon concentrations

are available.
103

The second approach for estimating ambient diesel PM concentrations based on monitor

data uses the chemical mass balance (CMB) model in conjunction with ambient PM

measurements to estimate ambient diesel PM concentrations. Inputs to the CMB model include

particulate matter measurements made at the receptor site as well as measurements made of each

of the source types suspected to affect the site. Because of the co-emission of diesel and gasoline

particulate matter in time and space, chemical molecular species that provide markers for

separation of these sources have been identified. Recent advances in chemical analytical

techniques have facilitated the development of sophisticated molecular source profiles, including

detailed speciation of organic compounds, which allow the apportionment of particulate matter to

gasoline and diesel sources with increased certainty. Older studies that made use of only

elemental carbon source profiles have been published and are summarized here, but are subject to

more uncertainty. It should be noted that since receptor modeling is based on the application of

source profiles to ambient measurements, this estimate of diesel particulate matter concentrations

includes the contribution from on-highway and nonroad sources of diesel PM. In addition, this

model accounts for primary emissions of diesel PM only; the contribution of secondary aerosols

is not included.

Ambient diesel PM concentration estimates using these two approaches are summarized

in Table V.A-3.

2. Modeled Ambient Concentrations

In this section, data on modeled ambient concentrations of air toxics are reviewed. 

Sources of data include the Agency’s Cumulative Exposure Project and the National Air Toxics

Assessment.

a. Cumulative Exposure Project

In 1998, EPA’s Office of Policy, Planning, and Evaluation released results of a modeling

study that estimated outdoor concentrations of hazardous air pollutants.10 This analysis was done

as part of the Cumulative Exposure Project (CEP). The study estimated 1990 annual average

outdoor concentrations of 148 toxics, nationally, and by census tract. In this study, county level

emissions were allocated to individual census tracts using spatial surrogates (for example,

roadway miles were used a surrogate for gasoline highway motor vehicle emissions). Emissions

were also allocated temporally into three-hour time blocks. The emission estimates were

obtained from an inventory developed specifically for the CEP. Since the time this inventory

was developed, higher quality and more recent emissions data have become available. 
104

Table V.A-3

Ambient Diesel Particulate Matter Concentrations from Receptor Modeling

and Elemental Carbon Measurements

Location Year of Sampling Diesel PM10

& PM2.5

)g/m3

(mean)

Diesel PM

% of

Total PM

Source of Data

West LA, CA

Pasadena, CA

Rubidoux, CA

Downtown LA, CA11

1982, annual 4.4 13% Source-Receptor

1982, annual 5.3 19% Modeling

1982, annual 5.4 13%

1982, annual 11.6 36%

Phoenix area, AZ12 Winter,1989-90 4-22* †

Phoenix, AZ13 1994-95, annual 0-5.3 (2.4) 0-27%

California, 15 Air Basins14 1988-92, annual 0.2-3.6* †

Manhattan, NY15 3 days, Spring, 1993 13.2-46.7* 31-68%

Welby, CO

Brighton, CO16

60 days, Winter, 1996-97 0-7.3 (1.7) 0-26%

60 days, Winter, 1996-97 0-3.4 (1.2) 0-38%

Boston, MA

Rochester, NY 

Quabbin, MA

Reading, MA

Brockport, NY17

1995, annual 0.7-1.7 (1.1) 3-15% Elemental Carbon

Measurement 1995, annual 0.4-0.8 (0.5) 2-9%

1995, annual 0.2-0.6 (0.4) 1-6%

1995, annual 0.4-1.3 (0.6) 2-7%

1995, annual 0.2-0.5 (0.3) 1-5%

Washington, DC18 1992-1995, annual 1.3-1.8 (1.6) 6-10%

South Coast Air Basin1 1995-1996, annual 2.4-4.5‡ †

*PM10 † Not Available

‡ The Multiple Air Toxics Exposure Study in the South Coast Air Basin reported values for maximum

monthly elemental carbon concentrations across a ten-site network. 

Concentrations were estimated from these inventory data using a dispersion model known

as ASPEN (Assessment System for Population Exposure Nationwide). The modeling estimated

concentrations attributable to major, area, and mobile sources. In order to model a large number

of pollutants nationwide, ASPEN makes a number of simplifying assumptions. For instance,

where specific latitude and longitude coordinates were not available, facilities were randomly

located within a county. Moreover, concentration estimates at the census tract level were

estimated using modeling assumptions to allocate emissions from the county level, and the model

is very sensitive to the assumptions used. In addition, dispersion of emissions from non-point

sources (e.g. on-highway and nonroad vehicles) was treated simplistically. For resident tracts

that have radii greater than 0.3 km, non-point source ambient concentrations are estimated on the
105

basis of five pseudo point sources. The average concentration for the census tract is determined

by spatially averaging the ambient concentrations associated with the receptors defined for the

five pseudo sources which fall within the bounds of the tract. For resident tracts with radii less

than 0.3 km, ambient concentrations are set equal to zero. Other limitations include: terrain

impacts on dispersion were not included; no long range transport was included; and reliance on

long term climate summary data. Because of these limitations, the results are most meaningfully

interpreted when viewed over large geographic areas (i.e., at the national or State level). 

Comparison of modeled concentrations to monitored concentrations indicate that the model is

more likely to underestimate monitored values than to overestimate them. However, the model

appears to be relatively accurate for benzene. 

Table V.A-4 presents the CEP’s estimated nationwide average concentrations of benzene,

1,3-butadiene, formaldehyde, and acetaldehyde from all sources, as well as the contribution

attributable to mobile sources, separated into on-highway and nonroad. The mobile source

concentration estimates were allocated to on-highway and nonroad sources based on the onhighway and nonroad shares of the nationwide CEP inventory. Allocation of aldehydes was

based on direct emissions. There is considerable uncertainty in apportioning concentrations of

aldehydes in this way, because much of the ambient concentration of aldehydes is formed

secondarily from other precursors.

Table V.A-4

Average estimated nationwide concentrations of selected air toxics in 1990 

from the Cumulative Exposure Project (μg/m3

)

Compound Conc.

(μg/m3

)

All sources

Mobile

Contribution to

Ambient Conc.

On-Highway

Contribution to

Ambient Conc.

(% of avg. conc.)

Nonroad

Contribution to

Ambient Conc.

(% of avg. conc.)

Benzene 2.10 1.1 0.87 (41) 0.23 (11)

1,3-Butadiene 0.15 0.11 0.08 (53) 0.03 (20)

Formaldehyde 1.50 0.76 0.50 (33) 0.26 (17)

Acetaldehyde 0.72 0.44 0.29 (40) 0.15 (21)

Source: Systems Applications International. 1998. Modeling Cumulative Outdoor

Concentrations of Hazardous Air Pollutants. Report No. SYSAPP 98-96/33, Prepared for U. S.

EPA, Office of Policy, Planning and Evaluation, February, 1998.
168 The nationwide numbers are for 48 States plus the Virgin Islands and Puerto Rico.

106

b. National Air Toxics Assessment Results for Mobile Sources

As part of its National Air Toxics Assessment (NATA) activities, EPA has conducted a

national-scale air toxics assessment using the ASPEN dispersion model, in conjunction with the

1996 National Toxics Inventory, to estimate ambient concentrations of 33 air toxics identified in

the IUATS, plus diesel PM. The NATA national scale assessment reported distributions of

concentrations across census tracts nationally and at the county level. Since this national scale

assessment, like the CEP analysis, uses ASPEN, it has similar limitations. Again, the results are

most meaningfully interpreted when viewed over large geographic areas. The NATA national

scale analysis also apportioned the contribution to ambient concentrations between major, area,

nonroad mobile, and on-highway sources. Results are available at

http://www.epa.gov/ttn/uatw/nata. Table V.A-5 presents draft mean and median nationwide

gaseous toxic ambient concentrations attributable to on-highway and nonroad mobile sources

using this modeling method.168 Estimates are provided for benzene, 1,3-butadiene,

formaldehyde, and acetaldehyde. Both mean and median values are reported, because high

outlying values may bias the means. The estimates take into account photochemical reactivity. 

Mean concentrations for other mobile source toxics estimated using ASPEN can be found in

Appendix 1. For pollutants which are on the list of hazardous air pollutants included in the

National Scale Analysis, the on-highway contribution, nonroad contribution, and the contribution

from all sources is provided. There are a number of additional compounds on the mobile source

air toxics list that are not included in the National Scale Analysis. For these compounds, mobile

source only contributions were estimated using ASPEN.19 Diesel PM estimates are being revised

to account for inventory changes and will be included in the release for EPA Science Advisory

Board review. 

EPA has performed “model to monitor” comparisons for several compounds in the

NATA assessment. Results are available on the NATA website given above and summarized in

Table V.A-6 below. In general, the statistics for benzene suggest good agreement between the

model and the monitors. The median of the ratios is close to one, with a small standard deviation;

this suggests that on average, the model estimates and monitor averages are close to each other.

For almost half the sites, the range of county model estimates covers the monitor average; the

remaining sites are missed on the low side and some on the high side, suggesting no clear bias. 

The model’s estimates are within a factor of two of the monitored concentrations for about 90%

of the benzene monitors in this study. Comparisons for formaldehyde and acetaldehyde do not

show such good agreement. However, they compare more favorably when the maximum

estimated modeled concentration is examined within 30 km of the monitoring site. This indicates

that emissions sources were not precisely located or the monitors were sited to find peak

concentrations. 
107

Table V.A-5

Draft average estimates of mobile source contributions to nationwide concentrations

of selected air toxics in 1996 from the NATA national scale assessment

Compound On-Highway Contribution to

Ambient Conc. (μg/m3

)

Nonroad Contribution to

Ambient Conc. (μg/m3)

Mean Median Mean Median

Benzene 0.55 0.45 0.24 0.16

1,3-Butadiene 0.05 0.04 0.02 0.01

Formaldehyde 0.38 0.29 0.48 0.20

Acetaldehyde 0.40 0.32 0.27 0.12

Table V.A-6 

Agreement of modeled ambient concentrations from the NATA national scale assessment

and monitored ambient concentrations on a point by point basis 

Compound Number of

Sites

Median of

Ratios

Percentage of

sites within a

factor of two

Percentage of sites

where monitored

concentrations

underpredicted

Benzene 87 0.92 89 59

Formaldehyde 32 0.65 53 88

Acetaldehyde 32 0.60 59 91

c. Diesel PM Estimates

Two dispersion model studies reporting diesel PM have been conducted in Southern

California. Results are summarized in Table V.A-7. Secondary formation of particulate matter

accounted for 27% to 67% of the total particulate matter associated with diesel engines.20 21 

Dispersion modeling conducted in Southern California reported that the on-highway contribution

to the reported diesel PM levels ranged from 63% to 89%. 
108

Table V.A-7 

Annual average diesel particulate matter concentrations predicted

from dispersion modeling

Location Year of Sampling Diesel PM2.5

)g/m3

(mean)

Diesel

PM2.5 % of

Total PM2.5

Azusa, CA

Pasadena, CA

Anaheim, CA

Long Beach, CA

Downtown LA, CA

Lennox, CA

West LA, CA22

1982, annual 1.4** 5%

1982, annual 2.0** 7%

1982, annual 2.7** 12%

1982, annual 3.5** 13%

1982, annual 3.5** 11%

1982, annual 3.8** 13%

1982, annual 3.8** 16%

Claremont, CA23 18-19 Aug 1987 2.4** 8% 

Long Beach, CA

Fullerton, CA

Riverside, CA24

24 Sept 96 1.9 8% 

24 Sept 96 2.4 9%

25 Sept 96 4.4 12%

+Value in parenthesis includes secondary diesel PM (nitrate, ammonium, sulfate and hydrocarbons) due to

atmospheric reactions of primary diesel emissions of NOx, SO2 and hydrocarbons.

**On-highway diesel vehicles only

B. Modeled Inhalation Exposures

As part of the National Air Toxics Assessment (NATA) national scale assessment, 1996

inhalation exposure estimates are being developed to assess the exposure concentrations

attributable to on-highway and nonroad mobile sources. As mentioned previously, this effort

uses a dispersion model, ASPEN, to model ambient concentrations of air toxics at the county

level. These data will then be used as input into version 4 of the Hazardous Air Pollutant

Exposure Model (HAPEM4). A report with exposure and risk characterization results using

HAPEM4 will be submitted to the Agency’s Science Advisory Board for review later this year,

and final results should be publicly available subsequently in 2001. HAPEM4 estimates

inhalation exposures to air toxics from outdoor sources. It predicts inhalation exposure through a

series of calculation routines. The model makes use of census data, human activity patterns,

ambient air quality levels, climate data, and microenvironmental factors (indoor/outdoor

concentration relationships) to estimate an expected range of inhalation exposure concentrations

for groups of individuals. The microenvironmental factors are based on empirical field data,

which is better for some pollutants than for others. Although this model is not designed to

estimate individual exposures, it can provide exposure distribution estimates for the general

population as well as for various subpopulations of interest (e.g., children aged 0-17 years).
109

Table V.B-1

California annual average diesel PM exposure estimates for all

mobile sources from the California Population Indoor Exposure Model

Year California Exposure Estimates (On-Highway & Nonroad) in

)g/m3

1990 California Annual Average 1.5

2007 Projected California Annual Average 1.3

2020 Projected California Annual Average 1.2

Source: CARB. Proposed Identification of Diesel Exhaust as a Toxic Air Contaminant

Appendix III Part A: Exposure Assessment. 

Exposure estimates for diesel PM from on-highway and nonroad sources were recently

modeled by CARB using the California Population Indoor Exposure Model (CPIEM). Results

from this model are presented in Table V.B-1 below and described in more detail in CARB’s 

“Proposed Identification of Diesel Exhaust as a Toxic Air Contaminant Appendix III Part A:

Exposure Assessment”.25 Other than these two efforts, the only available estimates of inhalation

exposure to motor vehicle related air toxics from ambient sources were developed using the

Hazardous Air Pollutant Exposure Model for Mobile Sources, version 3 (HAPEM-MS3).26, 27, 28

This model uses CO as a tracer for air toxics exposure, rather than using modeled ambient

concentrations of toxics as inputs like HAPEM4. Also, this version of the model is designed to

address exposure attributable to on-highway vehicle emissions, whereas HAPEM4 addresses

exposures attributable to all source categories. Methods used to develop exposure estimates

using this model are discussed below.

1. Methodology for Modeling Inhalation Exposures to Benzene, Formaldehyde,

Acetaldehyde, 1,3-Butadiene and Diesel PM: HAPEM-MS3

Estimates of exposure for gaseous air toxics using a previous version of the HAPEM-MS

model were published in the 1993 Motor Vehicle-Related Air Toxics Study.29 Based on peer

review comments, a number of improvements were made to the model, principally by EPA’s

Office of Research and Development, resulting in HAPEM-MS3. These improvements include:

• 1980 census and CO monitoring data were replaced with 1990 data for base-year

modeling;

• 32 additional micro-environments were added to the 5 micro-environments in the original

model (20 of these micro-environments were indoors);

• Activity data from three cities were used, rather than data from one city as in the original

model; and

• More detail on seasonal and regional exposures was retained.
169It should be noted that in some microenvironments, there are large additive terms attributable to motor

vehicles, such as at service stations and in garages. HAPEM-MS3 does not account for these non-ambient sources

of exposure to motor vehicle emissions.

110

Exposure modeling projections considering currently planned controls and using

HAPEM-MS3 are presented in the next section. This section focuses on methods used to

develop these estimates, limitations and uncertainties, and an evaluation of the reasonableness of

the baseline estimates for 1990 and 1996, based on a comparison to other data sources.

a. Modeling Approach 

Exposure modeling was done for 1990. Data from 10 urban areas were used. These areas

were Atlanta, GA, Chicago, IL, Denver, CO, Houston, TX, Minneapolis, MN, New York, NY,

Philadelphia, PA, Phoenix, AZ, Spokane, WA, and St. Louis, MO. As mentioned previously,

HAPEM-MS3 uses CO as a tracer for toxics. Thus, these areas were selected because a large

percentage of the population lived within reasonable proximity to CO monitors, and also to

represent good geographic coverage of the U.S. Since most ambient CO comes from cars and

light trucks, we believe CO exposure is a reasonable surrogate for exposure to other motor

vehicle emissions, including toxics emissions. The HAPEM model links human activity patterns

with ambient CO concentration to arrive at average exposure estimates for 22 different

demographic groups (e.g., outdoor workers, children 0 to 17, working men 18 to 44, women 65+)

and for the total population. The model simulates the movement of individuals between home

and work and through a number of different micro-environments. The CO concentration in each

micro-environment is determined by multiplying ambient concentration by a microenvironmental factor derived from regression analysis of ambient and personal monitor data. 

Each micro-environmental factor has a multiplicative term, which represents ambient exposure,

and an additive term, which represents exposure to emissions originating within microenvironments. These factors were derived by IT Corporation based on the results of regression

analyses using paired ambient and personal exposure monitor measurements from CO studies in

Denver and Washington.30, 31 In our modeling, we set the additive term to zero, to eliminate nonambient sources of CO, such as gas stoves.169 The multiplicative term has a component that

represents penetration from the ambient air into the micro-environment, and a factor that

represents the proximity of the micro-environment to monitors. Thus, even though a compound

may have a penetration rate of close to one, the microenvironmental factor could be significantly

less than one if the microenvironment is typically found a significant distance from where CO

monitors are located. HAPEM-MS3 micro-environmental factors are given in Appendix 2.

With the 1990 CO exposure estimates generated by the HAPEM-MS3 model for each

urban area, EPA determined the fraction of exposure attributable to on-highway vehicle

emissions. This calculation was accomplished by scaling the exposure estimates (which reflect

exposure to total ambient CO) by the fraction of the 1990 CO emissions inventory from onhighway motor vehicles, determined from the EPA Emission Trends database.32, 33 This scaling
111

takes into account the contribution of background CO to the inventory. Nationwide urban CO

exposure attributable to on-highway vehicle emissions was estimated by first calculating a

population-weighted average CO exposure for the ten modeled areas. This number was adjusted

by applying a ratio of population-weighted annual average CO ambient concentrations for urban

areas in the entire country versus average ambient CO concentration for the modeled areas. To

estimate rural exposure, the urban estimate was scaled downward using rough estimates of urban

versus rural exposure from the 1993 Motor Vehicle-Related Air Toxics Study (EPA 1993a). The

scaling factor was 0.56, based on an average CO concentration in rural areas of 470 μg/m3 and a

concentration in urban areas of 842 μg/m3.

Modeled CO exposure attributable to on-highway vehicle emissions for 1990 was divided

by 1990 CO grams per mile emission estimates to create a conversion factor. The conversion

factor was applied to modeled toxic emission estimates (in grams per mile) to determine

exposure to on-highway vehicle toxic emissions, as shown in Equation 6:

TOXExposure(μg/m3) = [COExposure(μg/m3)/COEF(g/mi)]1990 × TOXEF(g/mi) (6)

where:

TOXExposure(μg/m3) = exposure to on-highway vehicle toxic emissions

COExposure(μg/m3) = exposure to on-highway vehicle CO emissions

COEF(g/mi) = CO emission factor

TOXEF(g/mi) = toxic emission factor

 The exposure estimates for calendar years 1996, 2007, and 2020 were adjusted for VMT

growth relative to 1990. We also included in the model various assumptions regarding

transformation of the toxics. For example, benzene was treated as inert, but 1,3-butadiene

exposure was adjusted to account for its atmospheric transformation into other species. The

multiplicative factors used to adjust for this transformation were 0.44 for summer, 0.70 for spring

and fall, and 0.96 for winter.34 These factors account for the difference in reactivity between

relatively inert CO, which is being used as the tracer for toxics exposure, and the more reactive

1,3-butadiene. In contrast, estimated exposures to formaldehyde and acetaldehyde were based on

direct emissions. For these pollutants, removal of direct emissions in the afternoon was assumed

to be offset by secondary formation. Limitations and problems with this assumption are

discussed in the following section. Annual average exposure estimates to the gaseous air toxics

for the entire population in 1990 and 1996 are presented in Tables V.B-2 and V.B-3. Annual

average inhalation exposure to diesel PM was estimated to be 0.82 μg/m3 in 1990 and 0.73 μg/m3

in 1996. Estimates were also developed for outdoor workers, and children 0 - 17 years of age. 

Exposure among outdoor workers was higher than for the entire population, and among children

it was slightly lower.

As discussed in Chapter 4, gaseous toxic and diesel PM emission estimates for heavy

duty gasoline and diesel vehicles in 1996, 2007, and 2020 were revised for the 2007 heavy-duty
112

engine proposed rule. Thus, exposure estimates for these years were adjusted upward to account

for the discrepancy.

b. Limitations and Uncertainties

Use of the HAPEM-MS3 model to estimate exposure to toxic emissions from motor

vehicles introduces several notable sources of uncertainty. First, the model may underestimate

CO exposures of the maximally exposed population. Although a validation study of HAPEMMS3 has not been done, such an analysis has been done for the pNEM/CO Model (NAAQS

Exposure Model for CO), which uses an approach similar to that used in HAPEM-MS3 as well

as much of the same data.35 Generally speaking, pNEM/CO’s estimates of CO exposures for the

population in the 5th percentile were overestimated by about 33%, and those in the 98th

percentile were underestimated by about 30%. This result suggests that pNEM/CO

underestimates CO exposures of the maximally exposed population. These results would likely

also hold for HAPEM-MS3 estimates of toxics exposure as well, and suggest that the model is

probably best suited for estimating average exposures.

Second, the data used to derive micro-environmental factors are limited. As described

earlier, the data are obtained from only two cities. Thus, the regression equations used to derive

the micro-environmental factors are subject to substantial error. Moreover, activity data are very

limited for some demographic groups. For instance, there was very little activity data for African

Americans or Hispanic Americans in the database. 

Third, because we set the additive terms of the micro-environmental factors to zero, the

HAPEM-MS3 results do not account for exposures to emissions originating within microenvironments. For instance, the model does not account for indoor exposure to evaporative

benzene emissions from vehicles parked in attached garages. The potential impact of these

additional sources of emissions within micro-environments is discussed in Section V.C.

