# Control of Hazardous Air Pollutants From Mobile Sources > Briefs, arguments, decisions, and more. URL: https://www.frixlaw.com/law-library/documents/fr%3AE7-2667 ## Record - **Collection:** Federal Register - **Document type:** Rule - **Published:** February 26, 2007 - **Citation:** 72 FR 8428 ## Text ENVIRONMENTAL PROTECTION AGENCY 40 CFR Parts 59, 80, 85, and 86 [EPA-HQ-OAR-2005-0036; FRL-8278-4] RIN 2060-AK70 Control of Hazardous Air Pollutants From Mobile Sources AGENCY: Environmental Protection Agency (EPA). ACTION: Final rule. SUMMARY: EPA is adopting controls on gasoline, passenger vehicles, and portable fuel containers (primarily gas cans) that will 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 limiting the benzene content of gasoline to an annual refinery average of 0.62% by volume, beginning in 2011. In addition, for gasoline, we are establishing a maximum average standard for refineries of 1.3% by volume beginning on July 1, 2012, which acts as an upper limit on gasoline benzene content when credits are used to meet the 0.62 volume % standard. We are also limiting exhaust emissions of hydrocarbons from passenger vehicles when they are operated at cold temperatures. This standard will be phased in from 2010 to 2015. For passenger vehicles, we are also adopting evaporative emissions standards that are equivalent to those currently in effect in California. Finally, we are adopting a hydrocarbon emissions standard for portable fuel containers beginning in 2009, which will reduce evaporation and spillage of gasoline from these containers. These controls will significantly reduce emissions of benzene and other mobile source air toxics such as 1,3-butadiene, formaldehyde, acetaldehyde, acrolein, and naphthalene. There will be additional substantial benefits to public health and welfare because of significant reductions in emissions of particulate matter from passenger vehicles. DATES: This rule is effective on April 27, 2007. ADDRESSES: EPA has established a docket for this action under Docket ID No. EPA-HQ-2005-0036. All documents in the docket are listed on the www.regulations.gov Web site. 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, is not placed on the Internet and will be publicly available only in hard copy form. Publicly available docket materials are available either electronically through http://www.regulations.gov or in hard copy at the Air Docket, EPA/DC, EPA West, Room 3334, 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. 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; e-mail address: lieske.christopher@epa.gov, or Assessment and Standards Division Hotline; telephone number: (734) 214-4636; e-mail address: asdinfo@epa.gov . SUPPLEMENTARY INFORMATION: 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 will 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 332431 3089 3411 Portable fuel container manufacturers. 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. Outline of This Preamble I. Summary II. Overview of Final Rule A. Light-Duty Vehicle Emission Standards B. Gasoline Fuel Standards C. Portable Fuel Container (PFC) Controls III. Why Is EPA Taking This Action? A. Statutory Requirements 1. Clean Air Act Section 202(l) 2. Clean Air Act Section 183(e) 3. Energy Policy Act B. Public Health Impacts of Mobile Source Air Toxics (MSATs) 1. What Are MSATs? 2. Health Risk Associated With MSATs a. National Cancer Risk b. National Risk of Noncancer Health Effects c. Exposure Near Roads d. Exposure From Attached Garages 3. What Are the Health Effects of Air Toxics? a. Overview of Potential Cancer and Noncancer Health Effects b. Health Effects of Key MSATs i. Benzene ii. 1,3-Butadiene iii. Formaldehyde iv. Acetaldehyde v. Acrolein vi. Polycyclic Organic Matter (POM) vii. Naphthalene viii. Diesel Exhaust c. Gasoline PM d. Near-Roadway Health Effects C. Ozone 1. Background 2. Health Effects of Ozone 3. Plant and Ecosystem Effects of Ozone 4. Current and Projected 8-hour Ozone Levels D. Particulate Matter 1. Background 2. Health Effects of PM 3. Welfare Effects of PM a. Visibility i. Background ii Current Visibility Impairment iii. Future Visibility Impairment b. Atmospheric Deposition c. Materials Damage and Soiling 4. Current and Projected PM 2.5 Levels 5. Current PM 10 Levels IV. What Are the Emissions, Air Quality, and Public Health Impacts of This Rule? A. Emissions Impacts of All Rule Provisions Combined 1. How Will MSAT Emissions Be Reduced? 2. How Will VOC Emissions Be Reduced? 3. How Will PM Emissions Be Reduced? B. Emission Impacts by Provision 1. Vehicle Controls a. Volatile Organic Compounds (VOC) b. Toxics c. PM 2.5 2. Fuel Benzene Standard 3. PFC Standards a. VOC b. Toxics C. What Are the Air Quality, Exposure, and Public Health Impacts of This Rule? 1. Mobile Source Air Toxics 2. Ozone 3. PM D. What Other Mobile Source Emissions Control Programs Reduce MSATs? 1. Fuels Programs a. Gasoline Sulfur b. Gasoline Volatility c. Diesel Fuel d. Phase-Out of Lead in Gasoline 2. Highway Vehicle and Engine Programs 3. Nonroad Engine Programs 4. Voluntary Programs 5. Additional Programs Under Development That Will Reduce MSATs a. On-Board Diagnostics for Heavy-Duty Vehicles Over 14,000 Pounds b. Standards for Small Nonroad Spark-Ignition Engines c. Standards for Locomotive and Marine Diesel Engines E. How Do These Mobile Source Programs Satisfy the Requirements of Clean Air Act Section 202(l)? V. New Light-duty Vehicle Standards A. Introduction B. What Cold Temperature Requirements Are We Adopting? 1. Why Are We Adopting a New Cold Temperature NMHC Standard? 2. What Are the New NMHC Exhaust Emissions Standards? 3. Feasibility of the Cold Temperature NMHC Standards a. Currently Available Emission Control Technologies b. Feasibility Considering Current Certification Levels, Deterioration and Compliance Margin c. Feasibility and Test Programs 4. Standards Timing and Phase-In a. Phase-In Schedule b. Alternative Phase-In Schedules 5. Certification Levels 6. 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 Can Be Carried Forward f. Voluntary Heavy-Duty Vehicle Credit Program 7. Additional Vehicle Cold Temperature Standard Provisions a. Applicability b. Useful Life c. High Altitude d. In-Use Standards for Vehicles Produced During Phase-In 8. Monitoring and Enforcement C. What Evaporative Emissions Standards Are We Finalizing? 1. Current Controls and Feasibility of the New Standards 2. Evaporative Standards Timing 3. Timing for Flex Fuel Vehicles 4. In-Use Evaporative Emission Standards 5. Existing Differences Between California and Federal Evaporative Emission Test Procedures D. 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) VI. Gasoline Benzene Control Program A. Description of and Rationale for the Gasoline Benzene Control Program 1. Gasoline Benzene Content Standard a. Description of the Average Benzene Content Standard b. Why Are We Finalizing a Benzene Content Standard? i. Standards That Would Include Toxics Other Than Benzene ii. Control of Gasoline Sulfur and/or Volatility for MSAT Reduction iii. Diesel Fuel Changes c. Why Are We Finalizing a Level of 0.62 vol% for the Average Benzene Standard? i. General Technological Feasibility of Benzene Control ii. Appropriateness of the 0.62 vol% Average Benzene Content Standard iii. Timing of the Average Standard d. Upper Limit Benzene Standard 2. Description of the Averaging, Banking, and Trading (ABT) Program a. Overview b. Credit Generation i. Eligibility ii. Early Credit Generation iii. Standard Credit Generation c. Credit Use i. Early Credit Life ii. Standard Credit Life iii. Consideration of Unlimited Credit Life iv. Credit Trading Provisions 3. Provisions for Small Refiners and Refiners Facing Hardship Situations a. Provisions for Small Refiners i. Definition of Small Refiner for Purposes of the MSAT2 Small Refiner Provisions ii. Small Refiner Status Application Requirements iii. Small Refiner Provisions iv. The Effect of Financial and Other Transactions on Small Refiner Status and Small Refiner Relief Provisions b. Provisions for Refiners Facing Hardship Situations i. Temporary Waivers Based on Extreme Hardship Circumstances ii. Temporary Waivers Based on Unforeseen Circumstances c. Option for Early Compliance in Certain Circumstances B. How Will the Gasoline Benzene Standard Be Implemented? 1. General Provisions 2. Small Refiner Status Application Requirements 3. Administrative and Enforcement Provisions a. Sampling/Testing b. Recordkeeping/Reporting C. How Will the Program Relate to Other Fuel-Related Toxics Programs? D. How Does This Program Satisfy the Statutory Requirements of Clean Air Act Section 202(l)(2)? VII. Portable Fuel Containers A. What Are the New HC Emissions Standards for PFCs? 1. Description of Emissions Standard 2. Determination of Best Available Control 3. Diesel, Kerosene and Utility Containers 4. Automatic Shut-Off B. Timing of Standard C. 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 D. What Certification and In-Use Compliance Provisions Is EPA Adopting? 1. Certification 2. Emissions Warranty and In-Use Compliance 3. Labeling E. How Would State Programs Be Affected by EPA Standards? F. Provisions for Small PFC Manufacturers 1. First Type of Hardship Provision 2. Second Type of Hardship Provision VIII. What Are the Estimated Impacts of the Rule? A. Refinery Costs of Gasoline Benzene Reduction 1. Methodology a. Overview of the Benzene Program Cost Methodology b. Changes to the Cost Estimation Methodology Used in the Proposed Rule c. Linear Programming Cost Model d. Refinery-by-Refinery Cost Model e. Price of Chemical Grade Benzene 2. Summary of Costs a. Nationwide Costs of the Final Benzene Control Program b. Regional Costs c. Refining Industry Cost Study B. What Are the Vehicle Cost Impacts? C. What Are the PFC 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 Final 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 Final 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? IX. Public Participation X. 