# National Ambient Air Quality Standards for Lead > Briefs, arguments, decisions, and more. URL: https://www.frixlaw.com/law-library/documents/fr%3A2014-30681 ## Record - **Collection:** Federal Register - **Document type:** Proposed Rule - **Published:** January 5, 2015 - **Citation:** 80 FR 278 ## Text ENVIRONMENTAL PROTECTION AGENCY 40 CFR Part 50 [EPA-HQ-OAR-2010-0108; FRL-9915-57-OAR] RIN 2060-AQ44 National Ambient Air Quality Standards for Lead AGENCY: Environmental Protection Agency. ACTION: Proposed rule. SUMMARY: Based on the Environmental Protection Agency's (EPA's) review of the air quality criteria and the national ambient air quality standards (NAAQS) for lead (Pb), the EPA is proposing to retain the current standards, without revision. DATES: Comments must be received on or before April 6, 2015. Public Hearings: If, by January 26, 2015, the EPA receives a request from a member of the public to speak at a public hearing concerning the proposed decision, we will hold a public hearing, with information about the hearing provided in a subsequent notice in the Federal Register . ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-OAR-2010-0108 by one of the following methods: • Federal eRulemaking Portal: http://www.regulations.gov: Follow the on-line instructions for submitting comments. • Email: a-and-r-Docket@epa.gov. Include docket ID No. EPA-HQ-OAR-2010-0108 in the subject line of the message. • Fax: 202-566-9744. • Mail: Docket No. EPA-HQ-OAR-2010-0108, Environmental Protection Agency, Mail Code 28221T, 1200 Pennsylvania Ave. NW., Washington, DC 20460. • Hand Delivery: Docket No. EPA-HQ-OAR-2010-0108, Environmental Protection Agency, EPA WJC West Building, Room 3334, 1301 Constitution Ave. NW., Washington, DC. Such deliveries are only accepted during the Docket's normal hours of operation, and special arrangements should be made for deliveries of boxed information. Instructions: Direct your comments to Docket ID No. EPA-HQ-OAR-2010-0108. The EPA's policy is that all comments received will be included in the public docket without change and may be made available online at www.regulations.gov, including any personal information provided, unless the comment includes information claimed to be Confidential Business Information (CBI) or other information whose disclosure is restricted by statute. Do not submit information that you consider to be CBI or otherwise protected through www.regulations.gov or email. The www.regulations.gov Web site is an “anonymous access” system, which means the EPA will not know your identity or contact information unless you provide it in the body of your comment. If you send an email comment directly to the EPA without going through www.regulations.gov, your email address will be automatically captured and included as part of the comment that is placed in the public docket and made available on the Internet. If you submit an electronic comment, the EPA recommends that you include your name and other contact information in the body of your comment and with any disk or CD-ROM you submit. If the EPA cannot read your comment due to technical difficulties and cannot contact you for clarification, the EPA may not be able to consider your comment. Electronic files should avoid the use of special characters, any form of encryption, and be free of any defects or viruses. For additional information about the EPA's public docket, visit the EPA Docket Center homepage at http://www.epa.gov/epahome/dockets.htm. Public Hearing: To request a public hearing or information pertaining to a public hearing on this document, contact Ms. Eloise Shepherd, Health and Environmental Impacts Division, Office of Air Quality Planning and Standards (C504-02), U.S. Environmental Protection Agency, Research Triangle Park, NC 27711; telephone number (919) 541-5507; fax number (919) 541-0804; email address: shepherd.eloise@epa.gov. See the SUPPLEMENTARY INFORMATION for further information about a possible public hearing. Docket: All documents in the docket are listed on the www.regulations.gov Web site. This includes documents in the rulemaking docket (Docket ID No. EPA-HQ-OAR-2010-0108) and a separate docket, established for the Integrated Science Assessment for this review (Docket ID No. EPA-HQ-ORD-2011-0051) that has been incorporated by reference into the rulemaking docket. All documents in these dockets 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 may be viewed, with prior arrangement, at the EPA Docket Center. Publicly available docket materials are available either electronically in www.regulations.gov or in hard copy at the Air and Radiation Docket Information Center, EPA/DC, WJC West Building, 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 and Radiation Docket Information Center is (202) 566-1742. FOR FURTHER INFORMATION CONTACT: Dr. Deirdre L. Murphy, Health and Environmental Impacts Division, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Mail Code C504-06, Research Triangle Park, NC 27711; telephone: (919) 541-0729; fax: (919) 541-0237; email: murphy.deirdre@epa.gov. To request a public hearing or information pertaining to a public hearing on this document, contact Ms. Eloise Shepherd, Health and Environmental Impacts Division, Office of Air Quality Planning and Standards (C504-02), U.S. Environmental Protection Agency, Research Triangle Park, NC 27711; telephone number (919) 541-5507; fax number (919) 541-0804; email address: shepherd.eloise@epa.gov. SUPPLEMENTARY INFORMATION: General Information Preparing Comments for the EPA 1. Submitting CBI. Do not submit this information to the EPA through www.regulations.gov or email. Clearly mark the part or all of the information that you claim to be CBI. For CBI information in a disk or CD-ROM that you mail to the EPA, mark the outside of the disk or CD-ROM as CBI and then identify electronically within the disk or CD-ROM the specific information that is claimed as CBI. In addition to one complete version of the comment that includes information claimed as CBI, a copy of the comment that does not contain the information claimed as CBI must be submitted for inclusion in the public docket. Information so marked will not be disclosed except in accordance with procedures set forth in 40 CFR part 2. 2. Tips for Preparing Your Comments. When submitting comments, remember to: • Identify the rulemaking by docket number and other identifying information (subject heading, Federal Register date and page number). • Follow directions—the agency may ask you to respond to specific questions or organize comments by referencing a Code of Federal Regulations (CFR) part or section number. • Explain why you agree or disagree, suggest alternatives, and substitute language for your requested changes. • Describe any assumptions and provide any technical information and/or data that you used. • Provide specific examples to illustrate your concerns, and suggest alternatives. • Explain your views as clearly as possible, avoiding the use of profanity or personal threats. • Make sure to submit your comments by the comment period deadline identified. Availability of Information Related to This Action A number of the documents that are relevant to this action are available through the EPA's Office of Air Quality Planning and Standards (OAQPS) Technology Transfer Network (TTN) Web site at http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html. These documents include the Plan for Review of the National Ambient Air Quality Standards for Lead (USEPA, 2011a), available at http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_pd.html, the Integrated Science Assessment for Lead (USEPA, 2013a), available at http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_isa.html, the Review of the National Ambient Air Quality Standards for Lead: Risk and Exposure Assessment Planning Document (USEPA, 2011b), available at http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_pd.html, and the Policy Assessment for the Review of the Lead National Ambient Air Quality Standards (USEPA, 2014), available at http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_pa.html. These and other related documents are also available for inspection and copying in the EPA docket identified above. Information About a Possible Public Hearing To request a public hearing or information pertaining to a public hearing on this document, contact Ms. Eloise Shepherd, Health and Environmental Impacts Division, Office of Air Quality Planning and Standards (C504-02), U.S. Environmental Protection Agency, Research Triangle Park, NC 27711; telephone number (919) 541-5507; fax number (919) 541-0804; email address: shepherd.eloise@epa.gov. Table of Contents The following topics are discussed in this preamble: I. Background A. Legislative Requirements B. Related Lead Control Programs C. Review of the Air Quality Criteria and Standards for Lead D. Multimedia, Multipathway Aspects of Lead E. Air Quality Monitoring II. Rationale for Proposed Decision on the Primary Standard A. General Approach 1. Approach in the Last Review 2. Approach for the Current Review B. Health Effects Information 1. Array of Effects 2. Critical Periods of Exposure 3. Nervous System Effects in Children 4. At-Risk Populations 5. Potential Impacts on Public Health C. Blood Lead as a Biomarker of Exposure and Relationships With Air Lead D. Summary of Risk and Exposure Assessment Information 1. Overview 2. Summary of Design Aspects 3. Key Limitations and Uncertainties 4. Summary of Risk Estimates and Key Observations E. Conclusions on Adequacy of the Current Primary Standard 1. Evidence-Based Considerations in the Policy Assessment 2. Exposure/Risk-Based Considerations in the Policy Assessment 3. CASAC Advice 4. Administrator's Proposed Conclusions on the Adequacy of the Current Primary Standard III. Rationale for Proposed Decision on the Secondary Standard A. General Approach 1. Approach in the Last Review 2. Approach for the Current Review B. Welfare Effects Information C. Summary of Risk Assessment Information D. Conclusions on Adequacy of the Current Secondary Standard 1. Evidence- and Risk-Based Considerations in the Policy Assessment 2. CASAC Advice 3. Administrator's Proposed Conclusions on the Adequacy of the Current Standard IV. Statutory and Executive Order Reviews A. Executive Order 12866: Regulatory Planning and Review and Executive Order 13563: Improving Regulation and Regulatory Review B. Paperwork Reduction Act C. Regulatory Flexibility Act 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 and Advancement Act J. Executive Order 12898: Federal Actions To Address Environmental Justice in Minority Populations and Low-Income Populations K. Determination Under Section 307(d) References I. Background A. Legislative Requirements Two sections of the Clean Air Act (CAA or the Act) govern the establishment and revision of the NAAQS. Section 108 (42 U.S.C. 7408) directs the Administrator to identify and list certain air pollutants and then to issue air quality criteria for those pollutants. The Administrator is to list those air pollutants that in her “judgment, cause or contribute to air pollution which may reasonably be anticipated to endanger public health or welfare;” “the presence of which in the ambient air results from numerous or diverse mobile or stationary sources;” and “for which . . . [the Administrator] plans to issue air quality criteria . . .” Air quality criteria are intended to “accurately reflect the latest scientific knowledge useful in indicating the kind and extent of all identifiable effects on public health or welfare which may be expected from the presence of [a] pollutant in the ambient air . . .” 42 U.S.C. 7408(b). Section 109 (42 U.S.C. 7409) directs the Administrator to propose and promulgate “primary” and “secondary” NAAQS for pollutants for which air quality criteria are issued. Section 109(b)(1) defines a primary standard as one “the attainment and maintenance of which in the judgment of the Administrator, based on such criteria and allowing an adequate margin of safety, are requisite to protect the public health.” 1 A secondary standard, as defined in section 109(b)(2), must “specify a level of air quality the attainment and maintenance of which, in the judgment of the Administrator, based on such criteria, is requisite to protect the public welfare from any known or anticipated adverse effects associated with the presence of [the] pollutant in the ambient air.” 2 1 The legislative history of section 109 indicates that a primary standard is to be set at “the maximum permissible ambient air level . . . which will protect the health of any [sensitive] group of the population,” and that for this purpose “reference should be made to a representative sample of persons comprising the sensitive group rather than to a single person in such a group.” See S. Rep. No. 91-1196, 91st Cong., 2d Sess. 10 (1970). 2 Welfare effects as defined in section 302(h) (42 U.S.C. 7602(h)) include, but are not limited to, “effects on soils, water, crops, vegetation, man-made materials, animals, wildlife, weather, visibility and climate, damage to and deterioration of property, and hazards to transportation, as well as effects on economic values and on personal comfort and well-being.” The requirement that primary standards provide an adequate margin of safety was intended to address uncertainties associated with inconclusive scientific and technical information available at the time of standard setting. It was also intended to provide a reasonable degree of protection against hazards that research has not yet identified. See Lead Industries Association v. EPA, 647 F.2d 1130, 1154 (D.C. Cir 1980), cert. denied, 449 U.S. 1042 (1980); American Petroleum Institute v. Costle, 665 F.2d 1176, 1186 (D.C. Cir. 1981), cert. denied, 455 U.S. 1034 (1982); American Farm Bureau Federation v. EPA, 559 F.3d 512, 533 (D.C. Cir. 2009); Association of Battery Recyclers v. EPA, 604 F.3d 613, 617-18 (D.C. Cir. 2010). Both kinds of uncertainties are components of the risk associated with pollution at levels below those at which human health effects can be said to occur with reasonable scientific certainty. Thus, in selecting primary standards that provide an adequate margin of safety, the Administrator is seeking not only to prevent pollution levels that have been demonstrated to be harmful but also to prevent lower pollutant levels that may pose an unacceptable risk of harm, even if the risk is not precisely identified as to nature or degree. The CAA does not require the Administrator to establish a primary NAAQS at a zero-risk level or at background concentration levels, see Lead Industries v. EPA, 647 F.2d at 1156 n.51, but rather at a level that reduces risk sufficiently so as to protect public health with an adequate margin of safety. In addressing the requirement for an adequate margin of safety, the EPA considers such factors as the nature and severity of the health effects involved, the size of sensitive population(s) at risk, 3 and the kind and degree of the uncertainties that must be addressed. The selection of any particular approach to providing an adequate margin of safety is a policy choice left specifically to the Administrator's judgment. See Lead Industries Association v. EPA, 647 F.2d at 1161-62. 