Fourth, the modeling done in this assessment assumes that the on-highway fleet

emissions ratio of CO to diesel PM can be used as an adjustment factor to convert estimated CO

personal exposures to diesel PM exposures. However, most CO emitted from on-highway

vehicles is emitted by gasoline vehicles, while most on-highway diesel PM is emitted from

heavy-duty diesel engines. Even though gasoline- and diesel-fueled on-highway vehicles travel

the same roadways, temporal and spatial patterns for diesel vehicle operation are different than

gasoline-fueled vehicles. This could result in underestimates of diesel PM exposure, for instance,

in areas where the proportion of heavy-duty diesel vehicle traffic is significantly greater than

average relative to light-duty gasoline vehicle traffic. Conversely, overestimates of commuting

exposures could occur where there is very little heavy-duty diesel vehicle traffic.

Similarly, the model also does not take into account the fact that spatial and temporal

allocation of benzene evaporative emissions are different than CO emissions. However, in

modern technology vehicles, with evaporative emission controls, benzene emissions are
170 Comparisons to monitor data were not made, due to the difficulty in estimating mobile source

contributions with accuracy.

113

dominated by the exhaust component. The modeling approach also assumes that emissions of

toxics vary linearly with CO as a function of ambient temperature. Also, although we know that

emissions of CO as well as the toxic compounds modeled are all higher at lower temperatures,

we do not know if the relationship is linear. Moreover, the assumption that exposure increases

proportionally to VMT does not account for urban spreading or building of new roadways within

an urban area.

Finally, as mentioned previously, we assumed that estimated exposure to formaldehyde

and acetaldehyde was based on direct emissions. As will be discussed in Section V.C.4 below,

we believe this assumption results in an underestimate of acetaldehyde exposure by about a

factor of three. Thus, HAPEM-MS3 based estimates of acetaldehyde exposure must be adjusted

to account for this underestimate. 

c. Improvements to HAPEM

As mentioned previously, a new version of HAPEM (HAPEM4) has been developed for

use in the National Air Toxics Assessment. This new version has a number of major

modifications and improvements including the capability to model inhalation exposure for all

outdoor sources. Thus a separate version of HAPEM for motor vehicles is no longer needed. The

model has been revised to accept monitored or modeled toxics concentrations directly as input,

rather than using CO as a surrogate for toxics. The model also now incorporates a new timeactivity database derived from the CHAD (Consolidated Human Activity Database), developed

by EPA’s Office of Research and Development. It should be noted that HAPEM4 still has

limitations. It estimates only inhalation exposures to air toxics from outdoor sources, and cannot

estimate maximum exposures, only population exposures. Moreover, the microenvironmental

factors in the model are better for some pollutants than for others.

2. Comparison of Exposure Modeling Results to Modeled Ambient

Concentrations

In this section, we compare HAPEM-MS3 exposure modeling results to modeled ambient

concentrations from the Cumulative Exposure Project and NATA national scale assessment.170 It

should be noted that average ambient concentrations do not represent average inhalation

exposures because they do not take into account human activity patterns, intrusion of ambient air

toxics into specific micro-environments, or emissions of air toxics from micro-environmental

sources. Nonetheless, we expect them to be within the same order of magnitude, and in the

absence of other exposure estimates, these data represent the best surrogate source of information

with which to evaluate the reasonableness of HAPEM-MS3 results.

A number of other limitations and uncertainties make it difficult to directly compare
114

modeled ambient concentration estimates to exposure estimates. First, uncertainties result from

the surrogates (e.g., roadway miles and population density) used to allocate emissions from the

county to census tract level for use in dispersion modeling. Also, the ASPEN dispersion model

does not include a terrain component, and relies on long-term climate summary data. 

We first compared HAPEM-MS3 average 1990 nationwide exposure estimates for onhighway vehicles for the entire U.S. population to 1990 CEP ambient concentration estimates for

on-highway vehicles. Results are presented in Table V.B-2. These results indicate close

correspondence except for acetaldehyde, where CEP results are about 70% higher. 

We also compared HAPEM-MS3's 1996 average nationwide estimates of gaseous toxic

exposure from on-highway vehicle emissions to estimates of the on-highway vehicle contribution

to ambient concentrations from the draft NATA national scale analysis. Results are presented in

Table V.B-3. Overall, average modeled ambient concentrations from the national scale analysis

are within the same order of magnitude of the average HAPEM-MS3 exposure results. 

Agreement is fairly close for benzene,1,3-butadiene, and formaldehyde, while HAPEMMS3 estimates for acetaldehyde are low compared to ambient concentration estimates from the

NATA national scale analysis. HAPEM-MS3 exposure estimates for formaldehyde and

acetaldehyde do not account for photochemistry, and removal of primary emissions are assumed

to be offset by secondary formation. ASPEN, on the other hand, accounts for aldehyde

photochemistry. It assumes that about 68% of formaldehyde is primary but only about 20% of

acetaldehyde is assumed to be primary. Since most ambient acetaldehyde is secondary, the

HAPEM-MS3 exposure estimate based on direct emissions will underestimate acetaldehyde

exposure. Thus, we have adjusted HAPEM-MS3-based estimates of acetaldehyde exposure by a

factor of 3 to be consistent with NATA modeled ambient concentrations. Subsequent estimates

of acetaldehyde exposure will include this adjustment. 

Given the limitations inherent in making comparisons, the results available at this time

suggest that the HAPEM-MS3 approach provides reasonable estimates of inhalation exposure

with the exception of acetaldehyde, which we are adjusting to account for the model’s inherent

limitations
115

Table V.B-2

Comparison of 1990 average exposure attributable to on-highway vehicle emissions

(HAPEM-MS3) to 1990 ambient concentration estimates

attributable to on-highway vehicle emissions (CEP)

Compound HAPEM-MS3 Based

Exposure (μg/m3

)

CEP Ambient Conc. (μg/m3

)

Benzene 1.07 0.87

1,3-Butadiene 0.11 0.08

Formaldehyde 0.57 0.50

Acetaldehyde 0.17* 0.29

*Unadjusted estimate based on direct emissions – adjusted level which includes secondary

formation is 0.51 μg/m3.

Table V.B-3

Comparison of 1996 annual average exposures attributable to on-highway vehicles

(HAPEM-MS3) and the on-highway vehicle portion of 1996

 modeled ambient concentrations (National Scale Assessment)

Compound HAPEM-MS3 OnHighway Vehicle

Exposure (μg/m3)

NATA On-Highway

Vehicle Mean Ambient

Concentration (μg/m3)

Benzene 0.71 0.55

1,3-Butadiene 0.08 0.05

Formaldehyde 0.37 0.38

Acetaldehyde 0.13* 0.40

*Unadjusted estimate based on direct emissions – adjusted level which includes secondary

formation is 0.38 μg/m3

.
116

Benzene Exposures Attributable to OnHighway Vehicles, New York City, 1996

0

0.2

0.4

0.6

0.8

1

1.2

1.4

All

persons

Children,

0 to 17

Outdoor

workers

Demographic Group

Exposure (ug/m3)

1996 Average

Benzene Exposure

1996 95th

Percentile

Benzene Exposure

3. Variance in Exposures

a. Distribution of Exposures

HAPEM-MS3 reports average annual and seasonal CO exposures by demographic group,

as well as the distribution of exposures around the mean. These distributions for CO exposure

can be used to estimate distributions of toxics exposure. As mentioned previously, we believe

that HAPEM-MS3 overestimates low-end exposures and underestimates high-end exposures (by

about 30% for the 98th percentile). Figure V.B-1 presents the on-highway vehicle portion of both

average annual and the 95th percentile annual benzene exposures for the general population in

New York City. Exposures for the 95th percentile of the entire population are about 50% higher

than the average. Results are presented for children 0 to 17 and outdoor workers as well. The

distribution of exposures for children and outdoor workers are not as broad as the distribution for

the entire population. This could be due to the smaller database for these demographic groups as

well as less variability in activity patterns.

Differences in the amount of time individuals spend in various micro-environments

contributes significantly to the overall distribution in annual exposures. For instance, individuals

spending the greatest percentage of time in high-exposure micro-environments have annual CO

exposures about 30% higher than average. Conversely, individuals spending the greatest amount

of time in low-exposure micro-environments have annual CO exposures about 5% lower than

average.

Figure V.B-1

Average and 95th percentile benzene exposures

(attributable to on-highway vehicles) in New York City, 1996

[Figure revised to correct error]
117

b. Variance among demographic groups

We have analyzed average inhalation exposures for three demographic groups -- the

overall population, outdoor workers, and children 0 to 17. Since inhalation exposures to air

toxics from outdoor sources are typically lower indoors than outdoors, exposures for outdoor

workers are somewhat higher than the general population. Exposures for children are similar to

the general population, although slightly lower since children spend a little more time indoors

than most other demographic groups. Nationwide average inhalation exposures for the three

demographic groups in 1996 are presented in Table V.B-4. 

Table V.B-4

Highway vehicle portion of nationwide average inhalation exposures to benzene,

1,3-butadiene, formaldehyde, acetaldehyde, and diesel PM for three

demographic groups in 1996, based on HAPEM-MS3

Pollutant Overall Population

Exposure (μg/m3

)

Outdoor Worker

Exposure (μg/m3)

Children’s Exposure

(μg/m3)

Benzene 0.71 0.82 0.68

1,3-Butadiene 0.08 0.09 0.08

Formaldehyde 0.37 0.46 0.37

Acetaldehyde 0.38 0.45 0.38

Diesel PM 0.76 0.88 0.73

c. Geographic variation

HAPEM-MS3 modeling results indicate that average inhalation exposures vary

significantly between geographic locations. Toxics exposures are impacted by ambient

temperatures, local fuel properties, age of the in-use fleet, I/M programs, traffic density,

demographics, and many other factors. To illustrate, Table V.B-5 presents the on-highway

portion of the1996 average annual benzene inhalation exposure estimates for the 10 areas

modeled in the EPA 1999 Study, as well as the estimates for urban areas and rural areas

nationwide. Among the urban areas modeled, Phoenix had the highest level of annual onhighway vehicle contribution to benzene exposure in 1996. Phoenix had a high level of CO

exposure attributable to highway vehicles in 1996 (484 μg/m3

) combined with an average fuel

benzene level of 1.07% in summer and 1.40% in winter (based on AAMA fuel surveys). 

Average benzene exposure in Phoenix is expected to drop substantially by 2007 due to the

adoption of California reformulated gasoline and as a result of more stringent Federal emission

standards and fleet turnover. Minneapolis also has high benzene exposure levels relative to other
118

modeled areas in 1996; this is due to significantly higher than average fuel benzene levels of

1.81% in summer and 1.65% in winter (based on AAMA fuel survey data). 

Not surprisingly, individuals in rural areas, which have lower population and traffic

density than urban areas, are expected to experience lower benzene-related exposures than

individuals in urban areas (Table V.B-5). Moreover, data from the 14 cities modeled in Glen and

Shadwick (1998) demonstrate that average CO levels increase proportionally with population

density (Table V.B-6). HAPEM-MS3 toxics exposure estimates will follow the same trend, since

CO is used as a surrogate for toxics.
119

Table V.B-5

 On-Highway vehicle portion of 1996 benzene exposure estimates

for 10 urban areas, and urban and rural areas nationwide,

 based on HAPEM-MS3 exposure modeling

Urban Area Average Highway Vehicle

Benzene Concentration

(μg/m3) in 1996 

Atlanta 0.87

Chicago 0.50

Denver 0.74

Houston 0.55

Minneapolis 1.15

New York 0.82

Philadelphia 0.53

Phoenix 1.31

Spokane 0.95

St. Louis 0.49

Urban Area Average 0.77

Rural Area Average 0.45
120

Table V.B-6

Annual Average Ambient CO Levels as a Function

of Population Density, 14 Cities

Population Density at

Monitor (residents per square

mile)

Average CO Levels, 1990

(ppm)

< 300 1.10

300 - 1,000 1.01

1,000 - 2,000 1.19

2,000 - 5,000 1.35

5,000 - 10,000 1.41

> 10,000 1.97

Overall Average 1.32

d. Seasonal variation

Average nationwide exposures to on-highway vehicle air toxics are much higher in winter

than in summer (Table V.B-7). This is primarily due to higher cold start emissions in winter.

Table V.B-7

Seasonal Average Nationwide Exposures (μg/m3

) Attributable to On-Highway Vehicle

Emissions, for the General Population, 1996

Pollutant Winter Spring Summer Fall

Benzene 0.90 0.64 0.55 0.74

Acetaldehyde 0.55 0.35 0.29 0.42

Formaldehyde 0.53 0.35 0.30 0.40

1,3-Butadiene 0.13 0.06 0.03 0.08

Diesel PM 0.88 0.74 0.65 0.76
121

4. Impact of Current On-Highway Vehicle Control Programs on Toxics

Exposure

Projected emissions reductions resulting from programs currently in place will result in

proportional reductions in inhalation exposure levels attributable to on-highway vehicles. Figure

V.B-2 presents exposure estimates for benzene, formaldehyde, acetaldehyde,1,3-butadiene, and

diesel PM in 1990, 1996, 2007, and 2020, using the methodology described in Section V.B.1. 

These estimates assume implementation of Phase II reformulated gasoline, the National Low

Emission Vehicle (NLEV) program, Tier 2 emissions standards with 30 ppm sulfur gasoline,

2004 heavy-duty standards, and proposed 2007 heavy duty standards. With these controls, by

2020 we expect that inhalation exposure to benzene attributable to on-highway vehicles will

decrease from 1990 levels by 74 percent, exposure to formaldehyde by 75 percent, exposure to

acetaldehyde by 65 percent, exposure to 1,3-butadiene by 73 percent, and exposure to diesel PM

by 93 percent.

5. Sensitivity Analyses

 Below is a discussion of the key sources of uncertainty and variability in the models and

data affecting exposure. The Agency has conducted some sensitivity analyses to address these

issues. However, additional aspects of sensitivity and uncertainty must be explored before we

are ready to release results. 

1) Representativeness of, and Variability in, Measured Ambient Carbon Monoxide Levels.

Toxics exposure estimates are based on measured ambient CO concentrations averaged

over 10 selected urban areas. Important limitations of these data relate to variations in

CO levels both within and among urban areas, and to the spatial variations in CO levels

relative to exposure locations for particular potential highly exposed or sensitive groups

(e.g., children, the elderly, ethnic minorities).

2) Estimates of Present and Future HAPs Emissions. The MOBTOX5b and PART5

models include data sets related to vehicle and fleet characteristics, VMT accumulation,

climatic conditions, and fuel characteristics. These input data relate to the estimated

characteristics of both “current” (1990) and “future” (1996, 2007, and 2020) vehicle

fleets. 

3) Appropriateness of CO as a Proxy for Estimating Toxics Exposures. Aside from the

uncertainties associated with the ambient CO measurements themselves, the inhalation

exposure estimates assume that ambient CO concentrations are an appropriate starting

point for estimating toxics exposures. This assumption is only valid if (1) the average

contributions of mobile sources to ambient CO and toxics exposures levels are similar 
122

0

0.2

0.4

0.6

0.8

1

1.2

Benzene

Formaldehyde

Acetaldehyde

1,3-Butadiene

Diesel PM

Pollutant

Annual Ambient 

Exposure (ug/m3)

1990

1996

2007

2020

Figure V.B-2

Exposure levels for four gaseous toxics and diesel PM under currently

planned controls and with 2007 Standards for Heavy Duty Engines (ug/m3)

across exposure areas, and (2) degradation or secondary generation of toxics due to

photochemical and other reactions can be neglected or accurately modeled. Also,

HAPEM-MS3 accounts only for exposures to ambient air toxics. Micro-environmental

sources of exposure are not accounted for. If the generation patterns or atmospheric fate

and transport characteristics of the toxics differ significantly from those of CO, or if there

are significant sources of toxics emissions that are not addressed in the current exposure

assessment methodology, the toxics exposure estimates may underestimate true exposure.

4) Micro-environmental Factors and Time-Activity Patterns. The revised ME factors and

time use patterns supporting EPA’s exposure assessment have been criticized as

substantially underestimating exposures to certain potentially sensitive populations and

highly exposed demographic groups, and failing to capture important inter-individual

variability in behavior and exposure patterns within demographic groups.36

5) Methods Used to Extrapolate National Urban and Rural Exposures. To estimate urban

exposures, we developed CO and HAPs emission estimates for urban counties, and scaled

them to the estimated average exposure for the 10 modeled urban areas. National average
123

rural exposures were calculated by assuming that rural HAPs exposures were, on average,

a constant fraction of the average urban exposures, scaled to the estimated CO and HAPs

emissions in the individual counties. Both of these procedures have some uncertainties.

C. Exposures in Micro-environments

Exposures to air toxics result not only from intrusion of ambient air into microenvironments, but also from emissions of air toxics originating within micro-environments. If

the contribution to long-term exposure from mobile sources within micro-environments is large,

the above estimates of exposures to ambient concentrations could significantly underestimate the

actual risk from exposure to motor vehicle air toxics. Among the most significant microenvironments where such exposures might occur are in vehicles, at service stations during

refueling, inside homes with attached garages, and near roadways. Unfortunately, measurements

of toxics concentrations within specific micro-environments is very limited, and much of it is

dated. We are addressing some of these limitations in the technical analysis plan. This section

briefly summarizes what we know about micro-environmental exposures for diesel PM, benzene,

1,3-butadiene, formaldehyde, and acetaldehyde. It should be noted that the information

presented here addresses only level of exposure, not the amount of exposure.

1. Diesel PM

Micro-environmental levels of diesel PM can be estimated using elemental carbon as a

surrogate. This approach provides some estimates of diesel PM in micro-environments such as

in-vehicle concentrations (2.8-36.6 )g/m3

), near roadways with diesel traffic (diesel PM

concentrations are calculated to be 0.7-7.5 )g/m3

 higher than background), and in schools (0.9-

5.5 )g/m3).

Recently, elemental carbon measurements were reported for enclosed vehicles driving on

Los Angeles roadways.37 Applying a ratio of diesel PM mass to elemental carbon mass, diesel

PM concentrations in the vehicle ranged from approximately 2.8 )g/m3 to 36.6 )g/m3 depending

on the type of vehicle being followed; higher concentrations were observed when the vehicle

followed heavy-duty diesel vehicles. CARB also collected elemental carbon near the Long

Beach Freeway for four days in May, 1993, and for three days in December, 1993.38 Using

emission estimates from their EMFAC7G model, and elemental/organic carbon composition

profiles for diesel and gasoline exhaust, tire wear and road dust, CARB estimated the

contribution of the freeway traffic to diesel PM concentrations. For the two days of sampling in

December 1993, diesel exhaust from vehicles on the nearby freeway were estimated to contribute

average concentrations ranging from 0.7 )g/m3 to 4.0 )g/m3 excess diesel PM above background

concentrations with a maximum 24 hour measurement of 7.5 )g/m3.

In a study designed to investigate relationships between diesel exhaust exposure and

respiratory health of children in the Netherlands, elemental carbon measurements were collected

in 24 schools located from 47 to 377 meters from a freeway.39 Thirty-two samples were collected
124

inside schools and 46 samples were collected outside the schools. Preliminary estimates of

elemental carbon concentrations indoors and outdoors ranged from 1 )g/m3 to 6 )g/m3, with an

average between 3 and 4 )g/m3

. These results correspond to diesel PM concentrations ranging

from 0.9 )g/m3 to 5.5 )g/m3 with a mean of approximately 2.7-3.7 )g/m3. Total PM2.5

concentrations inside the schools averaged 23.0 )g/m3

 while PM2.5 outside was only slightly

higher (24.8 )g/m3), suggesting extensive intrusion of outdoor air into the school environment. 

2. Benzene

The information contained in Table V.C-1 summarizes data from several studies that

have measured micro-environmental exposures to benzene. These studies are the EPA's Total

Exposure Assessment Methodology (TEAM) Study,40 Commuter's Exposure to Volatile Organic

Compounds, Ozone, Carbon Monoxide, and Nitrogen Dioxide,41 In-Vehicle Air Toxics

Characterization Study in the South Coast Air Basin,42 Air Toxics Micro-environment Exposure

and Monitoring Study,43 a 1998 California EPA study of in-vehicle concentrations (California

EPA, 1998), a 2000 study of commuter exposures in Detroit, MI,44 and a 1993 NIOSH study of

concentrations at service stations.45

The TEAM Study was planned in 1979 and completed in 1985. The goals of this study

were: 1) to develop methods to measure individual total exposure (exposure through air, food

and water) and resulting body burden to toxic and carcinogenic chemicals, and 2) to apply these

methods with a probability-based sampling framework to estimate the exposures and body

burdens of urban populations in several U.S. cities. This was achieved through the use of small

personal samplers, a specially designed spirometer (used to measure the chemicals in exhaled

breath), and a survey designed to insure the inclusion of potentially highly exposed groups.

The study, Commuter's Exposure to Volatile Organic Compounds, Ozone, Carbon

Monoxide, and Nitrogen Dioxide (Chan et al., 1989), focused on the driver's exposure to VOC's

in the Raleigh, NC area. The primary objective of this study was to measure driver's exposure to

all possible VOC and some combustion gases during one rush-hour driving period (18 sampling

days, two trips per day). Factors that could influence drivers’ exposure, such as different

roadways, car models, vehicle ventilation modes and times of driving were also tested. Car

exterior samples were also collected from the exterior of the moving vehicles by setting sampling

probes on the middle of the car roof. Another objective was to find the relationships between

fixed-site measurements and drivers' exposure (one fixed-site monitor matched per trip). Lastly,

the pedestrian's exposure to VOC in urban walking was evaluated with six walking samples.

