[Federal Register: March 29, 2006 (Volume 71, Number 60)]
[Proposed Rules]
[Page 15803-15963]
[DOCID:fr29mr06-33]

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Part II

Environmental Protection Agency

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40 CFR Parts 59, 80, 85 and 86

Control of Hazardous Air Pollutants From Mobile Sources; Proposed Rule

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Parts 59, 80, 85 and 86

[EPA-HQ-OAR-2005-0036; FRL-8041-2]
RIN 2060-AK70

Control of Hazardous Air Pollutants From Mobile Sources

AGENCY: Environmental Protection Agency (EPA).

ACTION: Proposed rule.

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SUMMARY: Today EPA is proposing controls on gasoline, passenger
vehicles, and portable gasoline containers (gas cans) that would
significantly reduce emissions of benzene and other hazardous air
pollutants (``mobile source air toxics''). Benzene is a known human
carcinogen, and mobile sources are responsible for the majority of
benzene emissions. The other mobile source air toxics are known or
suspected to cause cancer or other serious health effects.
    We are proposing to limit the benzene content of gasoline to an
annual average of 0.62% by volume, beginning in 2011. We are also
proposing to limit exhaust emissions of hydrocarbons from passenger
vehicles when they are operated at cold temperatures. This standard
would be phased in from 2010 to 2015. For passenger vehicles we also
propose evaporative emissions standards that are equivalent to those in
California. Finally, we are proposing a hydrocarbon emissions standard
for gas cans beginning in 2009, which would reduce evaporation and
spillage of gasoline from these containers.
    These controls would significantly reduce emissions of benzene and
other mobile source air toxics such as 1,3-butadiene, formaldehyde,
acetaldehyde, acrolein, and naphthalene. This proposal would result in
additional substantial benefits to public health and welfare by
significantly reducing emissions of particulate matter from passenger
vehicles.
    We project annual nationwide benzene reductions of 35,000 tons in
2015, increasing to 65,000 tons by 2030. Total reductions in mobile
source air toxics would be 147,000 tons in 2015 and over 350,000 tons
in 2030. Passenger vehicles in 2030 would emit 45% less benzene. Gas
cans meeting the new standards would emit almost 80% less benzene.
Gasoline would have 37% less benzene overall. We estimate that these
reductions would have an average cost of less than 1 cent per gallon of
gasoline and less than $1 per vehicle. The average cost for gas cans
would be less than $2 per can. The reduced evaporation from gas cans
would result in significant fuel savings, which would more than offset
the increased cost for the gas can.

DATES: Comments must be received on or before May 30, 2006. Under the
Paperwork Reduction Act, comments on the information collection
provisions must be received by OMB on or before April 28, 2006.
    Hearing: We will hold a public hearing on April 12, 2006. The
hearing will start at 10 a.m. local time and continue until everyone
has had a chance to speak. If you want to testify at the hearing,
notify the contact person listed under FOR FURTHER INFORMATION CONTACT
by April 3, 2006.

ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-
OAR-2005-0036, by one of the following methods:
     http://www.regulations.gov: Follow the on-line

instructions for submitting comments.
     Fax your comments to:<PHONE_NUMBER>.
     Mail: Air Docket, Environmental Protection Agency,
Mailcode: 6102T, 1200 Pennsylvania Ave., NW., Washington, DC 20460. In
addition, please mail a copy of your comments on the information
collection provisions to the Office of Information and Regulatory
Affairs, Office of Management and Budget (OMB), Attn: Desk Officer for
EPA, 725 17th St. NW., Washington, DC 20503.
     Hand Delivery: EPA Docket Center, (EPA/DC) EPA West, Room
B102, 1301 Constitution Ave., NW., Washington, DC 20004. Such
deliveries are only accepted during the Docket's normal hours of
operation, and special arrangements should be made for deliveries of
boxed information.
    Instructions: Direct your comments to Docket ID No. EPA-HQ-OAR-
2005-0036. EPA's policy is that all comments received will be included
in the public docket without change and may be made available online at
http://www.regulations.gov, including any personal information provided,

unless the comment includes information claimed to be Confidential
Business Information (CBI) or other information whose disclosure is
restricted by statute. Do not submit information that you consider to
be CBI or otherwise protected through http://www.regulations.gov or e-mail.

The http://www.regulations.gov website is an ``anonymous access'' system,

which means EPA will not know your identity or contact information
unless you provide it in the body of your comment. If you send an e-
mail comment directly to EPA without going through http://www.regulations.gov

your e-mail address will be automatically captured and included as part
of the comment that is placed in the public docket and made available
on the Internet. If you submit an electronic comment, EPA recommends
that you include your name and other contact information in the body of
your comment and with any disk or CD-ROM you submit. If EPA cannot read
your comment due to technical difficulties and cannot contact you for
clarification, EPA may not be able to consider your comment. Electronic
files should avoid the use of special characters, any form of
encryption, and be free of any defects or viruses. For additional
information about EPA's public docket visit the EPA Docket Center
homepage at http://www.epa.gov/epahome/dockets.htm. For additional

instructions on submitting comments, go to section XI, Public
Participation, of the SUPPLEMENTARY INFORMATION section of this
document.
    Docket: All documents in the docket are listed in the
http://www.regulations.gov index. Although listed in the index, some

information is not publicly available, e.g., CBI or other information
whose disclosure is restricted by statute. Certain other material, such
as copyrighted material, will be publicly available only in hard copy.
Publicly available docket materials are available either electronically
in http://www.regulations.gov or in hard copy at the Air Docket, EPA/DC, EPA

West, Room B102, 1301 Constitution Ave., NW., Washington, DC. The
Public Reading Room is open from 8:30 a.m. to 4:30 p.m., Monday through
Friday, excluding legal holidays. The telephone number for the Public
Reading Room is<PHONE_NUMBER>, and the telephone number for the Air
Docket is<PHONE_NUMBER>.
    Hearing: The public hearing will be held at Sheraton Crystal City
Hotel, 1800 Jefferson Davis Highway, Arlington, Virginia 22202,
Telephone:<PHONE_NUMBER>. See section XI, Public Participation, for
more information about public hearings.

FOR FURTHER INFORMATION CONTACT: Mr. Chris Lieske, U.S. EPA, Office of
Transportation and Air Quality, Assessment and Standards Division
(ASD), Environmental Protection Agency, 2000 Traverwood Drive, Ann
Arbor, MI 48105; telephone number:<PHONE_NUMBER>; fax number: (734)
214-4816; email address<EMAIL_ADDRESS>or Assessment and
Standards Division

Hotline; telephone number:<PHONE_NUMBER>; e-mail address:
<EMAIL_ADDRESS>

SUPPLEMENTARY INFORMATION:

General Information

A. Does this Action Apply to Me?

    Entities potentially affected by this action are those that produce
new motor vehicles, alter individual imported motor vehicles to address
U.S. regulation, or convert motor vehicles to use alternative fuels. It
would also affect you if you produce gasoline motor fuel or manufacture
portable gasoline containers. Regulated categories include:

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                                   NAICS      SIC  codes
           Category              codes \a\       \b\             Examples of potentially affected entities
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Industry......................       336111         3711  Motor vehicle manufacturers.
Industry......................       335312         3621  Alternative fuel vehicle converters.
                                     424720         5172
                                     811198         7539
                                ...........         7549  ......................................................
Industry......................       811111         7538  Independent commercial importers.
                                     811112         7533  ......................................................
                                     811198         7549  ......................................................
Industry......................       324110         2911  Gasoline fuel refiners.
Industry......................       326199         3089  Portable fuel container manufacturers.
                                     332431         3411  ......................................................
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\a\ North American Industry Classification System (NAICS).
\b\ Standard Industrial Classification (SIC) system code.

    This table is not intended to be exhaustive, but rather provides a
guide for readers regarding entities likely to be regulated by this
action. This table lists the types of entities that EPA is now aware
could potentially be regulated by this action. Other types of entities
not listed in the table could also be regulated. To determine whether
your activities are regulated by this action, you should carefully
examine the applicability criteria in 40 CFR parts 59, 80, 85, and 86.
If you have any questions regarding the applicability of this action to
a particular entity, consult the person listed in the preceding FOR
FURTHER INFORMATION CONTACT section.

B. What Should I Consider as I Prepare My Comments for EPA?

1. Submitting CBI
    Do not submit this information to EPA through http://www.regulations.gov

or e-mail. Clearly mark the part or all of the information that you
claim to be confidential business information (CBI). For CBI
information in a disk or CD ROM that you mail to EPA, mark the outside
of the disk or CD ROM as CBI and then identify electronically within
the disk or CD ROM the specific information that is claimed as CBI. In
addition to one complete version of the comment that includes
information claimed as CBI, a copy of the comment that does not contain
the information claimed as CBI must be submitted for inclusion in the
public docket. Information so marked will not be disclosed except in
accordance with procedures set forth in 40 CFR part 2.
2. Tips for Preparing Your Comments
    When submitting comments, remember to:
     Explain your views as clearly as possible.
     Describe any assumptions that you used.
     Provide any technical information and/or data you used
that support your views.
     If you estimate potential burden or costs, explain how you
arrived at your estimate.
     Provide specific examples to illustrate your concerns.
     Offer alternatives.
     Make sure to submit your comments by the comment period
deadline identified.
     To ensure proper receipt by EPA, identify the appropriate
docket identification number in the subject line on the first page of
your response. It would also be helpful if you provided the name, date,
and Federal Register citation related to your comments.

Outline of This Preamble

I. Introduction
    A. Summary
    B. What Background Information is Helpful to Understand this
Proposal?
    1. What Are Air Toxics and Related Health Effects?
    2. What is the Statutory Authority for Today's Proposal?
    a. Clean Air Act Section 202(l)
    b. Clean Air Act Section 183(e)
    c. Energy Policy Act
    3. What Other Actions Has EPA Taken Under Clean Air Act Section
202(l)?
    a. 2001 Mobile Source Air Toxics Rule
    b. Technical Analysis Plan
II. Overview of Proposal
    A. Why Is EPA Making This Proposal?
    1. National Cancer Risk from Air Toxics
    2. Noncancer Health Effects
    3. Exposure Near Roads and From Attached Garages
    4. Ozone and Particulate Matter
    B. What Is EPA Proposing?
    1. Light-Duty Vehicle Emission Standards
    2. Gasoline Fuel Standards
    3. Portable Gasoline Container (Gas Can) Controls
III. What Are Mobile Source Air Toxics (MSATs) and Their Health
Effects?
    A. What Are MSATs?
    B. Compounds Emitted by Mobile Sources and Identified in IRIS
    C. Which Mobile Source Emissions Pose the Greatest Health Risk
at Current Levels?
    1. National and Regional Risk Drivers in 1999 National-Scale Air
Toxics Assessment
    2. 1999 NATA Risk Drivers with Significant Mobile Source
Contribution
    D. What Are the Health Effects of Air Toxics?
    1. Overview of Potential Cancer and Noncancer Health Effects
    2. Health Effects of Key MSATs
    a. Benzene
    b. 1,3-Butadiene
    c. Formaldehyde
    d. Acetaldehyde
    e. Acrolein
    f. Polycyclic Organic Matter (POM)
    g. Naphthalene
    h. Diesel Particulate Matter and Diesel Exhaust Organic Gases
    E. Gasoline PM
    F. Near-Roadway Health Effects
    G. How Would This Proposal Reduce Emissions of MSATs?
IV. What Are the Air Quality and Health Impacts of Air Toxics, and
How do Mobile Sources Contribute?
    A. What Is the Health Risk to the U.S. Population from
Inhalation Exposure to Ambient Sources of Air Toxics, and How Would
It be Reduced by the Proposed Controls?