3 As used here and similarly throughout this notice, the term population (or group) refers to persons having a quality or characteristic in common, such as a specific pre-existing illness or a specific age or life stage. As discussed more fully in section II.B.4 below, the identification of sensitive groups (called at-risk groups or at-risk populations) involves consideration of susceptibility and vulnerability. In setting primary and secondary standards that are “requisite” to protect public health and welfare, respectively, as provided in section 109(b), the EPA's task is to establish standards that are neither more nor less stringent than necessary for these purposes. In so doing, the EPA may not consider the costs of implementing the standards. See generally, Whitman v. American Trucking Associations, 531 U.S. 457, 465-472, 475-76 (2001). Likewise, “[a]ttainability and technological feasibility are not relevant considerations in the promulgation of national ambient air quality standards.” American Petroleum Institute v. Costle, 665 F.2d at 1185. Section 109(d)(1) requires that “not later than December 31, 1980, and at 5-year intervals thereafter, the Administrator shall complete a thorough review of the criteria published under section 108 and the national ambient air quality standards . . . and shall make such revisions in such criteria and standards and promulgate such new standards as may be appropriate. . . .” Section 109(d)(2) requires that an independent scientific review committee “shall complete a review of the criteria . . . and the national primary and secondary ambient air quality standards . . . and shall recommend to the Administrator any new . . . standards and revisions of existing criteria and standards as may be appropriate. . . .” Since the early 1980s, this independent review function has been performed by the Clean Air Scientific Advisory Committee (CASAC). 4 4 Lists of CASAC members and of members of the CASAC Lead Review Panel are available at: http://yosemite.epa.gov/sab/sabproduct.nsf/WebCASAC/CommitteesandMembership?OpenDocument. B. Related Lead Control Programs States are primarily responsible for ensuring attainment and maintenance of the NAAQS. Under section 110 of the Act (42 U.S.C. 7410) and related provisions, states are to submit, for EPA approval, state implementation plans (SIPs) that provide for the attainment and maintenance of such standards through control programs directed to sources of the pollutants involved. The states, in conjunction with the EPA, also administer the Prevention of Significant Deterioration program (42 U.S.C. 7470-7479) for these pollutants. The NAAQS is only one component of the EPA's programs to address Pb in the environment. Federal programs additionally provide for nationwide reductions in air emissions of these and other air pollutants through the Federal Motor Vehicle Control program under Title II of the Act (42 U.S.C. 7521-7574), which involves controls for automobile, truck, bus, motorcycle, nonroad engine, and aircraft emissions; the new source performance standards under section 111 of the Act (42 U.S.C. 7411); emissions standards for solid waste incineration units and the national emission standards for hazardous air pollutants (NESHAP) under sections 129 (42 U.S.C. 7429) and 112 (42 U.S.C. 7412) of the Act, respectively. The EPA has taken a number of actions associated with these air pollution control programs since the last review of the Pb NAAQS, including completion of several regulations which will result in reduced Pb emissions from stationary sources regulated under the CAA sections 112 and 129. For example, in January 2012, the EPA updated the NESHAP for the secondary lead smelting source category (77 FR 555, January 5, 2012). These amendments to the original maximum achievable control technology standards apply to facilities nationwide that use furnaces to recover Pb from Pb-bearing scrap, mainly from automobile batteries (15 existing facilities, one under construction). By the effective date in 2014, this action is estimated to result in a Pb emissions reduction of 13.6 tons per year (tpy) across the category (a 68% reduction). Somewhat lesser Pb emissions reductions are also expected from regulations completed in 2013 for commercial and industrial solid waste incineration units (78 FR 9112, February 7, 2013), as well as several other regulations since 2007 (72 FR 73179, December 26, 2007; 72 FR 74088, December 28, 2007; 73 FR 225, November 20, 2008; 78 FR 10006, February 12, 2013; 76 FR 15372, March 21, 2011; 78 FR 7138, January 31, 2013; 74 FR 51368, October 6, 2009; Policy Assessment, Appendix 2A). The presentation below briefly summarizes additional ongoing activities that, although not directly pertinent to the review of the NAAQS, are associated with controlling environmental Pb levels and human Pb exposures more broadly. Among those identified are the EPA programs intended to encourage exposure reduction programs in other countries. Reducing Pb exposures has long been recognized as a federal priority as environmental and public health agencies continue to grapple with soil and dust Pb levels from the historical use of Pb in paint and gasoline and from other sources (Alliance to End Childhood Lead Poisoning, 1991; 62 FR 19885, April 23, 1997; 66 FR 52013, October 11, 2001; 68 FR 19931, April 23, 2003). A broad range of federal programs beyond those that focus on air pollution control provide for nationwide reductions in environmental releases and human exposures. For example, pursuant to section 1412 of the Safe Drinking Water Act (SDWA), the EPA regulates Pb in public drinking water systems through corrosion control and other utility actions which work together to minimize Pb levels at the tap (40 CFR 141.80-141.91). Under section 1417 of the SDWA, pipes, fittings and fixtures for potable water applications may not be used or introduced into commerce unless they are considered “lead free” as defined by that Act (40 CFR 141.43). 5 Additionally, federal Pb abatement programs provide for the reduction in human exposures and environmental releases from in-place materials containing Pb ( e.g., Pb-based paint, urban soil and dust, and contaminated waste sites). Federal regulations on disposal of Pb-based paint waste help facilitate the removal of Pb-based paint from residences (68 FR 36487, June 18, 2003). 5 Effective in January 2014, the amount of Pb permitted in pipes, fittings, and fixtures was lowered (see “Summary of the Reduction of Lead in Drinking Water Act and Frequently Asked Questions” at http://water.epa.gov/drink/info/lead/index.cfm ). Federal programs to reduce exposure to Pb in paint, dust, and soil are specified under the comprehensive federal regulatory framework developed under the Residential Lead-Based Paint Hazard Reduction Act (Title X). Under Title X (codified as Title IV of the Toxic Substances Control Act [TSCA]), the EPA has established regulations and associated programs in six categories: (1) Training, certification and work practice requirements for persons engaged in Pb-based paint activities (abatement, inspection and risk assessment); accreditation of training providers; and authorization of state and tribal Pb-based paint programs; (2) training, certification, and work practice requirements for persons engaged in home renovation, repair and painting (RRP) activities; accreditation of RRP training providers; and authorization of state and tribal RRP programs; (3) ensuring that, for most housing constructed before 1978, information about Pb-based paint and Pb-based paint hazards flows from sellers to purchasers, from landlords to tenants, and from renovators to owners and occupants; (4) establishing standards for identifying dangerous levels of Pb in paint, dust and soil; (5) providing grant funding to establish and maintain state and tribal Pb-based paint programs; and (6) providing information on Pb hazards to the public, including steps that people can take to protect themselves and their families from Pb-based paint hazards. The most recent rule issued under Title IV of TSCA is for the Lead Renovation, Repair and Painting Program (73 FR 21692, April 22, 2008), which became fully effective in April 2010 and which applies to compensated renovators and maintenance professionals who perform RRP activities in housing and child-care facilities built prior to 1978. To foster adoption of the rule's measures, the EPA has been conducting an extensive education and outreach campaign to promote awareness of these new requirements among both the regulated entities and the consumers who hire them ( http://www2.epa.gov/lead/renovation-repair-and-painting-program ). In addition, the EPA is investigating whether Pb hazards are also created by RRP activities in public and commercial buildings, in which case the EPA plans to issue RRP requirements, where appropriate, for this class of buildings (79 FR 31072, May 30, 2014). Programs associated with the Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA or Superfund) and Resource Conservation Recovery Act (RCRA) also implement abatement programs, reducing exposures to Pb and other pollutants. For example, the EPA determines and implements protective levels for Pb in soil at Superfund sites and RCRA corrective action facilities. Federal programs, including those implementing RCRA, provide for management of hazardous substances in hazardous and municipal solid waste ( e.g., 66 FR 58258, November 20, 2001). Federal regulations concerning batteries in municipal solid waste facilitate the collection and recycling or proper disposal of batteries containing Pb. 6 Similarly, federal programs provide for the reduction in environmental releases of hazardous substances such as Pb in the management of wastewater ( http://www.epa.gov/owm/ ). 6 See, e.g., “Implementation of the Mercury-Containing and Rechargeable Battery Management Act” at http://www.epa.gov/epawaste/hazard/recycling/battery.pdf and “Municipal Solid Waste Generation, Recycling, and Disposal in the United States: Facts and Figures for 2005 http://www.epa.gov/epawaste/nonhaz/municipal/pubs/msw-2005.pdf. A variety of federal nonregulatory programs also provide for reduced environmental release of Pb-containing materials by encouraging pollution prevention, promotion of reuse and recycling, reduction of priority and toxic chemicals in products and waste, and conservation of energy and materials. These include the “Resource Conservation Challenge” ( http://www.epa.gov/epaoswer/osw/conserve/index.htm ), the “National Waste Minimization Program” ( http://www.epa.gov/epaoswer/hazwaste/minimize/leadtire.htm ), “Plug in to eCycling” (a partnership between the EPA and consumer electronics manufacturers and retailers; http://www.epa.gov/epaoswer/hazwaste/recycle/electron/crt.htm#crts ), and activities to reduce the practice of backyard trash burning ( http://www.epa.gov/msw/backyard/pubs.htm ). The EPA's research program identifies, encourages and conducts research needed to locate and assess serious risks and to develop methods and tools to characterize and help reduce risks related to Pb exposure. For example, the EPA's Integrated Exposure Uptake Biokinetic Model for Lead in Children (IEUBK model) is widely used and accepted as a tool that informs the evaluation of site-specific data. More recently, in recognition of the need for a single model that predicts Pb concentrations in tissues for children and adults, the EPA has been developing the All Ages Lead Model (AALM) to provide researchers and risk assessors with a pharmacokinetic model capable of estimating blood, tissue, and bone concentrations of Pb based on estimates of exposure over the lifetime of the individual (USEPA, 2006a, sections 4.4.5 and 4.4.8; USEPA, 2013a, section 3.6). The EPA's research activities on substances including Pb, such as those identified here, focus on improving our characterization of health and environmental effects, exposure, and control or management of environmental releases (see http://www.epa.gov/research/ ). Other federal agencies also participate in programs intended to reduce Pb exposures. For example, programs of the Centers for Disease Control and Prevention (CDC) provide for the tracking of children's blood Pb levels in the U.S. and provide guidance on levels at which medical and environmental case management activities should be implemented (CDC, 2012; ACCLPP, 2012). As a result of coordinated, intensive efforts at the national, state and local levels, including those programs described above, blood Pb levels in all segments of the population have continued to decline from levels observed in the past. For example, blood Pb levels for the general population of children 1 to 5 years of age have dropped to a geometric mean level of 1.17 μg/dL in the 2009-2010 National Health and Nutrition Examination Survey (NHANES) as compared to the geometric mean in 1999-2000 of 2.23 µg/dL and in 1988-1991 of 3.6 μg/dL (USEPA, 2013a, section 3.4.1; USEPA, 2006a, AX4-2). Similarly, blood Pb levels in non-Hispanic black, Mexican American and lower socioeconomic groups, which are generally higher than those for the general population, have also declined (USEPA, 2013a, sections 3.4.1, 5.2.3 and 5.2.4; Jones et al., 2009). The EPA also participates in a broad range of international programs focused on reducing environmental releases and human exposures in other countries. For example, the Partnership for Clean Fuels and Vehicles program engages governments and stakeholders in developing countries to eliminate Pb in gasoline globally. 