# Control of Hazardous Air Pollutants From Mobile Sources > Briefs, arguments, decisions, and more. URL: https://www.frixlaw.com/law-library/documents/fr%3A06-2315 ## Record - **Collection:** Federal Register - **Document type:** Proposed Rule - **Published:** March 29, 2006 - **Citation:** 71 FR 15804 ## Text 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. 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: (202) 566-1741. • 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 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 www.regulations.gov or e-mail. The 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 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 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 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 (202) 566-1744, and the telephone number for the Air Docket is (202) 566-1742. Hearing: The public hearing will be held at Sheraton Crystal City Hotel, 1800 Jefferson Davis Highway, Arlington, Virginia 22202, Telephone: (703) 486-1111. 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: (734) 214-4584; fax number: (734) 214-4816; email address: lieske.christopher@epa.gov , or Assessment and Standards Division Hotline; telephone number: (734) 214-4636; e-mail address: asdinfo@epa.gov . 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: Category NAICS codes a SIC codes b Examples of potentially affected entities 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 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 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 PM 2.5 Levels 4. Current PM 10 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. PM 2.5 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. PM 2.5 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 PM 2.5 ) by over 1 million tons in 2030. The proposed vehicle standards would reduce direct PM 2.5 emissions by 20,000 tons in 2030 and would also reduce secondary formation of PM 2.5 . Although ozone and PM 2.5 are considered criteria pollutants rather than “air toxics,” reductions in ozone and PM 2.5 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 PM 2.5 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 PM 2.5 , 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. 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 °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 °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 °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 (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 benzene) Nitrate. Acetaldehyde Cyclohexane N-Nitrosodiethylamine. Acetone Cyclohexanone N-Nitrosodimethylamine. Acetophenone Di(2-ethylhexyl)phthalate N-Nitroso-di-n-butylamine. Acrolein (2-propenal) Dibenz[a,h]anthracene N-Nitrosodi-N-propylamine. Ammonia Dibutyl phthalate N-Nitrosopyrrolidine. Anthracene Dichloromethane Pentachlorophenol. Antimony Diesel PM and Diesel exhaust organic gases Phenol. Arsenic, inorganic Diethyl phthalate Phosphorus. Barium and compounds Ethylbenzene Phthalic anhydride. Benz[a]anthracene Ethylene glycol monobutyl ether Pyrene. Benzaldehyde Fluoranthene Selenium and compounds. Benzene Fluorene Silver. Benzo[a]pyrene (BaP) Formaldehyde Strontium. Benzo[b]fluoranthene Furfural Styrene. Benzo[k]fluoranthene Hexachlorodibenzo-p-dioxin, mixture (dioxin/furans) Tetrachloroethylene. Benzoic acid n-Hexane Toluene. Beryllium and compounds Hydrogen cyanide Trichlorofluoromethane. Boron (Boron and Borates only) Hydrogen sulfide Vanadium. Bromomethane Indeno[1,2,3-cd]pyrene Xylenes. Butyl benzyl phthalate Lead and compounds (inorganic) Zinc and compounds. * 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 1999 NATA risk drivers Percent contribution from all mobile sources (percent) Percent contribution from on-road mobile sources (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 gases 100 38 * 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 ( 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 μg/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 × 10 − 6 to 7.8 × 10 − 6 per μg/m 3 . In other words, there is a risk of about two to eight excess leukemia cases in one million people exposed to 1 μg/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 μg/m 3 ). 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. EPA's inhalation reference concentration (RfC) for benzene is 30 μg/m 3 , 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/m 3 ) 46 and even at air levels of 1 ppm (about 3 mg/m 3 ) 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 μg/m 3 for 1-14 days exposure. 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. 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 3×10 −5 per μg/m 3 (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 μg/m 3 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. 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. 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 μg/m 3 . Confidence in the inhalation RfC is medium. 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. 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.” 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. 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. 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). 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 2.2×10 − 6 per μg/m 3 . In other words, it is estimated that about 2 persons in one million exposed to 1 μg/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 μg/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. 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. 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 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. 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 μg/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. 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 . 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. 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. 