    B. What is the Distribution of Exposure and Risk?
    1. Distribution of National-Scale Estimates of Risk from Air
Toxics
    2. Elevated Concentrations and Exposure in Mobile Source-
Impacted Areas
    a. Concentrations Near Major Roadways
    b. Exposures Near Major Roadways
    i. Vehicles
    ii. Homes and Schools
    iii. Pedestrians and Bicyclists
    c. Exposure and Concentrations in Homes with Attached Garages
    d. Occupational Exposure
    3. What Are the Size and Characteristics of Highly Exposed
Populations?
    4. What Are the Implications for Distribution of Individual
Risk?
    C. Ozone
    1. Background
    2. Health Effects of Ozone
    3. Current and Projected 8-hour Ozone Levels
    D. Particulate Matter
    1. Background
    2. Health Effects of PM
    3. Current and Projected PM2.5 Levels
    4. Current PM10 Levels
    E. Other Environmental Effects
    1. Visibility
    a. Background
    b. Current Visibility Impairment
    c. Future Visibility Impairment
    2. Plant Damage from Ozone
    3. Atmospheric Deposition
    4. Materials Damage and Soiling
V. What Are Mobile Source Emissions Over Time and How Would This
Proposal Reduce Emissions, Exposure and Associated Health Effects?
    A. Mobile Source Contribution to Air Toxics Emissions
    B. VOC Emissions from Mobile Sources
    C. PM Emissions from Mobile Sources
    D. Description of Current Mobile Source Emissions Control
Programs that Reduce MSATs
    1. Fuels Programs
    a. RFG
    b. Anti-dumping
    c. 2001 Mobile Source Air Toxics Rule (MSAT1)
    d. Gasoline Sulfur
    e. Gasoline Volatility
    f. Diesel Fuel
    g. Phase-Out of Lead in Gasoline
    2. Highway Vehicle and Engine Programs
    3. Nonroad Engine Programs
    4. Voluntary Programs
    E. Emission Reductions from Proposed Controls
    1. Proposed Vehicle Controls
    a. Volatile Organic Compounds (VOC)
    b. Toxics
    c. PM2.5
    2. Proposed Fuel Benzene Controls
    3. Proposed Gas Can Standards
    a. VOC
    b. Toxics
    4. Total Emission Reductions from Proposed Controls
    a. Toxics
    b. VOC
    c. PM2.5
    F. How Would This Proposal Reduce Exposure to Mobile Source Air
Toxics and Associated Health Effects?
    G. Additional Programs Under Development That Will Reduce MSATs
    1. On-Board Diagnostics for Heavy-Duty Vehicles Over 14,000
Pounds
    2. Standards for Small SI Engines
    3. Standards for Locomotive and Marine Engines
VI. Proposed New Light-duty Vehicle Standards
    A. Why are We Proposing New Standards?
    1. The Clean Air Act and Air Quality
    2. Technology Opportunities for Light-Duty Vehicles
    3. Cold Temperature Effects on Emission Levels
    a. How Does Temperature Affect Emissions?
    b. What Are the Current Emissions Control Requirements?
    c. Opportunities for Additional Control
    B. What Cold Temperature Requirements Are We Proposing?
    1. NMHC Exhaust Emissions Standards
    2. Feasibility of the Proposed Standards
    a. Currently Available Emission Control Technologies
    b. Feasibility Considering Current Certification Levels,
Deterioration and Compliance Margin
    c. Feasibility and Test Programs for Higher Weight Vehicles
    3. Standards Timing and Phase-in
    a. Phase-In Schedule
    b. Alternative Phase-In Schedules
    4. Certification Levels
    5. Credit Program
    a. How Credits Are Calculated
    b. Credits Earned Prior to Primary Phase-In Schedule
    c. How Credits Can Be Used
    d. Discounting and Unlimited Life
    e. Deficits Could Be Carried Forward
    f. Voluntary Heavy-Duty Vehicle Credit Program
    6. Additional Vehicle Cold Temperature Standard Provisions
    a. Applicability
    b. Useful Life
    c. High Altitude
    d. In-Use Standards for Vehicles Produced During Phase-in
    7. Monitoring and Enforcement
    C. What Evaporative Emissions Standards Are We Proposing?
    1. Current Controls and Feasibility of the Proposed Standards
    2. Evaporative Standards Timing
    3. Timing for Multi-Fueled Vehicles
    4. In-Use Evaporative Emission Standards
    5. Existing Differences Between California and Federal
Evaporative Emission Test Procedures
    D. Opportunities for Additional Exhaust Control Under Normal
Conditions
    E. Vehicle Provisions for Small Volume Manufacturers
    1. Lead Time Transition Provisions
    2. Hardship Provisions
    3. Special Provisions for Independent Commercial Importers
(ICIs)
VII. Proposed Gasoline Benzene Control Program
    A. Overview of Today's Proposed Fuel Control Program
    B. Description of the Proposed Fuel Control Program
    C. Development of the Proposed Gasoline Benzene Standard
    1. Why Are We Focusing on Controlling Benzene Emissions?
    a. Other MSAT Emissions
    b. MSAT Emission Reductions Through Lowering Gasoline Volatility
or Sulfur Content
    i. Gasoline Sulfur Content
    ii. Gasoline Vapor Pressure
    c. Toxics Performance Standard
    d. Diesel Fuel Changes
    2. Why Are We Proposing To Control Benzene Emissions By
Controlling Gasoline Benzene Content?
    a. Benzene Content Standard
    b. Gasoline Aromatics Content Standard
    c. Benzene Emission Standard
    3. How Did We Select the Level of the Proposed Gasoline Benzene
Content Standard?
    a. Current Gasoline Benzene Levels
    b. The Need for an Average Benzene Standard
    c. Potential Levels for the Average Benzene Standard
    d. Comparison of Other Benzene Regulatory Programs
    4. How Do We Address Variations in Refinery Benzene Levels?
    a. Overall Reduction in Benzene Level and Variation
    b. Consideration of an Upper Limit Standard
    i. Per-Gallon Cap Standard
    ii. Maximum Average Standard
    5. How Would the Proposed Program Meet or Exceed Related
Statutory and Regulatory Requirements?
    D. Description of the Proposed Averaging, Banking, and Trading
(ABT) Program
    1. Overview
    2. Standard Credit Generation (2011 and Beyond)
    3. Credit Use
    a. Credit Trading Area
    b. Credit Life
    4. Early Credit Generation (2007-2010)
    a. Establishing Early Credit Baselines
    b. Early Credit Reduction Criteria (Trigger Points)
    c. Calculating Early Credits
    5. Additional Credit Provisions
    a. Credit Trading
    b. Pre-Compliance Reporting Requirements
    6. Special ABT Provisions for Small Refiners
    E. Regulatory Flexibility Provisions for Qualifying Refiners
    1. Hardship Provisions for Qualifying Small Refiners
    a. Qualifying Small Refiners
    i. Regulatory Flexibility for Small Refiners
    ii. Rationale for Small Refiner Provisions
    b. How Do We Propose to Define Small Refiners for the Purpose of
the Hardship Provisions?
    c. What Options Would Be Available For Small Refiners?
    i. Delay in Standards
    ii. ABT Credit Generation Opportunities
    iii. Extended Credit Life
    iv. ABT Program Review
    d. How Would Refiners Apply for Small Refiner Status?

    e. The Effect of Financial and Other Transactions on Small
Refiner Status and Small Refiner Relief Provisions
    2. General Hardship Provisions
    a. Temporary Waivers Based on Unforeseen Circumstances
    b. Temporary Waivers Based on Extreme Hardship Circumstances
    c. Early Compliance with the Proposed Benzene Standard
    F. Technological Feasibility of Gasoline Benzene Reduction
    1. Benzene Levels in Gasoline
    2. Technologies for Reducing Gasoline Benzene Levels
    a. Why is Benzene Found in Gasoline?
    b. Benzene Control Technologies Related to the Reformer
    i. Routing Around the Reformer
    ii. Routing to the Isomerization Unit
    iii. Benzene Saturation
    iv. Benzene Extraction
    c. Other Benzene Reduction Technologies
    d. Impacts on Octane and Strategies for Recovering Octane Loss
    e. Experience Using Benzene Control Technologies
    f. What Are the Potential Impacts of Benzene Control on Other
Fuel Properties?
    3. Feasible Level of Benzene Control
    4. Lead time
    5. Issues
    a. Small Refiners
    b. Imported Gasoline
    G. How Does the Proposed Fuel Control Program Satisfy the
Statutory Requirements?
    H. Effect on Energy Supply, Distribution, or Use
    I. How Would the Proposed Gasoline Benzene Standard Be
Implemented?
    1. General provisions
    a. What Are the Implementation Dates for the Proposed Program?
    b. Which Regulated Parties Would Be Subject to the Proposed
Benzene Standards?
    c. What Gasoline Would Be Subject to the Proposed Benzene
Standards?
    d. How Would Compliance With the Benzene Standard Be Determined?
    2. Averaging, Banking and Trading Program
    a. Early Credit Generation
    b. How Would Refinery Benzene Baselines Be Determined?
    c. Credit Generation Beginning in 2011
    d. How Would Credits Be Used?
    3. Hardship and Small Refiner Provisions
    a. Hardship
    b. Small Refiners
    4. Administrative and Enforcement Related Provisions
    a. Sampling/Testing
    b. Recordkeeping/Reporting
    c. Attest Engagements, Violations, Penalties
    5. How Would Compliance With the Provisions of the Proposed
Benzene Program Affect Compliance With Other Gasoline Toxics
Programs?
VIII. Gas Cans
    A. Why Are We Proposing an Emissions Control Program for Gas
Cans?
    1. VOC Emissions
    2. Technological Opportunities to Reduce Emissions from Gas Cans
    3. State Experiences Regulating Gas Cans
    B. What Emissions Standard is EPA Proposing, and Why?
    1. Description of Emissions Standard
    2. Determination of Best Available Control
    3. Emissions Performance vs. Design Standard
    4. Automatic Shut-Off
    5. Consideration of Retrofits of Existing Gas Cans
    6. Consideration of Diesel, Kerosene and Utility Containers
    C. Timing of Standard
    D. What Test Procedures Would Be Used?
    1. Diurnal Test
    2. Preconditioning to Ensure Durable In-Use Control
    a. Durability cycles
    b. Preconditioning Fuel Soak
    c. Spout Actuation
    E. What Certification and In-Use Compliance Provisions Is EPA
Proposing?
    1. Certification
    2. Emissions Warranty and In-Use Compliance
    3. Labeling
    F. How Would State Programs Be Affected By EPA Standards?
    G. Provisions for Small Gas Can Manufacturers
    1. First Type of Hardship Provision
    2. Second Type of Hardship Provision
IX. What are the Estimated Impacts of the Proposal?
    A. Refinery Costs of Gasoline Benzene Reduction
    1. Tools and Methodology
    a. Linear Programming Cost Model
    b. Refiner-by-Refinery Cost Model
    c. Price of Chemical Grade Benzene
    d. Applying the Cost Model to Special Cases
    2. Summary of Costs
    a. Nationwide Costs of the Proposed Program
    b. Regional Distribution of Costs
    c. Cost Effects of Different Standards
    d. Effect on Cost Estimates of Higher Benzene Prices
    3. Economic Impacts of MSAT Control Through Gasoline Sulfur and
RVP Control and a Total Toxics Standard
    B. What Are the Vehicle Cost Impacts?
    C. What Are The Gas Can Cost Impacts?
    D. Cost Per Ton of Emissions Reduced
    E. Benefits
    1. Unquantified Health and Environmental Benefits
    2. Quantified Human Health and Environmental Effects of the
Proposed Cold Temperature Vehicle Standard
    3. Monetized Benefits
    4. What Are the Significant Limitations of the Benefit Analysis?
    5. How Do the Benefits Compare to the Costs of The Proposed
Standards?
    F. Economic Impact Analysis
    1. What Is an Economic Impact Analysis?
    2. What Is the Economic Impact Model?
    3. What Economic Sectors Are Included in this Economic Impact
Analysis?
    4. What Are the Key Features of the Economic Impact Model?
    5. What Are the Key Model Inputs?
    6. What Are the Results of the Economic Impact Modeling?
X. Alternative Program Options
    A. Fuels
    B. Vehicles
    C. Gas cans
XI. Public Participation
    A. How Do I Submit Comments?
    B. How Should I Submit CBI to the Agency?
    C. Will There Be a Public Hearing?
    D. Comment Period
    E. What Should I Consider as I Prepare My Comments for EPA?
XII. Statutory and Executive Order Reviews
    A. Executive Order 12866: Regulatory Planning and Review
    B. Paperwork Reduction Act
    C. Regulatory Flexibility Act (RFA), as amended by the Small
Business Regulatory Enforcement Fairness Act of 1996 (SBREFA), 5
U.S.C. 601 et. seq
    1. Overview
    2. Background
    3. Summary of Regulated Small Entities
    a. Highway Light-Duty Vehicles
    b. Gasoline Refiners
    c. Portable Gasoline Container Manufacturers
    4. Potential Reporting, Record Keeping, and Compliance
    5. Relevant Federal Rules
    6. Summary of SBREFA Panel Process and Panel Outreach
    a. Significant Panel Findings
    b. Panel Process
    c. Small Business Flexibilities
    i. Highway Light-Duty Vehicles
    (a) Highway Light-Duty Vehicle Flexibilities
    (b) Highway Light-Duty Vehicle Hardships
    ii. Gasoline Refiners
    (a) Gasoline Refiner Flexibilities
    (b) Gasoline Refiner Hardships
    iii. Portable Gasoline Containers
    (a) Portable Gasoline Container Flexibilities
    (b) Portable Gasoline Container Hardships
    D. Unfunded Mandates Reform Act
    E. Executive Order 13132: Federalism
    F. Executive Order 13175: Consultation and Coordination With
Indian Tribal Governments
    G. Executive Order 13045: Protection of Children from
Environmental Health and Safety Risks
    H. Executive Order 13211: Actions that Significantly Affect
Energy Supply, Distribution, or Use
    I. National Technology Transfer Advancement Act
    J. Executive Order 12898: Federal Actions To Address
Environmental Justice in Minority Populations and Low-Income
Populations
XIII. Statutory Provisions and Legal Authority

I. Introduction

A. Summary

    Mobile sources emit air toxics that can cause cancer and other
serious health effects. Section III of this preamble and Chapter 1 of
the