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. The Need for and Objectives of This Rule 3. Summary of the Significant Issues Raised by the Public Comments 4. Summary of Regulated Small Entities a. Highway Light-Duty Vehicles b. Gasoline Refiners c. Portable Fuel Container Manufacturers 5. Description of the Reporting, Recordkeeping, and Other Compliance Requirements of the Rule 6. Relevant Federal Rules 7. Steps Taken To Minimize the Significant Economic Impact on Small Entities a. Significant Panel Findings b. Outreach With Small Entities (and the Panel Process) c. Small Business Flexibilities i. Highway Light-Duty Vehicles ii. Gasoline Refiners iii. Portable Fuel Containers 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 K. Congressional Review Act XI. Statutory Provisions and Legal Authority I. Summary Mobile sources emit air toxics (also known as “hazardous air pollutants”) that can cause cancer and other serious 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. 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 gas-phase hydrocarbons except POM, which appears in the gas and particle phases. 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 is a mixture of pollutants that collectively poses one of the greatest relative cancer risks when compared with the other individual pollutants assessed. 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. In this rule, we are finalizing standards for passenger vehicles, gasoline, and portable fuel containers (typically gas cans). Specifically, we are finalizing standards for: • exhaust hydrocarbon emissions from passenger vehicles during cold temperature operation; • evaporative hydrocarbon emissions from passenger vehicles; • the benzene content of gasoline; and • hydrocarbon emissions from portable fuel containers that would reduce evaporation, permeation, and spillage from these containers. These standards will significantly reduce emissions of the many air toxics that are hydrocarbons, including benzene, 1,3-butadiene, formaldehyde, acetaldehyde, acrolein, and naphthalene. The fuel benzene standards and hydrocarbon standards for vehicles and portable fuel containers will together reduce total emissions of air toxics by 330,000 tons in 2030, including 61,000 tons of benzene. As a result of this final rule, in 2030 passenger vehicles will emit 45% less benzene, gas cans will emit almost 80% less benzene, and gasoline will have 38% less benzene overall. Mobile sources were responsible for over 70% of benzene emissions in 1999. The reductions in mobile source air toxics emissions will 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. Nationwide, the cancer risk attributable to total MSATs emitted by all mobile sources will be reduced by 30%, and the risk from mobile source benzene will be reduced by 37%. At 2030 exposure levels, the highway vehicle contribution to MSAT cancer risk will be reduced on average 36% across the U.S., and the highway vehicle contribution to benzene cancer risk will be reduced on average by 43% across the U.S. Nationwide, the mobile source contribution to the respiratory hazard index will be reduced by 23%. In addition, the hydrocarbon reductions from the vehicle and gas can standards will reduce VOC emissions (which are precursors to ozone and PM 2.5 ) by over 1.1 million tons in 2030. The vehicle standards will reduce direct PM 2.5 emissions by over 19,000 tons in 2030 and will 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 nevertheless important co-benefits of this proposal. Section I.B.2 of this preamble provides more discussion of the public health and environmental impacts of mobile source air toxics, ozone, and PM. Details on health effects, emissions, exposure, and cancer risks are also located in Chapters 1-3 of the Regulatory Impact Analysis (RIA) for this rule. We estimate that the benefits of this rule will 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 rule will be about $400 million in 2030 (expressed in 2003 dollars). These net social costs include the value of fuel savings from the proposed gas can standards, which will be worth about $92 million in 2030. The rule will have an average cost of 0.27 cents per gallon of gasoline, less than $1 per vehicle, and less than $2 per gas can. The reduced evaporation from gas cans will result in fuel savings that will more than offset the increased cost for the gas can. In 2030, the long-term cost per ton of the standards (in combination, and including fuel savings) will be $1,100 per ton of total mobile source air toxics reduced; $5,900 per ton of benzene reduced; and no cost for the hydrocarbon and PM reductions (because we expect the vehicle standards will have no cost in 2020 and beyond). Section VIII of the preamble and Chapters 8-13 of the RIA provide more details on the costs, benefits, and economic impacts of the standards. The impacts on small entities and the flexibilities we are finalizing are discussed in section X of this preamble and Chapter 14 of the RIA. II. Overview of Final Rule A. Light-Duty Vehicle Emission Standards As described in more detail in section V, we are adopting new standards for both exhaust and evaporative emissions from passenger vehicles. The new exhaust emissions standards will 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. As we discussed in the proposal, current vehicle emission standards are based on testing of NMHC that is generally 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 will also result in lower direct PM emissions at cold temperatures. Accordingly, consistent with the proposal, we are adopting a new NMHC exhaust emissions standard at 20 °F for light-duty vehicles, light-duty trucks, and medium-duty passenger vehicles. Vehicles at or below 6,000 pounds gross vehicle weight rating (GVWR) will 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 will be subject to a sales-weighted fleet average NMHC level of 0.5 grams/mile. For lighter vehicles, the standard will phase in between 2010 and 2013. For heavier vehicles, the new standards will phase in between 2012 and 2015. The standards include 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. These standards in combination are expected to lead to emissions control over a wide range of in-use temperatures, and not just at 20 °F and 75 °F. We are also establishing, as proposed, a set of nominally more stringent evaporative emission standards for all light-duty vehicles, light-duty trucks, and medium-duty passenger vehicles. The 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 codify the approach that most manufacturers are already taking for 50-state evaporative systems, and thus prevent backsliding in the future. The evaporative emission standards will take effect in 2009 for lighter vehicles and in 2010 for the heavier vehicles. Section V of this preamble provides details on the exhaust and evaporative vehicle standards. B. Gasoline Fuel Standards As we proposed, we are limiting the benzene content of all gasoline, both reformulated and conventional. Beginning January 1, 2011, refiners must meet a refinery average gasoline benzene content standard of 0.62% by volume on all their gasoline. The program is described in more detail in section VI of this preamble. The standard does not apply to gasoline produced and/or sold for use in California because such gasoline is already covered under California's Phase 3 Reformulated Gasoline (Ca3RFG) program. The benzene content standard, in combination with the existing gasoline sulfur standard, will result in air toxics emissions reductions that are greater than required under all existing gasoline toxics programs. As a result, upon full implementation in 2011, the regulatory provisions for the benzene control program will become the regulatory mechanism used to implement the reformulated gasoline (RFG) and Anti-dumping annual average toxics performance and benzene content requirements. The current RFG and Anti-dumping annual average provisions thus will be replaced by this benzene control program. This benzene control program will also replace the requirements of the 2001 MSAT rule (“MSAT1”). In addition, the program will 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 that Act. In all of these ways, the existing national fuel-related MSAT regulatory program will be significantly consolidated and simplified. We are finalizing a nationwide ABT program that allows refiners and importers to choose the most economical compliance strategy (investment in technology, credits, or both) for meeting the 0.62 vol% annual average standard. From 2007-2010, refiners can generate “early credits” by making qualifying benzene reductions earlier than required. Beginning in 2011 and continuing indefinitely, refiners and importers can generate “standard credits” by producing/importing gasoline with benzene levels below 0.62 volume percent (vol%) on an annual average basis. Credits may be used interchangeably towards company compliance with the 0.62 vol% standard, “banked” for future use, and/or transferred nationwide to other refiners/importers subject to the standard. In addition to the 0.62 vol% standard, refiners and importers must also meet a 1.3 vol% maximum average benzene standard beginning July 1, 2012. To comply with the maximum average standard, gasoline produced by a refinery or imported by an