7 From 2007 to 2011, the number of countries known to still be using leaded gasoline was reduced from just over 20 to six, with three of the six also offering unleaded fuel. All six were expected to eliminate Pb from fuel in the near future (USEPA, 2011c). The EPA is a contributor to the Global Alliance to Eliminate Lead Paint, a cooperative initiative jointly led by the World Health Organization and the United Nations Environment Programme (UNEP) to focus and catalyze the efforts to achieve international goals to prevent children's Pb exposure from paints containing Pb and to minimize occupational exposures to Pb paint. This alliance has the broad objective of promoting a phase-out of the manufacture and sale of paints containing Pb and eventually to eliminate the risks that such paints pose. The UNEP is also engaged on the problem of managing wastes containing Pb, including Pb-containing batteries. The Governing Council of the UNEP, of which the U.S. is a member, has adopted decisions focused on promoting the environmentally sound management of products, wastes and contaminated sites containing Pb and reducing risks to human health and the environment from Pb and cadmium throughout the life cycles of those substances (UNEP Governing Council, 2011, 2013). The EPA is also engaged in the issue of environmental impacts of spent Pb-acid batteries internationally through the Commission for Environmental Cooperation (CEC), where the EPA Administrator along with the cabinet-level or equivalent representatives of Mexico and Canada comprise the CEC's senior governing body (CEC Council). 8 7 International programs in which the U.S. participates, including those identified here, are described at: http://epa.gov/international/air/pcfv.html, http://www.unep.org/transport/pcfv/, http://www.unep.org/hazardoussubstances/Home/tabid/197/hazardoussubstances/LeadCadmium/PrioritiesforAction/GAELP/tabid/6176/Default.aspx. 8 The CEC was established to support cooperation among the North American Free Trade Agreement partners to address environmental issues of continental concern, including the environmental challenges and opportunities presented by continent-wide free trade. C. Review of the Air Quality Criteria and Standards for Lead Unlike pollutants such as particulate matter and carbon monoxide, air quality criteria had not been issued for Pb as of the enactment of the CAA of 1970, which first set forth the requirement to set NAAQS based on air quality criteria. In the years just after enactment of the CAA, the EPA did not list Pb under Section 108 of the Act, having determined to control Pb air pollution through regulations to phase out the use of Pb additives in gasoline (See 41 FR 14921, April 8, 1976). However, the decision not to list Pb under Section 108 was challenged by environmental and public health groups, and the U.S. District Court for the Southern District of New York concluded that the EPA was required to list Pb under Section 108. Natural Resources Defense Council v. EPA, 411 F. Supp. 864 21 (S.D. N.Y. 1976), affirmed, 545 F.2d 320 (2d Cir. 1978). Accordingly, on April 8, 1976, the EPA published a notice in the Federal Register that Pb had been listed under Section 108 as a criteria pollutant (41 FR 14921, April 8, 1976) and on October 5, 1978, the EPA promulgated primary and secondary NAAQS for Pb under Section 109 of the Act (43 FR 46246, October 5, 1978). Both primary and secondary standards were set at a level of 1.5 micrograms per cubic meter (μg/m 3 ), measured as Pb in total suspended particles (Pb-TSP), not to be exceeded by the maximum arithmetic mean concentration averaged over a calendar quarter. These standards were based on the 1977 Air Quality Criteria for Lead (USEPA, 1977). The first review of the Pb standards was initiated in the mid-1980s. The scientific assessment for that review is described in the 1986 Air Quality Criteria for Lead (USEPA, 1986a; henceforth referred to as the 1986 CD), the associated Addendum (USEPA, 1986b) and the 1990 Supplement (USEPA, 1990a). As part of the review, the agency designed and performed human exposure and health risk analyses (USEPA, 1989), the results of which were presented in a 1990 Staff Paper (USEPA, 1990b). Based on the scientific assessment and the human exposure and health risk analyses, the 1990 Staff Paper presented recommendations for consideration by the Administrator (USEPA, 1990b). After consideration of the documents developed during the review and the significantly changed circumstances since Pb was listed in 1976, the agency did not propose any revisions to the 1978 Pb NAAQS. In a parallel effort, the agency developed the broad, multi-program, multimedia, integrated U.S. Strategy for Reducing Lead Exposure (USEPA, 1991). As part of implementing this strategy, the agency focused efforts primarily on regulatory and remedial clean-up actions aimed at reducing Pb exposures from a variety of nonair sources judged to pose more extensive public health risks to U.S. populations, as well as on actions to reduce Pb emissions to air, such as bringing more areas into compliance with the existing Pb NAAQS (USEPA, 1991). The EPA continues this broad, multi-program, multimedia approach to reducing Pb exposures today, as described in section I.B above. The last review of the Pb air quality criteria and standards was initiated in November 2004 (69 FR 64926, November 9, 2004); the agency's plans for preparation of the Air Quality Criteria Document and conduct of the NAAQS review were presented in documents completed in 2005 and early 2006 (USEPA, 2005a; USEPA 2006b). 9 The schedule for completion of the review was governed by a judicial order in Missouri Coalition for the Environment v. EPA (No. 4:04CV00660 ERW, September 14, 2005; and amended on April 29, 2008 and July 1, 2008). 9 In the current review, these two documents have been combined in the Integrated Review Plan for the National Ambient Air Quality Standards for Lead (USEPA, 2011a). The scientific assessment for the review is described in the 2006 Air Quality Criteria for Lead (USEPA, 2006a; henceforth referred to as the 2006 CD), multiple drafts of which received review by CASAC and the public. The EPA also conducted human exposure and health risk assessments and a pilot ecological risk assessment for the review, after consultation with CASAC and receiving public comment on a draft analysis plan (USEPA, 2006c). Drafts of these quantitative assessments were reviewed by CASAC and the public. The pilot ecological risk assessment was released in December 2006 (ICF International, 2006), and the final health risk assessment report was released in November 2007 (USEPA, 2007a). The policy assessment, based on both of these assessments, air quality analyses and key evidence from the 2006 CD, was presented in the Staff Paper (USEPA, 2007b), a draft of which also received CASAC and public review. The final Staff Paper presented OAQPS staff's evaluation of the public health and welfare policy implications of the key studies and scientific information contained in the 2006 CD and presented and interpreted results from the quantitative risk/exposure analyses conducted for this review. Based on this evaluation, the Staff Paper presented OAQPS staff recommendations that the Administrator give consideration to substantially revising the primary and secondary standards to a range of levels at or below 0.2 μg/m 3 . Immediately subsequent to completion of the Staff Paper, the EPA issued an advance notice of proposed rulemaking (ANPR) that was signed by the Administrator on December 5, 2007 (72 FR 71488, December 17, 2007). 10 CASAC provided advice and recommendations to the Administrator with regard to the Pb NAAQS based on its review of the ANPR and the previously released final Staff Paper and risk assessment reports. In 2008, the proposed decision on revisions to the Pb NAAQS was signed on May 1 and published in the Federal Register on May 20 (73 FR 29184, May 20, 2008). Members of the public provided comments and the CASAC Pb Panel also provided advice and recommendations to the Administrator based on its review of the proposal notice. The final decision on revisions to the Pb NAAQS was signed on October 15, 2008, and published in the Federal Register on November 12, 2008 (73 FR 66964, November 12, 2008). 10 The ANPR, one of the features of the revised NAAQS review process that EPA instituted in 2006, was replaced by reinstatement of the Policy Assessment prepared by OAQPS staff (previously termed the OAQPS Staff Paper) in 2009 (Jackson, 2009). The November 2008 notice described the EPA's decision to revise the primary and secondary NAAQS for Pb, as discussed more fully in section II.A.1 below. In consideration of the much-expanded health effects evidence on neurocognitive effects of Pb in children, the EPA substantially revised the primary standard from a level of 1.5 μg/m 3 to a level of 0.15 μg/m 3 . The averaging time was revised to a rolling 3-month period with a maximum (not-to-be-exceeded) form, evaluated over a 3-year period. The indicator of Pb-TSP was retained, reflecting the evidence that Pb particles of all sizes pose health risks. The secondary standard was revised to be identical in all respects to the revised primary standard (40 CFR 50.16). Revisions to the NAAQS were accompanied by revisions to the data handling procedures, the treatment of exceptional events and the ambient air monitoring and reporting requirements, as well as emissions inventory reporting requirements. One aspect of the revised data handling requirements is the allowance for the use of monitoring for particulate matter with mean diameter below 10 microns (Pb-PM 10 ) for Pb NAAQS attainment purposes in certain limited circumstances at non-source-oriented sites. Subsequent to the 2008 rulemaking, additional revisions were made to the monitoring network requirements (75 FR 81126, December 27, 2010). Guidance on the approach for implementation of the new standards was described in the Federal Register notices for the proposed and final rules (73 FR 29184, May 20, 2008; 73 FR 66964, November 12, 2008). On February 26, 2010, the EPA formally initiated its current review of the air quality criteria and standards for Pb, requesting the submission of recent scientific information on specified topics (75 FR 8934, February 26, 2010). Soon after this, the EPA held a workshop to discuss the policy-relevant science, which informed identification of key policy issues and questions to frame the review of the Pb NAAQS (75 FR 20843, April 21, 2010). Drawing from the workshop discussions, the EPA developed the draft Integrated Review Plan (draft IRP, USEPA, 2011d). The draft IRP was made available in late March 2011 for consultation with the CASAC Pb Review Panel and for public comment (76 FR 20347, April 12, 2011). This document was discussed by the Panel via a publicly accessible teleconference consultation on May 5, 2011 (76 FR 21346, April 15, 2011; Frey, 2011a). The final Integrated Review Plan for the National Ambient Air Quality Standards for Lead (IRP), developed in consideration of the CASAC consultation and public comment, was released in November 2011 (USEPA, 2011a; 76 FR 76972, December 9, 2011). In developing the Integrated Science Assessment (ISA) for this review, the EPA held a workshop in December 2010 to discuss with invited scientific experts preliminary draft materials and released the first external review draft of the document for CASAC review and public comment in May 2011 (USEPA, 2011e; 76 FR 26284, May 6, 2011; 76 FR 36120, June 21, 2011). The CASAC Pb Review Panel met at a public meeting on July 20, 2011, to review the draft ISA (76 FR 36120, June 21, 2011). The CASAC provided comments in a December 9, 2011, letter to the EPA Administrator (Frey and Samet, 2011). The second external review draft ISA was released for CASAC review and public comment in February 2012 (USEPA, 2012a; 77 FR 5247, February 2, 2012) and was the subject of a public meeting on April 10-11, 2012 (77 FR 14783, March 13, 2012). The CASAC provided comments in a July 20, 2012, letter (Samet and Frey, 2012). The third external review draft was released for CASAC review and public comment in November 2012 (USEPA, 2012b; 77 FR 70776, November 27, 2012) and was the subject of a public meeting on February 5-6, 2013 (78 FR 938, January 7, 2013). The CASAC provided comments in a June 4, 2013, letter (Frey, 2013a). The final ISA was released in late June 2013 (USEPA, 2013a, henceforth referred to as the ISA; 78 FR 38318, June 26, 2013). In June 2011, the EPA developed and released the Risk and Exposure Assessment Planning Document (REA Planning Document) for consultation with CASAC and public comment (USEPA, 2011b; 76 FR 58509). This document presented a critical evaluation of the information related to Pb human and ecological exposure and risk ( e.g., data, modeling approaches) newly available in this review, with a focus on consideration of the extent to which new or substantially revised REAs for health and ecological risk might be warranted by the newly available evidence. Evaluation of the newly available information with regard to designing and implementing health and ecological REAs for this review led us to conclude that the currently available information did not provide a basis for developing new quantitative risk and exposure assessments that would have substantially improved utility for informing the agency's consideration of health and welfare effects and evaluation of the adequacy of the current primary and secondary standards, respectively (REA Planning Document, sections 2.3 and 3.3, respectively). The CASAC Pb Review Panel provided consultative advice on that document and its conclusions at a public meeting on July 21, 2011 (76 FR 36120, June 21, 2011; Frey, 2011b). Based on their consideration of the REA Planning Document analysis, the CASAC Pb Review Panel generally concurred with the conclusion that a new REA was not warranted in this review (Frey, 2011b; Frey, 2013b). In consideration of the conclusions reached in the REA Planning Document and CASAC's consultative advice, the EPA has not developed REAs for health and ecological risk for this review. Accordingly, we consider the risk assessment findings from the last review for human exposure and health risk (USEPA, 2007a, henceforth referred to as the 2007 REA) and ecological risk (ICF International, 2006; henceforth referred to as the 2006 REA) with regard to any appropriate further interpretation in light of the evidence newly available in this review. A draft of the Policy Assessment (PA) was released for public comment and review by CASAC in January 2013 (USEPA, 2013b; 77 FR 70776, November 27, 2012) and was the subject of a public meeting on February 5-6, 2013 (78 FR 938, January 7, 2013). Comments provided by the CASAC in a June 4, 2013 letter (Frey, 2013b), as well as public comments received on the draft PA were considered in preparing the final PA, which was released in May 2014 (USEPA, 2014; 79 FR 26751, May 9, 2014). D. Multimedia, Multipathway Aspects of Lead Since Pb distributes from air to other media and is persistent, our review of the NAAQS for Pb considers the protection provided against such effects associated both with exposures to Pb in ambient air and with exposures to Pb that makes its way into other media from ambient air. Additionally, in assessing the adequacy of protection afforded by the current NAAQS, we are mindful of the long history of greater and more widespread atmospheric emissions that occurred in previous years (both before and after