Review of the National Ambient Air Quality Standards for Lead

Federal RegisterOct 18, 2016

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 50

[EPA-HQ-OAR-2010-0108; FRL-9952-87-OAR]

RIN 2060-AQ44

Review of the National Ambient Air Quality Standards for Lead

AGENCY:

Environmental Protection Agency (EPA).

ACTION:

Final 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 retaining the current standards, without revision.

DATES:

This final rule is effective on November 17, 2016.

ADDRESSES:

The EPA has established a docket for this action under Docket ID No. EPA-HQ-OAR-2010-0108. Incorporated into this docket is a separate docket established for the Integrated Science Assessment for this review (Docket ID No. EPA-HQ-ORD-2011-0051). 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 will be publicly available only in hard copy form. It 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.

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

Integrated Review Plan for 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.

SUPPLEMENTARY INFORMATION:

Table of Contents

Executive Summary

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

F. Summary of Proposed Decisions

G. Organization and Approach to Final Decisions

II. Rationale for Decision on the Primary Standard

A. Introduction

1. Background on the Current Standard

2. Overview of Health Effects Evidence

3. Overview of Information on Blood Lead Relationships With Air Lead

4. Overview of Risk and Exposure Assessment Information

B. Conclusions on the Primary Standard

1. Basis for the Proposed Decision

2. CASAC Advice in This Review

3. Comments on the Proposed Decision

4. Administrator's Conclusions

C. Decision on the Primary Standard

III. Rationale for Decision on the Secondary Standard

A. Introduction

1. Overview of Welfare Effects Information

2. Overview of Risk Assessment Information

B. Conclusions on the Secondary Standard

1. Basis for the Proposed Decision

2. CASAC Advice in This Review

3. Comments on the Proposed Decision

4. Administrator's Conclusions

C. Decision on the Secondary 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 (PRA)

C. Regulatory Flexibility Act (RFA)

D. Unfunded Mandates Reform Act (UMRA)

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 Concerning Regulations 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)

L. Congressional Review Act

References

Executive Summary

This document describes the completion of our current review of the NAAQS for Pb. This review of the standards and the air quality criteria (the scientific information upon which the standards are based) is required by the Clean Air Act on a periodic basis. In conducting this review, the EPA has carefully evaluated the currently available scientific literature on the health and welfare effects of Pb, focusing particularly on the information newly available since the conclusion of the last review in 2008. Between 2008 and 2014, the EPA prepared draft and final versions of the Integrated Science Assessment and the Policy Assessment, multiple drafts of which were subject to public review and comment and were reviewed by the Clean Air Scientific Advisory Committee, an independent scientific advisory committee established pursuant to the Clean Air Act and charged with providing advice to the Administrator. The EPA issued a proposed decision on the standards on January 5, 2015 (80 FR 278), and provided a 3-month period for submission of comments from the public. After consideration of public comments on the proposed decision and advice from the Clean Air Scientific Advisory Committee, the EPA has developed this document, which is the final step in the review process.

The prior review of the NAAQS for Pb was completed in 2008. As a result of that review, we significantly revised

both the primary and secondary standards, including a lowering of the standard levels by an order of magnitude. The 2008 change to the primary standard was focused on providing the requisite protection for children and other at-risk populations against an array of adverse health effects, most notably including neurological effects in children, including neurocognitive effects (

e.g.,

IQ loss) and neurobehavioral effects. Although Pb has long been recognized to exert an array of adverse health effects, over the three decades from the time the standard was initially set in 1978 through its revision with the NAAQS review completed in 2008, the evidence base expanded considerably in a number of areas, including with regard to effects on neurocognitive function in young children at increasingly lower blood Pb levels. These effects formed the principal basis for the 2008 revisions to the primary standard.

The health effects evidence newly available in this review of the 2008 standard, as critically assessed in the ISA in conjunction with the full body of evidence, reaffirms conclusions on the broad array of effects recognized for Pb in the last review. Further, the currently available evidence is generally consistent with the evidence available in the last review, particularly with regard to key aspects of the evidence on which the current standard (set in 2008) is based. These key aspects include those regarding the relationships between air Pb concentrations and the associated Pb in the blood of young children as well as between total blood Pb levels and effects on children's IQ.