importer may not exceed 1.3 vol% benzene on an annual average basis. The ABT program allows us to set a numerically more stringent benzene standard than would otherwise be achievable (within the meaning of Clean Air Act section 202(l)(2)). The ABT program also allows implementation to occur earlier. Under this benzene content standard and ABT program, gasoline in all areas of the country will have lower benzene levels than they have today. Overall benzene levels will be 38% lower. This will reduce benzene emissions and exposure nationwide. The program includes special provisions for refiners facing hardship. Refiners approved as “small refiners” are eligible for certain temporary relief provisions. In addition, any refiner facing extreme unforeseen circumstances or extreme hardship circumstances can apply for similar temporary relief. C. Portable Fuel Container (PFC) Controls Portable fuel containers, such as gas cans and diesel and kerosene containers, are consumer products used to refuel a wide variety of equipment, including lawn and garden equipment, recreational equipment, and passenger vehicles that have run out of gas. As described in section VII, we are adopting standards for these containers that would reduce hydrocarbon emissions from evaporation, permeation, and spillage. The program we are finalizing is consistent with the proposal, except that instead of applying only to gasoline containers, it will also apply to diesel and kerosene containers. These standards will significantly reduce emissions of benzene and other gaseous toxics, as well as VOC. VOC is an ozone precursor, and certain aromatic species are believed to contribute to secondary organic PM 2.5 . We are finalizing a performance-based standard of 0.3 grams per gallon per day of hydrocarbons, determined based on the emissions from the can over a diurnal test cycle specified in the rule. The standard applies to containers manufactured on or after January 1, 2009. We are also establishing test procedures and a certification and compliance program, in order to ensure that containers meet the emission standard over a range of in-use conditions. The standards are based on the performance of best available control technologies, such as durable permeation barriers, automatically closing spouts, and cans that are well-sealed, and the standards will result in the use of these control technologies. 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 finalizing. Although a few aspects of the programs are different, we believe manufacturers will be able to meet both EPA and California requirements with the same container designs, resulting in equivalent emission reductions. III. Why Is EPA Taking This Action? 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 1 , 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, people that spend a large amount of time in vehicles or work with motorized equipment, and people living in homes with attached garages 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 are likely to remain a public health concern. Benzene will likely 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. Section III.B of this preamble discusses the risks posed by outdoor toxics now and in the future. Sections III.C and III.D discuss the health and welfare effects of ozone and PM, respectively. The controls in this rule will significantly reduce exposure to emissions of mobile source air toxics (and reduce exposure to ozone and PM 2.5 as well), thus reducing these public health concerns. 1 Based on quantitative estimates of risk, which do not include risks associated with diesel particulate matter and diesel exhaust organic gases. A. Statutory Requirements 1. 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 (“air toxics”) from motor vehicles 2 , 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. 2 “Motor vehicles” is a term of art, defined in Clean Air Act section 216(2) as “any self-propelled vehicle designed for transporting persons or property on a street or highway.” 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 issuing the vehicle emissions standards under this authority in conjunction with section 202(l)(2). 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 issuing the benzene standard for gasoline under this authority in conjunction with section 202(l)(2). Clean Air Act section 202(l)(2) also requires EPA to revise its regulations controlling hazardous air pollutants from motor vehicles and fuels, “from time to time.” EPA's first rule under Clean Air Act section 202(l) was published on March 29, 2001, entitled, “Control of Emissions of Hazardous Air Pollutants from Mobile Sources” (66 FR 17230). That rule committed to additional rulemaking that would evaluate the need for and feasibility of additional controls. Today's final rule fulfills that commitment. 2. 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), but it did not consider or list portable fuel containers. After analyzing these containers' emissions inventory impacts, we recently published a Federal Register notice that added portable fuel containers to the list of consumer products to be regulated. 3 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: 3 71 FR 28320, May 16, 2006, “Consumer and Commercial Products: Schedule for Regulation”. 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 issuing a hydrocarbon standard for portable fuel containers under the authority of section 183(e). 3. Energy Policy Act Section 1504(b) of the Energy Policy Act of 2005 requires EPA to adjust the toxics emissions baselines for individual refineries 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 VI of this preamble, we believe the benzene content standard we are finalizing today will in fact result in greater overall reductions than would be achieved by adjusting the individual baselines under the Energy Policy Act. Accordingly, under the provisions of the Energy Policy Act, this rule obviates the need for readjusting emissions baselines for reformulated gasoline. B. Public Health Impacts of Mobile Source Air Toxics (MSATs) 1. 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. Some MSATs are known or suspected to cause cancer. Some of these pollutants are also known to have adverse health effects on people's respiratory, cardiovascular, neurological, immune, reproductive, or other organ systems, and they may also have developmental effects. Some may pose particular hazards to more susceptible and sensitive populations, such as pregnant women, children, the elderly, or people with pre-existing illnesses. Some MSATs of particular concern include benzene, 1,3-butadiene, formaldehyde, acrolein, naphthalene, polycyclic organic matter, and diesel particulate matter and diesel exhaust organic gases. These are compounds that EPA's National-Scale Air Toxics Assessment (NATA) for 1999 4 identifies as the most significant contributors to cancer and noncancer health risk from breathing outdoor air toxics, and that have a significant contribution from mobile sources. Our understanding of what compounds pose the greatest risk will evolve over time, based on our understanding of the ambient levels and health effects associated with the compounds. 4 http://www.epa.gov/ttn/atw/nata1999/. EPA has compiled a Master List of Compounds Emitted by Mobile Sources, based on an extensive review of the literature on exhaust and evaporative emissions from onroad and nonroad equipment. The list currently includes approximately 1,000 compounds, and it is available in the public docket for this rule and on the Web ( http://www.epa.gov/otaq/toxics.htm ). Chapter 1 of the RIA provides a detailed discussion of information sources for identifying those compounds that have the potential for serious adverse health effects (i.e., could be considered “MSATs”). This discussion includes a list of those compounds that are emitted by mobile sources and listed in EPA's Integrated Risk Information System (IRIS). MSATs are emitted by motor vehicles, nonroad engines (such as lawn and garden equipment, farming and construction equipment, locomotives, and ships), aircraft, and their fuels. 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. There are other sources of air toxics, including 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. 2. Health Risk Associated With MSATs EPA's National-Scale Air Toxics Assessment (NATA) for 1999 provides some perspective on the average risk of cancer and noncancer health effects associated with breathing air toxics from outdoor sources, and the contribution of mobile sources to these risks. 5, 6 NATA assessed 177 pollutants. It is worth noting that NATA does not include indoor sources of air toxics. Also, it assumes uniform outdoor concentrations within a census tract, and therefore does not reflect elevated concentrations and exposures near roadways or other sources within a census tract. Additional limitations and uncertainties associated with NATA are discussed in Section 3.2.1.3 of the RIA. 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. Some of NATA's findings are discussed in the paragraphs below. 5 http://www.epa.gov/ttn/atw/nata1999/. 