establishment of the 1978 NAAQS) and that contributed to the Pb that exists in human populations and ecosystems today. Likewise, we also recognize the role of other, nonair sources of Pb now and in the past that also contribute to the Pb that exists in human populations and ecosystems today. Lead emitted to ambient air is transported through the air and is also distributed from air to other media. This multimedia distribution of Pb emitted into ambient air (air-related Pb) contributes to multiple air-related pathways of human and ecosystem exposure (ISA, sections 3.1.1 and 3.7.1). Air-related pathways may also involve media other than air, including indoor and outdoor dust, soil, surface water and sediments, vegetation and biota. Air-related Pb exposure pathways for humans include inhalation of ambient air or ingestion of food, water or other materials, including dust and soil, that have been contaminated through a pathway involving Pb deposition from ambient air (ISA, section 3.1.1.1). Ambient air inhalation pathways include both inhalation of air outdoors and inhalation of ambient air that has infiltrated into indoor environments. The air-related ingestion pathways occur as a result of Pb passing through the ambient air, being distributed to other environmental media and contributing to human exposures via contact with and ingestion of indoor and outdoor dusts, outdoor soil, food and drinking water. Lead exposures via the various inhalation and ingestion air-related pathways may vary with regard to the time in which they respond to changes in air Pb concentrations. For example, exposures resulting from human exposure pathways most directly involving Pb in ambient air and exchanges of ambient air with indoor air ( e.g., inhalation) can respond most quickly, while those for pathways involving exposure to Pb deposited from ambient air into the environment ( e.g., diet) may be expected to respond more slowly. The extent of this will be influenced by the magnitude of change, as well as—for deposition-related pathways—the extent of prior deposition and environment characteristics influencing availability of prior deposited Pb. Lead currently occurring in nonair media may also derive from sources other than ambient air (nonair Pb sources) (ISA, sections 2.3 and 3.7.1). For example, Pb in dust inside some houses or outdoors in some urban areas may derive from the common past usage of leaded paint, while Pb in drinking water may derive from the use of leaded pipe or solder in drinking water distribution systems (ISA, section 3.1.3.3). We also recognize the history of much greater air emissions of Pb in the past, such as that associated with leaded gasoline usage and higher industrial emissions which have left a legacy of Pb in other (nonair) media. The relative importance of different pathways of human exposure to Pb, as well as the relative contributions from Pb resulting from recent and historic air emissions and from nonair sources, vary across the U.S. population as a result of both extrinsic factors, such as a home's proximity to industrial Pb sources or its history of leaded paint usage, and intrinsic factors, such as a person's age and nutritional status (ISA, sections 5.1, 5.2, 5.2.1, 5.2.5 and 5.2.6). Thus, the relative contributions from specific pathways is situation specific (ISA, p. 1-11), although a predominant Pb exposure pathway for very young children is the incidental ingestion of indoor dust by hand-to-mouth activity (ISA, section 3.1.1.1). For adults, however, diet may be the primary Pb exposure pathway (2006 CD, section 3.4). Similarly, the relative importance of air-related and nonair-related Pb also varies with the relative magnitudes of exposure by those pathways, which may vary with different circumstances. The distribution of Pb from ambient air to other environmental media also influences the exposure pathways for organisms in terrestrial and aquatic ecosystems. Exposure of terrestrial animals and vegetation to air-related Pb can occur by contact with ambient air or by contact with soil, water or food items that have been contaminated by Pb from ambient air (ISA, section 6.2). Transport of Pb into aquatic systems similarly provides for exposure of biota in those systems, and exposures may vary among systems as a result of differences in sources and levels of contamination, as well as characteristics of the systems themselves, such as salinity, pH and turbidity (ISA, section 2.3.2). In addition to Pb contributed by current atmospheric deposition, Pb may occur in aquatic systems as a result of nonair sources such as industrial discharges or mine-related drainage, of historical air Pb emissions ( e.g., contributing to deposition to a water body or via runoff from soils near historical air sources) or combinations of different types of sources ( e.g., resuspension of sediments contaminated by urban runoff and surface water discharges). The persistence of Pb contributes an important temporal aspect to lead's environmental pathways, and the time (or lag) associated with realization of the impact of air Pb concentrations on concentrations in other media can vary with the media ( e.g., ISA, section 6.2.2). For example, exposure pathways most directly involving Pb in ambient air or surface waters can respond more quickly to changes in ambient air Pb concentrations while pathways involving exposure to Pb in soil or sediments generally respond more slowly. An additional influence on the response time for nonair media is the environmental presence of Pb associated with past, generally higher, air concentrations. For example, after a reduction in air Pb concentrations, the time needed for sediment or surface soil concentrations to indicate a response to reduced air Pb concentrations might be expected to be longer in areas of more substantial past contamination than in areas with lesser past contamination. Thus, considering the Pb concentrations occurring in nonair environmental media as a result of air quality conditions that meet the current NAAQS is a complexity of this review, as it also was, although to a lesser degree, with regard to the prior standard in the last review. E. Air Quality Monitoring Lead emitted to the air is predominantly in particulate form. Once emitted, particle-bound Pb can be transported long or short distances depending on particle size, which influences the amount of time spent in the aerosol phase. In general, larger particles tend to deposit more quickly, within shorter distances from emissions points, while smaller particles remain in aerosol phase and travel longer distances before depositing (ISA, section 1.2.1). Accordingly, airborne concentrations of Pb near sources are much higher (and the representation of larger particles generally greater) than at sites not directly influenced by sources (PA, Figure 2-11; ISA sections 2.3.1 and 2.5.3). Ambient air monitoring data for Pb, in terms of Pb-TSP, Pb-PM 10 or Pb in particulate matter with mean diameter smaller than 2.5 microns (Pb-PM 2.5 ), are currently collected in several national networks. Monitoring conducted for purposes of Pb NAAQS surveillance is regulated to ensure accurate and comparable data for determining compliance with the NAAQS. In order to be used in NAAQS attainment designations, ambient Pb concentration data must be obtained using either the federal reference method (FRM) or a federal equivalent method (FEM). The FRMs for sample collection and analysis are specified in 40 CFR part 50. The procedures for approval of FRMs and FEMs are specified in 40 CFR part 53. In 2013, after consultation with CASAC's Ambient Air Monitoring and Methods Subcommittee, the EPA adopted a new FRM for Pb-TSP, based on inductively coupled plasma-mass spectrometry (78 FR 40000, July 3, 2013). The previous FRM was retained as an FEM, and existing FEMs were retained as well. The Pb monitoring network design requirements (40 CFR part 58, Appendix D, paragraph 4.5) include two types of monitoring sites—source-oriented monitoring sites and non-source-oriented monitoring sites—as well as the collection of a year of Pb-TSP measurements at 15 specific airports. The indicator for the current Pb NAAQS is Pb-TSP, although in some situations, 11 ambient Pb-PM 10 concentrations may be used in judging nonattainment. Currently, approximately 260 Pb-TSP monitors are in operation; these are a mixture of source- and non-source-oriented monitors. 11 The Pb-PM 10 measurements may be used for NAAQS monitoring as an alternative to Pb-TSP measurements in certain conditions defined in 40 CFR part 58, Appendix C, section 2.10.1.2. These conditions include where Pb concentrations are not expected to equal or exceed 0.10 μg/m 3 as an arithmetic 3-month mean and where the source of Pb emissions is expected to emit a substantial majority of its Pb in the size fraction captured by PM 10 monitors. Since the phase-out of Pb in on-road gasoline, Pb is widely recognized as a source-oriented air pollutant. Variability in air Pb concentrations is highest in areas including a Pb source, “with high concentrations downwind of the sources and low concentration at areas far from sources” (ISA, p. 2-92). The current requirements for source-oriented monitoring include placement of monitor sites near sources of air Pb emissions which are expected to or have been shown to contribute to ambient air Pb concentrations in excess of the NAAQS. At a minimum, there must be one source-oriented site located to measure the maximum Pb concentration in ambient air resulting from each non-airport Pb source which emits 0.50 or more tons of Pb per year and from each airport which emits 1.0 or more tons of Pb per year. 12 The EPA Regional Administrators may require additional monitoring beyond the minimum requirements where the likelihood of Pb air quality violations is significant. Such locations may include those near additional industrial Pb sources, recently closed industrial sources and other sources of resuspended Pb dust, as well as airports where piston-engine aircraft emit Pb associated with combustion of leaded aviation fuel (40 CFR part 58, Appendix D, section 4.5(c)). A single year of monitoring was also required near 15 specific airports 13 in order to gather additional information on the likelihood of NAAQS exceedances due to the combustion of leaded aviation gasoline (75 FR 81126, December 27, 2010; 40 CFR part 58, Appendix D, 4.5(a)(iii)). These airport monitoring data along with other data gathering and analyses will inform the EPA's ongoing investigation into the potential for Pb emissions from piston-engine aircraft to cause or contribute to air pollution that may reasonably be anticipated to endanger public health or welfare. This investigation is occurring under section 231 of the CAA, separate from the Pb NAAQS review. As a whole, the various data gathering and analyses are expected to improve our understanding of Pb concentrations in ambient air near airports and conditions influencing these concentrations. 12 The Regional Administrator may waive this requirement for monitoring near Pb sources if the state or, where appropriate, local agency can demonstrate the Pb source will not contribute to a maximum 3-month average Pb concentration in ambient air in excess of 50 percent of the NAAQS level based on historical monitoring data, modeling, or other means (40 CFR part 58, Appendix D, section 4.5(a)(ii)). 13 These airports were selected based on three criteria: annual Pb inventory between 0.5 ton/year and 1.0 ton/year, ambient air within 150 meters of the location of maximum emissions ( e.g., the end of the runway or run-up location), and airport configuration and meteorological scenario that leads to a greater frequency of operations from one runway. These criteria are expected, collectively, to identify airports with the highest potential to have ambient air Pb concentrations approaching or exceeding the Pb NAAQS (75 FR 81126). Monitoring agencies are also required, under 40 CFR part 58, Appendix D, to conduct non-source-oriented Pb monitoring at the NCore sites 14 required in metropolitan areas with a population of 500,000 or more (as defined by the U.S. Census Bureau). 15 Either Pb-TSP or Pb-PM 10 monitoring may be performed at these sites. Currently, all 50 NCore Pb sites are operational and measuring Pb concentrations, with 28 measuring Pb in TSP and 24 measuring Pb in PM 10 (2 sites are measuring both Pb in TSP and Pb in PM 10 ). In a separate action addressing a range of issues related to monitoring requirements for criteria pollutants, the EPA is proposing to remove the requirement for Pb monitoring at NCore sites (79 FR 54395, September 11, 2014). This change is being proposed in consideration of current information indicating concentrations at these sites to be well below the Pb NAAQS and of the presence of other monitoring networks that provide information on Pb concentrations in urban areas not directly impacted by Pb sources. The data available for these sites indicate maximum 3-month average concentrations (of Pb-PM 10 or Pb-TSP) well below the level of the Pb NAAQS, with the vast majority of sites showing concentrations less than 0.01 μg/m 3 . Additionally, other monitoring networks provide data on Pb in PM 10 or PM 2.5 , at non-source-oriented urban, and some rural, sites. These include the National Air Toxics Trends Stations for PM 10 and the Chemical Speciation Network for PM 2.5 . Data on Pb in PM 2.5 are also provided at the rural sites of the Interagency Monitoring of Protected Visual Environments network. 14 The NCore network, that formally began in January 2011, is a subset of the state and local air monitoring stations network that is intended to meet multiple monitoring objectives ( e.g. , long-term trends analysis, model evaluation, health and ecosystem studies, as well as NAAQS compliance). The complete NCore network consists of 63 urban and 15 rural stations, with each state containing at least one NCore station; 46 of the states plus Washington, DC and Puerto Rico have at least one urban station. 