The study by the South Coast Air Quality Management District (SCAQMD), In-Vehicle

Air Toxics Characterization Study in the South Coast Air Basin (Shikiya et al., 1989), was

conducted to refine the assessment of health risk due to exposure to toxic air pollutants. This

study examined the relative contribution of in-vehicle exposure to airborne toxics to an

individual's total exposure by measuring concentrations within vehicle interiors during home-towork commutes. Other objectives of this study were to develop statistical and concentration
125

Table V.C-1

Micro-environmental concentrations of benzene (μg/m3)

Scenarios In-Vehicle Service Station Parking Garage O

Mean Max. Mean Max. Mean Max. Mea

TEAM Study (EPA, 1987b) -- 40-60a -- 3000b -- -- -- 

Raleigh, NC Studyc

(Chan et al., 1989)

10.9 42.8 -- -- -- -- – 

SCAQMD Studyd(Shikiya et al., 1989)

42.5 267.1 -- -- -- -- -- 

SCAQMD Studye(Wilson et al., 1991) -- -- -- 288 -- 67.1 -- Los Angeles, CA(Cal. EPA, 1998)

10-22 -- -- -- -- -- -- 

Sacramento, CA(Cal. EPA, 1998)

3-15 -- -- -- -- -- -- 

Detroit, MIf(Batterman, et. al., 2000)

5.3 --

NIOSH(Hartle, 1993)

 -- -- 195 -- -- -- -- 

aMaximum benzene concentrations could not be reliably determined because exposures were averaged over a 12-hour period; however

of 3 to 4 times normal exposures were calculated.

bThis concentration was estimated, rather than measured directly.cA one-hour measurement was taken for each experimental trip.dThe estimated sampling time period was 1.5 hours/round-trip.eThe measurements from this study are five-minute levels.fMeasurements taken from interiors of urban buses.
126

measurement methods for a vehicular survey and to identify measures which might reduce

commuters' exposure to toxic air pollutants. Vehicles of home-to-work commuters from a nonindustrial park were sampled for in-vehicle concentrations of 14 toxic air pollutants, carbon

monoxide, and lead.

The second study by SCAQMD, Air Toxics Micro-environment Exposure and

Monitoring Study (Wilson et al., 1991), attempted to monitor exposures to motor vehicle

emissions in micro-environments other than in-vehicle. The study randomly sampled 100 selfservice filling stations and took samples at 10 parking garages and 10 offices nears the garages in

Los Angeles, Orange, Riverside, and San Bernadino Counties of Southern California. The study

took five-minute samples of 13 motor vehicle air pollutants in each micro-environment and in

the ambient environment. 

The 1998 California EPA study characterized the concentration of several pollutants

inside vehicles during commutes in Sacramento and Los Angeles. A variety of scenarios were

assessed, based on such variables as roadway type, traffic congestion, ventilation setting, and

vehicle type. 

Another recent study conducted in Detroit characterized concentrations of benzene and a

number of other compounds inside urban buses and compared them to ambient samples collected

on the outside of passenger cars, and to ambient monitor values. The study found that

concentrations inside buses were representative of concentrations in the ambient air collected

along bus routes. The concentrations inside buses were three to five times higher than

concentrations at fixed site monitors in Detroit.

The 1993 NIOSH study assessed benzene and MTBE concentrations and service station

attendant exposures at service stations with and without Stage II vapor recovery. The study

found that Stage II vapor recovery did not significantly reduce exposure to benzene during

refueling. However, the efficiency of Stage II vapor recovery has improved over the years. 

NESCAUM has suggested that Stage II vapor recovery systems are greater than 90% effective at

capturing MTBE and benzene vapors during refueling.46 These systems would therefore be

expected to reduce exposure beyond that shown in this initial exposure assessment.

In general, these micro-environmental exposures are short in duration, and thus are of

greater relevance to potential short-term risks rather than potential chronic risks. One microenvironmental source of exposure which could be more significant is inside homes with attached

garages. Results of sensitivity analyses on HAPEM-MS3 enable us to estimate how significant

exposures from this micro-environmental source might be.47 HAPEM-MS3 was run with

alternative sets of micro-environmental factors. The only factors that differed were those for

residential garages and homes with attached garages. The second set of factors were designed to

account for evaporative benzene emissions in these micro-environments and were used to adjust

CO concentrations upward. However, these factors were developed using data collected before

vehicles had evaporative emission controls (circa 1980).48 Since MOBILE data indicate that in

conventional fuel areas with no I/M, evaporative emissions have declined 60% between 1980 and
127

1990, we scaled the CO concentrations to account for the reduction. The result is average

exposure concentrations that are 90% higher than the estimates in Figure V.B-2. Such an

estimate assumes all evaporative benzene emissions originating in attached garages are from

vehicles, with none from gasoline cans, lawnmowers, snowblowers, solvents, and so on. Thus,

this estimate of 90% higher exposure to motor vehicle benzene emissions should be viewed as an

upper bound.

3. Acetaldehyde

The only data on micro-environmental exposures to acetaldehyde from motor vehicles are

from the In-Vehicle Air Toxics Characterization Study in the South Coast Air Basin (Shikiya et

al., 1989), which focused on the driver's exposure to VOC's in the southern California area. The

in-vehicle exposure level of acetaldehyde was determined in this study to have a mean of 13.7

μg/m3 and a maximum measured level of 66.7 μg/m3.

4. Formaldehyde

The information contained in Table V.C-2 is excerpted from three studies that have

measured micro-environment exposures to formaldehyde. These two studies are the In-Vehicle

Air Toxics Characterization Study in the South Coast Air Basin (Shikiya et al., 1989), Air Toxics

Micro-environment Exposure and Monitoring Study (Wilson et al., 1991), and the 1998

California EPA Study of in-vehicle concentrations (California EPA, 1998).

Maximum micro-environment exposure levels of formaldehyde related to motor vehicles

were determined in these studies to range from 4.9 μg/m3

 for exhaust exposure at a service

station to 41.8 μg/m3 for exhaust exposure at a parking garage.

5. 1,3-Butadiene

There are very few data on micro-environmental exposures to 1,3-butadiene. Some invehicle measurements were taken as part of the Commuter's Exposure to Volatile Organic

Compounds, Ozone, Carbon Monoxide, and Nitrogen Dioxide (Chan et al., 1989). The invehicle exposure level of 1,3-butadiene was determined in this study to have a mean of 3.0 μg/m3

and a maximum measured level of 17.2 μg/m3. Exterior to the vehicle, the mean was determined

to also be 3.0 μg/m3 with a maximum level of 6.9 μg/m3. The 1998 California EPA study of invehicle concentrations (California EPA, 1998) also included 1,3-butadiene measurements. Invehicle concentrations of 1,3-butadiene ranged from 1 to 4 μg/m3

 in Sacramento, and 2 to 6

μg/m3 in Los Angeles.
128

Table V.C-2

Micro-environmental exposure to formaldehyde (μg/m3)

Scenarios In-Vehicle Service

Station

Parking

Garage

Office

Building

Mean Max

.

Mean Max. Mean Max. Mean Max.

SCAQMD Studya

(Shikiya et al.,

1989)

15.4 35.4 -- -- -- -- -- --

SCAQMD Studyb

(Wilson et al.,

1991)

-- -- -- 4.9 -- 41.8 -- 44.2

Los Angeles, CA

(Cal. EPA, 1998)

<MQLc

to 22

Sacramento, CA

(Cal. EPA, 1998)

5-14

a

The estimated sampling time period was 1.5 hours/round-trip.

b

The measurements from this study are five-minute levels.

c

<MQL - below method quantification limit
129

Appendix 1: Mean Highway and Nonroad Contributions to Nationwide Concentrations of

Mobile Source Air Toxics in 1996, from ASPEN Modeling Using the 1996 NTI

Pollutant

Mean Ambient Conc. (μg/m3)

Highway

Contribution

(% of Total)

Nonroad

Contribution

(% of Total)

Total

1,3-Butadiene 0.05 (63) 0.02 (25) 0.08

Acetaldehyde 0.40 (54) 0.27 (36) 0.74

Acrolein 0.05 (45) 0.04 (36) 0.11

Arsenic Compounds 6.5E-07 (0.4) 7.7E-06 (4.8) 1.6E-04

Benzene 0.55 (39) 0.24 (17) 1.39

Chromium Compounds 4.2E-05 (1.3) 1.4E-04 (4.2) 3.3E-03

Dioxins/Furans 2.9E-10 2.0E-10 N.A.

Ethylbenzene 0.32 0.11 N.A.

Formaldehyde 0.38 (30) 0.48 (38) 1.28

Lead Compounds 5.9E-05 3.4E-03 N.A.*

Manganese Compounds 1.7E-05 (0.4) 1.4E-04 (3.3) 4.3E-03

MTBE 0.44 0.29 N.A.

n-Hexane 0.24 0.08 N.A.

Nickel Compounds 3.3E-05 3.2E-04 N.A.

POM (as sum of 7-PAH) 1.2E-04 (10) 2.6E-05 (2.2) 1.2E-03

Styrene 0.04 0.005 N.A.

Toluene 2.18 0.43 N.A.

Xylenes 1.20 0.40 N.A.

*Included in the National Scale Analysis, but nationwide concentrations from all sources not yet

available
130

Appendix 2: HAPEM-MS3 Microenvironmental Factors

Lag=0 indicates current ambient value used,

Lag=-1 indicates previous hour’s ambient value used.

All additive terms are set to zero.

Micro-environment Multiplicative Factor Lag

In transit, car 0.960 0

In transit, bus 1.650 0

In transit, truck 1.140 0

In transit, van 0.960 0

Indoors, public garage 0.590 -1

Outdoors, in a parking lot 0.570 0

Outdoors, along a roadway 0.850 0

In transit, motorcycle 1.030 0

Indoors, service station 0.870 -1

Outdoors, service station 0.000 0

Indoors, residential garage 0.780 -1

Indoors, in a repair shop 1.320 0

Indoors, home 0.380 -1

Indoors, office 0.380 -1

Indoors, store 0.410 -1

Indoors, restaurant 0.710 -1

Indoors, mfg. facility 0.470 -1

Indoors, school 0.450 -1

Indoors, church 0.280 -1

Indoors, shopping mall 2.110 -1

Indoors, auditorium 0.120 -1

Indoors, health care facility 0.310 -1
131

Micro-environment Multiplicative Factor Lag

Indoors, public building 0.350 -1

Indoors, other location 0.790 -1

Indoors, not specified 0.790 -1

Outdoors, construction 0.960 0

Outdoors, residential grounds 0.550 0

Outdoors, school grounds 0.960 0

Outdoors, sports arena 0.280 0

Outdoors, park/golf course 0.280 0

Outdoors, other location 0.600 0

Outdoors, not specified 0.960 0

In transit, train 0.960 0

In transit, airplane 0.000 0
132

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454-R-00-003.

3. South Coast Air Quality Management District. 1999. Multiple Air Toxics Exposure

Study in the South Coast Air Basin – MATES-II. 

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Scheutzle D. and J. Butler. 1991. Quantitative Determination of Trucking Industry

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8. Warner-Selph, M. A., Dietzmann, H.E. 1984. Characterization of Heavy-Duty Motor

Vehicle Emissions Under Transient Driving Conditions. Southwest Research Institute. 

EPA-600/3-84-104.

9. U.S. EPA. 2000. Health Assessment Document for Diesel Exhaust: SAB Review Draft.

EPA/600/8-90/057E Office of Research and Development, Washington, D.C. The

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U. S. EPA, Office of Policy, Planning and Evaluation, February, 1998.

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Prepared by Mantech Environmental Technology, Inc. for the U.S. Environmental

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Arbor, MI. Report No. EPA 420-R-93-005.

30. Johnson, T., M. McCoy and J. E. Capel. 1993. Enhancements to the Hazardous Air

Pollutant Exposure Model (HAPEM) as Applied to Mobile Source Pollutants. Prepared

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Development by International Technology Corporation, September, 1993.

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to the Hazardous Air Pollutant Exposure Model (HAPEM-MS3). Prepared for U. S.

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Inventories and the Mobile Source Contribution in Selected Areas Using the 1990

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Assessment and Modeling Division, September, 1997. 

33. E. H. Pechan and Associates, Inc. 1999. CO Inventories and Mobile Source Contribution

for Atlanta. Prepared for U. S. EPA, Office of Mobile Sources, Assessment and

Modeling Division.
135

34. Systems Applications International. 1994. Projected Emission Trends and Exposure

Issues for 1,3-Butadiene. Prepared for the American Automobile Manufacturers

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of a probabilistic exposure model applied to carbon monoxide (pNEM/CO) using Denver

personal exposure monitoring data. Journal Air and Waste Manage. Assoc. 47:491-500.

36. Northeast States for Coordinated Air Use Management. Peer review of U.S. EPA’s Draft

Estimation of Motor Vehicle Emissions and Exposure in Selected Urban Areas.

37. California Environmental Protection Agency (1998b) Measuring Concentrations of

Selected Air Pollutants Inside California Vehicles. Final Report.

38. California Environmental Protection Agency (1998a) Report to the Air Resources Board

on the Proposed Identification of Diesel Exhaust as a Toxic Air Contaminant. Appendix

III, Part A: Exposure Assessment. April 1998. 

39. Brunekreef, B. (1999) Environmental Diesel Exhaust Exposure and Respiratory Health of

Children in the Netherlands. Presented at the Health Effects Institute Diesel Workshop:

Building a Research Strategy to Improve Risk Assessment, Stone Mountain, GA, March

7-9, 1999.

40. EPA. 1987. The Total Exposure Assessment Methodology (TEAM) Study: Summary

and Analysis: Volume I. Office of Research and Development, Washington, D.C. June

1987. EPA Report No. EPA/600/6-87/002a.

41. Chan, C.C., H. Ozkaynak, J.D. Spengler, L. Sheldon, W. Nelson, and L. Wallace. 1989. 

Commuter's exposure to volatile organic compounds, ozone, carbon monoxide, and

nitrogen dioxide. Prepared for the Air and Waste Management Association. AWMA

Paper 89-34A.4.

42. Shikiya, D.C., C.S. Liu, M.I. Kahn, J. Juarros, and W. Barcikowski. 1989. In-vehicle air

toxics characterization study in the south coast air basin. South Coast Air Quality

Management District, El Monte, CA. May, 1989.

43. Wilson, A. et al. 1991. Air toxics micro-environment exposure and monitoring study. 

South Coast Air Quality Management District, El Monte, CA. 

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Urban Air Toxics During Commuting: A Field Study in the Motor City. Air & Waste

Management Association 93rd Annual Meeting, Salt Lake City, UT, June 19-22, 2000.

45. Hartle, R. Exposure to Methyl tert-Butyl Ether and Benzene among Service Station

Attendants and operators. Environmental Health Perspectives, Supplements: 101
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46. NESCAUM. 1999. RFG/MTBE Findings and Recommendations. August, 1999.

47. Glen, G. and D. Shadwick. 1998. Sensitivity Analysis Report: Analysis of Carbon

Monoxide Exposure for Fourteen Cities Using HAPEM-MS3. Prepared for National

Exposure Research Laboratory, U.S. EPA by Mantech Environmental Technology, Inc.

48. Palma, T., M. Riley, and J. E. Capel. 1996. Development and Evaluation of

Enhancements to the Hazardous Air Pollutant Exposure Model (HAPEM-MS3). 

Prepared for U.S. EPA by International Technology Corporation, September, 1996. 
137

Chapter 6: Motor Vehicle-Based Controls of Mobile Source

Air Toxics

Introduction

The Chapters 4 and 5 discussed the reductions in toxics emissions and exposure that have

already resulted from the Agency’s mobile source volatile organic compound (VOC) and diesel

particulate matter (PM)) control programs. This chapter presents the rationale for our

determination that additional motor vehicle-based controls (beyond those already adopted) not be

established at this time under §202(l)(2). This is based on considerations of the technical

feasibility and cost of further controls at this time. The first section presents an overview of

vehicle-based emission control technologies and their role in reducing air toxics. The second

section reviews the Agency’s most recent actions to further reduce VOC and PM emissions from

on-highway vehicles and engines. 

A. Vehicle-Based Technologies that Control Air Toxics

To better understand the nature of mobile source air toxics (MSAT) and their control it is

helpful to categorize the MSAT into three groups: gaseous organic toxics, DPM + DEOG (as

measured by diesel PM), and metals. For each group, the following sections present an overview

of these toxics and the impact of emission control technology on these toxics. It is well

documented that the Agency’s effort to control criteria pollutants and their precursors through

motor vehicle based controls has dramatically reduced VOC emissions. As discussed below and

in Chapter 4, these VOC controls have contributed to large reductions in gaseous MSATs. 

Similarly, other EPA controls have had major impacts on the non-gaseous MSATs as well. 

1. Gaseous Organic Toxics

Fifteen of the 21 MSATs are gaseous organics. These 15 gaseous toxics can be further

categorized depending on whether they are fuel components or combustion products. Those that

are gasoline fuel components may be found in both evaporative and exhaust emissions, while the

non-fuel components that are combustion products are found only in exhaust emissions (see

Table IV-A.1).
138

Table VI.A-1

Gaseous MSATs

Gaseous Organic

Toxics

Fuel Component Exhaust Component

Acetaldehyde YES

Acrolein YES

Benzene YES YES

1,3-Butadiene YES

Dioxin/Furans YES

Ethylbenzene YES YES

Formaldehyde YES

n-Hexane YES YES

MTBE YES YES

Naphthalene YES YES

POM YES YES

Styrene YES

Toluene YES YES

Xylene YES YES

Vehicle-based controls are effective in reducing all 15 of the gaseous air toxics. The toxics that

are fuel components may result in vehicle exhaust emissions and evaporative emissions

(depending on the volatility of the compound), and can be reduced through exhaust and

evaporative emission control as well by controlling the fuel composition directly. For those

compounds that are formed during the combustion process, control strategies rely on exhaust

emission control technology and changes to fuel composition.

a. Exhaust Controls

This section describes our requirements for vehicle controls that result in the control of

exhaust VOC emissions in general. The Agency is not aware of any exhaust emission controls

that selectively work only on the gaseous toxics listed in Table VI.A-1. All of the control

technologies of which we are aware control other VOCs as well. It is worth noting that since

almost all of the compounds listed in Table VI.A-1 contain either oxygen functional groups or

unsaturated carbon bonds, the VOC controls that are described here are generally slightly more
171 Siegl, W.O., et al., A Comparison of Conversion Efficiencies of Individual Hydrocarbon Species

Across Pd- and Pt-Based Catalysts as a Function of Fuel-Air Ratio, SAE 982549.

172 EPA Speciate Database http://www.epa.gov/ttnchie1/spec/index.html

139

effective at oxidizing these toxics than many other exhaust VOCs.171 Table VI.A-2 shows typical

exhaust fractions of MSATs for a gasoline-fueled vehicle operating with a typical fuel. (Note:

actual in-use emissions can vary significantly for different vehicles and different fuels.) As is

true for this typical case, MSATs can comprise one-quarter of all exhaust VOC emissions from a

gasoline-fueled vehicle.

Table VI.A-2

Gaseous MSATs in Typical Gasoline-Fueled Vehicle Exhaust

Toxic Exhaust Fraction of VOC172

Acetaldehyde 0.5 %

1,3-Butadiene 0.5 %

Formaldehyde 1 %

Benzene 4 %

Toluene 10 %

Other Gaseous MSATs 9 %

Total 25%

VOCs are the result of incomplete combustion occurring in a vehicle’s engine. Some

VOC emissions are unburned fuel and engine oil, some are combustion byproducts from

partially-burned fuel and engine oil. This is true for both gasoline-fueled vehicles and diesel

vehicles. To reduce both types of VOC emissions from gasoline-fueled vehicles, manufacturers

have designed their engines to achieve virtually complete combustion and have installed catalytic

converters in the exhaust system. As discussed later in this section, a similar approach can be

used with diesel engines. In order for these controls to work well for gasoline-fueled vehicles, it

is necessary to maintain the mixture of air and fuel at a nearly stoichiometric ratio (that is, just

enough air to completely burn the fuel). Poor air-fuel mixture can result in significantly higher

emissions of incompletely combusted fuel. Current generation highway vehicles are able to

maintain stoichiometry by using closed-loop electronic feedback control of the fuel systems. As

part of these systems, technologies have been developed to closely meter the amount of fuel

entering the combustion chamber to promote complete combustion. Sequential multi-point fuel

injection delivers a more precise amount of fuel to each cylinder independently and at the

appropriate time increasing engine efficiency and fuel economy. Electronic throttle control

offers a faster response to engine operational changes than mechanical throttle control can
173 http://www.epa.gov/otaq/tr2home.htm#Documents. EPA 420-R-99-023

174 McDonald, J., L. Jones, Demonstration of Tier 2 Emission Levels for Heavy Light-Duty Trucks, SAE

2000-01-1957. 

175 "Analysis of Cold-Start Emission Controls", November 15, 2000, Docket #A-2000-

IV-B-6. 

140

achieve, but it is currently considered expensive and only used on some higher-price vehicles. 

The greatest gains in fuel control can be made through engine calibrations -- the algorithms

contained in the powertrain control module (PCM) software that control the operation of various

engine and emission control components/systems. As microprocessor speed becomes faster, it is

possible to perform quicker calculations and to increase response times for controlling engine

parameters such as fuel rate and spark timing. Other advances in engine design have also been

used to reduce engine-out emissions of VOCs, including: the reduction of crevice volumes in the

combustion chamber to prevent trapping of unburned fuel; "fast burn" combustion chamber

designs that promote swirl and flame propagation; and multiple valves with variable-valve timing

to reduce pumping losses and improve efficiency. Improvements in the overall efficiency of the

vehicle can also reduce emissions by reducing the amount of fuel that is consumed. These

technologies are discussed in more detail in the RIA for the Tier 2 FRM.173

As noted above, manufacturers are also using aftertreatment control devices to oxidize

VOCs emitted by the engine. The primary approach is to use a three-way catalyst (TWC) that

simultaneously controls VOCs, CO, and NOx. New three-way catalysts are so effective that once

a TWC reaches its operating temperature, VOC emissions are virtually undetectable (0.01 gpm or

less).174 Manufacturers are now working to improve the durability of the TWC and to reduce

light-off time (that is, the amount of time necessary after starting the engine before the catalyst

reaches its operating temperature and is effectively controlling VOCs and other pollutants). EPA

expects that manufacturers will be able to design their catalyst systems so that they light off

within less than thirty seconds of engine starting. Other potential exhaust aftertreatment systems

that could further reduce cold-start emissions are thermally insulated catalysts, electrically heated

catalysts, and HC adsorbers (or traps). Each of these technologies, which are discussed below,

offer the potential for VOC reductions in the future. There are technological, implementation,

and cost issues that still need to be addressed, and at this time, it appears that these technologies

would not be a cost-effective means of reducing toxic emissions on a nationwide basis. 