Regulatory Impact Analysis (RIA) for this rule describe these compounds
and their health effects. Mobile sources contribute significantly to
the nationwide risk from breathing outdoor sources of air toxics.
Mobile sources were responsible for about 44% of outdoor toxic
emissions, almost 50% of the cancer risk, and 74% of the noncancer risk
according to EPA's National-Scale Air Toxics Assessment (NATA) for
1999. In addition, people who live or work near major roads or live in
homes with attached garages are likely to have higher exposures and
risk, which are not reflected in NATA. Sections II.A and IV of this
preamble and Chapter 3 of the RIA provide more detail about NATA, as
well as our analysis of exposures near roadways.
    According to NATA for 1999, there are a few mobile source air
toxics that pose the greatest risk based on current information about
ambient levels and exposure. These include benzene, 1,3-butadiene,
formaldehyde, acrolein, naphthalene, and polycyclic organic matter
(POM). All of these compounds are hydrocarbons except POM. Benzene is
the most significant contributor to cancer risk from all outdoor air
toxics, according to NATA for 1999. NATA does not include a
quantitative estimate of cancer risk for diesel exhaust, but it
concludes that diesel exhaust (specifically, diesel particulate matter
and diesel exhaust organic gases) is one of the pollutants that pose
the greatest relative cancer risk. Although we expect significant
reductions in mobile source air toxics in the future, cancer and
noncancer health risks will remain a public health concern, and
exposure to benzene will remain the largest contributor to this risk.
    As discussed in detail in Section V of this preamble and Chapter 2
of the RIA, this proposal would significantly reduce emissions of the
many air toxics that are hydrocarbons, including benzene, 1,3-
butadiene, formaldehyde, acetaldehyde, acrolein, and naphthalene. The
proposed fuel benzene standard and hydrocarbon standards for vehicles
and gas cans would together reduce total emissions of mobile source air
toxics by 350,000 tons in 2030, including 65,000 tons of benzene.
Mobile sources were responsible for 68% of benzene emissions in 1999.
As a result of this proposal, in 2030 passenger vehicles would emit 45%
less benzene, gas cans would emit 78% less benzene, and the gasoline
would have 37% less benzene overall.
    In addition, EPA has already taken significant steps to reduce
diesel emissions from mobile sources, which will result in a 70%
reduction between 1999 and 2020. We have adopted stringent standards
for diesel trucks and buses, and nonroad diesel engines (engines used,
for example, in construction, agricultural, and industrial
applications). We also have additional programs underway to reduce
diesel emissions, including voluntary programs and a proposal that is
being developed to reduce emissions from diesel locomotives and marine
engines.
    The proposed reductions in mobile source air toxics emissions would
reduce exposure and predicted risk of cancer and noncancer health
effects, including in environments where exposure and risk may be
highest, such as near roads, in vehicles, and in homes with attached
garages. In addition, the hydrocarbon reductions from the vehicle and
gas can standards would reduce VOC emissions (which are a precursor to
ozone and PM2.5) by over 1 million tons in 2030. The
proposed vehicle standards would reduce direct PM2.5
emissions by 20,000 tons in 2030 and would also reduce secondary
formation of PM2.5. Although ozone and PM2.5 are
considered criteria pollutants rather than ``air toxics,'' reductions
in ozone and PM2.5 are important co-benefits of this
proposal. More details on emissions, cancer risks, and adverse health
and welfare effects associated with ozone and PM are found in sections
II.A, IV and V of this preamble and Chapters 2 and 3 of the RIA.
    Section II.B of this preamble provides an overview of the
regulatory program that EPA is proposing for passenger vehicles,
gasoline, and gas cans. We are proposing standards to limit the exhaust
hydrocarbons from passenger vehicles during cold temperature operation.
We are also proposing evaporative hydrocarbon emissions standards for
passenger vehicles. We are proposing to limit the average annual
benzene content of gasoline. Finally, we are proposing hydrocarbon
emissions standards for gas cans that would reduce evaporation,
permeation, and spillage from these containers. Detailed discussion of
each of these programs is in sections VI, VII, and VIII of the preamble
and Chapters 5, 6, and 7 of the RIA.
    We estimate that the benefits of this proposal would be about $6
billion in 2030, based on the direct PM2.5 reductions from
the vehicle standards, plus unquantified benefits from reductions in
mobile source air toxics and VOC. We estimate that the annual net
social costs of this proposal would be about $200 million in 2030
(expressed in 2003 dollars). These net social costs include the value
of fuel savings from the proposed gas can standards, which would be
worth $82 million in 2030.
    The proposed reductions would have an average cost of 0.13 cents
per gallon of gasoline, less than $1 per vehicle, and less than $2 per
gas can. The reduced evaporation from gas cans would result in fuel
savings that would more than offset the increased cost for the gas can.
In 2030, the long-term cost per ton of the proposed standards (in
combination, and including fuel savings) would be $450 per ton of total
mobile source air toxics reduced; $2,400 per ton of benzene reduced;
and no cost for the hydrocarbon and PM reductions (because the vehicle
standards would have no cost in 2020 and beyond). Section IX of the
preamble and Chapters 8-13 of the RIA provide more details on the
costs, benefits, and economic impacts of the proposed standards. The
impacts on small entities and the flexibilities we are proposing are
discussed in section XII.C of this preamble and Chapter 14 of the RIA.

B. What Background Information is Helpful to Understand this Proposal?

1. What Are Air Toxics and Related Health Effects?
    Air toxics, which are also known in the Clean Air Act as
``hazardous air pollutants,'' are those pollutants known or suspected
to cause cancer or other serious health or environmental effects. For
example, some of these pollutants are known to have negative effects on
people's respiratory, cardiovascular, neurological, immune,
reproductive, or other organ systems, and they may also have
developmental effects. They may pose particular hazards to more
susceptible and sensitive populations, such as children, the elderly,
or people with pre-existing illnesses.
    Mobile source air toxics (MSATs) are those toxics emitted by motor
vehicles, nonroad engines (such as lawn and garden equipment, farming
and construction equipment, aircraft, locomotives, and ships), and
their fuels. Toxics are also emitted by stationary sources such as
power plants, factories, oil refineries, dry cleaners, gas stations,
and small manufacturers. They can also be produced by combustion of
wood and other organic materials. There are also indoor sources of air
toxics, such as solvent evaporation and outgassing from furniture and
building materials.
    Some MSATs of particular concern include benzene, 1,3-butadiene,
formaldehyde, acrolein, naphthalene, and diesel particulate matter and
diesel exhaust organic gases. Benzene and 1,3-butadiene are both known
human

carcinogens. Section III of this preamble provides more detail on the
health effects of each of these pollutants.
    MSATs are emitted as a result of various processes. Some MSATs are
present in fuel or fuel additives and are emitted to the air when the
fuel evaporates or passes through the engine. Some MSATs are formed
through engine combustion processes. 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, some air toxics, such as metals, result from
engine wear or from impurities in oil or fuel.
2. What is the Statutory Authority for Today's Proposal?
a. Clean Air Act Section 202(l)
    Section 202(l)(2) of the Clean Air Act requires EPA to set
standards to control hazardous air pollutants from motor vehicles,
motor vehicle fuels, or both. These standards must reflect the greatest
degree of emission reduction achievable through the application of
technology which will be available, taking into consideration the motor
vehicle standards established under section 202(a) of the Act, the
availability and cost of the technology, and noise, energy and safety
factors, and lead time. The standards are to be set under Clean Air Act
sections 202(a)(1) or 211(c)(1), and they are to apply, at a minimum,
to benzene and formaldehyde emissions.
    Section 202(a)(1) of the Clean Air Act directs EPA to set standards
for new motor vehicles or new motor vehicle engines which EPA judges to
cause or contribute to air pollution which may reasonably be
anticipated to endanger public health or welfare. We are proposing a
cold-temperature hydrocarbon emission standard for passenger vehicles
under this authority.
    Section 211(c)(1)(A) of the Clean Air Act authorizes EPA (among
other things) to control the manufacture of fuel if any emission
product of such fuel causes or contributes to air pollution which may
reasonably be anticipated to endanger public health or welfare. We are
proposing a benzene standard for gasoline under this authority.
    Clean Air Act section 202(l)(2) requires EPA to ``from time to time
revise'' its regulations controlling hazardous air pollutants from
motor vehicles and fuels. As described in more detail in section I.F.
below, EPA has previously set standards under section 202(l), and we
committed in that rule to engage in further rulemaking to implement
section 202(l). This proposal fulfills that commitment.
b. Clean Air Act Section 183(e)
    Clean Air Act section 183(e)(3) requires EPA to list categories of
consumer or commercial products that the Administrator determines,
based on an EPA study of VOC emissions from such products, contribute
at least 80 percent of the VOC emissions from such products in areas
violating the national ambient air quality standard for ozone. EPA
promulgated this list at 60 FR 15264 (March 23, 1995). EPA plans to
publish a Federal Register notice announcing that EPA has added
portable gasoline containers to the list of consumer products to be
regulated. This action must be taken by EPA prior to issuing a final
rule for gas cans. EPA is required to develop rules reflecting ``best
available controls'' to reduce VOC emissions from the listed products.
``Best available controls'' are defined in section 183(e)(1)(A) as
follows:

    The term ``best available controls'' means the degree of
emissions reduction that the Administrator determines, on the basis
of technological and economic feasibility, health, environmental,
and energy impacts, is achievable through the application of the
most effective equipment, measures, processes, methods, systems, or
techniques, including chemical reformulation, product or feedstock
substitution, repackaging, and directions for use, consumption,
storage, or disposal.''

    Section 183(e)(4) also allows these standards to be implemented by
means of ``any system or systems of regulation as the Administrator may
deem appropriate, including requirements for registration and labeling,
self-monitoring and reporting * * * concerning the manufacture,
processing, distribution, use, consumption, or disposal of the
product.'' We are proposing a hydrocarbon standard for gas cans under
the authority of section 183(e).
c. Energy Policy Act
    Section 1504(b) of the Energy Policy Act of 2005 requires EPA to
adjust the toxics emissions baselines for reformulated gasoline to
reflect 2001-2002 fuel qualities. However, the Act provides that this
action becomes unnecessary if EPA takes action which results in greater
overall reductions of toxics emissions from vehicles in areas with
reformulated gasoline. As described in section VII of this preamble, we
believe today's proposed action would in fact result in greater
reductions than would be achieved by adjusting the baselines under the
Energy Policy Act. Accordingly, under the provisions of the Energy
Policy Act, this proposed action would obviate the need for readjusting
emissions baselines for reformulated gasoline.
3. What Other Actions Has EPA Taken Under Clean Air Act Section 202(l)?
a. 2001 Mobile Source Air Toxics Rule
    EPA published a final rule under Clean Air Act section 202(l) on
March 29, 2001, entitled, ``Control of Emissions of Hazardous Air
Pollutants from Mobile Sources'' (66 FR 17230). This rule established
toxics emissions performance standards for gasoline refiners. These
standards were designed to ensure that the over compliance to the
standard seen in the in-use fuels produced in the years of 1998-2000
would continue in the future.
    EPA adopted this anti-backsliding requirement as a near-term
control that could be implemented and take effect within a year or two.
We did not adopt long-term controls, those controls that require a
longer lead time to implement, because we lacked information to address
the costs and benefits of potential fuel controls in the context of the
fuel sulfur controls that we had finalized in February 2000. However,
the March 2001 rule did commit to additional rulemaking that would
evaluate the need for and feasibility of additional controls.\1\
Today's proposal fulfills that commitment, and represents the second
step of the two-step approach originally envisioned in the 2001 rule.
---------------------------------------------------------------------------

    \1\ See Sierra Club v. EPA, 325 F. 3d 374, 380 (D.C. Cir. 2003),
which upholds this approach.
---------------------------------------------------------------------------

    The 2001 rule did not set additional air toxics controls for motor
vehicles, because the technology-forcing Tier 2 light-duty vehicle
standards and 2007 heavy-duty engine and vehicle standards had just
been promulgated. We found that those standards represented the
greatest degree of toxics control achievable at that time under section
202(l).\2\
---------------------------------------------------------------------------

    \2\ 66 FR 17241-17245 (March 29, 2001).
---------------------------------------------------------------------------

b. Technical Analysis Plan
    The 2001 rulemaking also included a Technical Analysis Plan that
described toxics-related research and activities that would inform our
future rulemaking to evaluate the need for and appropriateness of
additional mobile source air toxic controls. Specifically, we
identified four critical areas where there were data gaps requiring
long-term efforts:
     Developing better air toxics emission factors for nonroad
sources;
     Improving estimation of air toxics exposures in
microenvironments;

     Improving consideration of the range of total public
exposures to air toxics; and
     Increasing our understanding of the effectiveness and
costs of vehicle, fuel and nonroad controls for air toxics.
    EPA and other outside researchers have conducted significant
research in these areas since 2001. The findings of this research are
described in more detail in other sections of this preamble and in the
regulatory impact analysis for this proposal. Following are some
highlights of our activities.
    Nonroad emissions testing. EPA has tested emissions of nonroad
diesel engines for a comprehensive suite of hydrocarbons and inorganic
compounds. These emissions tests employed steady-state as well as
transient test cycles, using typical nonroad diesel fuel and low-sulfur
nonroad diesel fuel. In addition, EPA tested small gasoline-powered
engines such as lawnmowers, leaf blowers, chainsaws and string
trimmers.
    Improved estimation of exposures in microenvironments and
consideration of the range of public exposures. EPA and other
researchers have conducted a substantial amount of research and
analysis in these areas, which is discussed in section IV of this
preamble and in the regulatory impact analysis. This research has
involved monitoring as well as the development and application of
enhanced modeling tools. For example, personal exposure monitoring and
ambient monitoring has been conducted at homes and schools near
roadways; in vehicles; in homes with attached garages; and in
occupational settings involving both diesel and gasoline nonroad
equipment. We have also applied dispersion modeling techniques with
greater spatial refinement to estimate gradients of toxic pollutants
near roadways. A variety of improvements to our emissions, dispersion,
and exposure modeling tools are improving our ability to consider the
range of exposure people experience. These include the MOBILE6
emissions model, improved spatial and temporal allocation of emissions,
development of the Community Multiscale Air Quality (CMAQ) model, and
updates to the HAPEM exposure model. Many of these improvements were
applied in EPA's National-Scale Air Toxics Assessment for 1999 and
other analyses EPA performed to support this proposal. In fact, EPA
developed a modification of the HAPEM exposure model to account for
higher pollutant concentrations near major roads.
    Research in these areas is continuing both inside and outside EPA,
including work under the auspices of the Health Effects Institute and
the Mickey Leland National Urban Air Toxics Research Center.
    Costs and effectiveness of vehicle, fuel, and nonroad controls for
air toxics. EPA's analysis of the costs and effectiveness of vehicle
and fuel controls is described in section IX of this preamble and in
the regulatory impact analysis. In addition, as described in section V,
EPA is currently developing rules that will examine controls of small
gasoline engines and diesel locomotive and marine engines.