Based on consideration of the currently available health effects evidence in the context of this framework, and with support from the exposure/risk information, recognizing the uncertainties attendant in both, as well as the increasing uncertainty of risk estimates for lower air Pb concentrations, the Administrator concludes that the current primary standard provides the requisite protection of public health with an adequate margin of safety, including protection of at-risk populations. With regard to the secondary standard, the EPA has considered the currently available welfare effects evidence and screening-level risk information, including the general consistency of the current evidence with that available in the last review and the substantial limitations in the current evidence that complicate conclusions regarding the potential for Pb emissions under the current, much lower standard to contribute to welfare effects. Based on these considerations, the Administrator concludes that the current secondary standard is requisite to protect public welfare from known or anticipated adverse effects. Thus, based on the EPA's review of the air quality criteria and the NAAQS for Pb, the EPA is retaining the current standards, without revision.

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.”

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.”

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).

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

EPA,

647 F.2d 1130, 1154 (D.C. Cir. 1980),

cert. denied,

449 U.S. 1042 (1980);

American Petroleum Institute

Costle,

665 F.2d 1176, 1186 (D.C. Cir. 1981),

cert. denied,

455 U.S. 1034 (1982);

American Farm Bureau Federation

EPA,

559 F. 3d 512, 533 (D.C. Cir. 2009);

Association of Battery Recyclers

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

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,

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

EPA,

647 F.2d at 1161-62.

As used here and similarly throughout this document, 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.A.2.d 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

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

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).

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 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 (completed in 2008), including completion of several regulations that 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 (13 existing facilities). This action was estimated to result in a Pb emissions reduction of 13.6 tons per year (tpy) across the category (a 68 percent 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.

Pursuant to section 1412 of the Safe Drinking Water Act (SDWA), EPA sets public health goals and enforceable standards for drinking water quality. The Lead and Copper Rule (LCR) is a treatment technique rule. The LCR requires public water systems to treat the water to reduce corrosion of Pb and copper from premise plumbing and drinking water distribution system components. When corrosion control treatment isn't enough, water systems must educate the public about Pb in drinking water and replace lead service lines, which are the pipes that connect buildings to the drinking water mains (40 CFR 141.80-141.91). The importance of corrosion control treatment was illustrated by the recent events in Flint, MI, when Pb levels in drinking water increased after the water system did not maintain corrosion control treatment when the system changed its water supply. Section 1417 of the SDWA additionally prohibits the use of any pipe, any pipe or plumbing fitting or fixture, any solder, or any flux in the installation or repair of any public water system or any plumbing in a residential or non-residential facility providing water for human consumption, that is not lead free as defined by the Act.

Effective in January 2014, the amount of Pb permitted in pipes, fittings, and fixtures was lowered (see “Section 1417 of the Safe Drinking Water Act: Prohibition on Use of Lead Pipes, Solder, and Flux” at

http://www.epa.gov/dwstandardsregulations/section-1417-safe-drinking-water-act-prohibition-use-lead-pipes-solder-and

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).

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.

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/

See,

e.g.,

“Implementation of the Mercury-Containing and Rechargeable Battery Management Act” available from

https://www.epa.gov/hw

and facts and figures on recycling and disposal in the U.S. at

https://www.epa.gov/smm/advancing-sustainable-materials-management-facts-and-figures.

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 “National Waste Minimization Program” (

https://archive.epa.gov/epawaste/hazard/wastemin/web/html/tools.html

), “Sustainable Management of Electronics” (

https://www.epa.gov/smm-electronics

), and the “Sustainable Materials Management (SMM) Electronics Challenge” (

https://www.epa.gov/smm-electronics/sustainable-materials-management-smm-electronics-challenge

The EPA's research program identifies, encourages and conducts research needed to develop methods and tools to characterize and help reduce risks related to Pb exposure. An example of one such effort is the EPA's Integrated Exposure Uptake Biokinetic Model for Lead in Children (IEUBK model), which 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, statistics for the distribution of blood Pb levels in non-Hispanic black and lower socioeconomic groups of young children, which are generally higher than those for that population as a whole, have also declined, as have the differences in these statistics between non-Hispanic black and other groups, as well as between lower and higher socioeconomic groups (USEPA, 2013a, sections 3.4.1, 5.2.3 and 5.2.4; Jones et al., 2009).