However, the cost-effectiveness of these technologies for reducing toxic emissions would depend

on the technology costs and emission reductions of these technologies, which remain somewhat

uncertain, as well as the costs of traditional exhaust emission control technologies.175 The costeffectiveness would also be dependent on the manner in which these costs are apportioned with

respect to the other exhaust pollutants (i.e., VOC, NOx, and CO).

Thermally insulated catalysts maintain sufficiently high catalyst temperatures by

surrounding the catalyst with an insulating vacuum. Prototypes of this technology have
176 Burch, S.D., and J.P. Biel, SULEV and "Off-Cycle" Emissions Benefits of a Vacuum-Insulated

Catalytic Convert, SAE 1999-01-0461.

177 Laing, P.M., Development of an Alternator-Powered Electrically-Heated Catalyst System, SAE

941042.

141

demonstrated the ability to store heat for more than 12 hours.176 Since ordinary catalysts typically

cool down below their light-off temperature in less than one hour, this technology could reduce

in-use emissions for vehicles that have multiple cold-starts in a single day. However, this

technology would have less impact on emissions from vehicles that have only one or two coldstarts per day. 

Electrically-heated catalysts reduce cold-start emissions by applying an electric current to

the catalyst before the engine is started to get the catalyst up to its operating temperature more

quickly.177 These systems require a modified catalyst, as well as an upgraded battery and

charging system. These can greatly reduce cold-start emissions, but could require the driver to

wait until the catalyst is heated before the engine would start to achieve optimum performance. 

Hydrocarbon adsorbers are designed to trap VOCs while the catalyst is cold and unable to

sufficiently convert them. They accomplish this by utilizing an adsorbing material which holds

onto the VOC molecules. Once the catalyst is warmed up, the trapped VOCs are automatically

released from the adsorption material and are converted by the fully functioning downstream

three-way catalyst. There are three principal methods for incorporating an adsorber into the

exhaust system. The first is to coat the adsorber directly on the catalyst substrate. The advantage

is that there are no changes to the exhaust system required, but the desorption process cannot be

easily controlled and usually occurs before the catalyst has reached light-off temperature. The

second method locates the adsorber in another exhaust pipe parallel with the main exhaust pipe,

but in front of the catalyst and includes a series of valves that route the exhaust through the

adsorber in the first few seconds after cold start, switching exhaust flow through the catalyst

thereafter. Under this system, mechanisms to purge the adsorber are also required. The third

method places the trap at the end of the exhaust system, in another exhaust pipe parallel to the

muffler, because of the low thermal tolerance of adsorber material. Again a purging mechanism

is required to purge the adsorbed VOCs back into the catalyst, but adsorber overheating is

avoided. One manufacturer who incorporates a zeolite hydrocarbon adsorber in its California

SULEV vehicle found that an electrically heated catalyst was necessary after the adsorber

because the zeolite acts as a heat sink and nearly negates the cold start advantage of the adsorber. 

This approach has been demonstrated to effectively reduce cold start emissions. 

Historically, control of VOC emissions from diesel engines has relied primarily on

technologies that improve combustion. Because diesel engines are designed to operate with very

high air/fuel ratios (that is, with excess oxygen), they have inherently lower VOC emissions than

gasoline-fueled engines. Nevertheless, since combustion is not always complete, diesels do have

significant VOC emissions. Recent efforts to lower PM emissions have led to much more
178 EPA Speciate Database http://www.epa.gov/ttnchie1/spec/index.html

142

complete combustion for diesel engines being produced today. This has resulted in VOC

emissions from diesel engines being about 0.2-0.3 g/bhp-hr. It is possible to achieve even lower

VOC emission levels by incorporating an oxidation catalyst in the exhaust. Since these catalysts

are generally used to control PM, they are discussed in more detail in that section.

b. Evaporative Controls

Evaporative emissions occur when fuel evaporates and is vented to the atmosphere. They

can occur during refueling, while the vehicle is operating, or while it is parked. This section

describes the control of evaporative VOC emissions from on-highway gasoline vehicles. Diesel

vehicles do not have significant evaporative emissions because diesel fuel has such a high boiling

point (over 300°F). Table VI.A-3 shows typical evaporative fractions of MSATs for a gasolinefueled vehicle operating with a typical fuel. MSATs can comprise one-tenth of all evaporative

VOC emissions from a gasoline-fueled vehicle.

Table VI.A-3

Gaseous MSATs in Typical Gasoline-Fueled Evaporative Emissions

Toxic Evaporative Fraction of VOC178

Acetaldehyde 0 %

1,3-Butadiene 0 %

Formaldehyde 0 %

Benzene 2 %

Toluene 4 %

Other MSATs 5 %

Total 11%

In general, evaporative emission control is accomplished by sealing the fuel system, and

forcing all vented vapors to go through a charcoal canister, which adsorbs any fuel vapors

present. If the canister is sufficiently large, evaporative emissions from venting can be virtually

eliminated for normal operating conditions. The canister is occasionally flushed with fresh air

which "purges" the fuel vapors from the canister. These purged gases are then routed into the

engine air intake system so that they can be combusted in the engine. Since using the purge

gases for intake air instead of fresh air changes the air/fuel ratio, it must be coordinated with the

fueling control to ensure that the engine does not run rich. However, with modern electronic

controls, this is relatively straightforward. 
143

Other sources of evaporative emissions are fuel vapor venting, fuel spit-back, and postfill drip during refueling; fuel permeation through the fuel tank and fuel lines; and leaking

connections. The refueling emissions can be controlled by optimizing the nozzle-vehicle

interface, including the fill neck design, and capturing the vapors with a charcoal cannister. 

These systems are called onboard refueling vapor recovery (ORVR) systems. For design

efficiency, ORVR systems are integrated with the evaporative systems. The refueling vapors are

vented to the same cannister that is used for other evaporative emissions and are purged into the

engine along with the other vapors. The primary physical difference between an evaporative

control system and an ORVR system is the fillneck seal. In most cases, the fillneck seal is

achieved using a liquid seal. The liquid seal can be as simple as incorporating a "J-tube" into the

fillneck, much like the trap in a sink drain. ORVR systems also include anti-spitback valves to

control fuel spillage during refueling. 

Permeation and leaks can be greatly reduced by reducing the number of hoses, fittings

and connections, and by using less permeable hoses and lower loss fittings and connections. 

Fluoropolymer materials can be added as liners to hose and component materials to yield large

reductions in permeability over such conventional materials as monowall nylon. In addition,

fluoropolymer materials can greatly reduce the adverse impact of alcohols in gasoline on

permeability of evaporative components, hoses and seals. Manufacturers are also beginning to

incorporate “returnless” fuel injection systems. These systems use more precise fuel pumping

and metering to eliminate the return of heated fuel from the injectors, which is a significant

source of fuel tank heat and vapor generation. The elimination of return lines also reduces the

total length of hose on the vehicle and also reduces the number of fittings and connections that

can leak.

The test procedures and requirements associated with EPA's evaporative and refueling

emission standards essentially require manufacturers to design for zero emission levels. 

Upgrades to evaporative emission requirements and expansion of the refueling standard coverage

as part of recent and proposed EPA rules (see Section B) have gone even further towards the goal

of eliminating gasoline evaporation as a potential source of MSATs. More information on

evaporative control technologies is contained in the RIAs for the 1994 "Refueling Emissions

Regulations for Light-duty Vehicles and Trucks and Heavy-duty Vehicles" and the recent Tier 2

Rulemaking.

2. Diesel Particulate Matter and Diesel Exhaust Organic Gases

Diesel exhaust is a complex mixture of carbon particles and associated organics and

inorganics, and it is not known what fraction or combination of fractions cause the health effects

discussed in Chapter 3 that have been observed with exposure to diesel exhaust. Gaseous

components of diesel exhaust include benzene, formaldehyde, acetaldehyde, 1,3-butadiene,

acrolein, and semi-volatile organic compounds, some of which are nitrated. Diesel PM has

historically been divided into three primary constituents: unburned elemental carbon particles (or

"soot"), which make up the largest portion of the total PM; the soluble organic fraction (SOF),
179 McClure, B'T', et al., The Influence of an Oxidation Catalytic Converter and Fuel Composition on the

Chemical and Biological Characteristics of Diesel Exhaust Emissions, SAE 920854.

180 Pataky, G.M., et al., Effects of an Oxidation Catalytic Converter on Regulated and Unregulated Diesel

Emissions, SAE 940243.

144

which consists of unburned hydrocarbons (including polycyclic organic matter and dioxins) that

have condensed into liquid droplets or have condensed onto unburned carbon particles; and

sulfates, which result from oxidation of fuel-borne sulfur in the engine's exhaust. Diesel exhaust

also includes metals, which are discussed in the next section. EPA and engine manufacturers

have historically focused on control of PM emissions rather than gas-phase organics for two

reasons. First, PM-reducing technologies generally also reduce gas-phase organic emissions. 

Second, controlling PM emissions has proven to be significantly more challenging than

controlling gas phase organic emissions from diesel engines. Thus, the remainder of this section

describes PM emission controls. The extent to which diesel exhaust organic gas emissions are

controlled by VOC or other hydrocarbon controls is discussed above in section 6.A.1.

Diesel engines have made great progress in lowering engine out emissions from

uncontrolled levels between 0.8 and 1.0 g/bhp-hr PM to 0.1 g/bhp-hr PM for current engines.

These reductions came initially with improvements to combustion and fuel systems. Several

exhaust aftertreatment devices have also been developed to control PM. They generally fall into

two categories: diesel oxidation catalysts (DOCs) and particulate filters (or traps). DOCs have

been shown to be durable in-use, but they control only a relatively small fraction of the total PM

mass (mostly the soluble fraction, which is typically less than 30 percent of the total). 

Nevertheless, DOCs have been shown to significantly reduce the emissions of toxic organics

from diesel engines.179, 180

PM traps work by passing the exhaust through a ceramic or metallic filter to collect the

PM. The collected PM must then be burned off the filter before the filter becomes plugged. This

burning off of collected PM is referred to as "regeneration," and can occur either: on a periodic

basis by using base metal catalysts or an active regeneration system such as an electrical heater, a

fuel burner, or a microwave heater; or, on a continuous basis by using precious metal catalysts. 

Uncatalyzed diesel particulate traps demonstrated high PM trapping efficiencies many years ago,

but the regeneration characteristics were not dependable. As a result, some systems employed

electrical heaters or fuel burners to improve upon regeneration, but these complicated the system

design and still did not provide the durability and dependability required for HD diesel

applications. 

Catalyzed diesel particulate traps have the potential to provide the same reductions in

diesel PM emissions and provide the durability and dependability required for diesel

applications. They have lower average backpressure than other traps and they need no extra

burners or heaters. Most importantly, however, they are highly efficient at trapping all forms of

diesel PM and are reliably regenerated under normal operating conditions typical of a diesel
181 Allansson, et al, European Experience of High Mileage Durability of Continuously Regenerating

Diesel Particulate Filter Technology. SAE 2000-01-0480.

182 Kleeman, M.J., Schauer, J.J., Cass, G. R., 2000, Size and Composition Distribution of Fine Particulate

Matter Emitted From Motor Vehicles, Environmental Science and Technology, Vol. 34, No. 7.

145

engine. These catalyzed PM traps are able to provide in excess of 90 percent control of diesel

PM. More than one aftertreatment manufacturer is developing these precious metal catalyzed,

passively regenerating PM traps. In field trials, they have demonstrated highly efficient PM

control and promising durability. A recent publication documents results from a sample of these

field test engines after years of use in real world applications. The sampled filters had on average

four years of use covering more than 225,000 miles in applications ranging from city buses to

garbage trucks to intercity trains. When tested on the U.S. Heavy-Duty Federal Test Procedure

(HD FTP), these in-use engines demonstrated PM reductions in excess of 90 percent.181 It

should be noted, however, these catalyzed traps work well only with diesel fuel with very low

sulfur content.

Modern catalyzed PM traps have been shown to be very effective at reducing not only

PM mass, but overall number of particles emitted. Hawker, et. al., found that a modern catalyzed

PM trap reduced the particle count by over 95 percent, including ultrafine particles (< 50 nm), at

most tested operating conditions.182 Particles smaller than 1,000 nanometers (nm) comprise more

than 90 percent of PM mass. Of these particles, approximately half of the mass is from particles

smaller than 100 to 200 nm. PM traps have very high particle capture efficiencies. Smaller

particles (<200 to 300 nm) are captured primarily by diffusional deposition to surfaces within the

trap walls. Capture efficiency of primary PM by diffusion actually increases for decreasing

particle size. Larger particles are captured primarily by inertial impaction on surfaces due to the

tortuous path of the exhaust gases as they pass through the porous trap walls. Capture

efficiencies for the elemental carbon fraction (soot) of diesel PM nearing 100 percent are possible

with PM traps, with the only remaining PM downstream of the trap being sulfate and a small

amount of organic material. 

3. Metals

Mobile source toxics include compounds of six metals: arsenic, chromium, lead,

manganese, mercury, and nickel. The source of these toxic emissions are trace amounts of these

compounds in engine oil or fuel that come from additives, impurities, and products of engine

wear. From a vehicle or engine perspective, the primary methods of reducing emission of toxic

metals would be to reduce engine wear and oil consumption. (Metal products of engine wear

collect in the engine oil, and can be emitted if the oil is burned in the cylinder or otherwise enters

the exhaust stream.) Manufacturers already have a strong incentive to reduce both engine wear

and oil consumption due to consumer demand. Moreover, manufacturers must limit oil

consumption to very low levels in order to comply with the existing PM standards. 
146

It is also worth noting that some engines are equipped with devices that intentionally

introduce small amounts of used crankcase oil into the fuel system as a means of disposing of the

used oil and capturing its energy content. The effects of using this type of system are essentially

the same as the effects of ordinary oil consumption. To the extent that there are toxic metals in

the oil, they would be emitted in the exhaust (generally associated with the PM emissions). We

currently require that these systems be certified to ensure that they do not cause noncompliance

with our standards. The very low heavy-duty on-highway engine PM standards that have been

proposed for 2007 may effectively preclude the use of these devices.

B. Emission Control Requirements

The previous section described the emission control technologies that are currently being

used as well as others that are projected to be used in the near future. This section describes

regulatory requirements that will force the introduction of these projected technologies in future

model years, and the impacts that these requirements will have on toxic emissions.

1. Tier 2 Standards for Light-Duty Vehicles

On February 10, 2000, EPA published new "Tier 2" emissions standards for all passenger

vehicles, including sport utility vehicles (SUVs), minivans, vans and pick-up trucks. The new

standards will ensure that exhaust VOC emissions be reduced to less than 0.1 g/mi on average

over the fleet, and that evaporative emissions be reduced by at least 50 percent. ORVR

requirements were also extended to medium-duty passenger vehicles. By 2020, these standards

will reduce VOC emissions from light-duty vehicles by more than 25 percent of the projected

baseline inventory. (See Chapter 4 for a more detailed discussion of the impact of the Tier 2

FRM on VOC inventories.) To achieve these reductions, manufacturers will need to incorporate

nearly all available emission controls, including: larger and improved close-coupled catalysts,

optimized spark timing and fuel control, improved exhaust systems, and improved evaporative

controls. However, the Tier 2 standards will be achievable without using HC traps or electrically

heated catalysts. In the Tier 2 rulemaking, EPA determined that these technologies were not

likely to be cost-effective in time to meet the standards.

The Tier 2 FRM also included the first federal formaldehyde emission standards for lightduty vehicles. However, it is actually the VOC controls that are expected to provide the toxic

emission reduction. According to the Tier 2 RIA, these controls will reduce benzene emissions

by more 20,000 tons per year, acetaldehyde by 2,000 tons per year, formaldehyde by 4,000 tons

per year, and 1,3-butadiene by more than 2,000 tons per year. Although not calculated for that

rule, the standards will also significantly reduce emission of the other gaseous toxics since it will

require reductions of exhaust and evaporative VOC emissions in general.

2. Heavy-Duty Engines and Vehicles

EPA recently set new emission standards that will significantly reduce VOC emissions
183 "Analysis of Cold-Start Emission Controls", November 15, 2000, Docket #A-2000-

IV-B-6.

147

from heavy-duty vehicles (65 FR 59896, October 6, 2000), and proposed to set more agressive

standards (65 Federal Register 35430, June 2, 2000). In the first rulemaking, we set new

standards for 2005 and later heavy-duty gasoline vehicles that are projected to reduce exhaust

VOC emissions by two-thirds or more. To comply with these 2005 standards, manufacturers are

expected to optimize existing emission controls, but are not expected to need to use the more

sophisticated controls projected for Tier 2 vehicles. The October 6, 2000 FRM will require all

complete vehicles under 10,000 pounds GVWR to comply with the ORVR requirements.

The other rulemaking includes new emission standards that would begin to take effect in

2007, and would apply to all heavy-duty highway engines and vehicles. These proposed

standards would require the use of high-efficiency catalytic aftertreatment devices as well as

advanced engine technologies. For diesel engines, manufacturers are expected to incorporate

catalyzed PM traps that could virtually eliminate both organic PM (elemental carbon and SOF)

and VOC emissions from diesel engines during normal operation. However, the engines will still

emit some sulfate PM, and can also emit some VOCs during start-up operation where the

catalysts are below minimum functional temperature. Fortunately, since diesels are used mostly

in commercial applications, almost all operation will occur with a warm catalyst. For gasoline

engines manufacturers are expected to incorporate the technologies similar to those that will be

used to comply with the Tier 2 light-duty standards. This will include improved fuel injection,

fast electronic throttle controls, reduction of crevice volumes, "fast burn" combustion chamber,

and improved three-way catalysts. The heavy-duty standards that we proposed are projected to

reduce PM emissions by 83,000 tons and VOC emissions by 230,000 tons.

C. Potential for Further Reductions from New Vehicle Standards

Given the technology-forcing nature of the recently finalized Tier 2 emission standards

for light-duty vehicles and the new emission standards for heavy-duty vehicles and engines, it is

not feasible that manufacturers would be able to further reduce toxic emissions significantly at

this time. For both gasoline and diesel vehicles, these standards will result in near-zero exhaust

VOC emissions for all operation other than engine starting. Since the only significant exhaust

emissions will occur within the first minute after engine starting, further reductions would

require manufacturers to develop technologies specifically for this very short window. While

start-up controls such as HC traps and electrically-heated catalysts exist, the issues of

technological feasibility and cost are significant enough that EPA does not believe it would be

appropriate at this time to promulgate more stringent standards based on these technologies.183

For diesels, carbonaceous PM emissions are expected to be near-zero for all operation, including

engine starting. The only PM that is expected to occur in significant amounts will be in the form

of sulfate, which cannot be reduced by vehicle-based controls.

Similarly, for evaporative emissions, manufacturers are already required to design their
184 58 FR 9467, February 19, 1993.

148

Tier 2 vehicles to have very low evaporative emissions, and must also account for the effect of

alcohol in the fuel on fuel line permeability and in-use performance. For an in-use Tier 2

vehicle, the primary evaporative emissions that are expected to occur would be the result of an

occasional leaking connection in the fuel or evaporative control system, or abnormal vehicle

operation (e.g. vehicles parked for several days without being driven). While manufacturers are

expected to minimize the number of fuel connections used in the vehicle and to use designs that

are not prone to leaking, some leaks are still likely to occur in use. 

Since metal emissions are primarily the result of the combination of engine wear and oil

consumption, manufacturers already have a very strong incentive to minimize metal emissions. 

Those metal emissions that are not a result of engine wear and oil consumption are caused by

contaminants or additives in the fuel, and are thus beyond a vehicle or engine manufacturer's

control. An EPA standard for metals set at a level that is feasible for manufacturers would only

enforce existing engine designs. Such a standard would not justify the administrative and testing

burden that it would cause. As discussed earlier, EPA is addressing in the 2007 heavy-duty

rulemaking the issue of blending used oil into diesel fuel.

D. Potential for Further Reductions from In-Use Vehicles

As described in the Response to Comment document, we are not pursuing in-use controls

in this rulemaking. Nevertheless, they could be an important part of our future attempts to

achieve further reductions in toxic emissions. With the new standards that are coming into

effect, manufacturers will be designing and building their vehicles and engines to have very low

toxic emissions. However, this does not guarantee that all of these vehicles and engines will

have low toxic emissions in use. Malmaintenance of and/or tampering with the emission

controls could result in increased toxic emissions. EPA is continually working to improve in-use

maintenance and enforce the tampering prohibition. To address the malmaintenance issue, EPA

has established onboard diagnostic (OBD) requirements for manufacturers.184 These OBD

provisions require that vehicle manufacturers install dashboard indicators that alert drivers to the

need for emission-related maintenance, and electronic monitors that store codes in the vehicle's

computer to assist mechanics in the diagnosis and repair of the malfunction. To address both the

malmaintenance and tampering issues, EPA is working with states to develop and optimize

inspection and maintenance (I/M) programs that monitor the emission performance of in-use

vehicles. Historically, these programs have relied on tailpipe testing to identify high-emitting

vehicles. However, these programs have begun to rely more on the OBD systems to identify the 

high-emitting vehicles, as well as the cause of the emission problem. 

For heavy-duty vehicles, I/M is more difficult because it is not as easy to test the larger

vehicles. However, we recently established new OBD requirements for heavy-duty gasoline

vehicles under 14,000 pounds GVWR, and expect to propose similar requirements for all other

heavy-duty vehicles in the near future. As these heavy-duty OBD programs take effect, it will be
149

much more practical to develop heavy-duty I/M programs that will achieve real emission

reductions, especially for PM.