II. Overview of Proposal

A. Why Is EPA Making This Proposal?

    People experience elevated risk of cancer and other noncancer
health effects from exposure to air toxics. Mobile sources are
responsible for a significant portion of this risk. For example,
benzene is the most significant contributor to cancer risk from all
outdoor air toxics,\3\ and most of the nation's benzene emissions come
from mobile sources. These risks vary depending on where people live
and work and the kinds of activities in which they engage. People who
live or work near major roads, or people that spend a large amount of
time in vehicles, are likely to have higher exposures and higher risks.
Although we expect significant reductions in mobile source air toxics
in the future, predicted cancer and noncancer health risks will remain
a public health concern. Benzene will remain the largest contributor to
this risk. In addition, some mobile source air toxics contribute to the
formation of ozone and PM2.5, which contribute to serious
public health problems, which are discussed further in section II.A.4.
---------------------------------------------------------------------------

    \3\ Based on quantitative estimates of risk, which do not
include diesel particular matter and diesel exhaust organic gases.
---------------------------------------------------------------------------

    Sections II.A.1-3 discuss the risks posed by outdoor toxics now and
in the future, based on national-scale estimates such as EPA's
National-Scale Air Toxics Assessment (NATA). EPA's NATA for 1999
provides some perspective on the average risk of cancer and noncancer
health effects resulting from breathing air toxics from outdoor
sources, and the contribution of mobile sources to these
risks.4 5 This assessment did not include indoor sources of
air toxics. Also, it estimates average concentrations within a census
tract, and therefore does not reflect elevated concentrations and
exposures near roadways within a census tract. Nevertheless, its
findings are useful in providing a perspective on the magnitude of
risks posed by outdoor sources of air toxics generally, and in
identifying what pollutants and sources are important contributors to
these health risks.
---------------------------------------------------------------------------

    \4\ http://www.epa.gov/ttn/atw/nata 1999.

    \5\ NATA does not include a quantitative estimate of cancer risk
for diesel particulate matter and diesel exhaust organic gases. EPA
has concluded that while diesel exhaust is likely to be a human
carcinogen, available data are not sufficient to develop a
confidential estimate of cancer unit risk.
---------------------------------------------------------------------------

    EPA also performed a national-scale assessment for future years,
using the same modeling tools and approach as the 1999 NATA. Finally,
we also performed national-scale exposure modeling that accounts for
the higher toxics concentrations near roads. This latter modeling
provides a perspective on the mobile source contribution to risk from
air toxics that is not reflected in our other national-scale
assessments.
1. National Cancer Risk from Air Toxics
    According to NATA, the average national cancer risk in 1999 from
all outdoor sources of air toxics was 42 in a million. That is, 42 out
of one million people would be expected to contract cancer from a
lifetime of breathing air toxics at 1999 levels. Mobile sources were
responsible for 44% of outdoor toxic emissions and almost 50% of the
cancer risk. Considering only the subset of compounds emitted by mobile
sources (see Table IV.C-2), the national average cancer risk in 1999,
including the stationary source contribution to these pollutants, was
23 in a million.
    Benzene is the largest contributor to cancer risk of all 133
pollutants quantitatively assessed in the 1999 NATA. The national
average cancer risk from benzene alone was 11 in a million. Over 120
million people in 1999 were exposed to a risk level above 10 in a
million due to chronic inhalation exposure to benzene. Mobile sources
were responsible for 68% of benzene emissions in 1999.
    Although air toxics emissions are projected to decline in the
future as a result of standards EPA has previously adopted, cancer risk
will continue to be a public health concern. The predicted national
average cancer risk from MSATs in 2030 will be 18 in a million,
according to EPA analysis (described in more detail in section IV of
this preamble and Chapter 3 of the Regulatory Impact Analysis). In
fact, in 2030 there will be more people exposed to the highest levels
of risk. The number of Americans above the 10 in a million cancer risk
level from exposure to MSATs is projected to increase from 214 million
in 1999 to 240 million in 2030. Mobile sources will continue to be a
significant contributor to risk in the future, accounting for 22% of
total air

toxic emissions in 2020, and 44% of benzene emissions.
2. Noncancer Health Effects
    According to the NATA for 1999, nearly the entire U.S. population
was exposed to an average level of air toxics that has the potential
for adverse respiratory health effects (noncancer).\6\ This will
continue to be the case in 2030, even though toxics levels will be
lower.
---------------------------------------------------------------------------

    \6\ That is, the respiratory hazard index exceeded 1. See
section III.D of this preamble for more information.
---------------------------------------------------------------------------

    Mobile sources were responsible for 74% of the noncancer
(respiratory) risk from outdoor air toxics in 1999. The majority of
this risk was from acrolein, and formaldehyde also contributed to the
risk of respiratory health effects. Mobile sources will continue to be
responsible for the majority of noncancer risk from outdoor air toxics
in 2030.
    Although not included in NATA's estimates of noncancer risk, PM
from gasoline and diesel mobile sources contribute significantly to the
health effects associated with ambient PM, for which EPA has
established a National Ambient Air Quality Standard. There is extensive
human data showing a wide spectrum of adverse health effects associated
with exposure to ambient PM.
3. Exposure Near Roads and From Attached Garages
    The national-scale risks described above do not account for higher
exposures experienced by people who live near major roadways, or people
who live in homes with attached garages. A substantial number of
studies show elevated concentrations of multiple MSATs in close
proximity to major roads. We also conducted an exposure modeling study
for three geographically distinct states (Colorado, New York, and
Georgia) and found that when the elevated concentrations near roadways
are accounted for, the distribution of benzene exposure is broader,
with a larger fraction of the population exposed to higher
concentrations. The largest effect on personal exposure occurs for the
population living near major roads. A U.S. Census survey of housing
found that in 2003 12.6% of U.S. housing units were within 300 feet of
a major transportation source.\7\ The potential population exposed to
elevated concentrations near major roadways is therefore large. In
addition, our analysis indicates that benzene exposure experienced by
people living in homes with attached garages may be twice the national
average benzene exposure estimated by NATA for 1999. More details on
exposure near roads and from attached garages can be found in section
IV of this preamble.
---------------------------------------------------------------------------

    \7\ United States Census Bureau. (2004) American Housing Survey
web page. [Online at http://www.cenus.gov/hhes/www/housing/ahs/ahs03/ahs03.html
] Table IA-6.

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4. Ozone and Particulate Matter
    Many MSATs are part of a larger category of mobile source emissions
known as volatile organic compounds (VOC), which contribute to the
formation of ozone and particulate matter (PM). In addition, some MSATs
are emitted directly as PM rather than being formed through secondary
processes. Thus, MSATs contribute to adverse health effects both as
individual pollutants, and as precursors to ozone and PM. Mobile
sources contribute significantly to national emissions of VOC and PM.
In addition, gas cans are a source of both VOC and benzene emissions.
    Both ozone and PM contribute to serious public health problems,
including premature mortality, aggravation of respiratory and
cardiovascular disease (as indicated by increased hospital admissions
and emergency room visits, school absences, work loss days, and
restricted activity days), changes in lung function and increased
respiratory symptoms, changes to lung tissues and structures, altered
respiratory defense mechanisms, chronic bronchitis, and decreased lung
function.
    In addition, ozone and PM cause significant harm to public welfare.
Specifically, ozone causes damage to vegetation, which leads to crop
and forestry economic losses, as well as harm to national parks,
wilderness areas, and other natural systems. PM contributes to the
substantial impairment of visibility in many parts of the U.S.,
including national parks and wilderness areas. The deposition of
airborne particles can also reduce the aesthetic appeal of buildings
and culturally important articles through soiling, and can contribute
directly (or in conjunction with other pollutants) to structural damage
by means of corrosion or erosion.
    Finally, atmospheric deposition and runoff of polycyclic organic
matter (POM), metals, and other mobile-source-related compounds
contribute to the contamination of water bodies such as the Great Lakes
and coastal waters (e.g., the Chesapeake Bay).

B. What Is EPA Proposing?

1. Light-Duty Vehicle Emission Standards
    As described in more detail in section VI, we are proposing new
standards for both exhaust and evaporative emissions from passenger
vehicles. The new exhaust emissions standards would significantly
reduce non-methane hydrocarbon (NMHC) emissions from passenger vehicles
at cold temperatures. These hydrocarbons include many mobile source air
toxics (including benzene), as well as VOC.
    Current vehicle emission standards require that the certification
testing of NMHC is performed at 75 [deg]F. Recent research and analysis
indicates that these standards are not resulting in robust control of
NMHC at lower temperatures. We believe that cold temperature NMHC
control can be substantially improved using the same technological
approaches that are generally already being used in the Tier 2 vehicle
fleet to meet the stringent standards at 75 [deg]F. These cold-
temperature NMHC controls would also result in lower direct PM
emissions at cold temperatures.
    Accordingly, we are proposing that light-duty vehicles, light-duty
trucks, and medium-duty passenger vehicles would be subject to a new
non-methane hydrocarbon (NMHC) exhaust emissions standard at 20 [deg]F.
Vehicles at or below 6,000 pounds gross vehicle weight rating (GVWR)
would be subject to a sales-weighted fleet average NMHC level of 0.3
grams/mile. Vehicles between 6,000 and 8,500 pounds GVWR and medium-
duty passenger vehicles would be subject to a sales-weighted fleet
average NMHC level of 0.5 grams/mile. For lighter vehicles, the
standard would phase in between 2010 and 2013. For heavier vehicles,
the new standards would phase in between 2012 and 2015. We are also
proposing a credit program and other provisions designed to provide
flexibility to manufacturers, especially during the phase-in periods.
These provisions are designed to allow the earliest possible phase-in
of standards and help minimize costs and ease the transition to new
standards.
    We are also proposing a set of nominally more stringent evaporative
emission standards for all light-duty vehicles, light-duty trucks, and
medium-duty passenger vehicles. The proposed standards are equivalent
to California's Low Emission Vehicle II (LEV II) standards, and they
reflect the evaporative emissions levels that are already being
achieved nationwide. The standards we are proposing today would codify
the approach that most

manufacturers are already taking for 50-state evaporative systems, and
the standards would thus prevent backsliding in the future. We are
proposing to implement the evaporative emission standards in 2009 for
lighter vehicles and in 2010 for the heavier vehicles.
    Section VI provides details on the proposed exhaust and evaporative
standards and their implementation, and our rationale for proposing
them.
2. Gasoline Fuel Standards
    As described in more detail in section VII, we are proposing to
limit the benzene content of all gasoline, both reformulated and
conventional. We propose that beginning January 1, 2011, refiners would
meet an average gasoline benzene content standard of 0.62% by volume on
all their gasoline. We are not proposing a standard for California,
however, because it is already covered by a similar state program.
    This proposed fuel standard would result in air toxics emissions
reductions that are greater than required under all existing gasoline
toxics programs. As a result, EPA is proposing that upon full
implementation in 2011, the regulatory provisions for the benzene
control program would become the single regulatory mechanism used to
implement the RFG and Anti-dumping annual average toxics requirements.
The current RFG and Anti-dumping annual average provisions thus would
be replaced by the proposed benzene control program. The MSAT2 benzene
control program would also replace the MSAT1 requirements. In addition,
the program would satisfy certain fuel MSAT conditions of the Energy
Policy Act of 2005 and obviate the need to revise toxics baselines for
reformulated gasoline otherwise required by the Energy Policy Act. In
all of these ways, we would significantly consolidate and simplify the
existing national fuel-related MSAT regulatory program.
    We also propose that refiners could generate benzene credits and
use or transfer them as a part of a nationwide averaging, banking, and
trading (ABT) program. From 2007-2010 refiners could generate benzene
credits by taking early steps to reduce gasoline benzene levels.
Beginning in 2011 and continuing indefinitely, refiners could generate
credits by producing gasoline with benzene levels below the 0.62%
average standard. Refiners could apply the credits towards company
compliance, ``bank'' the credits for later use, or transfer (``trade'')
them to other refiners nationwide (outside of California) under the
proposed program. Under this program, refiners could use credits to
achieve compliance with the benzene content standard.
    This proposed ABT program would allow us to set a more stringent
benzene standard than would otherwise be possible, and it would allow
implementation to occur earlier. Under this proposed benzene content
standard and ABT program, gasoline in all areas of the country would
have lower benzene levels than they have today. Overall benzene levels
would be 37% lower. This would reduce benzene emissions and exposure
nationwide.
    Finally, we propose hardship provisions. Refiners approved as
``small refiners'' would be eligible for certain temporary relief
provisions. In addition, any refiner facing extreme unforeseen
circumstances or extreme hardship circumstances could apply for similar
temporary relief.
    Section VII of this preamble provides a detailed explanation and
rationale for the proposed fuel program and its implementation. It also
discusses and seeks comment on a variety of alternatives that we
considered.
3. Portable Gasoline Container (Gas Can) Controls
    Portable gasoline containers, or gas cans, are consumer products
used to refuel a wide variety of gasoline-powered equipment, including
lawn and garden equipment, recreational equipment, and passenger
vehicles that have run out of gas. As described in section VIII, we are
proposing standards that would reduce hydrocarbon emissions from
evaporation, permeation, and spillage. These standards would
significantly reduce benzene and other toxics, as well as VOC more
generally. VOC is an ozone precursor.
    We propose a performance-based standard of 0.3 grams per gallon per
day of hydrocarbons, based on the emissions from the can over a diurnal
test cycle. The standard would apply to gas cans manufactured on or
after January 1, 2009. We also propose test procedures and a
certification and compliance program, in order to ensure that gas cans
would meet the emission standard over a range of in-use conditions. The
proposed standards would result in the use of best available control
technologies, such as durable permeation barriers, automatically
closing spouts, and cans that are well-sealed.
    California implemented an emissions control program for gas cans in
2001, and since then, several other states have adopted the program.
Last year, California adopted a revised program, which will take effect
July 1, 2007. The revised California program is very similar to the
program we are proposing. Although a few aspects of the program we are
proposing are different, we believe manufacturers would be able to meet
both EPA and California requirements with the same gas can designs.