6 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 confident estimate of cancer unit risk. For this rule, EPA also performed a national-scale assessment for 1999 and future years using the same modeling tools and approach as the 1999 NATA, but with updated emissions inventories and an updated exposure model. The exposure model accounts for higher toxics concentrations near roads. This updated national-scale analysis examined only those toxics that are emitted by mobile sources (i.e., a subset of the 177 pollutants included in NATA). However, the analysis includes all sources of those pollutants, including mobile, stationary, and area sources. The analysis is discussed in detail in Chapter 3 of the RIA, and some highlights of the findings are discussed immediately below. In addition to national-scale analysis, we have also evaluated more refined local-scale modeling, measured ambient concentrations, personal exposure measurements, and other data. This information is discussed in detail in Chapter 3 of the RIA. These data collectively show that while levels of air toxics are decreasing, potential public health risks remain a concern, and ambient levels and personal exposure vary significantly. These data indicate that concentrations of benzene and other air toxics can be higher near high-traffic roads, inside vehicles, and in homes with attached garages. a. National Cancer Risk According to NATA, the average national cancer risk in 1999 from all outdoor sources of air toxics was estimated to be 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. Benzene is the largest contributor to cancer risk of all 133 pollutants quantitatively assessed in the 1999 NATA, and mobile sources are the single largest source of ambient benzene. According to the national-scale analysis performed for this rule, the national average cancer risk in 1999 from breathing outdoor sources of MSATs was about 25 in a million. 7 Over 224 million people in 1999 were exposed to a risk level above 10 in a million due to chronic inhalation exposure to MSATs. About 130 million people in 1999 were exposed to a risk level above 10 in a million due to chronic inhalation exposure to benzene alone. Mobile sources were responsible for over 70% of benzene emissions in 1999. 7 This includes emissions from mobile and stationary sources of these pollutants. 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. Without additional controls, the predicted national average cancer risk from MSATs in 2030 is predicted to be above 20 in a million. In fact, in 2030 there will be more people exposed to levels of MSATs that result in the highest levels of risk. For instance, the number of Americans above the 10 in a million cancer risk level from exposure to MSATs is projected to increase from 223 million in 1999 to 272 million in 2030. Mobile sources will continue to be a significant contributor to risk in the future, accounting for 43% of total air toxic emissions in 2020, and 55% of benzene emissions. b. National Risk of Noncancer Health Effects According to national-scale modeling for 1999 done for this rule, 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). 8 We estimated this will continue to be the case in 2030, even though toxics levels will be lower. 8 That is, the respiratory hazard index exceeded 1. See section III.B.3.a for more information. Mobile sources were responsible for 74% of the noncancer (respiratory) risk from outdoor air toxics in the 1999 NATA. The majority of this risk was from acrolein, and formaldehyde also contributed to the risk of respiratory health effects. 9 9 Acrolein was assigned an overall confidence level of “lower” based on consideration of the combined uncertainties from the modeling estimates. In contrast, formaldehyde was assigned an overall confidence level of “medium.” Although not included in NATA's estimates of noncancer risk, PM from gasoline and diesel mobile sources contributes significantly to the health effects associated with ambient PM, for which EPA has established National Ambient Air Quality Standards. There are extensive human data showing a wide spectrum of adverse health effects associated with exposure to ambient PM. 10 10 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, p. 8-318. c. Exposure Near Roads A substantial number of modeling assessment and air quality monitoring studies show elevated concentrations of multiple MSATs in close proximity to major roads. Exposure studies also indicate that populations spending time near major roadways likely experience elevated personal exposures to motor vehicle-related pollutants. In addition, these populations may experience exposures to differing physical and chemical compositions of certain air toxic pollutants depending on the amount of time spent in close proximity to motor vehicle emissions. Chapter 3.1 of the RIA provides a detailed discussion of air quality monitoring, personal exposure monitoring, and modeling assessments near major roadways. As part of the analyses underlying the final rule, we employed a new version of the Hazardous Air Pollutant Exposure Model (HAPEM), the exposure model used in NATA. HAPEM6 explicitly accounts for the gradient in outdoor concentrations that occurs near major roads, and the fraction of the population living near major roads. 11 The HAPEM6 analysis highlights the fact that residence near a major road is a substantial contributor to overall differences in exposure to directly-emitted MSATs. As an example, while the average of within-tract median annual census tract exposure concentrations nationally is 1.4 μg/m 3 , the average 90th percentile of within-tract exposure concentration nationally is over 2 μg/m 3 . 11 U.S. EPA. 2007. The HAPEM6 User's Guide. Prepared for Ted Palma, Office of Air Quality Planning and Standards, Research Triangle Park, NC, by Arlene Rosenbaum and Michael Huang, ICF International, January 2007. This document is available in Docket EPA-HQ-OAR-2005-0036. http://www.epa.gov/ttn/fera/human_hapem.html . The potential population exposed to elevated concentrations near major roadways is large. A study of the populations nationally indicated that more than half of the population lives within 200 meters of a major road. 12 It should be noted that this analysis relied on the Census Bureau definition of a major road, which is not based on traffic volume. Thus, some of the roads designated as “major” may carry a low volume of traffic. This estimate is consistent with other studies that have examined the proximity of population to major roads. These studies are discussed in Section 3.5 of the RIA. In addition, analysis of data from the Census Bureau's American Housing Survey suggests that approximately 37 million people live within 300 feet (~100 meters) of a 4-or-more lane highway, railroad, or airport. 13 American Housing Survey statistics, as well as epidemiology studies, indicate that those houses located near major transportation sources are more likely to be lower in income or have minority residents than houses not located near major transportation sources. These data are also discussed in detail in Section 3.5 of the RIA. 12 Major roads are defined as those roads defined by the U.S. Census as one of the following: “limited access highway,” “highway,” “major road (primary, secondary and connecting roads ),” or “ramp.” 13 United States Census Bureau. (2004) American Housing Survey web page. [Online at http://www.census.gov/hhes/www/housing/ahs/ahs03/ahs03.html ] Table IA-6. Other population studies also indicate that a significant fraction of the population resides in locations near major roads. At present, the available studies use different indicators of “major road” and of “proximity,” but the estimates range from 12.4% of student enrollment in California attending schools within 150 meters of roads with 25,000 vehicles per day or more, to 13% of Massachusetts veterans living within 50 meters of a road with at least 10,000 vehicles per day. 14, 15 Using a more general definition of a “major road,” between 22% and 51% of different study populations live near such roads. 14 Green, R.S.; Smorodinsky, S.; Kim, J.J.; McLaughlin, R.; Ostro, B. (2004) Proximity of California public schools to busy roads. Environ. Health Perspect. 112: 61-66. 15 Garshick, E.; Laden, F.; Hart, J.E.; Caron, A. (2003) Residence near a major road and respiratory symptoms in U.S. veterans. Epidemiol. 14: 728-736. d. Exposure From Attached Garages People living in homes with attached garages are potentially exposed to substantially higher overall concentrations of benzene, toluene, and other VOCs from mobile source-related emissions. EPA has conducted a modeling analysis to examine the influence of attached garages on personal exposure to benzene (see Appendix 3A of RIA). Compared to national average exposure concentrations modeled in 1999 NATA, which does not account for emissions originating in attached garages, average exposure concentrations for people with attached garages could more than double. Other recent studies also emphasize the substantial role of attached garages in exposure to MSATs. Chapter 3 of the RIA discusses measurements of concentrations and exposure associated with attached garages and EPA's modeling analysis. 3. What Are the Health Effects of Air Toxics? a. Overview of Potential Cancer and Noncancer Health Effects Air toxics can cause of variety of cancer and noncancer health effects. Inhalation cancer risks are usually estimated by EPA as “unit risks,” which represent the excess lifetime cancer risk estimated to result from continuous exposure to an agent at a concentration of 1 mu g/m 3 in air. Some air toxics are known to be carcinogenic in animals but lack data in humans. Many of these have been assumed to be human carcinogens. Also, in the absence of evidence of a nonlinear dose-response curve, EPA assumes these relationships between exposure and probability of cancer are linear. 