Another potential approach that could reduce emissions from existing vehicles is to

retrofit these vehicles with improved emission control devices. This could be especially

beneficial with heavy-duty vehicles, which can have very long useful lives. A heavy-duty retrofit

program is thus appealing because the slow turnover of the diesel fleet makes it difficult to

achieve near-term air quality goals through new vehicle standards alone. Some of the exhaust

aftertreatment technologies being considered in the recent heavy-duty diesel rule are especially

appealing for use in retrofits because they can be fitted to an existing vehicle as add-on devices

without major engine modifications, although some of the more sophisticated systems that

require careful control of engine parameters may be more challenging. We believe that large

diesel PM emission benefits from the existing fleet could be realized as a result of retrofits. 

However, these technologies will require changes to the fuel. Therefore, we think that where we

can consider future fuel and technology changes it is reasonable to defer our analysis on the longterm feasibility of these controls until a later action.

Finally, MSATs can be reduced through Transportation Control Measures (TCMs), which

have been in use for several decades to control traffic congestion on major streets and highways. 

TCMs include a wide variety of measures used to reduce motor vehicle emissions, primarily by

reducing the total amount of vehicle miles of travel in an area. A few examples of TCMs include

mass transit improvements, ridesharing arrangements, telecommuting and work schedule

changes, parking management, and roadway tolls. As noted earlier, most emissions from cars

occur just after starting, when the emissions control devices are not fully warmed up. Therefore,

transportation control strategies that reduce short trips have the most emissions benefits. 

Although we have no rules or regulations requiring that states or cities implement TCMs, we are

developing guidance that will help more areas implement such programs that should reduce

MSAT emissions.
185 Petroleum Supply Annual 1998, Energy Information Administration, June 1999. Table 2.

150

Chapter 7: Fuel Controls

This Chapter contains background information and analyses supporting our antibacksliding program. We first summarize the refining industry's current gasoline production and

the reasons for the current overcompliance with the reformulated gasoline and anti-dumping

requirements. We then discuss the means through which we expect the industry to comply with

our anti-backsliding requirement. A description of the costs and emission benefits of our

program follow, and we end with a discussion of incremental volumes, compliance margins, and

the reasons we have excluded California gasoline from our anti-backsliding requirements.

A. Industry and product characterization

1. Description of entities subject to the toxics anti-backsliding requirements

Our toxics anti-backsliding program will apply to every domestic refinery that produces

gasoline, every importer of gasoline to the U.S., and every foreign refiner of gasoline that exports

to the U.S. There are no new standards applicable to parties who buy, sell, and/or trade gasoline

downstream of refineries. 

a. Domestic refiners

Approximately 146 domestic refineries collectively produced approximately 2.9 billion

barrels of gasoline in 1998 (however, not all refineries produce gasoline). This amounts to

approximately 7.9 million barrels per calendar day on average185. Refineries are often identified

by the Petroleum Administration for Defense District (PADD) in which they reside. PADDs are

shown in Figure VII.A-1, while the number of refineries in each PADD, along with gasoline

production and consumption in that PADD, are shown in Table VII.A-1. Although a refinery

may be located in a particular PADD, the gasoline produced at that refinery may not necessarily

be distributed in that same PADD. For example, most of the gasoline consumed in PADD I is

produced by PADD III refineries.
186 Petroleum Supply Annual 1998, Volume 1, Energy Information Administration, June 1999. 

187 Petroleum Marketing Annual 1998, Energy Information Administration, May 1999.

151

Figure VII.A-1

Location of PADDs in the Contiguous U.S.

IV

V I

II

III

Table VII.A-1 

Refinery Count and 1998 Gasoline Volumes by PADD

PADD

Number of

operating

refineries as

of 1/1/2000 

Gasoline

production

(million

barrels)186

Gasoline

consumption

(million

barrels)187

I 14 354 1092

II 30 673 886

III 59 1270 418

IV 15 94 96

V 28 490 521
188 Petroleum Supply Annual 1998, Volume 1, Energy Information Administration, June 1999. 

152

b. Gasoline importers

In 1998, approximately 113 million barrels of gasoline were imported into the U.S. 188

Gasoline is imported into each coast, as well as into Alaska and Hawaii. Gasoline imports by

PADD are shown in Table VII.A-2.

Table VII.A-2 

1998 Imported Gasoline

Millions of barrels

PADD I

PADD II

PADD III

PADD IV

PADD V

104

1

6

0.2

2

c. Foreign refiners

Only a few foreign refineries have approved individual anti-dumping baselines. We

approved some of these baselines in 1999, and some in 2000. Shipments of gasoline

(conventional only) subject to the individual baselines began late in 1999. 

2. Toxics emissions variations

a. Differences in 1997-99 data

Our analysis of refiner reports submitted for the years 1997 through 1999 showed little

difference in fuel benzene levels between the years, or for either type of gasoline, RFG or

conventional. The lack of variation between these years suggests that the results for even one of

these years would be representative of all years. Table VII.A-3 shows the results of our analysis.
153

Table VII.A-3

Annual Average Refinery Fuel Benzene Content (vol%)

1997 1998 1999

RFG 0.64 0.65 0.67

CG 1.12 1.11 1.10

Accurate data on annual average toxics performance was not available for years other than 1998,

so year-to-year variations in toxics performance could not be directly evaluated. However, since

fuel benzene content has such a large effect on toxics emissions (up to 70 percent), we believe

that the values in Table VII.A-3 suggests that toxics performance levels also varied little between

1997 and 1999.

b. Default anti-backsliding baseline

Under our anti-backsliding program, each refinery and importer will be subject to a toxics

performance baseline which is based on their annual average production of RFG and CG over the

1998 - 2000 baseline period. Under some conditions, described more fully in the preamble, a

refinery or importer will not be able to establish a toxics performance baseline that is specific to

their facility. In this case there must be a default baseline available.

We have calculated the default anti-backsliding toxics performance baseline using 1998 -

1999 batch report data submitted to EPA by refiners under the RFG and anti-dumping programs. 

We are unable at this time to develop a default baseline using data for the full baseline period of

1998 - 2000 because year 2000 production data is not yet available. However, given the yearly

consistency exhibited in toxics emissions in Table VII.A-3, we believe that a default baseline

which is based on 1998 - 1999 data will be very close to one that is based on 1998 - 2000 data. 

Once complete year 2000 data becomes available, we will re-evaluate our default baseline and

will publish a revised version. .

Though 1998 and 1999 were Phase I RFG years, we have used the Phase II version of the

Complex Model to develop our default baseline. This is consistent with the manner in which

toxics performance requirements for every refinery and importer will be established, since

compliance with the anti-backsliding program will be determined using the Phase II version of

the Complex Model. Thus, the 1998-1999 refinery information was evaluated using the Phase II

Complex Model, and volume-weighted to determine the values listed in Table VII.A-4 below. 

We have also added a compliance margin to assure that refiners need go no further than their

1998 - 2000 production in terms of toxics performance levels. Compliance margins are

discussed more fully in Section VII.E below.
189 "Economic Reasons for U.S. Refineries Overcompliance with Current Benzene Fuel Content in

Reformulated and Conventional Gasoline, and Toxic Emissions Performance Standards," ICF Consulting, prepared for

U.S. EPA under Contract 68-C-98-170. December, 2000.

154

Table VII.A-4

Toxics Anti-backsliding Default Baseline

Type of gasoline Reformulated Conventional

Form of toxic emissions Total Exhaust

Units % reduction form statutory

baseline

mg/mile

1998-1999 average value 26.01 % reduction 92.14 mg/mile

Compliance margin 0.7 % reduction 2.5 mg/mile

Default baseline 26.71 % 94.64 mg/mile

3. Refinery Production of Benzene

Though we are finalizing toxics anti-backsliding performance requirement, and not a

benzene content requirement as proposed, the impacts of the petrochemical benzene market and

the associated refiner actions are still critical to a toxics overcompliance discussion because

benzene emissions constitute 70 percent of toxics emissions on a mass basis, and fuel benzene

content is the fuel parameter with the largest effect on benzene emissions. Therefore, our

discussion of current overcompliance with the current RFG and anti-dumping requirements must

begin with a presentation of chemical-grade benzene production at refineries at demand for

benzene in the petrochemicals industry.

To better understand the market forces that have lead to the significant fuel benzene

content reductions we have seen in the last several years, EPA oversaw a study conducted by ICF

Consulting to evaluate the benzene industry189. Specifically, the study considered the technical

and economic factors associated with benzene production and disposition. The work assignment

was designed to provide information on the following:

1) Technologies and economics for benzene reduction at refineries

2) Benzene use in petrochemical complexes

3) Benzene market (production, use transportation, costs)

4) Locations of refineries and petrochemical complexes

5) Technical and economic inputs on benzene reductions in small refineries
190 Based on an analysis from Honeywell Hi-Spec Solutions (formerly Bonner & Moore), based on 1999

NPRA Petrochemical Survey for benzene. See EPA Air Docket A-2000-12, "Bonner & Moore Associates U.S. Benzene

Supply/Demand."

155

As discussed in the study, the factors that determine whether a refinery sells benzene in

the petrochemical market or includes it in its gasoline are based on the relative economic benefits

of the petrochemical market for benzene versus the incremental processing costs associated with

continuing to allow benzene to be included in gasoline which meets all applicable gasoline

composition requirements. The report states that, currently, refineries which extract benzene for

the purposes of selling it to the petrochemicals industry do so because it appears more profitable

to extract benzene than to include it in gasoline. This situation appears to be motivated largely

by regulatory benzene content limits. As stated in the report:

The incremental cost to extract more benzene in a refinery is insignificant

compared to the base cost to extract benzene down to the RFG limit. Therefore,

once the investment in benzene extraction is made, the decision on whether to sell

benzene to the petrochemical market is made by comparison of the petrochemical

feedstock net-back value to the octane-barrels gasoline blending value.

Benzene Consumption (Demand) Demand for styrene, which is the primary petrochemical

product that uses benzene as a feed, is expected to increase at 4.5 percent annually. World

consumption of benzene is expected to increase by 2-4 percent annually. In the U.S., benzene

consumption is predicted to increase by about 1-3 percent annually. Future forecasts from both

Dewitt & Company, Inc. and Honeywell Hi-Spec Solutions show continued increases for the

next several years. See Figure VII.A-2190. Also, the U.S. is a net importer of benzene, and no

change is expected in this status.
156

Figure VII.A-2

Chemical Benzene Demand in the U.S. (Honeywell Hi-Spec Solutions forecast)

1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005

1700

1800

1900

2000

2100

2200

2300

2400

Million gallons

Benzene production(supply) The petrochemical industry obtains benzene from a number of

sources, depending on company location, transport issues and supply-demand characteristics. 

These sources include:

1) A refinery owned by the same company as the petrochemical facility

2) Another refining company

3) Benzene extraction units of the petrochemical company

4) Benzene imports

Within a refinery, chemical-grade benzene can be produced from a number of sources. Table

VII.A-5 shows a typical refinery benzene supply pattern.
157

Table VII.A-5

Typical Refinery Benzene Supply Pattern

Refinery Process Unit Source of Benzene

Supply, vol%

Reformer/Straight Run Gasoline 33

Ethylene Unit/Pyrolysis Gasoline 39

TDA/TDP 22

FC Gasoline/Hydrocrackate/Coker Gasoline 6

Benzene Price Benzene price has ranged from $0.70 to $2.25 per gallon since 1981. Currently

benzene is selling for about $1.50 per gallon. 

Benzene Transportation Benzene can be transported by pipeline, barge, rail and tank truck. 

Benzene freezes at a relatively high temperature, thus pipeline transport is typically between a

refinery and a nearby petrochemical plant. Long distance pipeline transport is precluded because

of the high potential for freezing en route. Rail transport is increasingly the travel mode of

choice for benzene because of lower cost per volume and because inventories can be reduced due

to the availability of nearby rail access. Tank truck is not a favorable mode due to hazardous

materials (HAZMAT) restrictions. Barge is favored only if waterway transport is convenient. 

The ICF report notes that:

...margins on benzene sales are not high enough to justify significant

transportation costs ....transportation is optimized to minimize cost.

The report states that economists have predicted that the transportation infrastructure may

significantly influence the benzene market in the future, providing an edge to companies with the

best transportation “logistics”. Thus benzene production is likely to be most favorable in

situations where transportation between a production source and the point of consumption is

shortest.

B. Toxics inventory and overcompliance

In this Section we present a brief discussion of the toxics emission inventories and the

reductions in those inventories that have resulted from overcompliance with the RFG and antidumping requirements. We are finalizing a toxics performance requirement which covers the

five toxics identified in the Clean Air Act's RFG and anti-dumping provisions. These include

benzene, 1,3-butadiene, formaldehyde, acetaldehyde, and polycyclic organic matter (POM). 
191 "1996 American Petroleum Institute/National Petroleum refiners Association Survey of Refining

Operations and Product Quality," Final report, July 1997.

158

Chapter IV presented our estimates for toxics inventories for selected years. For toxics

compounds which are included in the RFG and anti-dumping programs, these inventories

represent current gasoline production including all overcompliance with the RFG and antidumping requirements. In order to determine the effect that this overcompliance has had on

toxics inventories, it was necessary for us to estimate a hypothetical case in which there was no

overcompliance (i.e. RFG and conventional gasoline (CG) exactly meet the applicable toxics

emission requirements). To do this, we relied on estimates of gasoline fuel properties and of

toxics emissions as predicted by the Complex Model.

The Complex Model was created to permit users to estimate the percent change in

emissions that would result from changes in various gasoline fuel properties. The Complex

Model also predicts emissions in mg/mi for a given fuel formulation to permit calculation of

percent change effects for the sum of all toxics. As a result, it is possible to use the Complex

Model to determine how the mg/mi values for total toxics emissions would change if the fuel

exactly met the requirements of the RFG and anti-dumping programs. The change in mg/mi

values can then be correlated with the inventories presented in Chapter IV to determine the net

reduction in toxics inventories that has resulted from overcompliance with the RFG and antidumping requirements.

In order to estimate the change in mg/mi emissions as predicted by the Complex Model

that results from overcompliance, we must first have fuel property data on actual RFG and CG

produced and sold in recent years to establish "baseline" mg/mi levels with the Complex Model. 

EPA collects batch reports from all refiners to ensure compliance with the RFG and antidumping regulations. The most recent database that was available for use in our analysis was for

calender year 1998. This database includes volumes and measured properties for all Complex

Model inputs. Using this database, we volume-weighted all values to determine the annual

average fuel properties for CG and RFG for both summer and winter. The one exception to this

was for oxygen content. The dataset for oxygenates used in CG appeared to have contained

blendstock and/or RBOB (Reformulated gasoline Blendstock for Oxygenate Blending) data, and

was therefore deemed unsuitable. Therefore, we based the CG oxygen levels on the 1996

API/NPRA survey.191 The 1998 average fuel properties are shown in Table VII.B-1.
192 "Phase II RFG Report on Performance Testing," April 5, 1999. U.S. EPA, Office of Transportation and Air

Quality. See EPA Air Docket A-2000-12.

159

Table VII.B-1

Average fuel properties from 1998 annual reports

Conventional gasoline Reformulated gasoline

Summer Winter Summer Winter

Oxygen, wt%a

Sulfur, ppm

RVP, psi

E200, vol%

E300, vol%

Aromatics, vol%

Olefins, vol%

Benzene, vol%

0.20

306

8.31

44.65

80.89

27.30

11.75

1.13

0.20

299

12.17

50.07

83.22

24.49

11.51

1.09

2.17

203

7.69

48.97

82.46

22.58

11.73

0.67

2.28

200

12.72

56.07

84.77

19.58

11.91

0.63

Volume fraction 0.324 0.386 0.133 0.157 a

 Oxygen was composed of approximately 70% MTBE, 30% ethanol. 

The most recent inventory is for 1996. Ideally, then, we would also have annual average

fuel properties for 1996. However, 1998 is the most recent year for which we have accurate fuel

property data. As shown in Table VII.A-3, we believe that fuel properties did not, on average,

vary significantly from year to year. Therefore, we considered the values in Table VII.B-1 to be

representative of gasoline produced in 1996. However, it may also be instructive to have a set of

representative fuel properties which represent gasoline production in 2007. Therefore we

adjusted the values in Table VII.B-1 to take into account the introduction of Phase II RFG in

2000 and low sulfur gasoline in 2004. First, we made use of the presumed fuel properties for

summer-grade Phase II RFG developed by the Phase II RFG Implementation Team in 1997

(winter-grade Phase II RFG was expected to be substantially similar to winter-grade Phase I

RFG).192 Second, we changed the sulfur levels of all gasoline to 30 ppm to reflect compliance

with the low sulfur requirements. For this analysis we have assumed that corresponding changes

in other fuel properties are negligible. Since we are doing a comparative and not an absolute

analysis as described more fully below, we do not believe that this assumption substantively

affects the results. Note that actual production and/or batch data on gasoline produced in year

2000 was not available at the time of this analysis. The resulting set of representative 2007 fuel

properties are given in Table VII.B-2.
160

Table VII.B-2

Representative 2007 Fuel Properties

Conventional gasoline Reformulated gasoline

Summer Winter Summer Winter

Oxygen, wt%a

Sulfur, ppm

RVP, psi

E200, vol%

E300, vol%

Aromatics, vol%

Olefins, vol%

Benzene, vol%

0.20

30

8.31

44.65

80.89

27.30

11.75

1.13

0.20

30

12.17

50.07

83.22

24.49

11.51

1.09

2.17

30

6.80

52.00

84.00

22.58

11.50

0.67

2.28

30

12.72

56.07

84.77

19.58

11.91

0.63

Volume fraction 0.324 0.386 0.133 0.157

a

 For calculation purposes, all oxygen was assumed to be MTBE.

The fuel properties from Tables VII.B-1 and VII.B-2 were then used as inputs into the

Complex Model to estimate total toxics emissions in terms of mg/mi. These emission estimates

are the per-vehicle equivalents of the inventories presented in Chapter IV, and are shown in

Table VII.B-3. Note that the 1996 values were derived from the Phase I version of the Complex

Model, which predicts significantly lower emissions than the Phase II version of the Complex

Model used to estimate the values for 2007.

Table VII.B-3

Baseline Toxics Emission Estimates From the Complex Model (mg/mi)

Conventional gasoline Reformulated gasoline Weighted

average Summer Winter Summer Winter

1996

2007

39.96

68.67

51.97

98.96

30.71

55.87

42.73

83.78

43.80

81.03

In order to determine the effect of overcompliance on toxics emissions, we then estimated

the mg/mi emissions that would result if both RFG and CG exactly met their respective standards

with respect to toxics. For RFG, this simply entailed applying the toxics standard given in 40

CFR §80.41 to the annual average statutory baseline for toxics to generate a "no overcompliance"

estimate of toxics emissions. For CG, we first calculated the average fuel properties for all

individual refinery 1990 baselines which are used as the foundation of compliance with antidumping, and then calculated the associated mg/mi values with the Complex Model. The results

are shown in Table VII.B-4.
193 "Analysis of the impacts of control programs on motor vehicle toxics emissions and exposure in urban areas

and nationwide," U.S. EPA report number EPA420-R-99-030, November 1999

161

Table VII.B-4

Total Toxics Emissions With and Without Overcompliance (mg/mi)

With Overcompliance Without Overcompliance Ratio

1996

2007

43.80

81.03

49.77

95.84

1.136

1.183

Since the mg/mi values in Table VII.B-4 are the per-vehicle equivalents of the inventory

estimates given in Chapter IV for gasoline-powered highway vehicles, the fractional increase in

mg/mi values due to removing the overcompliance should be the same as the fractional increase

in the inventories due to removing overcompliance. In other words, by applying the ratios given

in Table VII.B-4 to the inventories in Chapter IV, we can estimate the toxics inventories that

would have been produced had there been no overcompliance with the RFG and anti-dumping

requirements.

The estimated toxics inventories given in Table IV.B-3 include emissions from both

gasoline and diesel highway vehicles. Since the issue of overcompliance is limited to RFG and

CG, we used only the estimated tons for gasoline-powered vehicles from Sierra Research, Inc.193

These values are shown in Table VII.B-5, including our estimate of the effect of current

overcompliance on these inventories. Note that the study conducted by Sierra Research, Inc. did

not model POM. Therefore, the 1996 POM values in Table VII.B-5 were taken instead from the

1996 National Toxics Inventory, shown in Table IV.A-1. The reduction in the toxics inventories

between 1996 and 2007 is due to continuing reductions in the VOC inventory that result from the

compounding effects of existing control programs. 
162

 Table VII.B-5

Annual Emissions Inventory for Complex Model Toxics for the Total U.S.

Gasoline On-Highway Vehicles Only

(thousand short tons per year)

Compound

1996 Emissions 2007 Emissions

Actual

Without

overcomplianceReduction Actual

Without

overcomplianceReduction

Benzene 168 191 23 87 103 16

Acetaldehyde 21 24 3 9 11 2

Formaldehyde 66 75 9 22 26 4

1,3-Butadiene 22 25 3 10 12 2

POM 0.04 0.05 0.01 0.02 0.02 0.00

Total 277 315 38 128 151 23

Thus we estimate that, as a result of overcompliance with the RFG and anti-dumping

requirements, the on-highway toxics inventories are approximately 38,000 and 23,000 tons lower

than would otherwise be the case for the 1996 and 2007 inventories, respectively.

We do not have an accurate means for estimating the effects of overcompliance on toxics

emissions from nonroad engines. However, since a significant amount of toxics emissions arise

from nonroad engines, it nevertheless seems appropriate to calculate a rough estimate of the

effects of overcompliance on nonroad toxics inventories. In lieu of an emissions model specific

to nonroad engines, we applied the ratios from Table VII.B-4 to the nonroad inventories for

gasoline-powered vehicles. The nonroad inventories given in Table VIII.B-1 include both

gasoline and diesel sources of toxics emissions, so it was necessary to draw directly from the

1996 NTI study. Values for 2007 were adjusted on the basis of VOC inventories for nonroad in

1996 and 2007, consistent with the approach taken in developing the values in Table VIII.B-1. 

As before, the absent POM values were taken from Table IV.A-1. The results are shown in

Table VII.B-6.
163

 Table VII.B-6

Annual Emissions Inventory for Complex Model Toxics for the Total U.S.