Since the completion of the ISA, more recent NHANES data indicate the geometric mean blood Pb concentration for children in the U.S. population, aged one to five, to have declined to 0.97 μg/dL in the 2011-2012 survey (CDC, 2015).

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.

From 2007 to 2011, the number of countries known to still be using leaded gasoline was reduced from just over 20 to six (USEPA, 2011c). As of January, leaded gasoline for on-road use is known to be available (along with unleaded gasoline) in three countries.

International programs in which the U.S. participates, including those identified here, are described at:

https://www.epa.gov/international-cooperation, http://www.unep.org/transport/pcfv/, http://www.unep.org/hazardoussubstances/Home/tabid/197/hazardoussubstances/LeadCadmium/PrioritiesforAction/GAELP/tabid/6176/Default.aspx.

UNEP. “Leaded Petrol Phase-out: Global Status as at January 2016” map downloaded from

http://www.unep.org/transport/new/pcfv/.

The EPA is a contributor to the Global Alliance to Eliminate Lead Paint, a voluntary public-private partnership jointly led by the World Health Organization and the United Nations Environment Programme (UNEP) to prevent children's exposure to Pb from paints containing Pb and to minimize occupational exposures to Pb paint. The objective of this alliance is to promote 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).

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

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

), 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 air quality criteria and standards for Pb was initiated in November 2004 (69 FR 64926, November 9, 2004); the agency's plans for preparation of the Air Quality Criteria Document (AQCD) and conduct of the NAAQS review were presented in documents completed in 2005 and early 2006 (USEPA, 2005a; USEPA 2006b).

The schedule for completion of the review was governed by a judicial order in

Missouri Coalition for the Environment

EPA

(No. 4:04CV00660 ERW, September 14, 2005; and amended on April 29, 2008 and July 1, 2008).

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 the 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

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).

The 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. The 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).

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 preamble to the final rule described the EPA's decision to revise the primary and secondary standards for Pb, as discussed more fully in sections II.A.1 and III.A below. In consideration of the much-expanded health effects evidence on neurocognitive effects of Pb in children, the EPA substantially revised the primary standard level from 1.5 µg/m

to a level of 0.15 µg/m

. 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

) 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 preambles 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 (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).

As of this review, the document developed in NAAQS reviews in which the air quality criteria are assessed, previously the AQCD, is the ISA, and the document describing the OAQPS staff evaluation, previously the Staff Paper, is the PA. These documents are described in the IRP.

In June 2011, the EPA developed and released the

Risk and Exposure Assessment Planning Document

(REA Planning Document) for consultation with the 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 its 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. We have considered the 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, as described in the Policy Assessment (PA) and proposal.

A draft of the 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). The proposed decision (henceforth “proposal”) on this review of the NAAQS for Pb was signed on December 19, 2014, and published in the

Federal Register

on January 5, 2015. Written comments were received from twelve commenters during the public comment period on the proposal. Significant issues raised in the public comments and the EPA's responses to those comments are discussed in the preamble of this final action.

As in prior NAAQS reviews, the EPA is basing its decision in this review on studies and related information included in the ISA and PA,

which

have undergone CASAC and public review. The studies assessed in the ISA

and PA, and the integration of the scientific evidence presented in them, have undergone extensive critical review by the EPA, the CASAC, and the public. The rigor of that review makes these studies, and their integrative assessment, the most reliable source of scientific information on which to base decisions on the NAAQS, decisions that all parties recognize as of great import. Decisions on the NAAQS can have profound impacts on public health and welfare, and NAAQS decisions should be based on studies that have been rigorously assessed in an integrative manner not only by the EPA but also by the statutorily mandated independent scientific advisory committee, as well as the public review that accompanies this process. Some commenters have referred to and discussed individual scientific studies on the health effects of Pb that were not included in the ISA (“ `new' studies”). In considering and responding to comments for which such “new” studies were cited in support, the EPA has provisionally considered the cited studies in the context of the findings of the ISA. The EPA's provisional consideration of these studies did not and could not provide the kind of in-depth critical review described above.