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 3×10 − 5 per μg/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 μg/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. 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 . 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. 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 . 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 μg/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. 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. 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 μg/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 μg/m 3 provides adequate public health protection for ambient PM 2.5 . In fact, there may be benefits to reducing diesel PM below 5 μg/m 3 since diesel PM is a major contributor to ambient PM 2.5 . 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 PM 2.5 . 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). 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. 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. 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 secondary PM that is formed from chemical reactions in the atmosphere. The issue of secondary organic aerosol formation from aromatic precursors is an important one to which EPA and others are paying significant attention. This is discussed in more detail in Section 1.4.1 of the RIA. F. Near-Roadway Health Effects Over the years there have been a large number of studies that have examined associations between living near major roads and different adverse health endpoints. These studies generally examine people living near heavily-trafficked roadways, typically within several hundred meters, where fresh emissions from motor vehicles are not yet fully diluted with background air. Several studies have measured elevated concentrations of pollutants emitted directly by motor vehicles near road as compared to overall urban background levels. These elevated concentrations generally occur within approximately 200 meters of the road, although the distance may vary depending on traffic and environmental conditions. Pollutants measured with elevated concentrations include benzene, polycyclic aromatic hydrocarbons, carbon monoxide, nitrogen dioxide, black carbon, and coarse, fine, and ultrafine particulate matter. In addition, concentrations of road dust, and wear particles from tire and brake use also show concentration increases in proximity of major roadways. The near-roadway health studies provide stronger evidence for some health endpoints than others. Evidence of adverse responses to traffic-related pollution is strongest for non-allergic respiratory symptoms, cardiovascular effects, premature adult mortality, and adverse birth outcomes, including low birth weight and size. Some evidence for new onset asthma is available, but not all studies have significant orrelations. Lastly, among studies of childhood cancer, in particular childhood leukemia, evidence is inconsistent. Several small studies report positive associations, though such effects have not been observed in two larger studies. As described above, benzene and 1,3-butadiene are both known human leukemogens in adults. As previously mentioned, there is evidence of increased risk of leukemia among children whose parents have been occupationally exposed to benzene. Though the near-roadway studies are equivocal, taken together with the laboratory studies and other exposure environments, the data suggest a potentially serious children's health concern could exist. Additional research is needed to determine the significance of this potential concern. Significant scientific uncertainties remain in our understanding of the relationship between adverse health effects and near-road exposure, including the exposures of greatest concern, the importance of chronic versus acute exposures, the role of fuel type (e.g. diesel or gasoline) and composition (e.g., % aromatics), relevant traffic patterns, the role of co-stressors including noise and socioeconomic status, and the role of differential susceptibility within the “exposed” populations. For a more detailed discussion, see Chapter 3 of the Regulatory Impact Analysis. These studies provide qualitative evidence that reducing emissions from on-road mobile sources will provide public health benefits beyond those that can be quantified using currently available information. G. How Would This Proposal Reduce Emissions of MSATs? The benzene and hydrocarbon standards proposed in this action would reduce benzene, 1,3-butadiene, formaldehyde, acrolein, polycyclic organic matter, and naphthalene, as well as many other hydrocarbon compounds that are emitted by motor vehicles, including those that are listed in Table III.B-1 and discussed in more detail in Chapter 1 of the RIA. The emission reductions expected from today's controls are reported in section V.E of this preamble and Chapter 2 of the RIA. EPA believes that the emission reductions from the standards proposed today for motor vehicles and their fuels, combined with the standards currently in place, represent the maximum achievable reductions of emissions from motor vehicles through the application of technology that will be available, considering costs and the other factors listed in section 202(l)(2). This conclusion applies whether you consider just the compounds listed in Table III.B-1, or consider all of the compounds on the Master List of emissions, given the breadth of EPA's current and proposed control programs and the broad groups of emissions that many of the control technologies reduce. EPA has already taken significant steps to reduce diesel emissions from mobile sources. We have adopted stringent standards for on-highway 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 [Text truncated at 120,000 characters. The full text is on the page linked above.] --- Source: Frix Law Library, https://www.frixlaw.com/law-library/documents/fr%3A06-2315. Public record. Not legal advice.