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 estimate (MLE) 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 and dermal 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 interspecies extrapolation (animal to human) and intraspecies extrapolation (average human to sensitive human). Additional sources of uncertainty can include the use of 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 health 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. b. Health Effects of Key MSATs i. Benzene The EPA's IRIS database lists benzene, an aromatic hydrocarbon, as a known human carcinogen (causing leukemia) by all routes of exposure. 16 A number of adverse noncancer health effects including blood disorders and immunotoxicity have also been associated with long-term occupational exposure to benzene. 17 16 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. 17 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.pdf. Inhalation is the major source of human exposure to benzene in occupational and non-occupational settings. Long-term occupational inhalation exposure to benzene has been shown to cause cancers of the hematopoetic (blood cell) system in adults. 18 Among these are acute nonlymphocytic leukemia 19 and chronic lymphocytic leukemia. 20, 21 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 22, 23 and increased proliferation of mouse bone marrow cells. 24, 25 18 U.S. EPA (1998) Carcinogenic Effects of Benzene: An Update, National Center for Environmental Assessment, Washington, DC. EPA600-P-97-001F. Enter report number at the following search page, http://yosemite.epa.gov/ncepihom/nsCatalog.nsf//SearchPubs?Openform. 19 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 cell that is responsible for antibody and cell-mediated 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. 20 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. 21 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. 22 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. 23 U.S. EPA (1998) Carcinogenic Effects of Benzene: An Update, National Center for Environmental Assessment, Washington, DC. EPA600-P-97-001F. Enter report number at the following search page, http://yosemite.epa.gov/ncepihom/nsCatalog.nsf//SearchPubs?Openform. 24 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. 25 U.S. EPA (1998) Carcinogenic Effects of Benzene: An Update, National Center for Environmental Assessment, Washington, DC. EPA600-P-97-001F. Enter report number at the following search page, http://yosemite.epa.gov/ncepihom/nsCatalog.nsf//SearchPubs?Openform. The latest assessment by EPA estimates the excess risk of developing 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 an estimated risk of about two to eight excess leukemia cases in one million people exposed to 1 μg/m 3 of benzene over a lifetime. 26 This range of unit risks reflects 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 variation of the observed data used to develop dose-response values. 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. 26 U.S. EPA (1998) Carcinogenic Effects of Benzene: An Update, National Center for Environmental Assessment, Washington, DC. EPA600-P-97-001F. Enter report number at the following search page, http://yosemite.epa.gov/ncepihom/nsCatalog.nsf//SearchPubs?Openform. 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. 27 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. Such a relationship could support the inference that cancer risks are as high or are higher than the estimates provided in the existing EPA assessment. 28 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 μ/m 3 ). 29 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. 30, 31, 32 These data highlight the importance of ambient exposure levels and their contribution to benzene-related adducts. 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.” 33, 34, 35 These data are from the largest cohort studies 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 how they might influence low-dose risk estimates. A better understanding of the biological mechanism of benzene-induced leukemia is needed. 27 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. 28 U.S. EPA (1998) Carcinogenic Effects of Benzene: An Update. EPA/600/P-97/001F. 29 Rothman, N; Li, GL; Dosemeci, M; et al. (1996) Hematotoxicity among Chinese workers heavily exposed to benzene. Am. J. Indust. Med. 29:236-246. 30 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. 31 Rappaport, S.M.; Waidyanatha, S.; Qu, Q.; Yeowell-O'Connell, K.; Rothman, N.; Smith M.T.; Zhang, L.; Qu, Q.; Shore, R.; Li, G.; Yin, S. (2005) Protein adducts as biomarkers of human enzene metabolism. Chem Biol Interact. 153-154:103-109. 32 Lin, Y-S., Vermeulen, R., Tsai, C.H., Suramya, W., Lan, Q., Rothman, N., Smith, M.T., Zhang, L., Shen, M., Songnian, Y., Kim, S., Rappaport, S.M. (2006) Albumin adducts of electrophilic benzene metabolites in benzene-exposed and control workers. Environ Health Perspec. 33 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. 34 Hayes, R.B.; Songnian, Y.; Dosemeci, M.; and Linet, M. (2001) Benzene and lymphohematopoietic malignancies in humans. Am. J. Indust. Med. 40:117-126. 35 Lan, Q.; Zhang, L., Li, G., Vermeulen, R., et al. (2004). Hematotoxicity in Workers Exposed to Low Levels of Benzene. Science 306: 1774-1776. 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 lifetime risk of leukemia and other toxic effects from exposures occurring during childhood, if children 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. 36, 37 Data from animal studies have shown benzene exposures result in damage to the hematopoietic (blood cell formation) system during development. 38, 39, 40 Also, key changes related to the development of childhood leukemia occur in the developing fetus. 41 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. 42 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. 36 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. 37 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. 38 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. 39 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. 40 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. 41 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.pdf. 42 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. 43, 44 People with long-term occupational exposure to benzene have experienced harmful effects on the blood-forming tissues, especially in the 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, 45 a condition characterized by decreased numbers of circulating erythrocytes (red blood cells), leukocytes (white blood cells), and thrombocytes (blood platelets). 46, 47 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. 48, 49 The most sensitive noncancer effect observed in humans, based on current data, is the depression of the absolute lymphocyte count in blood. 50, 51 43 Aksoy, M. (1989) Hematotoxicity and carcinogenicity of benzene. Environ. Health Perspect. 82:193-197. 44 Goldstein, B.D. (1988) Benzene toxicity. Occupational medicine. State of the Art Reviews 3: 541-554. 45 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 skeletal system. 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. 46 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. 47 Goldstein, B.D. (1988) Benzene toxicity. Occupational medicine. State of the Art Reviews 3: 541-554. 48 Aksoy, M., S. Erdem, and G. Dincol. (1974) Leukemia in shoe-workers exposed chronically to benzene. Blood 44:837. 49 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. 50 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. 51 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, human reports of benzene's hematotoxic effects have been published 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 ) 52 and at air levels of 1 ppm (about 3 mg/m 3 ) or less among genetically susceptible populations. 53 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. 54 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. 52 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. 53 Lan, Q.; Zhang, L., Li, G., Vermeulen, R., et al. (2004). Hematotoxicity in Workers Exposed to Low Levels of Benzene. Science 306: 1774-1776. 54 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. ii. 1,3-Butadiene EPA has characterized 1,3-butadiene, a hydrocarbon, as a leukemogen, carcinogenic to humans by inhalation. 55 56 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 in humans 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. 57 58 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. A recent study extended the investigation of 1,3-butadiene exposure and leukemia among synthetic rubber industry workers. 59 The results of this study strengthen the evidence for the relationship between 1,3-butadiene exposure and lymphohematopoietic cancer. This relationship was found to persist after controlling for exposure to other toxics in this work environment. 55 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. 56 EPA 2005 “Full IRIS Summary for 1,3-butadiene (CASRN 106-99-0)” 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/0139.htm. 57 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. 58 EPA 2005 “Full IRIS Summary for 1,3-butadiene (CASRN 106-99-0)” 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/0139.htm. 59 Delzell, E., Sathiakumar, N., Graff, J., Macaluso, M., Maldonado, G., Matthews, R. (2006) An updated study of mortality among North American synthetic rubber industry workers. Health Effects Institute Report Number 132. 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. 60 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. 60 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. iii. 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. 61 EPA's current IRIS summary provides an upper bound cancer unit risk estimate of 1.3 × 10 −5 per μg/m 3 . 