As a new REA was not warranted in this review, the exposure and risk information from the last review (2007 REA; 2006 REA) is summarized in the PA in the context of the currently available health and welfare effects evidence.

Studies were identified for the Pb ISA based on the review's opening “call for information” (75 FR 8934), as well as literature searches 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” (ISA, p. 1-2). In a subsequent step, “[s]tudies that have undergone scientific peer review and have been published or accepted for publication and reports that have undergone review are considered for inclusion in the ISA” and “[a]nalyses conducted by EPA using publicly available data are also considered for inclusion in the ISA” (ISA, p. xlv). 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).

The decision to rely on studies and related information included in the ISA, REAs and PA, which have undergone CASAC and public review, is consistent with the EPA's practice in prior NAAQS reviews and its interpretation of the requirements of the CAA. Since the 1970 amendments, the EPA has taken the view that NAAQS decisions are to be based on scientific studies and related information that have been assessed as a part of the pertinent air quality criteria, and the EPA has consistently followed this approach. This longstanding interpretation was strengthened by new legislative requirements enacted in 1977, which added section 109(d)(2) of the Act concerning CASAC review of air quality criteria. See 71 FR 61144, 61148 (October 17, 2006, final decision on review of NAAQS for particulate matter) for a detailed discussion of this issue and the EPA's past practice.

As discussed in the EPA's 1993 decision not to revise the NAAQS for ozone, “new” studies may sometimes be of such significance that it is appropriate to delay a decision on revision of a NAAQS and to supplement the pertinent air quality criteria so the studies can be taken into account (58 FR at 13013-13014, March 9, 1993). In the present case, the EPA's provisional consideration of “new” studies concludes that, taken in context, the “new” information and findings do not materially change any of the broad scientific conclusions regarding the health and welfare effects and exposure pathways of Pb in ambient air made in the air quality criteria. For this reason, reopening the air quality criteria review would not be warranted.

Accordingly, the EPA is basing the final decisions in this review on the studies and related information included in the Pb air quality criteria that have undergone CASAC and public review. The EPA will consider the “new” studies for purposes of decision making in the next periodic review of the NAAQS for Pb, which the EPA expects to begin soon after the conclusion of this review and which will provide the opportunity to fully assess these studies through a more rigorous review process involving the EPA, CASAC, and the public.

D. Multimedia, Multipathway Aspects of Lead

Since Pb is distributed from air to other media and is persistent, our review of the NAAQS for Pb considers the protection provided against 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 is 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 is 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 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 are 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.

The time it takes for exposures to be reduced in response to reductions in air Pb concentrations varies with the various inhalation and ingestion exposure pathways. 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.

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, compared with smaller particles that remain in the 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

or Pb in particulate matter with mean aerodynamic diameter less than or equal to 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 the 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 NAAQS surveillance network regulations (40 CFR part 58, appendix D, paragraph 4.5) require source-oriented monitoring sites, and also the collection of one year of Pb-TSP measurements at 15 specific airports. The indicator for the current Pb NAAQS is Pb-TSP, although in some situations,

Pb-PM

concentrations may be used in judging nonattainment. Currently, more than 200 Pb-TSP monitors are in operation; these are a mixture of source- and non-source-oriented monitors (PA, p. 2-14).

The Pb-PM

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

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

monitors.

Since the phase-out of Pb in on-road gasoline, Pb is widely recognized as a near-source air pollutant, the ambient air concentrations of which generally fall off quickly with distance from sources. Variability in ambient 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 that 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 that emits 0.50 or more tons of Pb per year and from each airport that emits 1.0 or more tons of Pb per year.

The EPA Regional Administrators may require additional monitoring beyond the minimum requirements where the likelihood of Pb air quality violations is significant or where the emissions density, topography, or population locations are complex and varied. Such locations may include those near additional industrial Pb sources, recently closed industrial sources and other sources of re-entrained 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

in order to gather

additional information on ambient air Pb concentrations near airports, including specifically 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 under section 231(a)(2)(A) of the CAA of whether Pb emissions from piston-engine aircraft cause or contribute to air pollution which may reasonably be anticipated to endanger public health or welfare (see for example, EPA's Advance Notice of Proposed Rulemaking on Lead Emissions From Piston-Engine Aircraft Using Leaded Aviation Gasoline, 75 FR 22439, April 28, 2010). The EPA is conducting this investigation separate from the Pb NAAQS review. As a whole, the various data gathering efforts and analyses are expected to improve our understanding of Pb concentrations in ambient air near airports and conditions influencing these concentrations.