15 http://www.census.gov/population/www/metroareas/metroarea.html. The long-term record of Pb monitoring data documents the dramatic decline in atmospheric Pb concentrations that has occurred since the 1970s in response to reduced emissions (PA, Figures 2-1 and 2-7). Currently, the highest concentrations occur near some metals industries where some individual locations have concentrations that exceed the NAAQS (PA, Figure 2-10). Concentrations at non-source-oriented monitoring sites are much lower than those at source-oriented sites and well below the standard (PA, Figure 2-11). II. Rationale for Proposed Decision on the Primary Standard This section presents the rationale for the Administrator's proposed decision to retain the existing Pb primary standard. As discussed more fully below, this rationale is based on a thorough review, in the ISA, of the latest scientific information, generally published through September 2011, 16 on human health effects associated with Pb and pertaining to the presence of Pb in the ambient air. This proposal also takes into account: (1) The PA's staff assessments of the most policy-relevant information in the ISA and staff analyses of air quality, human exposure and health risks, upon which staff conclusions regarding appropriate considerations in this review are based; (2) CASAC advice and recommendations, as reflected in discussions of drafts of the ISA and PA at public meetings, in separate written comments, and in CASAC's letters to the Administrator; and (3) public comments received during the development of these documents, either in connection with CASAC meetings or separately. 16 In addition to the review's opening “call for information” (75 FR 8934), “literature searches were conducted routinely to identify studies published since the last review, focusing on studies published from 2006 (close of the previous scientific assessment) through September 2011,” and references “that were considered for inclusion or actually cited in this ISA can be found at http://hero.epa.gov/lead ” (ISA, p. 1-2). In presenting the rationale and its foundations, section II.A provides background on the general approach for review of the primary NAAQS for Pb, including a summary of the approach used in the last review (section II.A.1) and the general approach for the current review (section II.A.2). Sections II.B and II.C summarize the body of evidence supporting this rationale, focusing on consideration of key policy-relevant questions, and section II.D summarizes the exposure/risk information for this review. Section II.E presents the Administrator's proposed conclusions on adequacy of the current standard, drawing on both evidence-based and exposure/risk-based considerations (sections II.E.1 and II.E.2), and advice from CASAC (section II.E.3). A. General Approach The past and current approaches described below are both based, most fundamentally, on using the EPA's assessment of the current scientific evidence and associated quantitative analyses to inform the Administrator's judgment regarding a primary standard for Pb that protects public health with an adequate margin of safety. We note that in drawing conclusions with regard to the primary standard, the final decision on the adequacy of the current standard is largely a public health policy judgment to be made by the Administrator. The Administrator's final decision must draw upon scientific information and analyses about health effects, population exposure and risks, as well as judgments about how to consider the range and magnitude of uncertainties that are inherent in the scientific evidence and analyses. Our approach to informing these judgments, discussed more fully below, is based on the recognition that the available health effects evidence generally reflects a continuum, consisting of levels at which scientists generally agree that health effects are likely to occur, through lower levels at which the likelihood and magnitude of the response become increasingly uncertain. This approach is consistent with the requirements of the NAAQS provisions of the Act and with how the EPA and the courts have historically interpreted the Act. These provisions require the Administrator to establish primary standards that, in the judgment of the Administrator, are requisite to protect public health with an adequate margin of safety. In so doing, the Administrator seeks to establish standards that are neither more nor less stringent than necessary for this purpose. The Act does not require that primary standards be set at a zero-risk level, but rather at a level that avoids unacceptable risks to public health including the health of sensitive groups. 17 The four basic elements of the NAAQS (indicator, averaging time, level, and form) are considered collectively in evaluating the health protection afforded by the current standard. 17 The at-risk population groups identified in a NAAQS review may include low-income or minority groups. Where low-income/minority groups are among the at-risk populations, the rulemaking decision will be based on providing protection for these and other at-risk populations and lifestages ( e.g., children, older adults, persons with pre-existing heart and lung disease). To the extent that low-income/minority groups are not among the at-risk populations identified in the ISA, a decision based on providing protection of the at-risk lifestages and populations would be expected to provide protection for the low-income/minority groups. 1. Approach in the Last Review The last review of the NAAQS for Pb was completed in 2008 (73 FR 66964, November 12, 2008). The 2008 decision to substantially revise the primary standard was based on the extensive body of scientific evidence published over almost three decades, from the time the standard was originally set in 1978 through 2005-2006. In so doing, the 2008 decision considered the body of evidence as assessed in the 2006 CD (USEPA, 2006a), as well as the 2007 Staff Paper assessment of the policy-relevant information contained in the CD and the quantitative risk/exposure assessment (USEPA, 2007a, 2007b), the advice and recommendations of CASAC (Henderson 2007a, 2007b, 2008a, 2008b), and public comment. While recognizing that Pb has been demonstrated to exert “a broad array of deleterious effects on multiple organ systems,” the review focused on the effects most pertinent to ambient air exposures, which given ambient air Pb reductions over the past 30 years, are those associated with relatively lower exposures and associated blood Pb levels (73 FR 66975, November 12, 2008). In so doing, the EPA recognized the general consensus that the developing nervous system in children is among the most sensitive health endpoints associated with Pb exposure, if not the most sensitive one. Thus, primary attention was given to consideration of nervous system effects, including neurocognitive and neurobehavioral effects, in children (73 FR 66976, November 12, 2008). The body of evidence included associations of such effects in study populations of variously aged children with mean blood Pb levels below 10 µg/dL, extending from 8 down to 2 µg/dL (73 FR 66976, November 12, 2008). The public health implications of effects of air-related Pb on cognitive function ( e.g., IQ) in young children were given particular focus in the review. The conclusions reached by the Administrator in the last review were based primarily on the scientific evidence, with the risk- and exposure-based information providing support for various aspects of the decision. In reaching his conclusion on the adequacy of the then-current standard, which was set in 1978, the Administrator placed primary consideration on the large body of scientific evidence available in the review including significant new evidence concerning effects at blood Pb concentrations substantially below those identified when the standard was initially set (73 FR 66987, November 12, 2008; 43 FR 46246, October 5, 1978). Given particular attention was the robust evidence of neurotoxic effects of Pb exposure in children, recognizing: (1) That while blood Pb levels in U.S. children had decreased notably since the late 1970s, newer epidemiological studies had investigated and reported associations of effects on the neurodevelopment of children with those more recent lower blood Pb levels and (2) that the toxicological evidence included extensive experimental laboratory animal evidence substantiating well the plausibility of the epidemiological findings observed in human children and expanding our understanding of likely mechanisms underlying the neurotoxic effects (73 FR 66987, November 12, 2008). Additionally, within the range of blood Pb levels investigated in the available evidence base, a threshold level for neurocognitive effects was not identified (73 FR 66984, November 12, 2008; 2006 CD, p. 8-67). Further, the evidence indicated a steeper concentration-response (C-R) relationship for effects on cognitive function at those lower blood Pb levels than at higher blood Pb levels that were more common in the past, “indicating the potential for greater incremental impact associated with exposure at these lower levels” (73 FR 66987, November 12, 2008). As at the time when the standard was initially set in 1978, the health effects evidence and exposure/risk assessment available in the last review supported the conclusion that air-related Pb exposure pathways contribute to blood Pb levels in young children by inhalation and ingestion (73 FR 66987, November 12, 2008). The available information in the last review also indicated, however, a likely greater change in blood Pb per unit of air Pb than was estimated when the standard was initially set (73 FR 66987, November 12, 2008). In the Administrator's decision on the adequacy of the 1978 standard, the Administrator considered the evidence using a very specifically defined framework, referred to as an air-related IQ loss evidence-based framework. This framework integrates evidence for the relationship between Pb in air and Pb in young children's blood with evidence for the relationship between Pb in young children's blood and IQ loss (73 FR 66987, November 12, 2008). This evidence-based approach considers air-related effects on neurocognitive function (using the quantitative metric of IQ loss) associated with exposure in those areas with elevated air concentrations equal to potential alternative levels for the Pb standard. In simplest terms, the framework focuses on children exposed to air-related Pb in those areas with elevated air Pb concentrations equal to specific potential standard levels, providing for estimation of a mean air-related IQ decrement for young children in the high end of the national distribution of air-related exposures. Thus, the conceptual context for the framework is that it provides estimates of air-related IQ loss for the subset of U.S. children living in close proximity to air Pb sources that contribute to such elevated air Pb concentrations. In such cases, when a standard of a particular level is just met at a monitor sited to record the highest source-oriented concentration in an area, the large majority of children in the larger surrounding area would likely experience exposures to concentrations well below that level. The two primary inputs to the evidence-based air-related IQ loss framework are air-to-blood ratios and C-R functions for the relationship between blood Pb and IQ response in young children. Additionally taken into consideration in applying and drawing conclusions from the framework were the uncertainties inherent in these inputs. Application of the framework also entailed consideration of an appropriate level of protection from air-related IQ loss to be used in conjunction with the framework. The framework estimates of mean air-related IQ loss are derived through multiplication of the following factors: standard level (µg/m 3 ), air-to-blood ratio (albeit in terms of µg/dL blood Pb per µg/m 3 air concentration), and slope for the C-R function in terms of points IQ decrement per µg/dL blood Pb. Based on the application of the air-related IQ loss framework to the evidence, the Administrator concluded that, for exposures projected for air Pb concentrations at the level of the 1978 standard, the quantitative estimates of IQ loss associated with air-related Pb indicated risk of a magnitude that, in his judgment, was significant from a public health perspective, and that the evidence-based framework supported a conclusion that the 1978 standard did not protect public health with an adequate margin of safety (73 FR 66987, November 12, 2008). The Administrator further concluded that the evidence indicated the need for a substantially lower standard level to provide increased public health protection, especially for at-risk groups (most notably children), against an array of effects, most importantly including effects on the developing nervous system (73 FR 66987, November 12, 2008). In addition to giving primary consideration to the much expanded evidence base since the standard was set, the Administrator also took into consideration the exposure/risk assessments. In so doing, he observed that, while taking into consideration their inherent uncertainties and limitations, the quantitative estimates of IQ loss associated with air-related Pb in air quality scenarios just meeting the then-current standard also indicated risk of a magnitude that, in his judgment, was significant from a public health perspective. Thus, the Administrator concluded the exposure/risk estimates provided additional support to the evidence-based conclusion that the standard needed revision (73 FR 66987, November 12, 2008). In considering appropriate revisions to the prior standard in the review completed in 2008, each of the four basic elements of the NAAQS (indicator, averaging time, form and level) was evaluated. The rationale for decisions on those elements is summarized below. With regard to indicator, consideration was given to replacing Pb-TSP with Pb-PM 10 . The EPA recognized, however, that Pb in all particle sizes contributes to Pb in blood and associated health effects, additionally noting that the difference in particulate Pb captured by TSP and PM 10 monitors may be on the order of a factor of two in some areas (73 FR 66991, November 12, 2008). Further, the Administrator recognized uncertainty with regard to whether a Pb-PM 10 -based standard would also effectively control ultra-coarse 18 Pb particles, which may have a greater presence in areas near sources where Pb concentrations are highest (73 FR 66991, November 12, 2008). The Administrator decided to retain Pb-TSP as the indicator to provide sufficient public health protection from the range of particle sizes of ambient air Pb, including ultra-coarse particles (73 FR 66991, November 12, 2008). Additionally, a role was provided for Pb-PM 10 in the monitoring required for a Pb-TSP standard (73 FR 66991, November 12, 2008) based on the conclusion that use of Pb-PM 10 measurements at sites not influenced by sources of ultra-coarse Pb, and where Pb concentrations are well below the standard, would take advantage of the increased precision of these measurements and decreased spatial variation of Pb-PM 10 concentrations, without raising the same concerns over a lack of protection against health risks from all particulate Pb emitted to the ambient air that support retention of Pb-TSP as the indicator (versus revision to Pb-PM 10 ) (73 FR 66991, November 12, 2008). Accordingly, allowance was made for the use of Pb-PM 10 monitoring for Pb NAAQS attainment purposes in certain limited circumstances, at non-source-oriented sites, where the Pb concentrations are expected to be substantially below the standard and ultra-coarse particles are not expected to be present (73 FR 66991, November 12, 2008). 