62 In other words, there is an estimated risk of about thirteen excess leukemia cases in one million people exposed to 1 μg/m 3 of formaldehyde over a lifetime. 61 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. 62 U.S. EPA (1989). Integrated Risk Information System File for Formaldehyde. This material is available electronically at http://www.epa.gov/iris/subst/0419.htm. EPA is currently reviewing recently published epidemiological data. For instance, research conducted by the National Cancer Institute (NCI) found an increased risk of nasopharyngeal cancer and lymphohematopoietic malignancies such as leukemia among workers exposed to formaldehyde. 63 64 NCI is currently performing an update of these studies. 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. 65 Extended follow-up of a cohort of British chemical workers did not find evidence of an increase in nasopharyngeal or lymphohematopoeitic cancers, but a continuing statistically significant excess in lung cancers was reported. 66 63 Hauptmann, M.; Lubin, J. H.; Stewart, P. A.; Hayes, R. B.; Blair, A. 2003. Mortality from lymphohematopoietic malignancies among workers in formaldehyde industries. Journal of the National Cancer Institute 95: 1615-1623. 64 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. 65 Pinkerton, L. E. 2004. Mortality among a cohort of garment workers exposed to formaldehyde: an update. Occup. Environ. Med. 61: 193-200. 66 Coggon, D, EC Harris, J Poole, KT Palmer. 2003. Extended follow-up of a cohort of British chemical workers exposed to formaldehyde. J National Cancer Inst. 95:1608-1615. Based on the developments of the last decade, 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.” Recently the German Federal Institute for Risk Assessment determined that formaldehyde is a known human carcinogen. 67 67 Bundesinstitut fu r Risikobewertung (BfR) Toxicological Assessment of Formaldehyde. Opinion of BfR No. 023/2006 of 30 March 2006. www.bfr.bund.de/cm/290/toxicological_assessment_of_formaldehyde.pdf. 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. 68 69 70 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 were 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. 71 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). 72 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. 68 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. 69 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. 70 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. 71 Health Canada. 2001. Priority Substances List Assessment Report. Formaldehyde. Environment Canada, Health Canada, February 2001. 72 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. iv. Acetaldehyde Acetaldehyde, a hydrocarbon, is classified in EPA's IRIS database as a probable human carcinogen and is considered toxic by inhalation. 73 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. 74 75 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. 73 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. 74 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. 75 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. 76 Some asthmatics have been shown to be a sensitive subpopulation to decrements in functional expiratory volume (FEV1 test) and bronchoconstriction upon acetaldehyde inhalation. 77 76 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. 77 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. v. 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 . 78 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. 78 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. vi. 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, as well as impaired cognitive development at age three. 79, 80 These studies are discussed in the Regulatory Impact Analysis. 79 Perera, 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. 80 Perera, F.P.; Rauh, V.; Whyatt, R.M.; Tsai, W.Y.; Tang, D.; Diaz, D.; Hoepner, L.; Barr, D.; Tu, Y.H.; Camann, D.; Kinney, P. (2006) Effect of prenatal exposure to airborne polycyclic aromatic hydrocarbons on neurodevelopment in the first 3 years of life among inner-city children. Environ Health Perspect 114: 1287-1292. vii. 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 of a reassessment of the inhalation carcinogenicity of naphthalene. 81 The draft reassessment, External Review Draft, IRIS Reassessment of the Inhalation Carcinogenicity of Naphthalene, U.S. EPA, completed external peer review in 2004 by Oak Ridge Institute for Science and Education. 82 Based on external comments, additional analyses are being considered. California EPA has released a new risk assessment for naphthalene with a cancer unit risk estimate of 3×10 −5 per μg/m 3 . 83 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. 84 Current risk estimates for naphthalene are based on extrapolations from rodent studies conducted at higher doses. At present, human data are inadequate for developing estimates. 81 U.S. EPA (1998) Integrated Risk Information System (IRIS) summary on Naphthalene. 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/0436.htm . 82 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 . 83 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 . 84 International Agency for Research on Cancer (IARC). (2002) Monographs on the Evaluation of the Carcinogenic Risk of Chemicals for Humans. Vol. 82. Lyon, France. The current EPA IRIS assessment includes noncancer data on hyperplasia and metaplasia in nasal tissue that form the basis of an inhalation RfC of 3 μg/m 3 . 85 The principal study was given medium confidence because adequate numbers of animals were used, and the severity of nasal effects increased at the higher exposure concentration. However, the study produced high mortality and hematological evaluation was not conducted beyond 14 days. The database was given a low-to-medium confidence rating because there are no chronic or subchronic inhalation studies in other animal species, and there are no reproductive or developmental studies for inhalation exposure. In the absence of human or primate toxicity data, the assumption is made that nasal responses in mice to inhaled naphthalene are relevant to humans; however, it cannot be said with certainty that this RfC for naphthalene based on nasal effects will be protective for hemolytic anemia and cataracts, the more well-known human effects from naphthalene exposure. As a result, we have medium confidence in the RfC. 85 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 . viii. Diesel Exhaust In EPA's Diesel Health Assessment Document (HAD), 86 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. 86 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. An exploratory analysis was used to characterize a possible risk range 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. Noncancer health effects of acute and chronic exposure to 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. 87 88 89 90 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. The EPA Diesel HAD states, “With DPM [diesel particulate matter] being a ubiquitous component of ambient PM, there is an uncertainty about the adequacy of the existing DE [diesel exhaust] noncancer database to identify all of the pertinent DE-caused noncancer health hazards” (p. 9-19). 87 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. 88 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. 89 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. 90 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 discusses 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 PM 2.5 NAAQS is designed to provide protection from the noncancer and premature mortality effects of PM 2.5 as a whole, of which diesel PM is a constituent. c. 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. 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. 91 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 . 92 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). There is also emerging 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 in various animal and bioassay tests. 93 The authors suggest that emissions from gasoline engines are mutagenic and can induce inflammation and have cytotoxic effects. 91 U.S. EPA (2004) Air Quality Criteria for Particulate Matter: Volume 1. Research Triangle Park, NC: National Center for Environmental Assessment—RTP Office; Report No. EPA/600/P-99/002aF. Enter report number at the following search page, http://yosemite.epa.gov/ncepihom/nsCatalog.nsf//SearchPubs?Openform. 92 U.S. EPA (2004) Air Quality Criteria for Particulate Matter: Volume 1. Research Triangle Park, NC: National Center for Environmental Assessment—RTP Office; Report No. EPA/600/P-99/002aF, p. 8-318. Enter report number at the following search page, http://yosemite.epa.gov/ncepihom/nsCatalog.nsf//SearchPubs?Openform. 93 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. 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 shortly. Preliminary results from this work show the influence of high emitters on overall gasoline PM emissions and, also, that gasoline PM emissions increase at lower ambient temperatures in the in-use fleet. Some source apportionment studies show gasoline and diesel PM can result in larger contributions to ambient PM than predicted by EPA emission inventories. 94 95 These source apportionment studies were one impetus behind conducting the Kansas City study. 94 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. 95 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 such as toluene 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. d. Near-Roadway Health Effects Another approach to investigating the collective health effects of mobile source contaminants is to examine 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 roadways 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 correlations. 