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)).

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 or characteristics were selected as they were expected, “collectively, to identify airports with the highest potential to have ambient air Pb concentrations approaching or exceeding the Pb NAAQS” (75 FR 81132, December 27, 2010).

Monitoring agencies may also conduct non-source-oriented Pb monitoring at the NCore monitoring sites.

In 2015, all NCore sites with a population of 500,000 or more (as defined by the U.S. Census Bureau)

were measuring Pb concentrations, with a 2014 analysis indicating generally similar numbers of sites measuring Pb in TSP and Pb in PM

(Cavender, 2014). These numbers may change in the future as the requirement for Pb monitoring at these sites was recently eliminated in consideration of current information indicating concentrations at these sites to be well below the Pb NAAQS and of the existence of other monitoring networks that provide information on Pb concentrations at similar types of sites (81 FR 17248, March 28, 2016). The data available for the NCore sites indicate maximum 3-month average concentrations (of Pb-PM

or Pb-TSP) well below the level of the Pb NAAQS, with the large majority of these sites indicating maximum 3-month average concentrations at or below 0.01 µg/m

(Cavender, 2014). Other monitoring networks that provide data on Pb in PM

or PM

2.5

at non-source-oriented urban, and some rural, sites include the National Air Toxics Trends Stations for PM

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 (also known as the IMPROVE network).

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.

Metropolitan area population size information is available at the Census Bureau Web site (

http://www.census.gov/population/www/metroareas/metroarea.htm

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).

F. Summary of Proposed Decisions

For reasons discussed in the proposal and summarized in sections II.B.1 and III.B.1 below, the Administrator proposed to retain the current primary and secondary standards for Pb, without revision.

G. Organization and Approach to Final Decisions

This action presents the Administrator's final decisions in the current review of the primary and secondary Pb standards. The final decisions addressing standards for Pb are based on a thorough review in the ISA of scientific information on known and potential human health and welfare effects associated with exposure to Pb associated with levels typically found in the ambient air. These final decisions also take into account the following: (1) Staff assessments in the PA of the most policy-relevant information in the ISA as well as quantitative health and welfare exposure and risk information; (2) CASAC advice and recommendations, as reflected in its letters to the Administrator and its discussions of drafts of the ISA and PA at public meetings; (3) public comments received during the development of these documents, both in connection with CASAC meetings and separately; and (4) public comments received on the proposal.

The primary standard is addressed in section II and the secondary standard is addressed in section III. Section IV addresses applicable statutory and executive order reviews.

II. Rationale for Decision on the Primary Standard

This section presents the rationale for the Administrator's decision to retain the existing primary Pb standard. This rationale is based on a thorough review in the ISA of the latest scientific information, generally published through September 2011, on human health effects associated with Pb and pertaining to the presence of Pb in the ambient air. This decision 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 the CASAC's letters to the Administrator; (3) public comments received during the development of these documents, either in connection with CASAC meetings or separately, and (4) public comments received on the proposal.

Section II.A provides background on the general approach for review of the primary standard for Pb and brief summaries of key aspects of the currently available health effects and exposure/risk information. Section II.B presents the Administrator's conclusions on adequacy of the current standard, drawing on consideration of this information, advice from the CASAC, and comments from the public. Section II.C summarizes the Administrator's decision on the primary standard.

A. Introduction

As in prior reviews, the general approach to reviewing the current primary standard is 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. 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. The 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. 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.

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 in section II.A.1 below, 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.A.2 through II.A.4 below provide an overview of the current health effects and quantitative exposure and risk information with a focus on the specific policy-relevant questions identified for these categories of information in the PA (PA, chapter 3).