III. What Are Mobile Source Air Toxics (MSATs) and Their Health
Effects?

A. What Are MSATs?

    Section 202(l) refers to ``hazardous air pollutants from motor
vehicles and motor vehicle fuels.'' We use the term ``mobile source air
toxics (MSATs)'' to refer to compounds that are emitted by mobile
sources and have the potential for serious adverse health effects.
There are a variety of ways in which to identify compounds that have
the potential for serious adverse health effects. For example, EPA's
Integrated Risk Information System (IRIS) is EPA's database containing
information on human health effects that may result from exposure to
various chemicals in the environment. In addition, Clean Air Act
section 112(b) contains a list of hazardous air pollutants that EPA is
required to control through regulatory standards; other agencies or
programs such as the Agency for Toxic Substances and Disease Registry
and the California EPA have developed health benchmark values for
various compounds; and the International Agency for Research on Cancer
and the National Toxicology Program have assembled evidence of
substances that cause cancer in humans and issue judgments on the
strength of the evidence. Each source of information has its own
strengths and limitations. For example, there are inherent limitations
on the number of compounds that have been investigated sufficiently for
EPA to conduct an IRIS assessment. There are some compounds that are
not listed in IRIS but are considered to be hazardous air pollutants
under Clean Air Act section 112(b) and are regulated by the Agency
(e.g., propionaldehyde, 2,2,4-trimethylpentane).

B. Compounds Emitted by Mobile Sources and Identified in IRIS

    In its 2001 MSAT rule, EPA identified a list of 21 MSATs. We listed
a compound as an MSAT if it was emitted from mobile sources, and if the
Agency had concluded in IRIS that the compound posed a potential cancer
hazard and/or if IRIS contained an inhalation reference concentration
or ingestion reference dose for the compound. Since 2001, EPA has
conducted an extensive review of the

literature to produce a list of the compounds identified in the exhaust
or evaporative emissions from onroad and nonroad equipment, using
baseline as well as alternative fuels (e.g., biodiesel, compressed
natural gas). This list, the Master List of Compounds Emitted by Mobile
Sources (``Master List''), currently includes approximately 1,000
compounds. It is available in the public docket for this rule and on
the web (http://www.epa.gov/otaq/toxics.htm). Table III.B-1 lists those

compounds from the Master List that currently meet those 2001 MSAT
criteria, based on the current IRIS.
    Table III.B-1 identifies all of the compounds from the Master List
that are present in IRIS with (a) a cancer hazard identification of
known, probable, or possible human carcinogens (under the 1986 EPA
cancer guidelines) or carcinogenic to humans, likely to be carcinogenic
to humans, or suggestive evidence of carcinogenic potential (under the
2005 EPA cancer guidelines); and/or (b) an inhalation reference
concentration or an ingestion reference dose. Although all these
compounds have been detected in emissions from mobile sources, many are
emitted in trace amounts and data are not adequate to develop an
inventory. Those compounds for which we have developed an emissions
inventory are summarized in Table IV.C-2. There are several compounds
for which IRIS assessments are underway and therefore are not included
in Table III.B-1. These compounds are: Cerium, copper, ethanol, ethyl
tertiary butyl ether (ETBE), platinum, propionaldehyde, and 2,2,4-
trimethylpentane.
    The fact that a compound is listed in Table III.B-1 does not imply
a risk to public health or welfare at current levels, or that it is
appropriate to adopt controls to limit the emissions of such a compound
from motor vehicles or their fuels. 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 from motor vehicles cause or
contribute to air pollution which may reasonably be anticipated to
endanger public health or welfare.

 Table III.B-1.--Compounds Emitted by Mobile Sources That Are Listed in
                                  IRIS*
------------------------------------------------------------------------

------------------------------------------------------------------------
1,1,1,2-Tetrafluoroethane...  Cadmium.............  Manganese.
1,1,1-Trichloroethane.......  Carbon disulfide....  Mercury, elemental.
1,1-Biphenyl................  Carbon tetrachloride  Methanol.
1,2-Dibromoethane...........  Chlorine............  Methyl chloride.
1,2-Dichlorobenzene.........  Chlorobenzene.......  Methyl ethyl ketone
                                                     (MEK).
1,3-Butadiene...............  Chloroform..........  Methyl isobutyl
                                                     ketone (MIBK).
2,4-Dinitrophenol...........  Chromium III........  Methyl tert-butyl
                                                     ether (MTBE).
2-Methylnaphthalene.........  Chromium VI.........  Molybdenum.
2-Methylphenol..............  Chrysene............  Naphthalene.
4-Methylphenol..............  Crotonaldehyde......  Nickel.
Acenaphthene................  Cumene (isopropyl     Nitrate.
                               benzene).
Acetaldehyde................  Cyclohexane.........  N-
                                                     Nitrosodiethylamine
                                                     .
Acetone.....................  Cyclohexanone.......  N-
                                                     Nitrosodimethylamin
                                                     e.
Acetophenone................  Di(2-                 N-Nitroso-di-n-
                               ethylhexyl)phthalat   butylamine.
                               e.
Acrolein (2-propenal).......  Dibenz[a,h]anthracen  N-Nitrosodi-N-
                               e.                    propylamine.
Ammonia.....................  Dibutyl phthalate...  N-
                                                     Nitrosopyrrolidine.
Anthracene..................  Dichloromethane.....  Pentachlorophenol.
Antimony....................  Diesel PM and Diesel  Phenol.
                               exhaust organic
                               gases.
Arsenic, inorganic..........  Diethyl phthalate...  Phosphorus.
Barium and compounds........  Ethylbenzene........  Phthalic anhydride.
Benz[a]anthracene...........  Ethylene glycol       Pyrene.
                               monobutyl ether.
Benzaldehyde................  Fluoranthene........  Selenium and
                                                     compounds.
Benzene.....................  Fluorene............  Silver.
Benzo[a]pyrene (BaP)........  Formaldehyde........  Strontium.
Benzo[b]fluoranthene........  Furfural............  Styrene.
Benzo[k]fluoranthene........  Hexachlorodibenzo-p-  Tetrachloroethylene.
                               dioxin, mixture
                               (dioxin/furans).
Benzoic acid................  n-Hexane............  Toluene.
Beryllium and compounds.....  Hydrogen cyanide....  Trichlorofluorometha
                                                     ne.
Boron (Boron and Borates      Hydrogen sulfide....  Vanadium.
 only).
Bromomethane................  Indeno[1,2,3-         Xylenes.
                               cd]pyrene.
Butyl benzyl phthalate......  Lead and compounds    Zinc and compounds.
                               (inorganic).
------------------------------------------------------------------------
* Compounds listed in IRIS as known, probable, or possible human
  carcinogens and/or pollutants for which the Agency has calculated a
  reference concentration or reference dose.

C. Which Mobile Source Emissions Pose the Greatest Health Risk at
Current Levels?

    The 1999 National-Scale Air Toxics Assessment (NATA) provides some
perspective on which mobile source emissions pose the greatest risk at
current estimated ambient levels.\8\ We also conducted a national-scale
assessment for future years, which is discussed more fully in section
IV of this preamble and Chapters 2 and 3 of the RIA. Our understanding
of what emissions pose the greatest risk will evolve over time, based
on our understanding of the ambient levels and health effects
associated with the compounds.\9\
---------------------------------------------------------------------------

    \8\ It is, of course, not necessary for EPA to show that a
compound is a national or regional risk driver to show that its
emission from motor vehicles may reasonably cause or contribute to
endangerment of public health or welfare. A showing that motor
vehicles contribute some non-trivial percentage of the inventory of
a compound known to be associated with adverse health effects would
normally be sufficient. Cf. Bluewater Network v. EPA, 370 F. 3d 1,
15 (D.C. Cir. 2004).
    \9\ The discussion here considers risks other than those
attributed to ambient levels of criteria pollutants.
---------------------------------------------------------------------------

1. National and Regional Risk Drivers in 1999 National-Scale Air Toxics
Assessment
    The 1999 NATA evaluates 177 hazardous air pollutants currently
listed under CAA section 112(b), as well as

diesel PM.\10\ NATA is described in greater detail in Chapters 2 and 3
of the Regulatory Impact Analysis for this proposed rule. Additional
information can also be obtained from the NATA website (http://www.epa.gov/ttn/atw/nata1999
). Based on the assessment of inhalation

exposures associated with outdoor sources of these hazardous air
pollutants, NATA has identified cancer and noncancer risk drivers on a
national and regional scale (Table III.C-1). A cancer risk driver on a
national scale is a hazardous air pollutant for which at least 25
million people are exposed to risk greater than ten in one million.
Benzene is the only compound identified in the 1999 NATA as a national
cancer risk driver. A cancer risk driver on a regional scale is a
hazardous air pollutant for which at least one million people are
exposed to risk greater than ten in one million or at least 10,000
people are exposed to risk greater than 100 in one million. Twelve
compounds (or groups of compounds in the case of POM) were identified
as regional cancer risk drivers. The 1999 NATA concludes that diesel
particulate matter is among the substances that pose the greatest
relative risk, although the cancer risk cannot be quantified.
---------------------------------------------------------------------------

    \10\ NATA does not include a quantitative estimate of cancer
risk for diesel particulate matter and diesel exhaust organic gases.
---------------------------------------------------------------------------

    A noncancer risk driver at the national scale is a hazardous air
pollutant for which at least 25 million people are exposed at a
concentration greater than the inhalation reference concentration. The
RfC 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. Acrolein is the only compound
identified in the 1999 NATA as a national noncancer risk driver. A
noncancer risk driver on a regional scale is defined as a hazardous air
pollutant for which at least 10,000 people are exposed to an ambient
concentration greater than the inhalation reference concentration.
Sixteen regional-scale noncancer risk drivers were identified in the
1999 NATA (see Table III.C-1.).

 Table III.C-1.--National and Regional Cancer and Noncancer Risk Drivers
                              in 1999 NATA
------------------------------------------------------------------------
                Cancer \1\                            Noncancer
------------------------------------------------------------------------
National drivers \2\......................  National drivers \4\
Benzene...................................  Acrolein
Regional drivers \3\......................  Regional drivers \5\
Arsenic compounds.........................  Antimony
Benzidine.................................  Arsenic compounds
1,3-Butadiene.............................  1,3-Butadiene
Cadmium compounds.........................  Cadmium compounds
Carbon tetrachloride......................  Chlorine
Chromium VI...............................  Chromium VI
Coke oven.................................  Diesel PM
Ethylene oxide............................  Formaldehyde
Hydrazine.................................  Hexamethylene 1-6-
                                             diisocyanate
Naphthalene...............................  Hydrazine
Perchloroethylene.........................  Hydrochloric acid
Polycyclic organic matter.................  Maleic anhydride
                                            Manganese compounds
                                            Nickel compounds
                                            2,4-Toluene diisocyanate
                                            Triethylamine
------------------------------------------------------------------------
\1\ The list of cancer risk drivers does not include diesel particulate
  matter. However, the 1999 NATA concluded that it was one of the
  pollutants that posed the greatest relative cancer risk.
\2\ At least 25 million people exposed to risk >10 in 1 million.
\3\ At least 1 million people exposed to risk >10 in 1 million or at
  least 10,000 people exposed to risk >100 in 1 million.
\4\ At least 25 million people exposed to a hazard quotient > 1.0.
\5\ At least 10,000 people exposed to a hazard quotient > 1.

2. 1999 NATA Risk Drivers with Significant Mobile Source Contribution

    Among the national and regional-scale cancer and noncancer risk
drivers identified in the 1999 NATA, seven compounds have significant
contributions from mobile sources: benzene, 1,3-butadiene,
formaldehyde, acrolein, polycyclic organic matter (POM), naphthalene,
and diesel particulate matter and diesel exhaust organic gases (Table
III.C-2.). For example, mobile sources contribute 68% of the national
benzene inventory, with 49% from on-road sources and 19% from nonroad
sources.

  Table III.C-2.--Mobile Source Contribution to 1999 NATA Risk Drivers
------------------------------------------------------------------------
                                              Percent         Percent
                                           contribution    contribution
         1999 NATA risk drivers              from all      from on-road
                                          mobile sources  mobile sources
                                             (percent)       (percent)
------------------------------------------------------------------------
Benzene.................................              68              49
1,3-Butadiene...........................              58              41
Formaldehyde............................              47              27
Acrolein................................              25              14
Polycyclic organic matter *.............               6               3
Naphthalene.............................              27              21
Diesel PM and Diesel exhaust organic                 100             38
 gases..................................
------------------------------------------------------------------------
* This POM inventory includes the 15 POM compounds:
  benzo[b]fluoranthene, benz[a]anthracene, indeno(1,2,3-c,d)pyrene,
  benzo[k]fluoranthene, chrysene, benzo[a]pyrene, dibenz(a,h)anthracene,
  anthracene, pyrene, benzo(g,h,i)perylene, fluoranthene,
  acenaphthylene, phenanthrene, fluorene, and acenaphthene.