Gasoline Nonroad Vehicles Only

(thousand short tons per year)

Compound

1996 Emissions 2007 Emissions

Actual

Without

overcomplianceReduction Actual

Without

overcomplianceReduction

Benzene 176 200 24 70 83 13

Acetaldehyde 13 15 2 5 6 1

Formaldehyde 28 32 4 11 13 2

1,3-Butadiene 20 23 3 8 9 1

POM 0.02 0.02 0.00 0.02 0.02 0.00

Total 237 269 32 94 111 17

Our estimate of the total tons reduced as a result of overcompliance with the RFG and

anti-dumping requirements is shown in Table VII.B-7.

Table VII.B-7

Total Tons Reduced Due to Overcompliance (thousand tons)

Compound

1996 Inventory Reductions 2007 Inventory Reductions

Highway Nonroad Total Highway Nonroad Total

Benzene 23 24 47 16 13 29

Acetaldehyde 3 2 5 2 1 3

Formaldehyde 9 4 13 4 2 6

1,3-Butadiene 336213

POM 0.01 0.00 0.01 0.00 0.00 0.00

Total 38 32 70 23 17 40
164

Note that the derivation of the ratios in Table VII.B-4 and their application to the toxics

inventories was necessarily based on total toxics emissions, not emissions of the individual

pollutants benzene, acetaldehyde, formaldehyde, 1,3-butadiene, and POM. This is due to the fact

that compliance with the RFG and anti-dumping requirements is done on the basis of the sum of

toxics. As a result, we can place confidence only in the total tons reduced as given in Table

VII.B-7, not the tons reduced for the individual pollutants. We have provided estimates of tons

reduced for individual pollutants only to illustrate the relative reductions in each that we believe

are most likely. In fact the distribution of tons reduced for the individual pollutants could be

different in reality even though the totals remain the same. The analyses of the refinery modeling

has given us a solid indication of what the trends will be for fuel quality in the future as a result

of the RFG Phase II program, Tier 2 gasoline sulfur program and the ultra low sulfur diesel

program. 

C. Costs and Benefits of the Program

1. Technological Feasibility

a. Toxics Performance of RFG Program

The 1990 Clean Air Act Amendments directed EPA to issue regulations that require

gasoline to be “reformulated” to significantly reduce vehicle emissions of ozone-forming and

toxic air pollutants. This cleaner burning gasoline is called reformulated gasoline (RFG). RFG

contains the same components as conventional gasoline, but is blended to reduce air pollution. 

RFG is required to be used in the ten major metropolitan areas of the U.S. with the worst ozone

air pollution problems. Other areas with ozone levels exceeding the public health standard have

voluntarily chosen to use RFG. Phase I of the RFG program began in January of 1995 and Phase

II began in January 1, 2000. RFG has significantly reduced toxic emissions, including benzene. 

Analysis of fuel data submitted to EPA by industry for compliance purposes shows that emission

reductions from the RFG program have been more than the program requires each year since the

program’s introduction in 1995. Table VII.C-1 gives a comparison of the average toxics

emission reductions standards of RFG Phase I and Phase II, summarised from the standards

given in 40 CFR §80.41.

Table VII.C-1

Comparison of Average Emission Reductions Standards of RFG Phase I and RFG Phase II

RFG Phase I RFG Phase II

Volatile Organic Compounds 17% 27%

Nitrogen Oxides 2% 7%a

Toxics 17% 22%

a. Summertime only.
194 “Regulation of Fuels and Fuel Additives: Standards for Reformulated and

Conventional Gasoline - Final Rule,” 59 FR 7812 (February 16, 1994). See 40 CFR part 80

subparts D, E, and F.

195 “Negligible Cost Justification for Total Toxics Anti-Backsliding Program During the

Phase II RFG Program,” Memo to the Docket (A-2000-12) by Joe Sopata (USEPA), November

17, 2000.

165

The CAA also requires EPA to establish anti-dumping standards applicable to

conventional gasoline used in the rest of the country. The Administrator signed the final RFG

and anti-dumping regulations on December 15, 1993194 and these regulations became effective in

January 1995.

b. What is expected to happen with Air Toxics Performance due to RFG Phase

II Implementation?

Phase II RFG requirements began on January 1, 2000. However, since the compliance

period (the full calender year) has not been completed at the time of this writing, we do not yet

have complete information about the means refiners are using to comply with the new

requirements. Even so, we have information from refiners' compliance with the Phase I

requirements and their own voiced expectations regarding Phase II compliance that lead us to

gauge the means for complinace with the Phase II requirements. For instance, refiners are

expected meet the more stringent Phase II RFG VOC requirements by lowering the RVP of

Phase II RFG. To accomplish a lower RVP in Phase II RFG, one cost-effective option that

refiners may use is to blend less butane in Phase II RFG gasoline than Phase I RFG. The

reduction in butane will affect the toxics content of gasoline because butane dilutes toxics

components such as benzene, aromatics and olefins. In addition, blending less butane in gasoline

typically results in lower octane. To make up for the lost octane, refiners may rely on increased

reformate, which contains aromatics and benzene. 

To check the assumption that fuel benzene properties are likely to increase as a result of

compliance with Phase II RFG’s more stringent VOC standards, EPA performed a preliminary

analysis of second quarter benzene properties for 1998, 1999 and 2000 for those refineries in

three PADDs with available 2000 data. This analysis found that, contrary to EPA expectations,

that benzene content declined slightly from Phase I to Phase II RFG.195 

Oxygenates are added to RFG in order to meet the oxygen mandate of 2.0 weight percent

oxygen as mandated for RFG by the Clean Air Act. Methyl Tertiary Butyl Ether (MTBE) is the

most common oxygenate used in RFG to meet the oxygen mandate. Ethanol is the second most

common oxygenate used in RFG to meet the oxygen mandate. MTBE’s blending RVP is 8 psi,
196 U.S. Petroleum Refining, Assuring the Adequacy and Affordability of Cleaner Fuels,

National Petroleum Council, Committee on Refining, Lee R. Raymond, Chair, June 2000

197 “Control of Air Pollution from New Motor Vehicles: Tier 2 Motor Vehicles

Emissions Standards and Gasoline Sulfur Control Requirements - Final Rule,” 65 FR 6698

(February 10, 2000). See also 40 CFR part 80 subpart H for regulations applicable to gasoline

sulfur.

198 Regulatory Impact Analysis - Control of Air Pollution from New Motor Vehicles: Tier

2 Motor Vehicle Emission Standards and Gasoline Sulfur Control Requirements, EPA420-R-99-

023, December 1999.

166

whereas Ethanol’s blending RVP is 18 psi.196 Ethanol’s higher blending RVP requires that more

light-end hydrocarbons like butane and pentane be removed from the base gasoline blend stock in

the manufacturing of RFG, whereas, MTBE’s lower blending RVP may only require the removal

of some butanes in the manufacturing of RFG. 

c. Tier 2 Gasoline Sulfur Program

Recently, EPA issued regulations establishing lower sulfur content requirements for all

gasoline197 and establishing stricter tailpipe emissions standards for all passenger vehicles,

including sport utility vehicles (SUVs), minivans, vans and pick-up trucks (the “Tier 2" rule).

The low sulfur program will be phased-in beginning in 2004, and, in general, refiners must meet

a refinery average sulfur standard of 30 ppm beginning in 2005 and a per gallon cap standard of

80 ppm beginning in 2006 (with the exception of challenged refiners, and gasoline sold in certain

western states subject to geographic phase-in). Since less sulfur will be in gasoline as a result of

the Tier 2 gasoline sulfur rule, the vehicle emission control system will work more efficiently,

thus providing reductions in toxic pollutants.198 Some refiners will be generating credits early

under this program which will result in a decrease in toxic pollutants before 2004.

d. Summary of Refinery Modeling

In the Notice of Proposed Rulemaking, we proposed a benzene content requirement in

order to capture the significant amount of overcompliance above and beyond the requirements of

the federal reformulated gasoline and anti-dumping programs. The Agency asked for comment

on two other forms of the today’s rule: benzene emissions performance and toxics emissions

performance. 

In response to these comments, and based on refinery modeling performed for this rule,

the Agency finalized a toxics performance requirement instead of a benzene content requirement. 

The Agency’s general rationale is twofold: a toxics performance requirement captures a larger

amount of the overcompliance with the existing standards while imposing less costs on the

refining industry than the proposed benzene content requirement. 
199 The Complex Model is a regulatory tool for estimating emissions for the reformulated

gasoline and anti-dumping programs. The Complex Model inputs are eight specified fuel

parameters: benzene, oxygen content (by oxygenate type), sulfur, Reid Vapor Pressure,

aromatics, olefins and the percents evaporated at 200°F and 300°F (E200 and E300). Complex

Model outputs are the estimated emissions (VOC, toxics, NOx) resulting from the fuel

parameters specified. The Complex Model also calculates percent reductions of the input slate of

fuel parameters and resulting emissions compared to a base set of fuel parameters and resulting

base emissions.

167

As described in the preamble, the new toxic emissions performance requirement will

require, beginning with calendar year 2002, that a refinery’s or importer’s annual average total

toxics emissions performance for its reformulated gasoline (RFG) not exceed its 1998-2000

baseline RFG total toxics emissions performance. Likewise for conventional gasoline (CG), this

rule will require that the exhaust toxics emissions performance of a refinery’s or importer’s CG

not exceed its 1998-2000 baseline exhaust toxics emissions performance for CG. Incremental

volumes of either RFG or CG will be excluded from these requirements.

The 1998-2000 baseline RFG or CG toxics emissions performance value is the average

performance of the gasoline produced at the refinery (or imported) over the three year period

1998 through 2000. Emission values are determined using the Complex Model199, and

compliance with the program is determined separately for RFG and CG. Though this program

does not require new capital investments or changes in refinery operations, and thus should pose

no additional burden on refiners, we have included a number of compliance flexibilities, such as

deficit and credit carryforward, and a compliance margin, to offset unexpected or unusual

variances in the gasoline quality of a refinery (or importer).

The refinery modeling costs analysis is provided below.

Estimated Costs of Compliance with Toxics Emissions Performance Requirement

The Agency oversaw refinery modeling to investigate what impact the RFG Phase II

program, the Tier 2 sulfur gasoline program, and the proposed ultra low sulfur diesel fuel

program would have on the complex model fuel qualities for both conventional gasoline and

reformulated gasoline. We chose 1999 to represent the base case because it is the most recent

year to which we could calibrate the refinery model, and because it was the middle year of our

finalize baseline period (1998-2000). The modeling then compared the base case with what’s

known as a “reference case” to account for expected changes in fuel properties due to Phase II

RFG, Tier 2 low sulfur gasoline, and 15 ppm low sulfur diesel fuel (based on the proposed

heavy-duty 2007 rule ). Changes to diesel fuel quality will not directly affect gasoline quality,

but the increased hydrogen demand could put pressure to operate the reformer unit harder to

provide that needed hydrogen. Operating the reformer harder results in more benzene and other

aromatics in the gasoline. 
168

Table VII-C.2 lists 1999 baseline summer and winter conventional gasoline fuel quality

parameters and the volume fractions for PADDs I, II and III. Table VII-C.3 lists 1999 baseline

summer and winter RFG fuel quality parameters and the volume fractions for PADDs I, II and

III. Table VII-C.4 lists the projected 2005 summer and winter conventional gasoline fuel quality

parameters and the volume fractions for PADDs I, II and III. Table VII-C.5 lists the projected

2005 summer and winter RFG fuel quality parameters and the volume fractions for PADDs I, II

and III. The projected fuel quality parameters and volume fractions in 2005 account for the

implementation of the Phase II RFG program, the Tier 2 sulfur gasoline program and the

proposed ultra low sulfur diesel fuel program. Although PADD IV refiners and refiners outside

of California in PADD V were not modeled, these results would be expected to carry through for

these refiners because the effect of meeting the Tier 2 gasoline sulfur program should be the

same in these PADDs as they would be for PADDs I, II, and III. 

Table VII.C-2

Baseline (1999) conventional gasoline (summer & winter) fuel quality parameters 

and volume fraction in PADDs I, II and III.

Complex Model

Parameter

Summer

CG

PADD I

Winter

CG

PADD I

Summer

CG

PADD II

Winter

CG

PADD II

Summer

CG

PADD III

Winter

CG

PADD III

MTBE (wt% oxygen) 0 0 0 0 0 0

Ethanol (wt% oxygen) 0 0 0.4 0.4 0 0

Sulfur (ppm) 333 288 175.5 162.9 316 278

RVP (psi) 8.5 12.5 8.0 12.9 7.3 11.7

E200 (%) 40 45 47.1 52.3 40 46

E300 (%) 76 77 81.3 82.2 74 76

Aromatics (vol%) 35.4 30.0 25.9 25.8 30.6 28.4

Olefins (vol%) 18.8 15.5 9.7 9.8 14.2 12.1

Benzene (vol%) 0.90 1.4 1.4 1.3 0.90 1.1

Volume Fraction 0.4913 0.5087 0.5076 0.4924 0.5048 0.4952
169

Table VII.C-3

Baseline (1999) RFG (summer & winter) fuel quality parameters 

and volume fraction in PADDs I, II and III.

Complex Model

Parameter

Summer 

RFG 

PADD I

Winter 

RFG

PADD I

Summer

RFG 

PADD II

Winter

RFG

PADD II

Summer 

RFG 

PADD III

Winter 

RFG 

PADD III

MTBE (wt% oxygen) 2.1 2.1 0 0 2.1 2.1

Ethanol (wt% oxygen) 0 0 2.2 2.4 0 0

Sulfur (ppm) 200 164 209.1 244.5 117 282

RVP (psi) 7.9 12.5 7.8 12.9 6.9 11.7

E200 (%) 51 57 43.6 48.4 59 60

E300 (%) 80 83 77.1 80.5 89 88

Aromatics (vol%) 24.4 21.5 32.0 23.6 16.7 13.6

Olefins (vol%) 10.0 8.6 14.6 11.5 1.7 11.8

Benzene (vol%) 0.7 0.8 1.0 1.0 0.5 0.4

Volume Fraction 0.4984 0.5016 0.5092 0.4908 0.5167 0.4833
170

Table VII.C-4

Projected (2005) conventional gasoline (summer & winter) fuel quality parameters 

and volume fraction accounting for Phase II RFG, Tier 2 Sulfur Gasoline and Ultra-Low

Sulfur Diesel in PADDs I, II and III.

Complex Model

Parameter

Summer

CG

PADD I

Winter

CG

PADD I

Summer

CG

PADD II

Winter

CG

PADD II

Summer

CG

PADD III

Winter

CG

PADD III

MTBE (wt% oxygen) 0 0 0 0 0 0

Ethanol (wt% oxygen) 0 0 0.4 0.4 0 0

Sulfur (ppm) 40 29 32.1 26.7 38 25

RVP (psi) 8.5 12.5 8.0 12.9 7.3 11.7

E200 (%) 43 49 42.8 51 40 47

E300 (%) 76 80 76.5 81 74 77

Aromatics (vol%) 32.6 31.3 33.0 28.6 33.7 30.0

Olefins (vol%) 11.4 6.6 6.6 3.8 11.5 6.1

Benzene (vol%) 2.0 1.6 1.6 1.3 1.4 1.1

Volume Fraction 0.4498 0.5502 0.5118 0.4882 0.5048 0.4952
171

Table VII.C-5

Projected (2005) RFG (summer & winter) fuel quality parameters and volume fraction

accounting for Phase II RFG, Tier 2 Sulfur Gasoline and Ultra-Low Sulfur Diesel in

PADDs I, II and III.

Complex Model

Parameter

Summer

RFG

PADD I

Winter 

RFG

PADD I

Summer

RFG 

PADD II

Winter

RFG 

PADD II

Summer

RFG 

PADD III

Winter

RFG 

PADD III

MTBE (wt% oxygen) 1.8 2.4 0.52 0.54 2.1 2.1

Ethanol (wt% oxygen) 0 0 1.38 1.77 0 0

Sulfur (ppm) 37 28 40 24.8 32 11

RVP (psi) 6.8 12.5 6.7 12.9 6.7 11.7

E200 (%) 50 58 57.5 56.3 62 62

E300 (%) 80 82 93.4 86.7 94 93

Aromatics (vol%) 24.1 19.3 7.4 17.5 4.8 6.8

Olefins (vol%) 11.2 5.4 2.5 5.4 4.1 3.6

Benzene (vol%) 0.9 0.8 0.4 0.70 0.3 0.4

Volume Fraction 0.5128 0.4872 0.5086 0.4914 0.5167 0.4833

Even though the ultra low-sulfur diesel fuel requirements were not proposed to begin until 2006,

we have assumed that they began in 2005 for the purposes of modeling.

In order to determine the impact of the RFG Phase II program, the Tier 2 gasoline sulfur

program and the ultra low sulfur diesel program on exhaust and total toxic emissions, the fuel

quality parameters listed above were entered into the complex model for the 1999 baseline and

the projected year 2005 case separately for conventional gasoline and RFG. Table VII.C-6 lists

the results of the analysis for conventional gasoline on a PADD basis for exhaust toxic

emissions. Table VII.C-7 lists the results of the analysis for RFG on a PADD basis for total toxic

emissions. 
172

Table VII.C-6

Conventional gasoline (CG) exhaust toxic emissions performance for the 1999 base case

and projected year 2005 case on a PADD basis

CG

Case

PADD I, Exhaust 

Toxic Emissions

(mg/mi)

PADD II, Exhaust

Toxic Emissions

(mg/mi)

PADD III, Exhaust

Toxic Emissions

(mg/mi)

Base 100.27 86.70 93.28

Reference 100.23 87.85 88.52

For conventional gasoline (Table VII.C-6), the complex model analysis of predicted fuel

properties for PADDs I, II and III demonstrated that toxic emissions are likely to remain at or

below 1999 levels despite significant changes necessary to comply with future fuel regulations. 

The refinery modeling predicted a slight increase in toxic emissions in PADD II due to

compliance with future fuel regulations, but that increase is only 1.15 mg/mi, or about 1.3

percent above the 1999 base. The compliance margin established for conventional gasoline is

2.5 mg/mi, and thus the predicted increase is well within the compliance margin. Although

PADD IV refiners and refiners outside of California in PADD V were not modeled, these results

would be expected to carry through for these refiners because the effect of meeting the Tier 2

gasoline sulfur program should be the same in these PADDs as they would be for PADDs I, II,

and III. 

The model did not include any limits on the type of desulfurization technology to be used. 

In implementing the Tier 2 gasoline sulfur requirements, we believe that refiners may choose

desulfurization technologies such as Mobil Octgain or Scanfining which has the ability to both

recover lost octane and reduce olefins, at the same time that sulfur is being removed from FCC

Naptha. This type of technology would actually result in lower exhaust toxic emissions for

PADD II than predicted by the model on average. Even though the refinery modeling did not

assume these more advanced technologies, based on the refinery modeling and complex model

analysis presented here, today’s rule is expected to impose only negligible costs on the refining

industry.

Table VII.C-7

RFG exhaust toxic emissions performance for the 1999 base case and 

projected year 2005 case on a PADD basis

RFG

Case

PADD I, Total 

Toxic Emissions

(mg/mi)

PADD II, Total

Toxic Emissions

(mg/mi)

PADD III, Total

Toxic Emissions

(mg/mi)
173

Base 75.12 86.74 67.42

Reference 71.89 66.82 60.22

For RFG, the estimated emissions resulting from base and future fuel properties predicted

by the refinery modeling show that refineries are likely to be able to meet or exceed the new

baseline requirements even after implementing changes to comply with future fuel regulations. 

Table VII.C-7 lists the results of the analysis for RFG on a PADD basis for total toxic emissions. 

Based on the refinery modeling and analysis presented here, we expect that the new toxic

emissions performance requirement finalized in today’s action will impose only negligible costs

on the refining industry for RFG and for conventional gasoline. 

These fuel quality trends are averaged over PADD I, PADD II and PADD III separately

for RFG and conventional gasoline. Because we did not model PADD IV and PADD V and also

because we are not able to predict what each individual refiner will do to meet the fuels programs

in the year 2005, to help ensure that this toxic emissions anti-backsliding program will be a

negligible cost program for refiners we are also implementing several flexibilities for refiners. 

These flexibilities are a deficit and credit carry forward flexibility, a compliance margin

flexibility and an expanded baseline period flexibility.

Estimated Cost of Proposed Benzene Fuel Content Requirement

The Agency oversaw refinery modeling to investigate the costs of the proposed benzene

fuel content requirement, where benzene levels were not allowed to above a 1998-99 baseline for

an average refinery in PADDs I, II and III. This analysis was similar to the analysis performed

for the toxic emissions performance requirement.

Table VII.C-8

Annual Aggregate Cost Increase and Cent per Gallon Cost of a Benzene Anti-backsliding

Program for PADDs I, II and III and Nationally

Annual Aggregate Cost

Increase (including amortized

capital and all the operating

costs) $MM

Cost

(Cents/Gallon)

PADD I 0.9 0.01

PADD II 32 0.10

PADD III 41 0.07

Aggregate Costs 74 0.07 (volume-weighted)
174

Table VII-C.8 lists the annual aggregate cost increase (including amortized capital and all

the operating costs), and the cents per gallons cost of a benzene fuel content requirement for

PADDs I, II, and III. According to 1999 Energy Information Administration (EIA) data on

refinery motor gasoline volumes, PADDs I, II and III represent approximately 91 percent of the

gasoline produced in the United States, excluding California gasoline. PADD IV and refiners

outside of California in PADD V represent approximately 9 percent of the gasoline produced in

the Unites States. National gasoline domestic production in 1999 was estimated by EIA at 99

billion gallons. Since the aggregate costs in Table VII.C-8 represents about 91 percent of the

national gasoline supply, if these costs are extrapolated out to the rest of the United States,

excluding California, the national annualized aggregate cost increase would be $81 million.

D. Treatment of Incremental Volumes

There are several situations in which a refinery's production of gasoline could increase

above the annual average volumes of RFG and CG for that refinery in the 1998 - 2000 baseline

period. Incremental volumes are defined here as those volumes of RFG or CG that exceed the

volumes produced 0Examples of these situations include entering the RFG market when

heretofore the refinery has produced no RFG, shifting the balance from RFG to CG production or

vice-versa due to changes in the geographic applicability of the RFG program, or increasing

production volumes simply to keep up with growing demand. 