1. Background on the Current Standard

The current primary standard was established in the last review, which was completed in 2008 (73 FR 66964, November 12, 2008), and is set at a level that is one-tenth the level of the prior standard. 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. While recognizing that Pb has been demonstrated to exert “a broad array of deleterious effects on multiple organ systems,” the 2008 review focused on the effects most pertinent to recent ambient air exposures, which are those associated with relatively lower exposures and associated blood Pb levels (73 FR 66975, November 12, 2008). Given the general scientific 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, 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). Particular focus was given to the public health implications of effects of air-related Pb on cognitive function (

e.g.,

IQ).

The conclusions reached by the Administrator in the 2008 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). He gave particular attention to 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).

Based on consideration of the health effects evidence, supported by the quantitative risk analyses, 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 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 sensitive or 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 identifying the appropriate revised standard, revisions to each of the four basic elements of the NAAQS (indicator, averaging time, form and level) were considered.

With regard to indicator, the Administrator decided to retain Pb-TSP as the indicator. The EPA recognized that the difference in particulate Pb captured by TSP and PM

monitors may be on the order of a factor of two in some areas, and that ultra-coarse Pb particles may have a greater presence in areas near sources where Pb concentrations are highest, contributing uncertainty with regard to whether a Pb-PM

-based standard would also effectively control ultra-coarse Pb particles (73 FR 66991, November 12, 2008). Accordingly, Pb-TSP was retained as the indicator in order to provide sufficient public health protection from the broad range of particle sizes of ambient air Pb, including ultra-coarse particles, given the recognition that Pb in all particle sizes contributes to Pb in blood and associated health effects (73 FR 66991, November 12, 2008).

However, in order to take advantage of the increased precision of Pb-PM

measurements and decreased spatial variation of Pb-PM

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

), a role was provided for Pb-PM

measurements in the monitoring required for a Pb-TSP standard (73 FR 66991, November 12, 2008) at sites not influenced by sources of ultra-coarse Pb, and where Pb concentrations are well below the standard (73 FR 66991, November 12, 2008).

With regard to averaging time and form for the revised standard, after giving consideration 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, two changes were made. These were to a rolling 3-month average, thus giving equal weight to all 3-month periods, and to the method for deriving the 3-month average to provide equal weighting to each month. Both of these changes afford greater weight to each individual month than did the calendar quarter form of the 1978 standard, thus tending to control both the likelihood that any month will exceed the level of the standard and the magnitude of any such exceedance. The Administrator decided on these changes in recognition of the complexity inherent in this aspect of the standard which is greater for Pb 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 in an integrated manner 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, recognizing that some factors might imply support for a period as short as a month for averaging time, and others supporting use of a longer time, with all having associated uncertainty. Based on such 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 (73 FR 66996, November 12, 2008).

In reaching the decision on level for the revised standard, that, in combination with the specified choice of indicator, averaging time, and form, the Administrator judged requisite to protect public health, including the health of sensitive groups, with an adequate margin of safety, he considered the evidence using a very specifically defined framework, referred to as an air-related IQ loss evidence-based framework (73 FR 67004, November 12, 2008). 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 with air-related exposures that are in the high end of the national distribution of such 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. Consideration of this framework additionally recognizes that 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 air-related IQ loss evidence-based framework are air-to-blood ratios

and C-R functions for the relationship between blood Pb concentration and IQ response in young children (73 FR 67004, November 12, 2008). In applying and drawing conclusions from the framework, the Administrator additionally took into consideration the uncertainties inherent in these two 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

), air-to-blood ratio (albeit in terms of µg/dL blood Pb per µg/m

air concentration), and slope for the C-R function in terms of points of IQ decrement per µg/dL blood Pb. In light of the uncertainties and limitations associated with the evidence on these relationships, and other considerations, application of the air-related IQ loss evidence-based framework was recognized to provide “no evidence- or risk-based bright line that indicates a single appropriate level” for the standard (73 FR 67005-67006, November 12, 2008). Rather, the framework was seen as a useful guide, in the context of the specified averaging time and form, for consideration of health risks from exposure to levels of Pb in the ambient air to inform 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).

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

). Ratios are presented in the form of 1:x, with the 1 representing air Pb (in µg/m

) 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).