D. What Are the Health Effects of Air Toxics?

1. Overview of Potential Cancer and Noncancer Health Effects
    Air toxics can cause a variety of cancer and noncancer health
effects. A number of the mobile source air toxic pollutants described
in section III are known or likely to pose a cancer hazard in humans.
Many of these compounds also cause adverse noncancer health effects
resulting from chronic,\11\ subchronic,\12\ or acute \13\ inhalation
exposures. These include neurological, cardiovascular, liver, kidney,
and respiratory effects as well as effects on the immune and
reproductive systems. Section III.D.2 discusses the health effects of
air toxic compounds listed in Table III.C-2, as well as acetaldehyde.
The compounds in Table III.C-2 were all identified as national and
regional-scale cancer and noncancer risk drivers in the 1999 National-
Scale Air Toxics Assessment (NATA), and have significant inventory
contributions from mobile sources. Acetaldehyde is included because it
is a likely human carcinogen, has a significant inventory contribution
from mobile sources, and was identified as a risk driver in the 1996
NATA. We are also including diesel particulate matter and diesel
exhaust organic gases in this discussion. Although 1999 NATA did not
quantify cancer risks associated with exposure to this pollutant, EPA
has concluded that diesel exhaust ranks with the other substances that
the national-scale assessment suggests pose the greatest relative
risk.\14\
---------------------------------------------------------------------------

    \11\ Chronic exposure is defined in the glossary of the
Integrated Risk Information (IRIS) database (http://www.epa.gov/iris) as

repeated exposure by the oral, dermal, or inhalation route for more
than approximately 10 of the life span in humans (more than
approximately 90 days to 2 years in typically used laboratory animal
species).
    \12\ Defined in the IRIS database as exposure to a substance
spanning approximately 10 of the lifetime of an organism.
    \13\ Defined in the IRIS database as exposure by the oral,
dermal, or inhalation route for 24 hours or less.
    \14\ http://www.epa.gov/ttn/atw/nata1999.

---------------------------------------------------------------------------

    Inhalation cancer risks are usually estimated by EPA as ``unit
risks,'' which represent the excess lifetime cancer risk estimated to
result from continuous exposure to an agent at a concentration of 1
[mu]g/m\3\ in air. Some air toxics are known to be carcinogenic in
animals but lack data in humans. These have been assumed to be human
carcinogens. Also, relationships between exposure and probability of
cancer are assumed to be linear. In addition, these unit risks are
typically upper bound estimates. Upper bound estimates are more likely
to overestimate than underestimate risk. Where there are strong
epidemiological data, a maximum likelihood (MLE) estimate may be
developed. An MLE is a best scientific estimate of risk. The benzene
unit risk is an MLE. A discussion of the confidence in a quantitative
cancer risk estimate is provided in the IRIS file for each compound.
The discussion of the confidence in the cancer risk estimate includes
an assessment of the source of the data (human or animal),
uncertainties in dose estimates, choice of the model used to fit the
exposure and response data and how uncertainties and potential
confounders are handled.
    Potential noncancer chronic inhalation health risks are quantified
using reference concentrations (RfCs) and noncancer chronic ingestion
health risks are quantified using reference doses (RfDs). The RfC 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. Sources of uncertainty in the development of the
RfCs and RfDs include intraspecies extrapolation (animal to human) and
interspecies extrapolation (average human to sensitive human).
Additional sources of uncertainty can be using a lowest observed
adverse effect level in place of a no observed adverse effect level,
and other data deficiencies. A statement regarding the confidence in
the RfC and/or RfD is developed to reflect the confidence in the
principal study or studies on which the RfC or RfD are based and the
confidence in the underlying database. Factors that affect the
confidence in the principal study include how well the study was
designed, conducted and reported. Factors that affect the confidence in
the database include an assessment of the availability of information
regarding identification of the critical effect, potentially
susceptible populations and exposure scenarios relevant to assessment
of risk.
    The RfC may be used to estimate a hazard quotient, which is the
environmental exposure to a substance divided by its RfC. A hazard
quotient greater than one indicates adverse health effects are
possible. The hazard quotient cannot be translated to a probability
that adverse health effects will occur, and is unlikely to be
proportional to risk. It is especially important to note that a hazard
quotient exceeding one does not necessarily mean that adverse effects
will occur. In NATA, hazard quotients for different respiratory
irritants were also combined into a hazard index (HI). A hazard index
is the sum of hazard quotients for substances that affect the same
target organ or organ system. Because different pollutants may cause
similar adverse health effects, it is often appropriate to combine
hazard quotients associated with different substances. However, the HI
is only an approximation of a combined effect because substances may
affect a target organ in different ways.
2. Health Effects of Key MSATs
a. Benzene
    The EPA's IRIS database lists benzene, an aromatic hydrocarbon, as
a known human carcinogen (causing leukemia) by all routes of
exposure.\15\ A number of adverse noncancer health effects including
blood disorders and immunotoxicity have also been associated with long-
term occupational exposure to benzene.
---------------------------------------------------------------------------

    \15\ U.S. EPA (2000). Integrated Risk Information System File
for Benzene. This material is available electronically at http://www.epa.gov/iris/subst/0276.htm
.

---------------------------------------------------------------------------

    Inhalation is the major source of human exposure to benzene in the
occupational and non-occupational setting. Long-term inhalation
occupational exposure to benzene has been shown to cause cancer of the
hematopoetic (blood cell) system in adults. Among these are acute
nonlymphocytic leukemia \16\ and chronic lymphocytic
leukemia.17 18

Leukemias, lymphomas, and other tumor types have been observed in
experimental animals exposed to benzene by inhalation or oral
administration. Exposure to benzene and/or its metabolites has also
been linked with chromosomal changes in humans and animals
19 20 and increased proliferation of mouse bone marrow
cells.21 22
---------------------------------------------------------------------------

    \16\ 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. This
type of leukemia may also involve erythroblastic cell types
(immature red blood cells). Lymphocytic leukemia involves the
lymphocyte type of white blood cells that are responsible for the
immune responses. Both nonlymphocytic and lymphocytic leukemia may,
in turn, be separated into acute (rapid and fatal) and chronic
(lingering, lasting) forms. For example; in acute myeloid leukemia
there is diminished production of normal red blood cells
(erythrocytes), granulocytes, and platelets (control clotting),
which leads to death by anemia, infection, or hemorrhage. These
events can be rapid. In chronic myeloid leukemia (CML) the leukemic
cells retain the ability to differentiate (i.e., be responsive to
stimulatory factors) and perform function; later there is a loss of
the ability to respond.
    \17\ U.S. EPA (1985) Environmental Protection Agency, Interim
quantitative cancer unit risk estimates due to inhalation of
benzene, prepared by the Office of Health and Environmental
Assessment, Carcinogen Assessment Group, Washington, DC, for the
Office of Air Quality Planning and Standards, Washington, DC, 1985.
    \18\ U.S. EPA. (1993). Motor Vehicle-Related Air Toxics Study.
Office of Mobile Sources, Ann Arbor, MI. http://www.epa .gov/otaq/

regs/toxics /tox--archive.htm.
    \19\ International Agency for Research on Cancer (IARC) (1982)
IARC monographs on the evaluation of carcinogenic risk of chemicals
to humans, Volume 29, Some industrial chemicals and dyestuffs,
International Agency for Research on Cancer, World Health
Organization, Lyon, France, p. 345-389.
    \20\ U.S. EPA (1998) Environmental Protection Agency,
Carcinogenic Effects of Benzene: An Update, National Center for
Environmental Assessment, Washington, DC. EPA600-P-97-001F. http://www.epa.gov
 /ncepihom/Catalog /EPA600P97001F.html.

    \21\ Irons, R.D., W.S. Stillman, D.B. Colagiovanni, and V.A.
Henry (1992) Synergistic action of the benzene metabolite
hydroquinone on myelopoietic stimulating activity of granulocyte/
macrophage colony-stimulating factor in vitro, Proc. Natl. Acad.
Sci. 89:3691-3695.
    \22\ U.S. EPA (1998) Environmental Protection Agency,
Carcinogenic Effects of Benzene: An Update, National Center for
Environmental Assessment, Washington, DC. EPA600-P-97-001F. http://www.epa.gov/ncepihom/Catalog/EPA600P97001F.html
.

---------------------------------------------------------------------------

    The latest assessment by EPA places the excess risk of developing
acute nonlymphocytic leukemia from inhalation exposure to benzene at
2.2 x 10-\6\ to 7.8 x 10-\6\ per [mu]g/m\3\. In
other words, there is a risk of about two to eight excess leukemia
cases in one million people exposed to 1 [mu]g/m\3\ of benzene over a
lifetime.\23\ This range of unit risks are the MLEs calculated from
different exposure assumptions and dose-response models that are linear
at low doses. At present, the true cancer risk from exposure to benzene
cannot be ascertained, even though dose-response data are used in the
quantitative cancer risk analysis, because of uncertainties in the low-
dose exposure scenarios and lack of clear understanding of the mode of
action. A range of estimates of risk is recommended, each having equal
scientific plausibility. There are confidence intervals associated with
the MLE range that reflect random variation of the observed data. For
the upper end of the MLE range, the 5th and 95th percentile values are
about a factor of 5 lower and higher than the best fit value. The upper
end of the MLE range was used in NATA.
---------------------------------------------------------------------------

    \23\ U.S. EPA (1998). Environmental Protection Agency,
Carcinogenic Effects of Benzene: An Update, National Center for
Environmental Assessment, Washington, DC. EPA600-P-97-001F. http://www.epa.gov/ncepihom/Catalog/EPA600P97001F.html
.

---------------------------------------------------------------------------

    It should be noted that not enough information is known to
determine the slope of the dose-response curve at environmental levels
of exposure and to provide a sound scientific basis to choose any
particular extrapolation/exposure model to estimate human cancer risk
at low doses. EPA risk assessment guidelines suggest using an
assumption of linearity of dose response when (1) there is an absence
of sufficient information on modes of action or (2) the mode of action
information indicates that the dose-response curve at low dose is or is
expected to be linear.\24\ Since the mode of action for benzene
carcinogenicity is unknown, the current cancer unit risk estimate
assumes linearity of the low-dose response. Data that were considered
by EPA in its carcinogenic update suggested that the dose-response
relationship at doses below those examined in the studies reviewed in
EPA's most recent benzene assessment may be supralinear. They support
the inference that cancer risks are as high or are higher than the
estimates provided in the existing EPA assessment.\25\ Data discussed
in the EPA IRIS assessment suggest that genetic abnormalities occur at
low exposure in humans, and the formation of toxic metabolites plateaus
above 25 ppm (80,000 [mu]g/m3).\26\ More recent data on
benzene adducts in humans, published after the most recent IRIS
assessment, suggest that the enzymes involved in benzene metabolism
start to saturate at exposure levels as low as 1 ppm.\27\ Because there
is a transition from linear to saturable metabolism below 1 ppm, the
assumption of low-dose linearity extrapolated from much higher
exposures could lead to substantial underestimation of leukemia risks.
This is consistent with recent epidemiological data which also suggest
a supralinear exposure-response relationship and which ``[extend]
evidence for hematopoietic cancer risks to levels substantially lower
than had previously been established.'' 28 29 These data are
from the largest cohort study done to date with individual worker
exposure estimates. However, these data have not yet been formally
evaluated by EPA as part of the IRIS review process, and it is not
clear whether these data provide sufficient evidence to reject a linear
dose-response curve. A better understanding of the biological mechanism
of benzene-induced leukemia is needed.
---------------------------------------------------------------------------

    \24\ U.S. EPA (2005) Guidelines for Carcinogen Risk Assessment.
Report No. EPA/630/P-03/001F. http://cfpub.epa.gov/ncea/raf/recordisplay.cfm?deid=116283
.

    \25\ U.S. EPA (1998) Carcinogenic Effects of Benzene: An Update.
EPA/600/P-97/001F.
    \26\ Rothman, N; Li, GL; Dosemeci, M; et al. (1996)
Hematotoxicity among Chinese workers heavily exposed to benzene. Am.
J. Indust. Med. 29:236-246.
    \27\ Rappaport, S.M.; Waidyanatha, S.; Qu, Q.; Shore, R.; Jin,
X.; Cohen, B.; Chen, L.; Melikian, A.; Li, G.; Yin, S.; Yan, H.; Xu,
B.; Mu, R.; Li, Y.; Zhang, X.; and Li, K. (2002) Albumin adducts of
benzene oxide and 1,4-benzoquinone as measures of human benzene
metabolism. Cancer Research 62:1330-1337.
    \28\ Hayes, R.B.; Yin, S.; Dosemeci, M.; Li, G.; Wacholder, S.;
Travis, L.B.; Li, C.; Rothman, N.; Hoover, R.N.; and Linet, M.S.
(1997) Benzene and the dose-related incidence of hematologic
neoplasms in China. J. Nat. Cancer Inst. 89:1065-1071.
    \29\ Hayes, R.B.; Songnian, Y.; Dosemeci, M.; and Linet, M.
(2001) Benzene and lymphohematopoietic malignancies in humans. Am.
J. Indust. Med. 40:117-126.
---------------------------------------------------------------------------

    Children may represent a subpopulation at increased risk from
benzene exposure, due to factors that could increase their
susceptibility. Children may have a higher unit body weight exposure
because of their heightened activity patterns which can increase their
exposures, as well as different ventilation tidal volumes and
frequencies, factors that influence uptake. This could entail a greater
risk of leukemia and other toxic effects to children if they are
exposed to benzene at similar levels as adults. There is limited
information from two studies regarding an increased risk to children
whose parents have been occupationally exposed to
benzene.30 31 Data from animal studies have shown benzene
exposures result in damage to the hematopoietic (blood cell formation)
system during development.32 33 34 Also, key changes related
to the development of childhood leukemia occur in the developing
fetus.\35\ Several studies have reported that genetic changes related
to eventual leukemia development occur before birth. For example, there
is one study of genetic changes in twins who developed T cell leukemia
at 9 years of

age.\36\ An association between traffic volume, residential proximity
to busy roads and occurrence of childhood leukemia has also been
identified in some studies, although some studies show no association.
---------------------------------------------------------------------------

    \30\ Shu, X.O,; Gao, Y.T.; Brinton, L.A.; et al. (1988) A
population-based case-control study of childhood leukemia in
Shanghai. Cancer 62:635-644.
    \31\ McKinney, P.A.; Alexander, F.E.; Cartwright, R.A.; et al.
(1991) Parental occupations of children with leukemia in west
Cumbria, north Humberside, and Gateshead, Br. Med. J. 302:681-686.
    \32\ Keller, KA; Snyder, CA. (1986) Mice exposed in utero to low
concentrations of benzene exhibit enduring changes in their colony
forming hematopoietic cells. Toxicology 42:171-181.
    \33\ Keller, KA; Snyder, CA. (1988) Mice exposed in utero to 20
ppm benzene exhibit altered numbers of recognizable hematopoietic
cells up to seven weeks after exposure. Fundam. Appl. Toxicol.
10:224-232.
    \34\ Corti, M; Snyder, CA. (1996) Influences of gender,
development, pregnancy and ethanol consumption on the hematotoxicity
of inhaled 10 ppm benzene. Arch. Toxicol. 70:209-217.
    \35\ U.S. EPA. (2002). Toxicological Review of Benzene
(Noncancer Effects). National Center for Environmental Assessment,
Washington, DC. Report No. EPA/635/R-02/001F. http://www.epa.gov/iris/toxreviews/0276-tr
[1].pdf.