In the NPRM we raised the question of whether the "incremental volumes" of RFG would

be likely to contain higher concentrations of benzene than the baseline volumes. Higher benzene

concentrations could theoretically arise if refineries producing greater volumes of gasoline did so

by converting a larger portion of their crude oil into gasoline instead of simply processing more

crude oil. In converting a larger portion of their crude into gasoline, they would be processing

that portion of crude oil which tends to be incrementally heavier and more aromatic than the

portion of crude oil used to produce gasoline up to their 1998 - 2000 baseline volume. As a

result, the benzene concentration of gasoline could increase.

At the time of the NPRM, we did not have any data or modeling that suggested higher

benzene concentrations would occur for incremental volumes of RFG. But the potential for

higher benzene concentrations in incremental volumes was theoretically great enough to warrant

taking comment on the issue. However, the comments we received in response to the NPRM

provided essentially no data on this subject, though most of the regulated community did agree

with the need to exclude incremental volumes from the anti-backsliding program.

In response to the need for a more quantitative analysis on this subject, we reviewed

historical data on RFG production volumes and benzene concentrations to determine if there was

a correlation between the two. By-refinery annual average volumes and benzene concentrations

were culled from EPA's batch report database for 1997, 1998, and 1999 for RFG. For any case in
175

which total production volumes increased from 1997 to 1998, or from 1998 to 1999, the ratio of

the change in benzene concentration to the percent increase in gasoline volume was calculated. A

distribution of these values for can be seen in Figures VII.D-1.

Figure VII.D-1

Effect of Incremental Volumes on Benzene for Reformulated Gasoline

-0.03

-0.025

-0.02

-0.015

-0.01

-0.005

0

0.005

0.01

0.015

0.02

0.025

0.03

0.035

0.04

0.045

0.05

Delta benzene content (vol%) / Percent change in gasoline volume

0

5

10

15

20

25

Number of observations

The majority of observations indicate that fuel benzene content did in fact increase when

total volume increased, though the reasons (processing more crude, greater use of FCC or

reformer units) are unclear. In addition, there was a statistically significant (at the 95 percent

confidence level) average increase in benzene concentration when total RFG production volume

increased. Although the average increase was small, 0.003 vol% benzene for a one percent

increase in gasoline volume, these results do suggest that, at least in the past, increases in RFG

production volume were in fact accompanied by increases in benzene content.

We also repeated the analysis for CG. The results are shown in Figure VII.D-2. Even

though a majority of the observations were above zero, and there was no statistically significant

average effect.
176

-0.22

-0.2

-0.18

-0.16

-0.14

-0.12

-0.1

-0.08

-0.06

-0.04

-0.02

0

0.02

0.04

0.06

0.08

0.1

0.12

0.14

Delta benzene content (vol%) / Percent change in gasoline volume

0

10

20

30

40

Number of observations

Figure VII.D-2

Effect of Incremental Volumes on Benzene for Conventional Gasoline

Since we are finalizing a toxics performance requirement instead of the benzene content

standard we proposed in the NPRM, it seemed prudent to determine how potential increases in

RFG benzene content for incremental volumes might impact toxics emissions. To do this we

used the RFG fuel properties from Table VII.B-1 as representative of the average refinery

baseline, and increased both benzene content and total aromatics content by an amount equal to

the average expected increase in RFG benzene content derived above. The increase in benzene

content was calculated for a total RFG pool volume increase of approximately 14 percent, which

represents the expected growth in RFG demand between the baseline period and 2008. Calender

year 2008 was chosen because by this time the Tier 2 low sulfur standard will be phased-in. 

However, other years could also have served to illustrate how potential increases in benzene

content due to increasing pool volumes might affect total toxics emissions. The resulting

increase in benzene content was approximately 0.04 vol%. When this benzene content increase

was added to the baseline RFG and the results evaluated with the Complex Model, the result

was that total toxics emissions in terms of percent change from the statutory baseline increased

by 0.5 percent. Given that the compliance margin, as described more fully in Section VII.E

below, is only 0.7 percent, it would appear that potential future increases in RFG benzene content

which are associated with incremental volumes may in fact erode the cushion that the compliance

margin is intended to establish.
177

Our analysis focused only on fuel benzene content. There is some reason to believe that

other changes in fuel properties which are associated with incremental volumes may also

contribute to toxics emissions. As described in the preamble, these could include greater

volumes of imports from foreign refiners to satisfy growing demand for gasoline, or greater use

of existing domestic reformer and FCC units. In addition to increases in aromatic and benzene

content, the increased use of these units may also lead to increases in sulfur or olefin content

which can also increase toxics emissions. The impact that these incremental volumes could have

on fuel properties and, thus, toxics emissions may be just as likely for CG as for RFG, since

incremental volumes are a function primarily of growth in demand for gasoline which affects

both CG and RFG. 

Requiring refiners, however, to meet a more stringent toxics standard for these

incremental volumes could require additional capital investment and thereby impose a constraint

on incremental gasoline production. As a result, we have decided to exclude incremental

volumes from our anti-backsliding program for both RFG and CG.

Exclusion of incremental volumes from the compliance calculations is not

straightforward, because the incremental volumes are not specific gallons produced during the

last few weeks of the year, but instead arise as increased production volume throughout the year. 

As a result it is impossible to identify the specific gallons, and their associated fuel properties,

that can be labeled as incremental volumes and thus excluded from the compliance calculations. 

Instead, it was necessary to adjust the compliance calculations in such a way that incremental

volumes have no impact on a refinery's compliance with its 1998 - 2000 toxics performance

baseline.

In determining compliance, a refinery must compare its annual average toxics

performance for any given year to its baseline toxics performance. If the annual average toxics

performance exceeds the baseline toxics performance, the refinery is out of compliance (credit

carryovers and other flexibilities in our final rule notwithstanding). , Consistent with the

approach described above, the baseline must be adjusted so that incremental volumes, as part of a

refinery's total annual volume, are compared only to the existing RFG or anti-dumping toxics

standards. Using this approach, incremental volumes remain as part of the calculation of annual

average toxics performance according to the following equation:

(1)

( )

T

V T

V

a

i i

i

n

i

i

= n

× =

=

∑

∑

1

1

Where:

Ta = The refinery or importer annual average toxics value, as applicable. Units

are mg/mi for CG and percent reduction from statutory baseline for RFG.

Vi = The volume of applicable gasoline produced or imported in batch i.
178

Ti = The toxics value of batch i. Units are mg/mi for CG and percent reduction

from statutory baseline for RFG.

n = The total number of batches of applicable gasoline produced or imported

during the averaging period.

i = Individual batch of gasoline produced or imported during the averaging

period.

However, even though incremental volumes remain as part of the calculation of annual average

toxics performance, the baseline to which the annual average is compared is adjusted to eliminate

the effect of the incremental volumes. To do this we developed a "compliance baseline" which

combines a refinery's 1998 - 2000 toxics baseline and the applicable RFG or CG toxics standard:

T (2)

TV TV

V V

CBase

Base Base Exist inc

Base inc

=

×+ ×

+

where

TCBase = Compliance baseline toxics value. Units are mg/mi for CG and percent

reduction from statutory baseline for RFG.

TBase = Baseline toxics value for the refinery or importer. Units are mg/mi for CG

and percent reduction from statutory baseline for RFG.

VBase = Baseline volume, equal to the annual average volume of gasoline produced

or imported during January 1, 1998 through December 31, 2000. 

TExist = Existing toxics standard. For RFG, this value is 21.5 percent. For CG, this

value is equal to the refinery's or importer's CG standard in mg/mi.

Vinc = Volume of gasoline produced over and above VBase

If a refinery's gasoline production for either RFG or CG does not exceed its 1998 - 2000 annual

average production, then Vinc in equation (2) is zero and the compliance baseline reverts to the

refinery's 1998 - 2000 toxics baseline. TBase is a refinery's 1998 - 2000 toxics baseline calculated

from:
179

(3)

( )

T

V T

V

Base M

i i

i

n

i

i

= n

×

+ =

=

∑

∑

1

1

Where: 

TBase = Baseline toxics value. Units are mg/mi for CG and percent reduction from

statutory baseline for RFG.

Vi

 = Volume of gasoline batch i produced or imported during January 1, 1998

through December 31, 2000. 

Ti

 = Toxics value of gasoline batch i produced or imported during January 1,

1998 through December 31, 2000. Units are mg/mi for CG and percent

reduction from statutory baseline for RFG.

n = Total number of batches of gasoline produced or imported during January

1, 1998 through December 31, 2000.

i = Individual batch of gasoline produced or imported during January 1, 1998

through December 31, 1999.

M = Compliance margin, described in Section VII.E below

To determine compliance, a refinery or importer will calculate its annual average toxics

performance according to equation (1) for either RFG or CG, and will compare the result to the

compliance baseline calculated according to equation (2). Any incremental volumes will, in the

course of the comparison, be held only to the existing RFG or CG toxics standards, while all

production volumes up to the refinery's baseline volume will be held to that refinery's 1998 -

2000 annual average toxics performance. 

E. Compliance Margins

Whenever gasoline is required by regulation to meet a standard for either individual fuel

properties or an emission performance standard such as those administered via the Complex

Model, the refiner plans its operations in such as way as to provide reasonable assurance that the

standard will never be breeched. In practical terms, the refiner aims for some level below the

standard so that it can assure compliance even though fuel properties often vary due to imprecise

test methods, blending tolerances, commingling and other factors. The difference between the

standard and the level that the refiner actually targets to assure compliance is termed the

compliance margin.

In today's action we are finalizing an anti-backsliding program which is intended to

indefinitely preserve the benefits of the overcompliance exhibited by gasoline in the 1998 - 2000

timeframe. Our program is not intended to produce additional emission benefits. However, if

we set the anti-backsliding requirements for toxics emissions at exactly the annual average levels

exhibited in 1998 - 2000, refiners would actually target toxics emissions below those 1998 - 2000
180

levels and would therefore be generating additional emission benefits, potentially at some nonnegligible cost. To avoid this, we have determined that it is appropriate to add a compliance

margin to the toxics performance requirement applicable to RFG and CG at every refinery. 

The overcompliance with the RFG and anti-dumping toxics standards that occurred in the

1998 - 2000 timeframe far exceeded what might be expected from typical compliance margins. 

Refiners were clearly producing gasoline with lower than necessary toxics emissions for reasons

other than simply applying a compliance margin to their applicable standard, as described more

fully in Section VII.A.3 above. Therefore, we could not directly assess from historical data the

magnitude of an appropriate compliance margin to apply to the toxics performance requirements

that will be applicable to individual refineries under our anti-backsliding program. Instead, it

was necessary for us to conduct a statistical analysis of the distribution of toxic performance

values to estimate the value of an appropriate compliance margin. 

Under the RFG and anti-dumping programs, refiners are required to report to EPA the

fuel properties and associated toxics emission levels, as estimated by the Complex Model, for

every batch of gasoline they produce. To date our most complete and accurate set of batch

reports is from 1998. Beginning with this set of over 40,000 batch reports, we separated the data

on the basis of whether a refinery produced only CG, only RFG, or produced both CG and RFG. 

We then randomly selected ten refineries in each of these three categories of refineries and

collected all of their applicable 1998 batch reports to produce a selection of refineries which

varied in terms of annual gasoline volume, geographic location, and whether it produced CG only

or CG and RFG. For each selected refinery we then calculated the compliance margin that would

result if the refinery in question intended to meet an anti-backsliding standard equal to the

average toxics performance for its 1998 gasoline production. To do this, we used a one-tailed ttest at the 95 percent confidence level. This approach allowed us to determine the buffer that

would need to be added to a refinery's 1998 average toxics performance to assure that its future

average toxics performance fell below the anti-backsliding requirement. In mathematical terms

this calculation was:

Compliance margin = t · STDS ÷ OBSERVATIONS

Where

t = Critical value of t for a 95% confidence level

STDS = Sample standard deviation

OBSERVATIONS = Number of observations (batch reports)

The results of this calculation are given in Table VII.E-1. The CG data represented a total of

1141 batch reports, while the RFG data represented 686 batch reports. The calculated

compliance margins could not be correlated with the annual average toxics levels for 1998 -

2000. Therefore, we have calculated the average compliance margins for the refineries we

randomly selected for the analysis. The average compliance margins of 2.5 mg/mi for CG and
181

0.7 percent for RFG will be added to the anti-backsliding baselines approved by the EPA for

every refinery and importer in the U.S.

Table VII.E-1

Compliance Margins for Selected Refineries

Refinery

Exhaust toxics

for CG (mg/mi)

Total toxics for RFG (% change

from statutory baseline)

A

B

C

D

E

F

G

H

I

J

1.76

1.37

2.75

1.04

4.57

n/a

5.53

2.10

0.74

n/a

0.91

n/a

n/a

n/a

n/a

0.79

n/a

0.49

n/a

0.61

Average 2.5 0.7

F. Exclusion of California gasoline

We are not requiring gasoline intended for use in California to be included in a refiner’s

or importer’s compliance determination under the toxics anti-backsliding rule. This action is

consistent with other Agency actions on similar fuel issues - California gasoline is exempt from

the recently promulgated federal gasoline sulfur requirements [65 FR 6698, February 10, 2000],

and while subject to the RFG and anti-dumping provisions, California refineries have been

exempted from several of the enforcement and compliance mechanisms of those programs.

Most of the gasoline used in California is produced by California refineries which are

subject to the California Cleaner Burning Gasoline (CBG) requirements. The current set of

Phase 2 CBG requirements began in 1996 and run through 2002; beginning in 2003, the

California Phase 3 gasoline requirements take effect. The sulfur, benzene, aromatics and olefins

standards for Phase 2 and Phase 3 are shown in Table VII.F-1. The Flat Limits in Table VII.F-1

are equivalent to per-gallon caps.
182

Table VII.F-1

Select California Phase 2 and Phase 3 Gasoline Standards

Property Flat Limit Averaging Limit Cap Limit

Phase 2 Phase 3 Phase 2 Phase 3 Phase 2 Phase 3

Sulfur 

(ppm)

40 20 30 15 80 60/30

Benzene

(vol%)

1.0 0.8 0.8 0.7 1.2 1.1

Aromatics

(vol%)

25.0 25.0 22.0 22.0 30.0 35.0

Olefins

(vol%)

6.0 6.0 4.0 4.0 10.0 10.0

In 1998, under the 0.8 vol% Phase 2 benzene standard, California refineries averaged

0.57 vol%. Because of this overcompliance, and the upcoming more stringent Phase 3 standards

on all the other fuel parameters, it is likely that toxics emissions under Phase 3 will not be greater

than toxics emissions under Phase 2. Thus, we do not expect California refineries, on average, to

backslide relative to their 1998-2000 average toxic emission level. Additionally, given the

compliance margin we are including in today’s rule, it is highly unlikely that any backsliding

would exceed the combination of the actual 1998-2000 baseline plus the compliance margin. 
200 “Nonroad Engine and Vehicle Study - Report and Appendices,” EPA-21A-201, November 1991

(available in Air Docket A-96-40).

201 HC stands for hydrocarbon. HC and VOC are very similar and are generally used interchangeably.

202 59 FR 31306, June 17, 1994.

183

Chapter 8: Nonroad Mobile Source Air Toxics

In this chapter we first describe our current nonroad engine emission control programs

and then present our estimates of the impacts of these programs on future air toxics inventories. 

We are looking at nonroad MSATs emissions separately from motor vehicle emissions of

MSATs primarily because our understanding of nonroad MSAT emissions is much more limited

than that of motor vehicle MSAT emissions. Therefore, this chapter ends with a discussion of

the significant uncertainty and data gaps that exist with respect to toxics emissions from nonroad

engines. We will need to fill these gaps in our data before we can assess the need for, and

appropriateness of, programs intended to further reduce nonroad MSATs. Under our Technical

Analysis Plan, described in Section VII of the preamble for this rule, we will seek to gather this

information by 2003. We intend to evaluate potential strategies relating to hazardous air

pollutants from nonroad engines and vehicles.

A. Overview of Current Nonroad Engine Emission Control Programs

The 1990 Clean Air Act Amendments specifically directed us to study the contribution of

nonroad engines to air pollution which may reasonably be anticipated to endanger public health

or welfare, and regulate them if warranted. "Nonroad" is a term that covers a diverse collection of

engines, equipment, and vehicles. Also referred to as "off-road" or "off-highway," the nonroad

category includes outdoor power equipment, recreational equipment, farm equipment,

construction equipment, lawn and garden equipment, and marine vessels. Though dealt with

separately in the Clean Air Act, locomotives and aircraft can also be considered categories of

nonroad engines. Except for aircraft, we did not regulate emissions from nonroad engines prior to

the mid-1990s.

In 1991, we released a study documenting emission levels across a broad spectrum of

nonroad equipment that were higher than expected.200 The study showed that emissions from

nonroad engines are a significant source of oxides of nitrogen (NOx), volatile organic compound

(VOC), and particulate matter (PM) emissions. In some areas of the country, emissions from

nonroad engines represent a third of the total mobile source NOx and VOC inventory and over

two-thirds of the mobile source PM inventory. Based on the results of this study, referred to as

NEVES, we determined that emissions of NOx, HC,201 and CO from nonroad engines and

equipment contribute significantly to ozone and CO concentrations in more than one

nonattainment area.202 Thus, we initiated regulatory programs for several categories of nonroad

engines as required by section 213(a)(3) of the Clean Air Act.
203 59 FR 31306, June 17, 1994.

184

In addition to the determination of significance for NOx, HC, and CO emissions just

discussed, we made a determination, under section 213(a)(4) of the Clean Air Act, that smoke

and PM emissions from nonroad engines and equipment significantly contribute to air pollution

that may be reasonably anticipated to endanger public health or welfare.203 Under this

determination we are authorized to establish smoke and PM emission standards for nonroad

engines and equipment. While we have established smoke and PM regulations for many

categories of nonroad engines and equipment, our efforts to date have been more focused on

achieving NOx reductions from diesel nonroad engines, and HC and CO reductions from

gasoline nonroad engines.

The broad category of nonroad equipment encompasses a large variety of equipment

types, from hand-held lawn and garden equipment to locomotives and large marine vessels. The

engines used in nonroad equipment also vary dramatically, from very small two-stroke sparkignited (SI) gasoline engines to very large two-, and four-stroke diesel engines. Many of these

engines are designed and manufactured specifically for their nonroad applications. Others are

adaptations of on-highway engine designs, or even other nonroad engines. For example, most

land-based nonroad diesel engines are based on on-highway engines, with modifications as

necessary for nonroad application. Likewise, most small and medium size diesel marine engines

are modified land-based nonroad engines.

Even though many nonroad engines are derived from on-highway engines, the

technologies applied to on-highway engines to reduce emissions are often not readily

transferrable to nonroad engines, or are transferrable to different nonroad applications in different

degrees. The physical limitations of nonroad equipment, as well as different operating

environments and duty cycles, sometimes limit the application of on-highway emission reduction

technologies. For example, charge air cooling is widely used as a NOx reduction technique for

large diesel truck engines. With the aftercooler mounted on the front of the truck, the ram air

available as a truck travels down the road can afford a large degree of cooling. However, with

land-based nonroad equipment the available cooling tends to be significantly lower, both because

of the physical limitations of the equipment in terms of mounting the aftercooler, as well as the

typically slower speeds at which such equipment tends to operate. Conversely, there is a large

amount of cooling available in marine applications through the use of the surrounding water to

cool the charge air.

Due to the variety of nonroad engine and equipment types and sizes, combustion

processes, uses, and potential for emissions reductions, we placed nonroad engines into several

categories for regulatory purposes. These categories include land-based diesel engines (e.g., farm

and construction equipment), small land-based spark-ignition (SI) engines (e.g., lawn and garden

equipment), large land-based SI engines (e.g., forklifts, airport ground service equipment),

marine engines (including diesel and SI, propulsion and auxiliary, commercial and recreational),
204 59 FR 31306, June 17, 1994.

205 The Mine Safety and Health Administration is responsible for setting requirements for underground

mining equipment. Locomotives and marine vessels are covered by separate EPA programs.

206 63 FR 56968, October 23, 1998.

185

locomotives, aircraft, and recreational vehicles (e.g., large land-based SI engines used in off-road

motorcycles, all-terrain vehicles and snowmobiles). Summaries of our current or anticipated

programs for these nonroad categories follow. The information presented for these programs is,

in many cases, taken directly from the preambles and supporting documents of the final rules. 

Following the discussion of the specific nonroad control programs, we present a general

overview of the nonroad fuels issue.

1. Land-Based Nonroad Diesel Engines

Nonroad diesel (also referred to as compression-ignition) engines dominate the large

nonroad engine market and comprise approximately 25 percent of the current mobile source NOx

emissions inventory and 40 percent of the current mobile source PM emissions inventory.

Examples of applications falling into this category include agricultural equipment such as

tractors, construction equipment such as backhoes, material handling equipment such as heavy

forklifts, and utility equipment such as generators and pumps.

Under our regulations, diesel engines greater than 50 horsepower (hp) must comply with

Tier 1 emissions standards that are being phased in between 1996 and 2000, depending on the

size of the engine.204 Under the Tier 1 standards, we project that NOx emissions from new diesel

nonroad equipment will be reduced by over 30 percent from uncontrolled levels. The Tier 1

standards do not apply to engines used in underground mining equipment, locomotives, and

marine vessels.205

In August 1998, we adopted more stringent emission standards for NOx, HC, and PM for

new nonroad diesel engines, to be phased in over several years beginning in 1999.206 Engines

used in underground mining equipment, locomotives, and marine engines over 50 hp are not

included. This comprehensive new program includes the first set of standards for nonroad diesel

engines less than 50 hp. Standards for these small engines will be phased in from 1999 to 2000. 