18 The term “ultra-coarse” refers to particles collected by a TSP sampler but not by a PM 10 sampler. This terminology is consistent with the traditional usage of “fine” to refer to particles collected by a PM 2.5 sampler, and “coarse” to refer to particles collected by a PM 10 sampler but not by a PM 2.5 sampler, recognizing that there will be some overlap in the particle sizes in the three types of collected material. With regard to averaging time and form for the revised standard, consideration was given to a monthly averaging time, with a form of second maximum, and to 3-month and calendar quarter averaging times, with not-to-be exceeded forms. While the Administrator recognized that there were some factors that might imply support for a period as short as a month for averaging time, he also noted other factors supporting use of a longer time. He additionally took note of the complexity inherent in this consideration for the primary Pb standard, which is greater than in the case of other criteria pollutants due to the multimedia nature of Pb and its multiple pathways of human exposure. In this situation for Pb, the Administrator emphasized the importance of considering all of the relevant factors, both those pertaining to the human physiological response to changes in Pb exposures and those pertaining to the response of air-related Pb exposure pathways to changes in airborne Pb, in an integrated manner. As discussed further in the PA, the evidence on human physiological response to changes in Pb exposure available in the last review indicated that children's blood Pb levels respond quickly to increased Pb exposure, particularly during the time of leaded gasoline usage but likely with lessened immediacy since that time as children's exposure pathways have changed (PA, section 4.1.1.2). The Administrator also recognized limitations and uncertainties in the evidence and variability with regard to the information regarding the response time of indoor dust Pb to ambient airborne Pb. In consideration of the uncertainty associated with the evidence, the Administrator noted that the two changes in form for the standard (to a rolling 3-month average and to providing equal weighting to each month in deriving the 3-month average) both afford greater weight to each individual month than did the calendar quarter form of the 1978 standard, tending to control both the likelihood that any month will exceed the level of the standard and the magnitude of any such exceedance. Thus, based on an integrated consideration of the range of relevant factors, the averaging time was revised to a rolling 3-month period with a maximum (not-to-be-exceeded) form, evaluated over a 3-year period. As compared to the previous averaging time and form of calendar quarter (not-to-be exceeded), this revision was considered to be more scientifically appropriate and more health protective (73 FR 66996, November 12, 2008). The rolling average gives equal weight to all 3-month periods, and the new calculation method gives equal weight to each month within each 3-month period (73 FR 66996, November 12, 2008). Further, the rolling average yields twelve 3-month averages each year to be compared to the NAAQS versus four averages in each year for the block calendar quarters pertaining to the previous standard (73 FR 66996, November 12, 2008). Lastly, based on the body of scientific evidence and information available, as well as CASAC recommendations and public comment, the Administrator decided on a standard level that, in combination with the specified choice of indicator, averaging time, and form, he judged requisite to protect public health, including the health of sensitive groups, with an adequate margin of safety (73 FR 67006, November 12, 2008). In reaching the decision on level for the revised standard, the Administrator considered as a useful guide the evidence-based framework developed in that review. As described above, that framework integrates evidence for the relationship between Pb in air and Pb in children's blood and the relationship between Pb in children's blood and IQ loss. Application of the air-related IQ loss evidence-based framework was recognized, however, to provide “no evidence- or risk-based bright line that indicates a single appropriate level” for the standard (73 FR 67006, November 12, 2008). Rather, the framework was seen as a useful guide for consideration of health risks from exposure to ambient levels of Pb in the air, in the context of a specified averaging time and form, with regard to the Administrator's decision on a level for a revised NAAQS that provides public health protection that is sufficient but not more than necessary under the Act (73 FR 67004, November 12, 2008). As noted above, use of the evidence-based air-related IQ loss framework to inform selection of a standard level involved consideration of the evidence with regard to two input parameters. The two input parameters are an air-to-blood ratio and a C-R function for population IQ response associated with blood Pb level (73 FR 67004, November 12, 2008). The evidence at the time of the last review indicated a broad range of air-to-blood ratio estimates, 19 each with limitations and associated uncertainties. Based on the then-available evidence, the Administrator concluded that 1:5 to 1:10 represented a reasonable range to consider and identified 1:7 as a generally central value on which to focus (73 FR 67004, November 12, 2008). With regard to C-R functions, in light of the evidence of nonlinearity and of steeper slopes at lower blood Pb levels, the Administrator concluded it was appropriate to focus on C-R analyses based on blood Pb levels that most closely reflected the then-current population of children in the U.S., 20 recognizing the EPA's identification of four such analyses and giving weight to the central estimate or median of the resultant C-R functions (73 FR 67003, November 12, 2008, Table 3; 73 FR 67004, November 12, 2008). The median estimate for the four C-R slopes of −1.75 IQ points decrement per µg/dL blood Pb was selected for use with the framework. With the framework, potential alternative standard levels (µg/m 3 ) are multiplied by estimates of air-to-blood ratio (µg/dL blood Pb per µg/m 3 air Pb) and the median slope for the C-R function (points IQ decrement per µg/dL blood Pb), yielding estimates of a mean air-related IQ decrement for a specific subset of young children ( i.e., those children exposed to air-related Pb in areas with elevated air Pb concentrations equal to specified alternative levels). As such, the application of the framework yields estimates for the mean air-related IQ decrements of the subset of children expected to experience air-related Pb exposures at the high end of the distribution of such exposures. The associated mean IQ loss estimate is the average for this highly exposed subset and is not the average air-related IQ loss projected for the entire U.S. population of children. Uncertainties and limitations were recognized in the use of the framework and in the resultant estimates (73 FR 67000, November 12, 2008). 19 The term “air-to-blood ratio” describes the increase in blood Pb (in µg/dL) estimated to be associated with each unit increase of air Pb (in µg/m 3 ). Ratios are presented in the form of 1:x, with the 1 representing air Pb (in µg/m 3 ) and x representing blood Pb (in µg/dL). Description of ratios as higher or lower refers to the values for x ( i.e., the change in blood Pb per unit of air Pb). 20 The geometric mean blood Pb level for U.S. children aged 5 years and below, reported for NHANES in 2003-04 (the most recent years for which such an estimate was available at the time of the 2008 decision) was 1.8 µg/dL and the 5th and 95th percentiles were 0.7 µg/dL and 5.1 µg/dL, respectively (73 FR 67002). In considering the use of the evidence-based air-related IQ loss framework to inform his judgment as to the appropriate degree of public health protection that should be afforded by the NAAQS to provide requisite protection against risk of neurocognitive effects in sensitive populations, such as IQ loss in children, the Administrator recognized in the 2008 review that there were no commonly accepted guidelines or criteria within the public health community that would provide a clear basis for such a judgment. During the 2008 review, CASAC commented regarding the significance from a public health perspective of a 1-2 point IQ loss in the entire population of children and along with some commenters, emphasized that the NAAQS should prevent air-related IQ loss of a significant magnitude, such as on the order of 1-2 IQ points, in all but a small percentile of the population. Similarly, the Administrator stated that “ideally air-related (as well as other) exposures to environmental Pb would be reduced to the point that no IQ impact in children would occur” (73 FR 66998, November 12, 2008). The Administrator further recognized that, in the case of setting a NAAQS, he was required to make a judgment as to what degree of protection is requisite to protect public health with an adequate margin of safety (73 FR 66998, November 12, 2008). The NAAQS must be sufficient but not more stringent than necessary to achieve that result, and the Act does not require a zero-risk standard (73 FR 66998, November 12, 2008). The Administrator additionally recognized that the evidence-based air-related IQ loss framework did not provide estimates pertaining to the U.S. population of children as a whole. Rather, the framework provided estimates (with associated uncertainties and limitations) for the mean of a subset of that population, the subset of children assumed to be exposed to the level of the standard. As described in the final decision “[t]he framework in effect focuses on the sensitive subpopulation that is the group of children living near sources and more likely to be exposed at the level of the standard” (73 FR 67000, November 12, 2008). As further noted in the final decision (73 FR 67000, November 12, 2008): EPA is unable to quantify the percentile of the U.S. population of children that corresponds to the mean of this sensitive subpopulation. Nor is EPA confident in its ability to develop quantified estimates of air-related IQ loss for higher percentiles than the mean of this subpopulation. EPA expects that the mean of this subpopulation represents a high, but not quantifiable, percentile of the U.S. population of children. As a result, EPA expects that a standard based on consideration of this framework would provide the same or greater protection from estimated air-related IQ loss for a high, albeit unquantifiable, percentage of the entire population of U.S. children. In reaching a judgment as to the appropriate degree of protection, the Administrator considered advice and recommendations from CASAC and public comments and recognized the uncertainties in the health effects evidence and related information as well as the role of, and context for, a selected air-related IQ loss in the application of the framework, as described above. Based on these considerations, the Administrator identified an air-related IQ loss of 2 points for use with the framework, as a tool for considering the evidence with regard to the level for the standard (73 FR 67005, November 12, 2008). In so doing, the Administrator was not determining that such an IQ decrement value was appropriate in other contexts (73 FR 67005, November 12, 2008). Given the various uncertainties associated with the framework and the scientific evidence base, and the focus of the framework on the sensitive subpopulation of children that are more highly exposed to air-related Pb, a standard level selected in this way, in combination with the selected averaging time and form, was expected to significantly reduce and limit for a high percentage of U.S. children the risk of experiencing an air-related IQ loss of that magnitude (73 FR 67005, November 12, 2008). At the standard level of 0.15 µg/m 3 , with the combination of the generally central estimate of air-to-blood ratio of 1:7 and the median of the four C-R functions (−1.75 IQ point decrement per µg/dL blood Pb), the framework estimates of air-related IQ loss were below 2 IQ points (73 FR 67005, November 12, 2008, Table 4). In reaching the decision in 2008 on a level for the revised standard, the Administrator also considered the results of the quantitative risk assessment to provide a useful perspective on risk from air-related Pb. In light of important uncertainties and limitations for purposes of evaluating potential standard levels, however, the Administrator placed less weight on the risk estimates than on the evidence-based assessment. Nevertheless, in recognition of the general comparability of quantitative risk estimates for the case studies considered most conceptually similar to the scenario represented by the evidence-based framework, he judged the quantitative risk estimates to be “roughly consistent with and generally supportive” of the evidence-based framework estimates (73 FR 67006, November 12, 2008). Based on consideration of the entire body of evidence and information available in the review, as well as the recommendations of CASAC and public comments, the Administrator decided that a level for the primary Pb standard of 0.15 µg/m 3 , in combination with the specified choice of indicator, averaging time and form, was requisite to protect public health, including the health of sensitive groups, with an adequate margin of safety (73 FR 67006, November 12, 2008). In reaching decisions on level as well as the other elements of the revised standard, the Administrator took note of the complexity associated with consideration of health effects caused by different ambient air concentrations of Pb and with uncertainties with regard to the relationships between air concentrations, exposures, and health effects. For example, selection of a maximum, not to be exceeded, form in conjunction with a rolling 3-month averaging time over a 3-year span was expected to have the effect that the at-risk population of children would be exposed below the standard most of the time (73 FR 67005, November 12, 2008). The Administrator additionally considered the provision of an adequate margin of safety in making decisions on each of the elements of the standard, including, for example “selection of TSP as the indicator and the rejection of the use of PM 10 scaling factors; selection of a maximum, not to be exceeded form, in conjunction with a 3-month averaging time that employs a rolling average, with