    \36\ Ford, AM; Pombo-de-Oliveira, MS; McCarthy, KP; MacLean, JM;
Carrico, KC; Vincent, RF; Greaves, M. (1997) Monoclonal origin of
concordant T-cell malignancy in identical twins. Blood 89:281-285.
---------------------------------------------------------------------------

    A number of adverse noncancer health effects, including blood
disorders such as preleukemia and aplastic anemia, have also been
associated with long-term exposure to benzene.37 38 People
with long-term occupational exposure to benzene have experienced
harmful effects on the blood-forming tissues, especially in bone
marrow. These effects can disrupt normal blood production and suppress
the production of important blood components, such as red and white
blood cells and blood platelets, leading to anemia (a reduction in the
number of red blood cells), leukopenia (a reduction in the number of
white blood cells), or thrombocytopenia (a reduction in the number of
blood platelets, thus reducing the ability of blood to clot). Chronic
inhalation exposure to benzene in humans and animals results in
pancytopenia,\39\ a condition characterized by decreased numbers of
circulating erythrocytes (red blood cells), leukocytes (white blood
cells), and thrombocytes (blood platelets).40 41 Individuals
that develop pancytopenia and have continued exposure to benzene may
develop aplastic anemia, whereas others exhibit both pancytopenia and
bone marrow hyperplasia (excessive cell formation), a condition that
may indicate a preleukemic state.42 43 The most sensitive
noncancer effect observed in humans, based on current data, is the
depression of the absolute lymphocyte count in blood.44 45
---------------------------------------------------------------------------

    \37\ Aksoy, M. (1989) Hematotoxicity and carcinogenicity of
benzene. Environ. Health Perspect. 82:193-197.
    \38\ Goldstein, B.D. (1988) Benzene toxicity. Occupational
medicine. State of the Art Reviews 3: 541-554.
    \39\ 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).
In adults, all three major types of blood cells are produced in the
bone marrow of the vertebra, sternum, ribs, and pelvis. The bone
marrow contains immature cells, known as multipotent myeloid stem
cells, that later differentiate into the various mature blood cells.
Pancytopenia results from a reduction in the ability of the red bone
marrow to produce adequate numbers of these mature blood cells.
    \40\ 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.
    \41\ Goldstein, B.D. (1988) Benzene toxicity. Occupational
medicine. State of the Art Reviews 3: 541-554.
    \42\ Aksoy, M., S. Erdem, and G. Dincol. (1974) Leukemia in
shoe-workers exposed chronically to benzene. Blood 44:837.
    \43\ Aksoy, M. and K. Erdem. (1978) A follow-up study on the
mortality and the development of leukemia in 44 pancytopenic
patients associated with long-term exposure to benzene. Blood 52:
285-292.
    \44\ 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.
    \45\ EPA 2005 ``Full IRIS Summary for Benzene (CASRN 71-43-2)''
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/iris/subst/0276.htm
.

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    EPA's inhalation reference concentration (RfC) for benzene is 30
[mu]g/m3, based on suppressed absolute lymphocyte counts as
seen in humans under occupational exposure conditions. The overall
confidence in this RfC is medium. Since development of this RfC, there
have appeared human reports of benzene's hematotoxic effects in the
literature that provides data suggesting a wide range of hematological
endpoints that are affected at occupational exposures of less than 5
ppm (about 16 mg/m3) \46\ and even at air levels of 1 ppm
(about 3 mg/m3) or less among genetically susceptible
populations.\47\ One recent study found benzene metabolites in mouse
liver and bone marrow at environmental doses, indicating that even
concentrations in urban air can elicit a biochemical response in
rodents that indicates toxicity.\48\ EPA has not formally evaluated
these recent studies as part of the IRIS review process to determine
whether or not they will lead to a change in the current RfC. EPA does
not currently have an acute reference concentration for benzene. The
Agency for Toxic Substances and Disease Registry Minimal Risk Level for
acute exposure to benzene is 160 [mu]g/m3 for 1-14 days
exposure.
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    \46\ Qu, Q., R. Shore, G. Li, X. Jin, L.C. Chen, B. Cohen, et
al. (2002). Hematological changes among Chinese workers with a broad
range of benzene exposures. Am. J. Industr. Med. 42: 275-285.
    \47\ Lan, Qing, Zhang, L., Li, G., Vermeulen, R., et al. (2004).
Hematotoxically in Workers Exposed to Low Levels of Benzene. Science
306: 1774-1776.
    \48\ Turtletaub, K.W. and Mani, C. (2003). Benzene metabolism in
rodents at doses relevant to human exposure from Urban Air. Res Rep
Health Effect Inst 113.
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b. 1,3-Butadiene
    EPA has characterized 1,3-butadiene, a hydrocarbon, as a
leukemogen, carcinogenic to humans by inhalation.49 50 The
specific mechanisms of 1,3-butadiene-induced carcinogenesis are
unknown; however, it is virtually certain that the carcinogenic effects
are mediated by genotoxic metabolites of 1,3-butadiene. Animal data
suggest that females may be more sensitive than males for cancer
effects; nevertheless, there are insufficient data from which to draw
any conclusions on potentially sensitive subpopulations. The upper
bound cancer unit risk estimate is 0.08 per ppm or 3x10-5
per [mu]g/m3 (based primarily on linear modeling and
extrapolation of human data). In other words, it is estimated that
approximately 30 persons in one million exposed to 1 [mu]g/
m3 of 1,3-butadiene continuously for their lifetime would
develop cancer as a result of this exposure. The human incremental
lifetime unit cancer risk estimate is based on extrapolation from
leukemias observed in an occupational epidemiologic study.\51\ This
estimate includes a two-fold adjustment to the epidemiologic-based unit
cancer risk applied to reflect evidence from the rodent bioassays
suggesting that the epidemiologic-based estimate (from males) may
underestimate total cancer risk from 1,3-butadiene exposure in the
general population, particularly for breast cancer in females.
Confidence in the excess cancer risk estimate of 0.08 per ppm is
moderate.
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    \49\ U.S. EPA. (2002). Health Assessment of 1,3-Butadiene.
Office of Research and Development, National Center for
Environmental Assessment, Washington Office, Washington, DC. Report
No. EPA600-P-98-001F. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54499
.

    \50\ U.S. EPA (1998). A Science Advisory Board Report: Review of
the Health Risk Assessment of 1,3-Butadiene. EPA-SAB-EHC-98.
    \51\ Delzell, E, N. Sathiakumar, M. Macaluso, et al. (1995). A
follow-up study of synthetic rubber workers. Submitted to the
International Institute of Synthetic Rubber Producers. University of
Alabama at Birmingham. October 2, 1995.
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    1,3-Butadiene also causes a variety of reproductive and
developmental effects in mice; no human data on these effects are
available. The most sensitive effect was ovarian atrophy observed in a
lifetime bioassay of female mice.\52\ Based on this critical effect and
the benchmark concentration methodology, an RfC was calculated. This
RfC for chronic health effects is 0.9 ppb, or about 2 [mu]g/
m3. Confidence in the inhalation RfC is medium.
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    \52\ Bevan, C.; Stadler, J.C.; Elliot, G.S.; et al. (1996)
Subchronic toxicity of 4-vinylcyclohexene in rats and mice by
inhalation. Fundam. Appl. Toxicol. 32:1-10.
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c. Formaldehyde
    Since 1987, EPA has classified formaldehyde, a hydrocarbon, as a

probable human carcinogen based on evidence in humans and in rats,
mice, hamsters, and monkeys.\53\ Recently released research conducted
by the National Cancer Institute (NCI) found an increased risk of
nasopharyngeal cancer among workers exposed to
formaldehyde.54 55 A recent National Institute of
Occupational Safety and Health (NIOSH) study of garment workers also
found increased risk of death due to leukemia among workers exposed to
formaldehyde.\56\ In 2004, the working group of the International
Agency for Research on Cancer concluded that formaldehyde is
carcinogenic to humans (Group 1 classification), on the basis of
sufficient evidence in humans and sufficient evidence in experimental
animals--a higher classification than previous IARC evaluations. In
addition, the National Institute of Environmental Health Sciences
recently nominated formaldehyde for reconsideration as a known human
carcinogen under the National Toxicology Program. Since 1981 it has
been listed as a ``reasonably anticipated human carcinogen.''
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    \53\ U.S. EPA (1987). Assessment of Health Risks to Garment
Workers and Certain Home Residents from Exposure to Formaldehyde,
Office of Pesticides and Toxic Substances, April 1987.
    \54\ Hauptmann, M.; Lubin, J. H.; Stewart, P. A.; Hayes, R. B.;
Blair, A. 2003. Mortality from lymphohematopoetic malignancies among
workers in formaldehyde industries. Journal of the National Cancer
Institute 95: 1615-1623.
    \55\ Hauptmann, M.; Lubin, J. H.; Stewart, P. A.; Hayes, R. B.;
Blair, A. 2004. Mortality from solid cancers among workers in
formaldehyde industries. American Journal of Epidemiology 159: 1117-
1130.
    \56\ Pinkerton, L. E. 2004. Mortality among a cohort of garment
workers exposed to formaldehyde: an update. Occup. Environ. Med. 61:
193-200.
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    In the past 15 years there has been substantial research on the
inhalation dosimetry for formaldehyde in rodents and primates by the
CIIT Centers for Health Research, with a focus on use of rodent data
for refinement of the quantitative cancer dose-response
assessment.57 58 59 CIIT's risk assessment of formaldehyde
incorporated mechanistic and dosimetric information on formaldehyde.
The risk assessment analyzed carcinogenic risk from inhaled
formaldehyde using approaches that are consistent with EPA's draft
guidelines for carcinogenic risk assessment. In 2001, Environment
Canada relied on this cancer dose-response assessment in their
assessment of formaldehyde.\60\ In 2004, EPA also relied on this cancer
unit risk estimate during the development of the plywood and composite
wood products national emissions standards for hazardous air pollutants
(NESHAPs).\61\ In these rules, EPA concluded that the CIIT work
represented the best available application of the available mechanistic
and dosimetric science on the dose-response for portal of entry cancers
due to formaldehyde exposures. EPA is reviewing the recent work cited
above from the NCI and NIOSH, as well as the analysis by the CIIT
Centers for Health Research and other studies, as part of a
reassessment of the human hazard and dose-response associated with
formaldehyde.
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    \57\ Conolly, RB, JS Kimbell, D Janszen, PM Schlosser, D
Kalisak, J Preston, and FJ Miller. 2003. Biologically motivated
computational modeling of formaldehyde carcinogenicity in the F344
rat. Tox. Sci. 75: 432-447.
    \58\ Conolly, RB, JS Kimbell, D Janszen, PM Schlosser, D
Kalisak, J Preston, and FJ Miller. 2004. Human respiratory tract
cancer risks of inhaled formaldehyde: Dose-response predictions
derived from biologically-motivated computational modeling of a
combined rodent and human dataset. Tox. Sci. 82: 279-296.
    \59\ Chemical Industry Institute of Toxicology (CIIT). 1999.
Formaldehyde: Hazard characterization and dose-response assessment
for carcinogenicity by the route of inhalation. CIIT, September 28,
1999. Research Triangle Park, NC.
    \60\ Health Canada. 2001. Priority Substances List Assessment
Report. Formaldehyde. Environment Canada, Health Canada, February
2001.
    \61\ U.S. EPA. 2004. National Emission Standards for Hazardous
Air Pollutants for Plywood and Composite Wood Products Manufacture:
Final Rule. (69 FR 45943, 7/30/04).
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    Noncancer effects of formaldehyde have been observed in humans and
several animal species and include irritation to eye, nose and throat
tissues in conjunction with increased mucous secretions.
d. Acetaldehyde
    Acetaldehyde, a hydrocarbon, is classified in EPA's IRIS database
as a probable human carcinogen and is considered moderately toxic by
inhalation.\62\ Based on nasal tumors in rodents, the upper confidence
limit estimate of a lifetime extra cancer risk from continuous
acetaldehyde exposure is about 2.2x10-\6\ per [mu]g/m\3\. In
other words, it is estimated that about 2 persons in one million
exposed to 1 [mu]g/m\3\ acetaldehyde continuously for their lifetime
(70 years) would develop cancer as a result of their exposure, although
the risk could be as low as zero. In short-term (4 week) rat studies,
compound-related histopathological changes were observed only in the
respiratory system at various concentration levels of
exposure.63 64 Data from these studies showing degeneration
of the olfactory epithelium were found to be sufficient for EPA to
develop an RfC for acetaldehyde of 9 [mu]g/m\3\. Confidence in the
principal study is medium and confidence in the database is low, due to
the lack of chronic data establishing a no observed adverse effect
level and due to the lack of reproductive and developmental toxicity
data. Therefore, there is low confidence in the RfC. The agency is
currently conducting a reassessment of risk from inhalation exposure to
acetaldehyde.
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    \62\ U.S. EPA. 1988. Integrated Risk Information System File of
Acetaldehyde. This material is available electronically at http://www.epa.gov/iris/subst/0290.htm
.