The rule also phases in more stringent Tier 2 standards for all engine sizes from 2001 to 2006,

and yet more stringent Tier 3 standards for engines over 50 hp from 2006 to 2008. Finally, the

new program includes a voluntary program to encourage the production of advanced, very-low

emitting engines. Under these new standards, we project that emissions from new nonroad diesel

equipment will be further reduced by 60 percent for NOx and 40 percent for PM compared to the

emission levels of engines meeting the Tier 1 standards. We are currently working on the

Nonroad Tier 3 technology review for 2001. We intend to consider the control of sulfur in

nonroad diesel fuel as part of our Tier 3 technology review. This could potentially allow more
207 60 FR 34582, July 3, 1995.

208 64 FR 15208, March 30, 1999 and 65 FR 24267, April 25, 2000.

186

effective diesel PM control technologies such as catalysts to be applied to nonroad engines and

vehicles.

2. Small Land-Based SI Engines

Small spark-ignition (SI) engines (e.g., engines operating on gasoline, natural gas,

propane, or methanol) at or below 25 hp comprise about 9 percent of the mobile source VOC

inventory. These small engines are used primarily in lawn and garden equipment, such as

lawn-mowers, string trimmers, edgers, chain saws, commercial turf equipment, and lawn and

garden tractors.

Under Phase 1 of our nonroad small SI engine regulations, new small SI engines must

comply with emission standards for HC, CO, and NOx beginning in 1997. 207 The Phase 1

standards apply to all SI engines at or below 25 hp, except for those used in aircraft, marine

vessels, and recreational equipment. We expect that these Phase 1 standards will result in a 32

percent reduction in HC emissions from small SI engines (approximately 340,000 tons from

uncontrolled levels). 

We finalized Phase 2 nonroad small SI engine regulations in March 1999 for

nonhandheld engines, and in March 2000 for handheld engines.208 The Phase 2 programs include

more stringent emission levels and new provisions to ensure low in-use emissions. We expect

the Phase 2 program for nonhandheld engines, when fully phased in, to achieve approximately

350,000 tons of HC + NOx emission reductions, and the program for handheld engines to

achieve approximately 450,00 tons of reduction in HC + NOx emissions. These reductions

represent reductions in HC+NOX beyond the Phase 1 levels of 60 percent for nonhandheld

engines and 70 percent for handheld engines.

3. Large Land-Based Spark-Ignition Engines

We do not currently have emission standards in place for spark-ignition engines above 25

hp used in commercial applications. These engines are used in a variety of industrial equipment,

including forklifts, airport ground-service equipment, generators, and compressors. We are

currently developing an emission control program for these engines (65 FR 76797, December 7,

2000).

4. Marine Engines

Like land-based nonroad engines, marine engines serve a wide variety of applications.

The smallest marine engines, virtually all of which use gasoline, are used in recreational
209 61 FR 52088, October 4, 1996.

210 64 FR 73300, December 29, 1999.

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outboards and personal watercraft. Small gasoline or diesel marine engines provide auxiliary

power on many vessels. Larger marine engines provide propulsion for both recreational and

commercial applications. Recreational sterndrive and inboard engines tend to be gasoline,

though diesel engines are making inroads into that market. Commercial engines, virtually all

diesel, power vessels such as tugs, ferries, and crew/supply boats. These engines also provide

auxiliary power on larger vessels. The largest marine diesel engines, sometimes exceeding

60,000 hp, propel ocean-going vessels. We group engines under three control programs

reflecting their application and, to some extent, the fuel they use.

a. Gasoline Outboards and Personal Watercraft Marine Engines 

Gasoline outboards and personal watercraft contribute about 5 percent of the national

mobile source VOC inventory. However, in areas with large boat populations, the contribution

of these recreational marine engines may exceed 10 percent of the regional mobile source VOC

inventory. These engines typically employ 2-stroke technology, which has changed very little

over the last 50 years. Regulations to control exhaust emissions from new outboards and

personal watercraft went into effect beginning with the 1998 model year.209 The emission

controls for these engines involve increasingly stringent standards over the course of a nine-year

phase-in period beginning in model year 1998. By the end of the phase-in, each manufacturer

must meet an emission standard, on a corporate-average basis, that represents a 75-percent

reduction (on the order of 500,000 tons) in HC compared to unregulated levels. The gradually

decreasing emission standard allows manufacturers to determine the best approach to achieving

the targeted reductions over time. Manufacturers are able to phase in the types of control

technologies in the most sensible way, while minimizing the cost impact to the consumer. 

b. Commercial Diesel Marine Engines 

Commercial diesel marine engines contribute about 8 percent of the national mobile

source NOx inventory, and about 1 percent of the national mobile source PM inventory. In areas

with large commercial ports or near busy shipping lanes, the contribution of diesel marine

engines to the local mobile source NOx and PM inventory may be much higher. We published

regulations for the control of exhaust emissions from new marine diesel engines in December

1999.210 The emission limits, which vary depending on the size of the engine, are similar to

emission limits for corresponding land-based nonroad or locomotive engines. These limits apply

beginning with engines manufactured in 2004, and will result in 13-percent VOC and 26-percent

diesel PM reductions from uncontrolled levels. The emission limits for very large commercial

marine diesel engines are the same as those contained in Annex VI of the International

Convention on the Prevention of Pollution from Ships (MARPOL). Consistent with MARPOL

Annex VI, these limits will apply to engines installed on ships constructed on or after January 1,

2000.
211 63 FR 18978, April 16, 1998.

212 Locomotives are typically overhauled to “as new” condition every four to eight years in a process

known as remanufacturing.

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c. Recreational Sterndrive and Inboard Engines 

Recreational sterndrive and inboard engines can be either gasoline or diesel engines.

While their contribution to national mobile VOC and NOx levels is smaller than the other two

marine engine categories, their emissions are expected to increase due to the growing number of

recreational vessels. We did not finalize emission limits for gasoline sterndrive and inboard

engines as part of the 1996 marine rule. Likewise, we did not propose limits for recreational

diesel engines in the commercial diesel engine rule. We do not currently have emission

regulations in place for this category of marine engine, but have begun developing them (65 FR

76797, December 7, 2000).

5. Locomotives 

Locomotives are estimated to contribute about 9 percent of the nationwide mobile source

NOx emissions inventory. These engines are generally larger and last longer than any land-based

nonroad diesel engines. In April 1998, we published emission standards for NOx, HC, CO, PM,

and smoke for locomotives.211 The new standards are ultimately expected to reduce NOx

emissions by two-thirds, while HC and PM emissions from these engines will be decreased by 50

percent.

A unique feature of the locomotive program is that it includes emission standards for

remanufactured engines, including all those that were originally built since 1973.212 Regulation

of the remanufacturing process is critical because locomotives are generally remanufactured 5 to

10 times during their total service lives, which is typically 40 years or more.

Three separate sets of emission standards have been adopted, with applicability of the

standards dependent on the date a locomotive is first manufactured. The first set of standards

(Tier 0) applies to locomotives and locomotive engines originally manufactured from 1973

through 2001, any time they are manufactured or remanufactured. The second set of standards

(Tier 1) applies to locomotives and locomotive engines originally manufactured from 2002

through 2004. These locomotives and locomotive engines will be required to meet the Tier 1

standards at the time of original manufacture and at each subsequent remanufacture. The final

set of standards (Tier 2) applies to locomotives and locomotive engines originally manufactured

in 2005 and later. Tier 2 locomotives and locomotive engines will be required to meet the

applicable standards at the time of original manufacture and at each subsequent remanufacture.

Electric locomotives, historic steam-powered locomotives, and locomotives originally

manufactured before 1973 do not contribute significantly to the emissions problem and, thus, are

not subject to the locomotive regulations.
213 International Civil Aviation Organization (ICAO) Annex 16, Volume II, Environmental Protection,

Aircraft Engine Emissions.

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While the Tier 0 and Tier 1 regulations are primarily intended to reduce NOx emissions,

the Tier 2 regulations will result in 50 percent reductions in VOC and diesel PM from

unregulated levels, as well as additional NOx reductions beyond the Tier 0 and Tier 1

regulations. As a result, almost half of the NOx reductions we ultimately expect will be achieved

by 2005. In contrast, the VOC and diesel PM reductions are achieved more slowly, due to the

very slow fleet turnover. By 2040 we expect VOC reductions of about 18,000 tons per year and

diesel PM reductions of about 12,000 tons per year. About one third of these VOC and diesel

PM reductions will be realized by 2010.

6. Aircraft

Aircraft emissions comprise less than 2 percent of the mobile source NOx emissions

inventory, but they are significant contributors to the NOx inventory in some cities. In addition,

commercial aircraft emissions are a fast growing segment of the transportation emissions

inventory. Aircraft emissions are potentially important contributors to global climate change and

may also contribute to the depletion of the stratospheric ozone layer.

Emission standards for gas turbine engines that power civil aircraft have been in place for

about 20 years. Such engines are used in virtually all commercial aircraft, including both

passenger and freight airlines. The standards do not apply to military or general aviation aircraft.

Controls on engine smoke and prohibitions on fuel venting were instituted in 1974 and have been

revised several times since then. Beginning in 1984, limits were placed on the amount of

unburned HC gas turbine engines can emit per landing and takeoff cycle.

In April 1997, we adopted the existing International Civil Aviation Organization (ICAO)

NOx and CO emission standards for gas turbine engines.213 ICAO, a specialized agency of the

United Nations, is the most appropriate forum for first establishing commercial aircraft engine

emission standards due to the international nature of the aviation industry.

None of the actions just discussed have resulted in significant emissions reductions, but

rather have largely served to prevent increases in aircraft emissions. We are also exploring other

ways to reduce the environmental effects associated with air travel throughout the nation. We are

working with the Federal Aviation Administration (FAA) to encourage continuing progress in

reducing emissions from airport ground service equipment and aircraft auxiliary power units. 

We sponsored compilation of technical data and emission inventory methods, which the FAA

will use to develop an Advisory Circular for airlines and airport authorities interested in reducing

emissions from these sources.

Some municipalities are taking an interest in toxic air pollution from airports and are
214 “Preliminary Study and Analysis of Toxic Air Pollutant Emissions from O’Hare International Airport

and the Resulting Health Risks Created by these Toxic Emissions in Surrounding Residential Communities,” City of

Park Ridge, IL, August, 2000.

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undertaking their own studies. An example is a study being undertaken by the City of Park

Ridge, Illinois concerning O’Hare International Airport.214

7. Recreational Vehicles

We do not have standards in place for large land-based SI engines used in recreational

vehicles, such as off-road motorcycles, all-terrain vehicles, and snowmobiles. However, we are

currently developing emission regulations for recreational vehicles. As part of this regulatory

process, we intend to consider toxics emissions from these vehicles (65 FR 76797, December 7,

2000).

8. Fuels

In addition to the above engine technology-based emission control programs, fuel

controls will also reduce emissions of air toxics from nonroad engines. For example, gasoline

formulation (the removal of lead, limits on gasoline volatility and reformulated gasoline) will

reduce nonroad MSATs because most gasoline-fueled nonroad vehicles are fueled with the same

gasoline used in on-highway motor vehicles. An exception to this is lead in aviation gasoline. 

Aviation gasoline is a high octane fuel used in a relatively small number of aircraft (those with

piston engines). Such aircraft are generally used for personal transportation, sightseeing, crop

dusting, and similar activities. 

As just discussed, most of our fuel controls aimed at gasoline cover both on-highway and

nonroad vehicle fuel. The same is not true for diesel fuel. We have regulations in place which 

will dramatically reduce the sulfur levels in on-highway diesel fuel. These controls do not apply

to nonroad diesel fuel, and prior to these controls there was no distinction between on-highway

and nonroad diesel fuel. We intend to consider the control of sulfur in nonroad diesel fuel as part

of our Tier 3 technology review. This could potentially allow more effective diesel PM control

technologies such as catalysts to be applied to nonroad engines and vehicles.

B. Impacts of Nonroad Control Programs on Air Toxics

As a whole, our nonroad programs significantly reduce the impact of nonroad equipment

on the nation’s air quality. As with motor vehicle controls, while we’ve focused our controls on

achieving reductions in criteria pollutants (NOx, HC, and PM), our control programs have also

been effective in reducing emissions of air toxics.

As is the case with motor vehicle emissions, we expect nonroad emissions of gaseous

toxics to decrease over the next 20 years under our current control programs. By 2020, we
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estimate that benzene emissions will decrease by 31 percent (over 31,000 tons) and formaldehyde

emissions will decrease by 49 percent (over 38,000 tons), as compared with 1990 levels. 

However, nonroad emissions of diesel PM are not decreasing dramatically. We estimate that by

2020, nonroad engines will emit more that 310,000 tons per year of diesel PM emissions, as

compared with 346,000 tons in 1996, a 10-percent decrease. Our land-based nonroad Tier 3

technology review will examine nonroad engine diesel PM emissions. Although we are not

required to address nonroad MSATs under §202(l) of the Act, as part of our Technical Analysis

Plan, described in the preamble to the regulation, we also intend to evaluate potential strategies

relating to hazardous air pollutants from nonroad engines and vehicles.

1. Nonroad MSAT Baseline Inventories

We previously presented the 1996 baseline inventories for several key nonroad MSATs in

Table IV.A-1. This nonroad MSAT data was taken from the 1996 National Toxics Inventory

(NTI). In general, the data shows that nonroad vehicles tend to be significant contributors of

those MSATs for which motor vehicles are also significant contributors. Nonroad vehicles

contribute as much as 39 percent of the national inventory of some MSATs, such as acetaldehyde

and MTBE, and contribute significantly to the national inventories of several others, including

1,3-butadiene, acrolein, benzene, formaldehyde, lead compounds, n-hexane, toluene and xylene.

2. Emission Reductions from Current Programs

The programs summarized in Section A of this chapter are expected to result in

reductions of national inventories of the MSATs. This section summarizes our estimates of

nonroad MSAT inventories into the future, based on the nonroad emission control programs we

currently have in place. The discussion in this section consists of three parts. First, we discuss

the inventories of four MSATs: benzene, formaldehyde, acetaldehyde and 1,3-butadiene. 

Second, we discuss nonroad VOC emissions inventories as a surrogate for the other nonroad

gaseous MSATs. Finally, we discuss the trend of nonroad diesel PM emissions. We focused on

these pollutants for nonroad mobile sources primarily to allow comparisons with the on-highway

analyses presented in earlier chapters. The inventories presented here are based only on

regulations that we have completed. As previously discussed, we are developing the first

national regulations applicable to recreational vehicles and recreational marine sterndrive and

inboard engines (65 FR 76797, December 7, 2000). We are also conducting a technology review

through regulation for land-based nonroad diesel engines. As part of this review, we intend to

consider whether additional VOC (and, thus, gaseous MSAT) reductions would be appropriate. 

We intend to consider the control of sulfur in nonroad diesel fuel as part of our Tier 3 technology

review. This could potentially allow more effective diesel PM control technologies such as

catalysts to be applied to nonroad engines and vehicles.

We are not reporting inventory trends for the metals on our list of MSATs (arsenic

compounds, chromium compounds, mercury compounds, nickel compounds, manganese 

compounds, and lead compounds) or for dioxin/furans. Metals in mobile source exhaust can
215 The draft NONROAD model is a model we are developing which is used to project emissions

inventories from nonroad mobile sources. Because this is a draft model and subject to future revisions, the

inventories derived from the draft NONROAD model and presented here are subject to change.

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come from fuel, fuel additives, engine oil, engine oil additives, or engine wear. Formation of

dioxin and furans requires a source of chlorine. Thus, while metal emissions and dioxins/furans

emissions are associated with particles and it is possible that these compounds track PM

emissions to some extent, there are a number of other factors that contribute to emission levels

and we do not have good data on these relationships.

a. Benzene, Acetaldehyde, Formaldehyde, and 1,3-Butadiene 

Table VIII.B-1 shows our estimates of the nonroad emissions of these four gaseous

MSATs . These estimates were based on the 1996 inventories contained in the 1996 NTI study. 

The 1990 estimates were derived by applying a ratio of nationwide 1990 to 1996 VOC

inventories from the draft NONROAD model to the 1996 NTI numbers.215 Toxic fractions

represent the fraction of total VOC that a given MSAT makes up. The toxic fractions were

derived from speciated emissions data on different engines and come from a variety of studies

which are discussed in Chapter 2. By knowing the total VOC inventory and the toxic fraction

for a given MSAT, we can estimate the inventory of that specific MSAT indirectly. The 2007

and 2020 estimates were also derived from the draft NONROAD model, with the toxic fractions

applied to the VOC results. The draft NONROAD model does not include locomotives,

commercial diesel marine engines, or aircraft. We do not have enough information to estimate

the inventories of the four gaseous MSATs for these three nonroad vehicle categories. Thus,

they are not included in the 1990, 2007 and 2020 estimates. For consistency’s sake, we have

excluded these categories from the 1996 NTI numbers as well. Thus, the 1996 estimates shown

here differ slightly from those shown in Table IV.A-2. However, these three nonroad categories

only represent about three percent of the total nonroad VOC. Using VOC as a surrogate for

gaseous toxics, as discussed in the next section, we conclude that the exclusion of locomotives,

commercial diesel marine engines, and aircraft from our estimates of gaseous MSATs does not

have a significant impact on those estimates.
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Table VIII.B-1

Annual Emissions for Benzene, Acetaldehyde, Formaldehyde, and 1,3-Butadiene from

Nonroad Sources 

(thousand short tons per year)

Compound 1990 Emissions 1996 Emissions 2007 Emissions 2020 Emissions

Benzene 100.2 98.7 75.4 69

Acetaldehyde 37.7 40.8 26.3 20

Formaldehyde 79.2 86.4 53.8 40.7

1,3-Butadiene 9.4 9.9 8.8 7.8

Table VIII.B-2 summarizes the percent reductions in 2007 and 2020 from 1990 and 1996

levels represented by the inventories in Table VIII.B-1. This table shows that the reductions

expected from our existing nonroad control programs are significant, although not as substantial

as the reductions of these pollutants for on-highway motor vehicles presented in Chapter 4.

Table VIII.B-2

 Emission Reductions for Benzene, Acetaldehyde, Formaldehyde, and 1,3-Butadiene 

from Nonroad Sources

Reduction in 2007 Reduction in 2020

Compound From 1990 From 1996 From 1990 From 1996

Benzene 25% 24% 31% 30%

Acetaldehyde 30% 36% 47% 51%

Formaldehyde 32% 38% 49% 53%

1,3-Butadiene 7% 11% 18% 21%

b. VOCs

With the exception of the four MSATs shown in Table VIII.B-1, we cannot estimate 

emissions from nonroad mobile sources for the other gaseous MSATs because we do not have

toxic fraction information for the other gaseous MSAT emissions. Therefore, to estimate

projected inventory impacts from our current nonroad mobile source emission control programs,

we use VOC inventories. We believe this is appropriate because the gaseous MSATs are

constituents of total VOC emissions. By using VOC emissions as a surrogate, we are assuming

that MSAT emissions track VOC reductions. In reality, however, as can be seen from Table

VIII.B-2, some gaseous MSATs may not decrease at the same rate as VOCs overall. Without
216 “National Air Pollutant Emission Trends, 1900-1996,” EPA-454/R-97-011, December, 1997.

194

having more detailed emission data for each of the MSATs, however, we are unable to offer any

insights on how those rates may differ. This is one of the issues we intend to address as part of

the Technical Analysis Plan described in the preamble to the regulation.

Our VOC emission inventories were developed using the draft NONROAD model. 

Because the draft NONROAD model does not include locomotives, commercial marine diesel

engines, or aircraft we supplemented the draft NONROAD model inventories with locomotive

and diesel marine inventories developed in support of our regulations for those categories, and

with aircraft emission inventories from the National Air Pollutant Emissions Trends, 1900-1996

report.216 The results of this analysis shows that VOC inventories are projected to decrease

approximately 44 percent between 1996 and 2020 due to existing nonroad mobile source

emission control programs. This analysis, however, shows that our existing nonroad emission

control programs will nonetheless result in significant gaseous MSAT reductions (assuming, as

previously discussed, that gaseous MSATs emissions track VOC reductions).

Table VIII.B-3

Annual VOC Emissions 

From Nonroad Sources

Year 1996 2007 2020

Million short tons per year 3.6 2.2 2.0

Cumulative Percent Reduction *** 39% 44%

c. Diesel PM

We estimated the nonroad diesel PM inventories using the draft NONROAD model. We

are using diesel PM as a surrogate for diesel PM and diesel exhaust organic gases. As noted

above, because the draft NONROAD model does not include locomotives, commercial marine

diesel engines, or aircraft we supplemented the draft NONROAD model inventories with

locomotive and diesel marine inventories developed in support of our regulations for those

categories, and with aircraft emission inventories from the National Air Pollutant Emissions

Trends, 1900-1996 report. Table VIII.B-4 shows our estimates of nonroad diesel PM emissions

inventories. As can be seen, we expect nonroad diesel PM emissions to begin to drop with the

implementation of some of our nonroad regulations. However, in the absence of additional

controls, we expect that nonroad diesel PM emission inventories will begin to increase due to

expected growth in the populations of nonroad vehicles and equipment.
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Table VIII.B-4

 Diesel PM Emissions 

From Nonroad Sources

Year 1996 2007 2020

Thousand short tons per year 345,800 282,800 310,800

Cumulative percent reduction

from 1996

*** 18% 10%

C. Data Gaps and Uncertainties

There are significant gaps in data on MSAT emissions from nonroad engines. These data

gaps contribute to a less developed understanding of nonroad MSAT inventories compared to our

understanding of on-highway vehicle MSAT emissions. The largest single data gap is in the area

of emission factors. While we have basic emission factors for VOC and PM for most of the

nonroad categories, we have very little VOC speciation data for the given categories that would

allow us to use VOC as a surrogate to estimate emissions of specific MSATs. Given the large

variety of nonroad engine sizes, types and uses, as well as the likelihood that this variety will

result in some differences in VOC composition, it is important that we obtain or develop

speciated VOC data specific to each nonroad category in order to more accurately project

nonroad MSAT inventories. These gaps, too, must be filled in order to accurately assess the need

for, and the most appropriate direction of, any future MSAT control program targeted specifically

at nonroad mobile sources. Our Technical Analysis Plan, described in the preamble to our rule,

contains a strategy to obtain and evaluate this data so we can evaluate potential strategies relating

to hazardous air pollutants from nonroad engines and vehicles.