the requirement that each month in the 3-month period be weighted equally (rather than being averaged by individual data) and that a 3-year span be used for comparison to the standard; and the use of a range of inputs for the evidence-based framework, that includes a focus on higher air-to-blood ratios than the lowest ratio considered to be supportable, and steeper rather than shallower C-R functions, and the consideration of these inputs in selection of 0.15 μg/m 3 as the level of the standard” (73 FR 67007, November 12, 2008). The Administrator additionally noted that a standard with this level would reduce the risk of a variety of health effects associated with exposure to Pb, including effects indicated in the epidemiological studies at lower blood Pb levels, particularly including neurological effects in children, and the potential for cardiovascular and renal effects in adults (73 FR 67006, November 12, 2008). The Administrator additionally considered higher and lower levels for the standard, concluding that a level of 0.15 µg/m 3 provided for a standard that was neither more or less stringent than necessary for this purpose, recognizing that the Act does not require that primary standards be set at a zero-risk level, but rather at a level that reduces risk sufficiently so as to protect public health with an adequate margin of safety (73 FR 67007, November 12, 2008). For example, the Administrator additionally considered potential public health protection provided by standard levels above 0.15 µg/m 3 , which he concluded were insufficient to protect public health with an adequate margin of safety. The Administrator also noted that in light of all of the evidence, including the evidence-based framework, the degree of public health protection likely afforded by standard levels below 0.15 µg/m 3 would be greater than what is necessary to protect public safety with an adequate margin of safety. The Administrator concluded, based on review of all of the evidence (including the evidence-based framework), that when taken as a whole the selected standard, including the indicator, averaging time, form, and level, would be “sufficient but not more than necessary to protect public health, including the health of sensitive subpopulations, with an adequate margin of safety” (73 FR 67007, November 12, 2008). 2. Approach for the Current Review The approach in this review of the current primary standard takes into consideration the approach used in the last Pb NAAQS review, addressing key policy-relevant questions in light of currently available scientific and technical information. To evaluate whether it is appropriate to consider retaining the current primary Pb standard, or whether consideration of revision is appropriate, the EPA has adopted an approach in this review that builds upon the general approach used in the last review and reflects the broader body of evidence and information now available. As summarized above, the Administrator's decisions in the prior review were based on an integration of information on health effects associated with exposure to Pb with that on relationships between ambient air Pb and blood Pb; expert judgments on the adversity and public health significance of key health effects; and policy judgments as to when the standard is requisite to protect public health with an adequate margin of safety. These considerations were informed by air quality and related analyses, quantitative exposure and risk assessments, and qualitative assessment of impacts that could not be quantified. Similarly in this review, as described in the PA, we draw on the current evidence and quantitative assessments of exposure pertaining to the public health risk of Pb in ambient air. In considering the scientific and technical information here as in the PA, we consider both the information available at the time of the last review and information newly available since the last review, including most particularly that which has been critically analyzed and characterized in the current ISA. We additionally consider the quantitative exposure/risk assessments from the last review that estimated Pb-related IQ decrements associated with different air quality conditions in simulated at-risk populations in multiple case studies (PA, section 3.4; 2007 REA). The evidence-based discussions presented below draw upon evidence from epidemiological studies and experimental animal studies evaluating health effects related to exposures to Pb, as discussed in the ISA. The exposure/risk-based discussions have drawn from the quantitative health risk analyses for Pb performed in the last Pb NAAQS review in light of the currently available evidence (PA, section 3.4; 2007 REA; REA Planning Document). Sections II.B through II.D below summarize the current health effects and exposure/risk information with a focus on the specific policy-relevant questions identified for these categories of information in the PA (PA, chapter 3). B. Health Effects Information 1. Array of Effects Lead has been demonstrated to exert a broad array of deleterious effects on multiple organ systems as described in the assessment of the evidence available in this review and consistent with conclusions of past CDs (ISA, section 1.6; 2006 CD, section 8.4.1). A sizeable number of studies on Pb health effects are newly available in this review and are critically assessed in the ISA as part of the full body of evidence. The newly available evidence reaffirms conclusions on the broad array of effects recognized for Pb in the last review (see ISA, section 1.10). 21 Consistent with those conclusions, in the context of pollutant exposures considered relevant to the Pb NAAQS review, 22 the ISA determines that causal relationships 23 exist for Pb with effects on the nervous system in children (cognitive function decrements and the group of externalizing behaviors comprising attention, impulsivity and hyperactivity), the hematological system (altered heme synthesis and decreased red blood cell survival and function), and the cardiovascular system (hypertension and coronary heart disease), and on reproduction and development (postnatal development and male reproductive function) (ISA, Table 1-2). Additionally, the ISA describes relationships between Pb and effects on the nervous system in adults, on immune system function and with cancer 24 as likely to be causal 25 (ISA, Table 1-2, sections 1.6.4 and 1.6.7). 21 Since the last Pb NAAQS review, the ISAs which have replaced CDs in documenting each review of the scientific evidence (or air quality criteria) employ a systematic framework for weighing the evidence and describing associated conclusions with regard to causality using established descriptors: “causal” relationship with relevant exposure, “likely” to be a causal relationship, evidence is “suggestive” of a causal relationship, “inadequate” evidence to infer a causal relationship, and “not likely” to be a causal relationship (ISA, Preamble). 22 In drawing judgments regarding causality for the criteria air pollutants, the ISA places emphasis “on evidence of effects at doses ( e.g., blood Pb concentration) or exposures ( e.g., air concentrations) that are relevant to, or somewhat above, those currently experienced by the population. The extent to which studies of higher concentrations are considered varies . . . but generally includes those with doses or exposures in the range of one to two orders of magnitude above current or ambient conditions. Studies that use higher doses or exposures may also be considered . . . [t]hus, a causality determination is based on weight of evidence evaluation . . ., focusing on the evidence from exposures or doses generally ranging from current levels to one or two orders of magnitude above current levels” (ISA, pp. lx-lxi). 23 In determining a causal relationship to exist for Pb with specific health effects, the EPA concludes that “[e]vidence is sufficient to conclude that there is a causal relationship with relevant pollutant exposures ( i.e., doses or exposures generally within one to two orders of magnitude of current levels)” (ISA, p. lxii). 24 The EPA concludes that a causal relationship is likely to exist between Pb exposure and cancer, based primarily on consistent, strong evidence from experimental animal studies, but inconsistent epidemiological evidence (ISA, section 4.10.5). Lead has also been classified as a probable human carcinogen by the International Agency for Research on Cancer, based mainly on sufficient animal evidence, and as reasonably anticipated to be a human carcinogen by the U.S. National Toxicology Program (ISA, section 4.10). 25 In determining that there is likely to be a causal relationship for Pb with specific health effects, the EPA has concluded that “[e]vidence is sufficient to conclude that a causal relationship is likely to exist with relevant pollutant exposures, but important uncertainties remain” (ISA, p. lxii). In some categories of health effects, there is newly available evidence regarding some aspects of the effects described in the last review or that strengthens our conclusions regarding aspects of Pb toxicity on a particular physiological system. Among the nervous system effects of Pb, the newly available evidence is consistent with conclusions in the previous review which recognized that “[t]he neurotoxic effects of Pb exposure are among those most studied and most extensively documented among human population groups” (2006 CD, p. 8-25) and took note of the diversity of studies in which such effects of Pb exposure early in development (from fetal to postnatal childhood periods) have been observed (2006 CD, p. E-9). Nervous system effects that receive prominence in the current review, as in previous reviews, include those affecting cognitive function and behavior in children (ISA, section 4.3), with conclusions that are consistent with findings of the last review. Across the broad array of Pb effects for systems and processes other than the nervous system, the evidence base has been augmented with additional epidemiological investigations in a number of areas, including developmental outcomes, such as puberty onset, and adult outcomes related to cardiovascular function, for which several large cohorts have been analyzed (ISA, Table 1-8 and sections 4.4 and 4.8). Conclusions on these other systems and processes are generally consistent with conclusions reached in the last review, while also extending our conclusions on some aspects of these effects (ISA, section 4.4 and Table 1-8). Based on the extensive assessment of the full body of evidence available in this review, the major conclusions drawn by the ISA regarding health effects of Pb in children include the following (ISA, p. lxxxvii). Multiple epidemiologic studies conducted in diverse populations of children consistently demonstrate the harmful effects of Pb exposure on cognitive function (as measured by IQ decrements, decreased academic performance and poorer performance on tests of executive function). . . . Evidence suggests that some Pb-related cognitive effects may be irreversible and that the neurodevelopmental effects of Pb exposure may persist into adulthood (Section 1.9.4). Epidemiologic studies also demonstrate that Pb exposure is associated with decreased attention, and increased impulsivity and hyperactivity in children (externalizing behaviors). This is supported by findings in animal studies demonstrating both analogous effects and biological plausibility at relevant exposure levels. Pb exposure can also exert harmful effects on blood cells and blood producing organs, and is likely to cause an increased risk of symptoms of depression and anxiety and withdrawn behavior (internalizing behaviors),decreases in auditory and motor function, asthma and allergy, as well as conduct disorders in children and young adults. There is some uncertainty about the Pb exposures contributing to the effects and blood Pb levels observed in epidemiologic studies; however, these uncertainties are greater in studies of older children and adults than in studies of young children (Section 1.9.5). Based on the extensive assessment of the full body of evidence available in this review, the major conclusions drawn by the ISA regarding health effects of Pb in adults include the following (ISA, p. lxxxviii). A large body of evidence from both epidemiologic studies of adults and experimental studies in animals demonstrates the effect of long-term Pb exposure on increased blood pressure (BP) and hypertension (Section 1.6.2). In addition to its effect on BP, Pb exposure can also lead to coronary heart disease and death from cardiovascular causes and is associated with cognitive function decrements, symptoms of depression and anxiety, and immune effects in adult humans. The extent to which the effects of Pb on the cardiovascular system are reversible is not well-characterized. Additionally, the frequency, timing, level, and duration of Pb exposure causing the effects observed in adults has not been pinpointed, and higher past exposures may contribute to the development of health effects measured later in life. As in prior reviews of the Pb NAAQS, this review is focused on those effects most pertinent to ambient air Pb exposures. Given the reductions in ambient air Pb concentrations over the past decades, these effects are generally those associated with the lowest levels of Pb exposure that have been evaluated. Additionally, we recognize the limitations on our ability to draw conclusions regarding the exposure conditions contributing to the findings from epidemiological analyses of blood Pb levels in populations of older children and adults, particularly in light of their history of higher Pb exposures. Evidence available in future reviews may better inform this issue. In the last review, while recognizing the range of health effects in variously aged populations related to Pb exposure, we focused on the health effects for which the evidence was strongest with regard to relationships with the lowest exposure levels, neurocognitive effects in young children. As is the case for studies of nervous system effects in children (discussed in more detail in section II.B.3 below), newly available studies of other effects in child and adult cohorts include cohorts with similar or somewhat lower mean blood Pb levels than in previously available studies. Categories of effects for which a causal relationship has been concluded in the ISA and for which there are a few newly available epidemiological studies indicating blood Pb associations with effects in study groups with somewhat lower blood Pb levels than previously available for these effects include effects on development (delayed puberty onset) and reproduction (male reproductive function) and on the cardiovascular system (hypertension) (ISA, sections 4.4 and 4.8; 2006 CD, sections 6.5 and 6.6). With regard to the former category, study groups in the newly available studies include groups composed of older children ranging up to age 18 years, for which there is increased uncertainty regarding historical exposures and their role in the observed effects. 