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. C. Ozone Many MSATs are part of a larger category of mobile source emissions known as volatile organic compounds (VOCs), which contribute to the formation of ozone. Mobile sources contribute significantly to national emissions of VOCs. In addition, PFCs are a source of VOCs. The vehicle and PFC standards in this final rule will help reduce emissions of VOCs. 1. Background Ground-level ozone pollution is formed by the reaction of VOCs and nitrogen oxides (NO X ) in the lower atmosphere in the presence of heat and sunlight. These pollutants, often referred to as ozone precursors, are emitted by many types of pollution sources, such as highway and nonroad motor vehicles and engines, power plants, chemical plants, refineries, makers of consumer and commercial products, industrial facilities, and smaller area sources. The PFC controls being finalized in this action will help reduce VOC emissions by reducing evaporation, permeation and spillage from PFCs. The vehicle controls being finalized will also reduce VOC emissions; however, because these reductions will occur at cold temperatures the ozone benefits will be limited. The science of ozone formation, transport, and accumulation is complex. 96 Ground-level ozone is produced and destroyed in a cyclical set of chemical reactions, many of which are sensitive to temperature and sunlight. When ambient temperatures and sunlight levels remain high for several days and the air is relatively stagnant, ozone and its precursors can build up and result in more ozone than typically would occur on a single high-temperature day. Ozone also can be transported into an area from pollution sources found hundreds of miles upwind, resulting in elevated ozone levels even in areas with low VOC or NO X emissions. 96 U.S. EPA, Air Quality Criteria for Ozone and Related Photochemical Oxidants (Final). U.S. Environmental Protection Agency, Washington, DC, EPA/600/R-05/004aF-cF, 2006. This document is available in Docket EPA-HQ-OAR-2005-0036. The current ozone National Ambient Air Quality Standards (NAAQS) established by EPA in 1997 has an 8-hour averaging time. 97 The 8-hour ozone NAAQS is based on well-documented science demonstrating that more people were experiencing adverse health effects at lower levels of exertion, over longer periods, and at lower ozone concentrations than addressed by the previous one-hour ozone NAAQS. The current ozone NAAQS addresses ozone exposures of concern for the general population and populations most at risk, including children active outdoors, outdoor workers, and individuals with pre-existing respiratory disease, such as asthma. The 8-hour ozone NAAQS is met at an ambient air quality monitoring site when the average of the annual fourth-highest daily maximum 8-hour average ozone concentration over three years is less than or equal to 0.084 ppm. 97 EPA's review of the ozone NAAQS is underway and a proposal is scheduled for June 2007 with a final rule scheduled for March 2008. 2. Health Effects of Ozone The health and welfare effects of ozone are well documented and are assessed in the EPA's 2006 ozone Air Quality Criteria Document (ozone AQCD) and EPA staff papers. 98 99 Ozone can irritate the respiratory system, causing coughing, throat irritation, and/or uncomfortable sensation in the chest. Ozone can reduce lung function and make it more difficult to breathe deeply, and breathing may become more rapid and shallow than normal, thereby limiting a person's activity. Ozone can also aggravate asthma, leading to more asthma attacks that require a doctor's attention and/or the use of additional medication. Animal toxicologic evidence indicates that with repeated exposure, ozone can inflame and damage the lining of the lungs, which may lead to permanent changes in lung tissue and irreversible reductions in lung function. People who are more susceptible to effects associated with exposure to ozone include children, the elderly, and individuals with respiratory disease such as asthma. There is also suggestive evidence that certain people may have greater genetic susceptibility. Those with greater exposures to ozone, for instance due to time spent outdoors (e.g., outdoor workers), are also of concern. 98 U.S. EPA, Air Quality Criteria for Ozone and Related Photochemical Oxidants (Final). U.S. Environmental Protection Agency, Washington, DC, EPA/600/R-05/004aF-cF, 2006. This document is available in Docket EPA-HQ-OAR-2005-0036. 99 U.S. EPA (2007) Review of National Ambient Air Quality Standards for Ozone, Assessment of Scientific and Technical Information, OAQPS Staff Paper, EPA-452/R-07-003. This document is available in Docket EPA-HQ-OAR-2005-0036. The recent ozone AQCD also examined relevant new scientific information which has emerged in the past decade, including the impact of ozone exposure on such health effects as changes in lung structure and biochemistry, inflammation of the lungs, exacerbation and causation of asthma, respiratory illness-related school absence, hospital admissions and premature mortality. Animal toxicologic studies have suggested potential interactions between ozone and PM with increased responses observed to mixtures of the two pollutants compared to either ozone or PM alone. The respiratory morbidity observed in animal studies along with the evidence from epidemiologic studies supports a causal relationship between acute ambient ozone exposures and increased respiratory-related emergency room visits and hospitalizations in the warm season. In addition, there is suggestive evidence of a contribution of ozone to cardiovascular-related morbidity and non-accidental and cardiopulmonary mortality. 3. Plant and Ecosystem Effects of Ozone Ozone contributes to many environmental effects, with impacts to plants and ecosystems being of most concern. Ozone can produce both acute and chronic injury in sensitive species depending on the concentration level and the duration of the exposure. Ozone effects also tend to accumulate over the growing season of the plant, so that even lower concentrations experienced for a longer duration have the potential to create chronic stress on vegetation. Ozone damage to plants includes visible injury to leaves and a reduction in food production through impaired photosynthesis, both of which can lead to reduced crop yields, forestry production, and use of sensitive ornamentals in landscaping. In addition, the reduced food production in plants and subsequent reduced root growth and storage below ground, can result in other, more subtle plant and ecosystems impacts. These include increased susceptibility of plants to insect attack, disease, harsh weather, interspecies competition and overall decreased plant vigor. The adverse effects of ozone on forest and other natural vegetation can potentially lead to species shifts and loss from the affected ecosystems, resulting in a loss or reduction in associated ecosystem goods and services. Lastly, visible ozone injury to leaves can result in a loss of aesthetic value in areas of special scenic significance like national parks and wilderness areas. The final 2006 ozone AQCD presents more detailed information on ozone effects on vegetation and ecosystems. 4. Current and Projected 8-hour Ozone Levels Currently, ozone concentrations exceeding the level of the 8-hour ozone NAAQS occur over wide geographic areas, including most of the nation's major population centers. 100 As of October 2006 approximately 157 million people live in the 116 areas that are currently designated as not in attainment with the 8-hour ozone NAAQS. There are 461 full or partial counties that make up the 116 8-hour ozone nonattainment areas. 100 A map of the 8-hour ozone nonattainment areas is included in the RIA for this rule. EPA has already adopted many emission control programs that are expected to reduce ambient ozone levels. These control programs include the Clean Air Interstate Rule (70 FR 25162, May 12, 2005), as well as many mobile source rules (many of which are described in section V.D). As a result of these programs, the number of areas that fail to meet the 8-hour ozone NAAQS is expected to decrease. Based on the recent ozone modeling performed for the CAIR analysis, 101 barring additional local ozone precursor controls, we estimate 37 Eastern counties (where 24 million people are projected to live) will exceed the 8-hour ozone NAAQS in 2010. An additional 148 Eastern counties (where 61 million people are projected to live) are expected to be within 10 percent of violating the 8-hour ozone NAAQS in 2010. 101 Technical Support Document for the Final Clean Air Interstate Rule Air Quality Modeling. This document is available in Docket EPA-HQ-OAR-2005-0036. States with 8-hour ozone nonattainment areas will be required to take action to bring these areas into compliance in the future. Based on the final rule designating and classifying 8-hour ozone nonattainment areas (69 FR 23951, April 30, 2004), most 8-hour ozone nonattainment areas will be required to attain the 8-hour ozone NAAQS in the 2007 to 2013 time frame and then be required to maintain the 8-hour ozone NAAQS thereafter. 102 The expected ozone inventory reductions from the standards being finalized in this action may be useful to states in attaining or maintaining the 8-hour ozone NAAQS. 