    \63\ Appleman, L. M., R. A. Woutersen, V. J. Feron, R. N.
Hooftman, and W. R. F. Notten. (1986). Effects of the variable
versus fixed exposure levels on the toxicity of acetaldehyde in
rats. J. Appl. Toxicol. 6: 331-336.
    \64\ Appleman, L.M., R.A. Woutersen, and V.J. Feron. (1982).
Inhalation toxicity of acetaldehyde in rats. I. Acute and subacute
studies. Toxicology. 23: 293-297.
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    The primary acute effect of exposure to acetaldehyde vapors is
irritation of the eyes, skin, and respiratory tract.\65\ Some
asthmatics have been shown to be a sensitive subpopulation to
decrements in functional expiratory volume (FEV1 test) and
bronchoconstriction upon acetaldehyde inhalation.\66\
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    \65\ U.S. EPA (1988). Integrated Risk Information System File of
Acetaldehyde. This material is available electronically at http://www.epa.gov/iris/subst/0290.htm
.

    \66\ Myou, S.; Fujimura, M.; Nishi K.; Ohka, T.; and Matsuda, T.
(1993) Aerosolized acetaldehyde induces histamine-mediated
bronchoconstriction in asthmatics. Am. Rev. Respir.Dis.148(4 Pt 1):
940-3.
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e. Acrolein
    Acrolein, a hydrocarbon, is intensely irritating to humans when
inhaled, with acute exposure resulting in upper respiratory tract
irritation and congestion. The Agency has developed an RfC for acrolein
of 0.02 [mu]g/m\3\.\67\ The overall confidence in the RfC assessment is
judged to be medium. The Agency is also currently in the process of
conducting an assessment of acute health effects for acrolein. EPA
determined in 2003 using the 1999 draft cancer guidelines that the
human carcinogenic potential of acrolein could not be determined
because the available data were inadequate. No information was
available on the carcinogenic effects of acrolein in humans and the
animal data provided inadequate evidence of carcinogenicity.
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    \67\ U.S. Environmental Protection Agency (2003) Integrated Risk
Information System (IRIS) on Acrolein. National Center for
Environmental Assessment, Office of Research and Development,
Washington, D.C. 2003. This material is available electronically at
http://www.epa.gov/iris/subst/0364.htm.

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f. Polycyclic Organic Matter (POM)
    POM is generally defined as a large class of organic compounds
which have multiple benzene rings and a boiling point greater than 100
degrees Celsius. Many of the compounds included in the class of
compounds known as POM are classified by EPA as probable human
carcinogens based on animal data. One

of these compounds, naphthalene, is discussed separately below.
    Polycyclic aromatic hydrocarbons (PAHs) are a chemical subset of
POM. In particular, EPA frequently obtains data on 16 of these POM
compounds. Recent studies have found that maternal exposures to PAHs in
a population of pregnant women were associated with several adverse
birth outcomes, including low birth weight and reduced length at
birth.\68\ These studies are discussed in the Regulatory Impact
Analysis.
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    \68\ Perara, F.P.; Rauh, V.; Tsai, W-Y.; et al. (2002) Effect of
transplacental exposure to environmental pollutants on birth
outcomes in a multiethnic population. Environ Health Perspect. 111:
201-205.
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g. Naphthalene
    Naphthalene is a PAH compound consisting of two benzene rings fused
together with two adjacent carbon atoms common to both rings. In 2004,
EPA released an external review draft (External Review Draft, IRIS
Reassessment of the Inhalation Carcinogenicity of Naphthalene, U.S.
EPA. http://www.epa.gov/iris) of a reassessment of the inhalation

carcinogenicity of naphthalene.\69\ The draft reassessment completed
external peer review in 2004 by Oak Ridge Institute for Science and
Education.\70\ Based on external comments, additional analyses are
being considered. California EPA has also released a new risk
assessment for naphthalene with a cancer unit risk estimate of
3x10-\5\ per [mu]g/m\3\.\71\ The California EPA value was
used in the 1999 NATA and in the analyses done for this rule. In
addition, IARC has reevaluated naphthalene and re-classified it as
Group 2B: possibly carcinogenic to humans.\72\ The cancer data form the
basis of an inhalation RfC of 3 [mu]g/m\3\.\73\ A low to medium
confidence rating was given to this RfC, in part because it cannot be
said with certainty that this RfC will be protective for hemolytic
anemia and cataracts, the more well-known human effects from
naphthalene exposure.
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    \69\ U.S. EPA. (2004) External Review Draft, IRIS Reassessment
of the Inhalation Carcinogenicity of Naphthalene. http://www.epa.gov/iris
    \70\ Oak Ridge Institute for Science and Education. (2004)

External Peer Review for the IRIS Reassessment of the Inhalation
Carcinogenicity of Naphthalene. August 2004. http://cfpub2.epa.gov/ncea/cfm/recordisplay.cfm?deid=86019
    \71\ California EPA. (2004) Long Term Health Effects of Exposure

to Naphthalene. Office of Environmental Health Hazard Assessment.
http://www.oehha.ca.gov/air/toxic_contaminants/draftnaphth.html
    \72\ International Agency for Research on Cancer (IARC). (2002)

Monographs on the Evaluation of the Carcinogenic Risk of Chemicals
for Humans. Vol. 82. Lyon, France.
    \73\ EPA 2005 ``Full IRIS Summary for Naphthalene (CASRN 91-20-
3)'' 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/iris/subst/0436.htm
.

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h. Diesel Particulate Matter and Diesel Exhaust Organic Gases
    In EPA's Diesel Health Assessment Document (HAD),\74\ diesel
exhaust was classified as likely to be carcinogenic to humans by
inhalation at environmental exposures, in accordance with the revised
draft 1996/1999 EPA cancer guidelines. A number of other agencies
(National Institute for Occupational Safety and Health, the
International Agency for Research on Cancer, the World Health
Organization, California EPA, and the U.S. Department of Health and
Human Services) have made similar classifications. EPA concluded in the
Diesel HAD that it is not possible currently to calculate a cancer unit
risk for diesel exhaust due to a variety of factors that limit the
current studies, such as limited quantitative exposure histories in
occupational groups investigated for lung cancer.
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    \74\ U.S. EPA (2002) Health Assessment Document for Diesel
Engine Exhaust. EPA/600/8-90/057F Office of Research and
Development, Washington DC. This document is available
electronically at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=29060
.

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    However, in the absence of a cancer unit risk, the EPA Diesel HAD
sought to provide additional insight into the significance of the
cancer hazard by estimating possible ranges of risk that might be
present in the population. The possible risk range analysis was
developed by comparing a typical environmental exposure level for
highway diesel sources to a selected range of occupational exposure
levels. The occupationally observed risks were then proportionally
scaled according to the exposure ratios to obtain an estimate of the
possible environmental risk. A number of calculations are needed to
accomplish this, and these can be seen in the EPA Diesel HAD. The
outcome was that environmental risks from diesel exhaust exposure could
range from a low of 10-\4\ to 10-\5\ to as high
as 10-\3\, reflecting the range of occupational exposures
that could be associated with the relative and absolute risk levels
observed in the occupational studies. Because of uncertainties, the
analysis acknowledged that the risks could be lower than
10-\4\ or 10-\5\, and a zero risk from diesel
exhaust exposure was not ruled out.
    The acute and chronic exposure-related effects of diesel exhaust
emissions are also of concern to the Agency. EPA derived an RfC from
consideration of four well-conducted chronic rat inhalation studies
showing adverse pulmonary effects.75 76 77 78 The RfC is 5
[mu]g/m\3\ for diesel exhaust as measured by diesel PM. This RfC does
not consider allergenic effects such as those associated with asthma or
immunologic effects. There is growing evidence, discussed in the Diesel
HAD, that diesel exhaust can exacerbate these effects, but the
exposure-response data are presently lacking to derive an RfC.
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    \75\ Ishinishi, N; Kuwabara, N; Takaki, Y; et al. (1988) Long-
term inhalation experiments on diesel exhaust. In: Diesel exhaust
and health risks. Results of the HERP studies. Ibaraki, Japan:
Research Committee for HERP Studies; pp. 11-84.
    \76\ Heinrich, U; Fuhst, R; Rittinghausen, S; et al. (1995)
Chronic inhalation exposure of Wistar rats and two different strains
of mice to diesel engine exhaust, carbon black, and titanium
dioxide. Inhal. Toxicol. 7:553-556.
    \77\ Mauderly, JL; Jones, RK; Griffith, WC; et al. (1987) Diesel
exhaust is a pulmonary carcinogen in rats exposed chronically by
inhalation. Fundam. Appl. Toxicol. 9:208-221.
    \78\ Nikula, KJ; Snipes, MB; Barr, EB; et al. (1995) Comparative
pulmonary toxicities and carcinogenicities of chronically inhaled
diesel exhaust and carbon black in F344 rats. Fundam. Appl. Toxicol.
25:80-94.
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    The Diesel HAD also briefly summarizes health effects associated
with ambient PM and the EPA's annual National Ambient Air Quality
Standard (NAAQS) of 15 [mu]g/m\3\. There is a much more extensive body
of human data showing a wide spectrum of adverse health effects
associated with exposure to ambient PM, of which diesel exhaust is an
important component. The RfC is not meant to say that 5 [mu]g/m\3\
provides adequate public health protection for ambient
PM2.5. In fact, there may be benefits to reducing diesel PM
below 5 [mu]g/m\3\ since diesel PM is a major contributor to ambient
PM2.5.

E. Gasoline PM

    Beyond the specific areas of quantifiable risk discussed above in
section III.C, EPA is also currently investigating gasoline PM.
Gasoline exhaust is a complex mixture that has not been evaluated in
EPA's IRIS, in contrast to diesel exhaust, which has been evaluated in
IRIS. However, there is evidence for the mutagenicity and cytotoxicity
of gasoline exhaust and gasoline PM. Seagrave et al. investigated the
combined particulate and semivolatile organic fractions of gasoline
engine emissions.\79\ Their results demonstrate that emissions from
gasoline engines are mutagenic and can induce inflammation and have
cytotoxic effects. Gasoline exhaust is a ubiquitous

source of particulate matter, contributing to the health effects
observed for ambient PM which is discussed extensively in the EPA
Particulate Matter Criteria Document.\80\ The PM Criteria Document
notes that the PM components of gasoline and diesel engine exhaust are
hypothesized, important contributors to the observed increases in lung
cancer incidence and mortality associated with ambient
PM2.5.\81\ Gasoline PM is also a component of near-roadway
emissions that may be contributing to the health effects observed in
people who live near roadways (see section III.F).
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    \79\ Seagrave, J.; McDonald, J.D.; Gigliotti, A.P.; Nikula,
K.J.; Seilkop, S.K.; Gurevich, M. and Mauderly, J.L. (2002)
Mutagenicity and in Vivo Toxicity of Combined Particulate and
Semivolatile Organic Fractions of Gasoline and Diesel Engine
Emissions. Toxicological Sciences 70:212-226.
    \80\ U.S. Environmental Protection Agency (2004) Air Quality
Criteria for Particulate Matter. Research Triangle Park, NC:
National Center for Environmental Assessment--RTP Office; Report No.
EPA/600/P-99/002aF (PM Criteria Document).
    \81\ PM Criteria Document, p. 8-318.
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    EPA is working to improve the understanding of PM emissions from
gasoline engines, including the potential range of emissions and
factors that influence emissions. EPA led a cooperative test program
that recently completed testing approximately 500 randomly procured
vehicles in the Kansas City metropolitan area. The purpose of this
study was to determine the distribution of gasoline PM emissions from
the in-use light-duty fleet. Results from this study are expected to be
available in 2006. Some source apportionment studies show gasoline and
diesel PM can result in larger contributions to ambient PM than
predicted by EPA emission inventories.82 83 These source
apportionment studies were one impetus behind the Kansas City study.
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    \82\ Fujita, E.; Watson, M.J.; Chow, M.C.; et al. (1998)
Northern Front Range Air Quality Study, Volume C: Source
apportionment and simulation methods and evaluation. Prepared for
Colorado State University, Cooperative Institute for Research in the
Atmosphere, by Desert Research Institute, Reno, NV.
    \83\ Schauer, J.J.; Rogge, W.F.; Hildemann, L.M.; et al. (1996)
Source apportionment of airborne particulate matter using organic
compounds as tracers. Atmos. Environ. 30(22):3837-3855.
---------------------------------------------------------------------------

    Another issue related to gasoline PM is the effect of gasoline
vehicles and engines on ambient PM, especially secondary PM. Ambient PM
is composed of primary PM emitted directly into the atmosphere and