Use of the air-related IQ loss evidence-based framework to inform selection of the standard level involved consideration of the evidence for the two primary input parameters mentioned above. With regard to air-to-blood ratio estimates, the evidence in the 2008 review indicated a broad range of estimates, each with limitations and associated uncertainties. Based on this evidence, the Administrator concluded that 1:5 to 1:10 represented a reasonable range to consider and focused on 1:7 as a generally central value (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 young children in the U.S.,

recognizing the EPA's identification of four such analyses and giving weight to the central estimate or median of the resultant linear 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

) are multiplied by estimates of air-to-blood ratio (µg/dL blood Pb per µg/m

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).

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). Using the air-to-blood ratio 1:7, the estimated air-related blood Pb level associated with the final standard level is approximately 1 µg/dL. In the 2008 decision, the EPA noted that even if it assumed, as an extreme hypothetical example, that the mean for the general population of U.S. children included zero contribution from air-related sources and added that to the estimate of air-related Pb, the result would still be below the lowest mean blood Pb level among the set of C-R analyses (73 FR 67002).

In considering the use of the air-related IQ loss evidence-based 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 national ambient air quality standard, 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 air-related IQ loss evidence-based 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). Further description of the EPA's consideration of this issue is provided in the preamble to the final decision rule (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

, 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

, 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

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

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

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

, 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

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. Overview of Health Effects Evidence

In this section, we provide an overview of the information presented in section II.B of the proposal on policy-relevant aspects of the health effects evidence available for consideration in this review. Section II.B of the proposal provides a detailed summary of key information contained in the ISA and in the PA on health and public health effects of Pb, focusing particularly on the information most relevant to consideration of effects associated with the presence of Pb in ambient air (80 FR 290-297, January 5, 2015). The subsections below briefly outline this information in the five topic areas addressed in section II.B of the proposal.

a. 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).

Consistent with those conclusions, in the context of pollutant exposures considered relevant to the Pb NAAQS review,

the ISA determines that causal relationships

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 certain types of effects on the nervous system in adults, and on immune system function, as well as with cancer,

as likely to be causal

(ISA, Table 1-2, sections 1.6.4 and 1.6.7).

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).

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).

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).

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).

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).

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). While some studies are newly available of other effects in children with somewhat lower blood Pb levels than previously available for these effects, nervous system effects continue to receive prominence in the current review, as in previous reviews, with particular emphasis on those affecting cognitive function and behavior in children (ISA, section 4.3), with conclusions that are consistent with findings of the last review. For example, 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).

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. For example, the evidence newly available for Pb relationships with cardiovascular effects in adults includes some studies with somewhat lower blood Pb levels than in the last review. However, 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).

Evidence available in future reviews may better inform this issue. Recognizing this, the extensive assessment of the full body of evidence available in this review contributed to the following major conclusions drawn by the ISA regarding health effects of Pb in adults (ISA, p. lxxxviii).

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).

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.

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. Similarly, given the strength of the evidence, including the greater confidence in conclusions regarding the exposures contributing to the observed effects, we focus in this review, as in the last, on neurocognitive effects in young children.

b. 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 (as discussed further in section II.B.3 of the proposal). 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.

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).

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, 5.2.1). 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).

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).

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).

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.,

at age 2 years) or concurrent blood Pb levels (ISA, section 4.3.11).

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.

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.).

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 exposure circumstances contributing to blood Pb levels measured in epidemiological studies. For example, the evidence does not indicate the exposure magnitude and timing that are eliciting such effects. 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.

c. Nervous System Effects in Children

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).

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).

Newly available in this review are two studies reporting association of blood Pb levels prior to 3 years of age with academic performance on standardized tests in primary school; mean blood Pb levels in these studies were 4.2 and 4.8 μg/dL (ISA, section 4.3.2.5; Chandramouli et al., 2009; Miranda et al., 2009). One of these two studies, which represented integer blood Pb levels as categorical variables, indicated a small effect on end-of-grade reading score of blood Pb levels as low as 2 μg/dL, after adjustment for age of measurement, race, sex, enrollment in free or reduced lunch program, parental education, and school type (Miranda et al., 2009).