102 The Los Angeles South Coast Air Basin 8-hour ozone nonattainment area will have to attain before June 15, 2021. EPA's review of the ozone NAAQS is currently underway and a proposed decision in this review is scheduled for June 2007 with a final rule scheduled for March 2008. If the ozone NAAQS is revised, then new nonattainment areas could be designated. While EPA is not relying on it for purposes of justifying this rule, the emission reductions from this rulemaking would also be helpful to states if there is an ozone NAAQS revision. D. Particulate Matter The cold temperature vehicle controls being finalized here will result in reductions of primary PM being emitted by vehicles. In addition, both the vehicle controls and the PFC controls will reduce VOCs that react in the atmosphere to form secondary PM 2.5 , namely organic carbonaceous PM 2.5 . 1. Background Particulate matter (PM) represents a broad class of chemically and physically diverse substances. It can be principally characterized as discrete particles that exist in the condensed (liquid or solid) phase spanning several orders of magnitude in size. PM is further described by breaking it down into size fractions. PM 10 refers to particles generally less than or equal to 10 micrometers (μm) in diameter. PM 2.5 refers to fine particles, those particles generally less than or equal to 2.5 μm in diameter. Inhalable (or “thoracic”) coarse particles refer to those particles generally greater than 2.5 μm but less than or equal to 10 μm in diameter. Ultrafine PM refers to particles with diameters generally less than 100 nanometers (0.1 μm). Larger particles (>10 μm) tend to be removed by the respiratory clearance mechanisms, whereas smaller particles are deposited deeper in the lungs. Fine particles are produced primarily by combustion processes and by transformations of gaseous emissions (e.g., SO x , NO X and VOCs) in the atmosphere. The chemical and physical properties of PM 2.5 may vary greatly with time, region, meteorology and source category. Thus, PM 2.5 may include a complex mixture of different pollutants including sulfates, nitrates, organic compounds, elemental carbon and metal compounds. These particles can remain in the atmosphere for days to weeks and travel through the atmosphere hundreds to thousands of kilometers. EPA has recently amended the PM NAAQS (71 FR 61144, October 17, 2006). The final rule, signed on September 21, 2006 and published on October 17, 2006, addressed revisions to the primary and secondary NAAQS for PM to provide increased protection of public health and welfare, respectively. The primary PM 2.5 NAAQS include a short-term (24-hour) and a long-term (annual) standard. The level of the 24-hour PM 2.5 NAAQS has been revised from 65 μg/m 3 to 35 μg/m 3 to provide increased protection against health effects associated with short-term exposures to fine particles. The current form of the 24-hour PM 2.5 standard was retained ( e.g., based on the 98th percentile concentration averaged over three years). The level of the annual PM 2.5 NAAQS was retained at 15 μg/m 3 continuing protection against health effects associated with long-term exposures. The current form of the annual PM 2.5 standard was retained as an annual arithmetic mean averaged over three years, however, the following two aspects of the spatial averaging criteria were narrowed: (1) The annual mean concentration at each site shall be within 10 percent of the spatially averaged annual mean, and (2) the daily values for each monitoring site pair shall yield a correlation coefficient of at least 0.9 for each calendar quarter. With regard to the primary PM 10 standards, the 24-hour PM 10 NAAQS was retained at a level of 150 μg/m 3 not to be exceeded more than once per year on average over a three-year period. Given that the available evidence does not suggest an association between long-term exposure to coarse particles at current ambient levels and health effects, EPA has revoked the annual PM 10 standard. With regard to the secondary PM standards, EPA has revised these standards to be identical in all respects to the revised primary standards. Specifically, EPA has revised the current 24-hour PM 2.5 secondary standard by making it identical to the revised 24-hour PM 2.5 primary standard, retained the annual PM 2.5 and 24-hour PM 10 secondary standards, and revoked the annual PM 10 secondary standards. This suite of secondary PM standards is intended to provide protection against PM-related public welfare effects, including visibility impairment, effects on vegetation and ecosystems, and material damage and soiling. 2. Health Effects of PM Scientific studies show ambient PM is associated with a series of adverse health effects. These health effects are discussed in detail in the 2004 Particulate Matter Air Quality Criteria Document (PM AQCD) as well as the 2005 PM Staff Paper. 103, 104 Further discussion of health effects associated with PM can also be found in the RIA for this final rule. 103 U.S. EPA (2004) Air Quality Criteria for Particulate Matter (Oct 2004), Volume I Document No. EPA600/P-99/002aF and Volume II Document No. EPA600/P-99/002bF. This document is available in Docket EPA-HQ-OAR-2005-0036. 104 U.S. EPA (2005) Review of the National Ambient Air Quality Standard for Particulate Matter: Policy Assessment of Scientific and Technical Information, OAQPS Staff Paper. EPA-452/R-05-005. This document is available in Docket EPA-HQ-OAR-2005-0036. Health effects associated with short-term exposures (e.g. hours to days) in ambient PM 2.5 include premature mortality, increased hospital admissions, heart and lung diseases, increased cough, adverse lower-respiratory symptoms, decrements in lung function and changes in heart rate rhythm and other cardiac effects. Studies examining populations exposed to different levels of air pollution over a number of years, including the Harvard Six Cities Study and the American Cancer Society Study, show associations between long-term exposure to ambient PM 2.5 and both total and cardiorespiratory mortality. In addition, the reanalysis of the American Cancer Society cohort shows an association between fine particle and sulfate concentrations and lung cancer mortality. Recently, several studies have highlighted the adverse effects of PM specifically from mobile sources. 105, 106 Studies have also focused on health effects due to PM exposures on or near roadways. 107 Although these studies include all air pollution sources, including both spark-ignition (gasoline) and diesel powered vehicles, they indicate that exposure to PM emissions near roadways, thus dominated by mobile sources, are associated with health effects. Additional information on near-roadway health effects can be found in section III.B.2.d of this preamble. 105 Laden, F.; Neas, L.M.; Dockery, D.W.; Schwartz, J. (2000) Association of Fine Particulate Matter from Different Sources with Daily Mortality in Six U.S. Cities. Environmental Health Perspectives 108: 941-947. 106 Janssen, N.A.H.; Schwartz, J.; Zanobetti, A.; Suh, H.H. (2002) Air Conditioning and Source-Specific Particles as Modifiers of the Effect of PM 10 on Hospital Admissions for Heart and Lung Disease. Environmental Health Perspectives 110: 43-49. 107 Riediker, M.; Cascio, W.E.; Griggs, T.R.; Herbst, M.C.; Bromberg, P.A.; Neas, L.; Williams, R.W.; Devlin, R.B. (2003) Particulate Matter Exposures in Cars is Associated with Cardiovascular Effects in Healthy Young Men. Am. J. Respir. Crit. Care Med. 169: 934-940. 3. Welfare Effects of PM a. Visibility i. Background Visibility can be defined as the degree to which the atmosphere is transparent to visible light. 108 Visibility impairment manifests in two principal ways: as local visibility impairment and as regional haze. 109 Local visibility impairment may take the form of a localized plume, a band or layer of discoloration appearing well above the terrain as a result from complex local meteorological conditions. Alternatively, local visibility impairment may manifest as an urban haze, sometimes referred to as a “brown cloud.” This urban haze is largely caused by emissions from multiple sources in the urban areas and is not typically attributable to only one nearby source or to long-range transport. The second type of visibility impairment, regional haze, usually results from multiple pollution sources spread over a large geographic region. Regional haze can impair visibility over large regions and across states. 108 National Research Council, 1993. Protecting Visibility in National Parks and Wilderness Areas. National Academy of Sciences Committee on Haze in National Parks and Wilderness Areas. National Academy Press, Washington, DC. This document is available in Docket EPA-HQ-OAR-2005-0036. This book can be viewed on the National Academy Press Web site at http://www.nap.edu/books/0309048443/html/ . 109 See discussion in U.S. EPA, National Ambient Air Quality Standards for Particulate Matter; Proposed Rule; January 17, 2006, Vol 71, p. 2676. This information is available electronically at http://epa.gov/fedrgstr/EPA-AIR/2006/January/Day-17/a177.pdf . Visibility is important because it has direct significance to people's enjoyment of daily activities in all parts of the country. Individuals value good visibility for the well-being it provides them directly, where they live and work, and in places where they enjoy recreational opportunities. Visibility is also highly valued in significant natural areas such as national parks and wilderness areas, and special emphasis is given to protecting visibility in these areas. For more information on visibility see the 2004 PM AQCD as well as the 2005 PM Staff Paper. 110 111 110 U.S. EPA (2004) Air Quality Crite [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%3AE7-2667. Public record. Not legal advice.