26 An additional factor that handicaps our consideration of exposure levels associated with these findings is the appreciable uncertainty associated with our understanding of Pb biokinetics during this lifestage (ISA, sections 3.2, 3.3, and 4.8.6). The evidence newly available for Pb relationships with cardiovascular effects in adults include some studies with somewhat lower blood Pb levels than in the last review. The long exposure histories of these cohorts, as well as the generally higher Pb exposures of the past, complicate conclusions regarding exposure levels that may be eliciting observed effects (ISA, sections 4.4.2.4 and 4.4.7). 27 Accordingly, as discussed further below, we focus in this review, as in the last, on neurocognitive effects in young children. 26 Several of these studies involve NHANES III cohorts for which early childhood exposures were generally much higher than those common in the U.S. today (ISA, section 4.8.5). 27 Studies from the late 1960s and 1970s suggest that adult blood Pb levels during that period ranged from roughly 13 to 16 μg/dL and from 15 to 30 μg/dL in children aged 6 and younger (ISA, section 4.4.1). 2. Critical Periods of Exposure As in the last review, we base our current understanding of health effects associated with different Pb exposure circumstances at various stages of life or in different populations on the full body of available evidence and primarily on epidemiological studies of health effects associated with population Pb biomarker levels (discussed further in section II.B.3 below). The epidemiological evidence is overwhelmingly composed of studies that rely on blood Pb for the exposure metric, with the remainder largely including a focus on bone Pb. Because these metrics reflect Pb in the body ( e.g., as compared to Pb exposure concentrations) and, in the case of blood Pb, reflect Pb available for distribution to target sites, they strengthen the evidence base for purposes of drawing causal conclusions with regard to Pb generally. The complexity of Pb exposure pathways and internal dosimetry, however, tends to limit the extent to which these types of studies inform our more specific understanding of the Pb exposure circumstances ( e.g., timing within lifetime, duration, frequency and magnitude) eliciting the various effects. As at the time of the last review (and discussed more fully in section II.B.3 below), assessment of the full evidence base, including evidence newly available in this review, demonstrates that Pb exposure prenatally and also in early childhood can contribute to neurocognitive impacts in childhood, with evidence also indicating the potential for effects persisting into adulthood (ISA, sections 1.9.4, 1.9.5, and 1.10). In addition to the observed associations of prenatal and childhood blood Pb with effects at various ages in childhood, there is also evidence of Pb-related cognitive function effects in non-occupationally exposed adults (ISA, section 4.3.11). This includes evidence of associations of such effects in adulthood with childhood blood Pb levels and in other cohorts, with concurrent (adult) blood Pb levels (ISA, sections 4.3.2.1, 4.3.2.7 and 4.3.11). As the studies finding associations of adult effects with childhood blood Pb levels did not examine adult blood Pb levels, the relative influence of adult Pb exposure cannot be ascertained, and a corresponding lack of early life exposure or biomarker measurements for the latter studies limits our ability to draw conclusions regarding specific Pb exposure circumstances eliciting the observed effects (4.3.11). Findings of stronger associations for adult neurocognitive effects with bone Pb, however, indicate the role of historical or cumulative exposures for those effects (ISA, section 4.3). A critical aspect of much of the epidemiological evidence, particularly studies focused on adults (and older children) in the U.S. today, is the backdrop of generally declining environmental Pb exposure (from higher exposures during their younger years) that is common across many study populations (ISA, p. 4-2). 28 An additional factor complicating the interpretation of health effect associations with blood Pb measurements in older children and younger adults is the common behaviors of younger children ( e.g., hand-to-mouth contact) that generally contribute to relatively greater exposures earlier in life (ISA, sections 3.1.1, 4.2.1). Such exposure histories for adults and older children complicate our ability to draw conclusions regarding critical time periods and lifestages for Pb exposures eliciting the effects for which associations with Pb biomarkers have been observed in these populations ( e.g., ISA, section 1.9.6). 29 Thus, our confidence is greatest in the role of early childhood exposure in contributing to Pb-related neurocognitive effects that have been associated with blood Pb levels in young children. This is due, in part, to the relatively short exposure histories of young children (ISA, sections 1.9.4, 1.9.6 and 4.3.11). 28 The declines in Pb exposure concentrations occurring from the 1970s through the early 1990s (and experienced by middle aged and older adults of today), as indicated by NHANES blood Pb information, were particularly dramatic (ISA, section 3.4.1). 29 The evidence from experimental animal studies can be informative with regard to key aspects of exposure circumstances in eliciting specific effects, thus informing our interpretation of epidemiological evidence. For example, the animal evidence base with regard to Pb effects on blood pressure demonstrates the etiologically-relevant role of long-term exposure (ISA, section 4.4.1). This finding then informs consideration of epidemiological studies of adult populations for whom historical exposures were likely more substantial than concurrent ones, suggesting that the observed effects may be related to the past exposure (ISA, section 4.4.1). For other health effects, the animal evidence base may or may not be informative in this manner. Epidemiological analyses evaluating risk of neurocognitive impacts ( e.g., reduced IQ) associated with different blood Pb metrics in cohorts with differing exposure patterns (including those for which blood Pb levels at different ages were not highly correlated) also indicate associations with blood Pb measurements concurrent with full scale IQ (FSIQ) tests at ages of approximately 6-7 years. The analyses did not, however, conclusively demonstrate stronger findings for early ( e.g., age 2 years) or concurrent blood Pb (ISA, section 4.3.11). 30 The experimental animal evidence additionally indicates early life susceptibility (ISA, section 4.3.15 and p. 5-21). Thus, while uncertainties remain with regard to the role of Pb exposures during a particular age of life in eliciting nervous system effects, such as cognitive function decrements, the full evidence base continues to indicate prenatal and early childhood lifestages as periods of increased Pb-related risk (ISA, sections 4.3.11 and 4.3.15). We recognize increasing uncertainty, however, in our understanding of the relative impact on neurocognitive function of additional Pb exposure of children by school age or later that is associated with limitations of the currently available evidence, including epidemiological cohorts with generally similar temporal patterns of exposure. 30 In the collective body of evidence of nervous system effects in children, it is difficult to distinguish exposure in later lifestages ( e.g., school age) and its associated risk from risks resulting from exposure in prenatal and early childhood (ISA, section 4.3.11). While early childhood is recognized as a time of increased susceptibility, a difficulty in identifying a discrete period of susceptibility from epidemiological studies has been that the period of peak exposure, reflected in peak blood Pb levels, is around 18-27 months when hand-to-mouth activity is at its maximum (ISA, section 3.4.1 and 5.2.1.1; 2006 CD, p. 6-60). The task is additionally complicated by the role of maternal exposure history in contributing Pb to the developing fetus (ISA, section 3.2.2.4.). As in the last review, there is also substantial evidence of other neurobehavioral effects in children, including effects on externalizing behaviors (reduced attention span, increased impulsivity, hyperactivity, and conduct disorders) and on internalizing behaviors. The evidence for many of these endpoints, as with neurocognitive effects, also includes associations of effects at various ages in childhood and for some effects, into adulthood, with blood Pb levels reflective of several different lifestages ( e.g., prenatal and several different ages in childhood) (ISA, sections 4.3.3 and 4.3.4). There is similar or relatively less extensive evidence to inform our understanding of such effects associated with specific time periods of exposure at specific lifestages than is the case for effects on cognitive function. Across the range of Pb effects on physiological systems and processes other than the nervous system, the evidence base for blood pressure and hypertension is somewhat more informative with regard to the circumstances of Pb exposure eliciting the observed effects than are the evidence bases for many other effects. In the case of Pb-induced increases in blood pressure, the evidence indicates an importance of long-term exposure (ISA, sections 1.6.2 and 4.4.7.1). The greater uncertainties regarding the time, duration and magnitude of exposure contributing to these observed health effects complicate identification of sensitive lifestages and associated exposure patterns that might be compared with our understanding of the sensitivity of young children to neurocognitive impacts of Pb. Thus, while augmenting the evidence base on these additional endpoints, the newly available evidence does not lead us to identify a health endpoint expected to be more sensitive to Pb exposure than neurocognitive endpoints in children, leading us to continue to conclude that the appropriate primary focus for our review is on neurocognitive endpoints in children. In summary, as in the last review, we continue to recognize a number of uncertainties regarding the circumstances of Pb exposure, including timing or lifestages, eliciting specific health effects. Consideration of the evidence newly available in this review has not appreciably changed our understanding on this topic. The relationship of long-term exposure to Pb with hypertension and increased blood pressure in adults is substantiated despite some uncertainty regarding the exposures circumstances ( e.g., magnitude and timing) contributing to blood Pb levels measured in epidemiological studies. Across the full evidence base, the effects for which our understanding of relevant exposure circumstances is greatest are neurocognitive effects in young children. Moreover, available evidence does not suggest a more sensitive endpoint. Thus, we continue to recognize and give particular attention to the role of Pb exposures relatively early in childhood in contributing to neurocognitive effects, some of which may persist into adulthood. 3. Nervous System Effects in Children In considering the question of levels of Pb exposure at which health effects occur, we recognize, as discussed in sections II.B.1 and II.B.2 above, that the epidemiological evidence base for our consideration in this review, as in the past, includes substantial focus on internal biomarkers of exposure, such as blood Pb, with relatively less information specific to exposure levels, including those derived from air-related pathways. Given that blood and bone Pb are integrated markers of aggregate exposure across all sources and exposure pathways, our interpretation of studies relying on them is informed by what is known regarding the historical context and exposure circumstances of the study populations. For example, a critical aspect of much of the epidemiological evidence is the backdrop of generally declining Pb exposure over the past several decades ( e.g., ISA, sections 2.5 and 3.4.1; 2006 CD, section 3.4). Thus, as a generality, recent epidemiological studies of populations with similar characteristics as those studied in the past tend to involve lower overall Pb exposures and accordingly lower blood Pb levels. This has been of particular note in the evidence of blood Pb associations with nervous system effects, particularly impacts on cognitive function in children, for which we have seen associations with progressively lower childhood blood Pb levels across past reviews (ISA, section 4.3.12; 1986 CD; USEPA, 1990a; 2006 CD; 73 FR 66976, November 12, 2008). The evidence currently available with regard to the magnitude of blood Pb levels associated with neurocognitive effects in children is generally consistent with that available in the review completed in 2008. Nervous system effects in children, specifically effects on cognitive function, continue to be the effects that are best substantiated as occurring at the lowest blood Pb concentrations (ISA, pp. lxxxvii-lxxxviii). Associations of blood Pb with effects on cognitive function measures in children have been reported in many studies across a range of childhood blood Pb levels, including study group (mean/median) levels ranging down to 2 μg/dL ( e.g., ISA, p. lxxxvii and section 4.3.2). 31 31 The value of 2 μg/dL refers to the regression analysis of blood Pb and end-of-grade test scores, in which blood Pb was represented by categories for integer values of blood Pb from 1 μg/dL to 9 and >10 μg/dL from large statewide database. A significant effect estimate was reported for test scores with all blood Pb categories in comparison to the reference category (1 μg/dL), which included results at and below the limit of detection. Mean levels are not provided for any of the categories (Miranda et al., 2009). Among the analyses of lowest study group blood Pb levels at the youngest ages are analyses available in the last review of Pb associations with neurocognitive function decrement in study groups with mean levels on the order of 3-4 μg/dL in children aged 24 months or ranging from 5 to 7 years (73 FR 66978-66979, November 12, 2008; ISA, sections 4.3.2.1 and 4.3.2.2; Bellinger and Needleman, 2003; Canfield et al., 2003; Lanphear et al., 2005; Tellez-Rojo et al., 2006; Bellinger, 2008; Canfield, 2008; Tellez-Rojo, 2008; Kirrane and Patel, 2014). 32 Newly avai [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%3A2014-30681. Public record. Not legal advice.