The tests for cognitive function in these studies include age-appropriate Wechsler intelligence tests (Lanphear et al., 2005; Bellinger and Needleman, 2003), the Stanford-Binet intelligence test (Canfield et al., 2003), and the Bayley Scales of Infant Development (Tellez-Rojo et al., 2006). The Wechsler and Stanford-Binet tests are widely used to assess neurocognitive function in children and adults. These tests, however, are not appropriate for children under age 3. For such children, studies generally use the age-appropriate Bayley Scales of Infant Development as a measure of cognitive development.

Newly available in this review are also several studies in older children on neurocognitive effects and other nervous system effects. As described in section II.B.3 of the proposal, however, these studies are focused on population groups of ages for which the available information indicates exposure levels were higher earlier in childhood. Thus, in light of this information, although the blood Pb levels in the studies in older child population groups are lower (at the time of the study) than the younger child study levels, the studies of older

children do not provide a basis for concluding a role for lower Pb exposure levels than those experienced by the younger study groups. Rather, this information makes these studies relatively uninformative with regard to evidence of effects associated with lower exposure levels than provided by evidence previously available.

Recognizing the complexity associated with interpretation of studies involving older cohorts,

as well as the potential role of higher exposure levels in the past, we continue to focus our consideration of this question on the evidence of effects in young children for which our understanding of exposure history is less uncertain.

Within this evidence base, we recognize the lowest study group blood Pb levels to be associated with effects on cognitive function measures, indicating that to be the most sensitive endpoint. As described above, the evidence available in this review is generally consistent with that available in the last review with regard to blood Pb levels at which such effects had been reported (ISA, section 4.3.2; 2006 CD, section 8.4.2.1; 73 FR 66976-66979, November 12, 2008). As blood Pb levels are a reflection of exposure history, particularly in early childhood (ISA, section 3.3.2), we conclude, by extension, that the currently available evidence does not indicate Pb effects at exposure levels appreciably lower than recognized in the last review.

Our conclusions regarding exposure levels at which Pb health effects occur, particularly with regard to such levels that might be common in the U.S. today, are complicated now, as in the last review, by several factors. These factors include the scarcity of information in epidemiological studies on cohort exposure histories, as well as by the backdrop of higher past exposure levels which frame the history of most, if not all, older study cohorts.

In focusing on effects associated with blood Pb levels in early childhood, however, we additionally recognize the evidence across categories of effects that relate to blood Pb levels in older child study groups (for which early childhood exposure may have had an influence) which provides additional support to an emphasis on nervous system effects (ISA, sections 4.3, 4.4, 4.5, 4.6, 4.7, 4.8).

We additionally note that, as in the last review, a threshold blood Pb level with which nervous system effects, and specifically cognitive effects, occur in young children cannot be discerned from the currently available studies (ISA, sections 1.9.3 and 4.3.12). Epidemiological analyses have reported blood Pb associations with cognitive effects (FSIQ or BSID MDI

) for young child population subgroups (age 5 years or younger) with individual blood Pb measurements as low as approximately 1 μg/dL and mean concentrations as low as 2.9 to 3.8 μg/dL (ISA, section 4.3.12; Bellinger and Needleman, 2003; Bellinger, 2008; Canfield el al., 2003; Canfield, 2008; Tellez-Rojo et al., 2006; Tellez-Rojo, 2008). As concluded in the ISA, however, “the current evidence does not preclude the possibility of a threshold for neurodevelopmental effects in children existing with lower blood levels than those currently examined” (ISA, p. 4-274).

The Bayley Scales of Infant Development, Mental Development Index (BSID MDI) is a well-standardized and widely used assessment measure of infant cognitive development. Scores earlier than 24 months are not necessarily strongly correlated with later FSIQ scores in children with normal development (ISA, section 4.3.15.1).

Important uncertainties associated with the evidence of effects at low exposure levels are similar to those recognized in the last review, including the shape of the concentration-response relationship for effects on neurocognitive function at low blood Pb levels in today's young children. Also of note is our interpretation of associations between blood Pb levels and effects in epidemiological studies, with which we recognize uncertainty with regard to the specific exposure circumstances (timing, duration, magnitude and frequency) that have elicited the observed effects, as well as uncertainties in relating ambient air concentrations (and associated air-related exposures) to blood Pb levels in early childhood, as recognized in section II.A.2.b above. We additionally recognize uncertainties associated with conclusions drawn with regard to the nature of the epidemiological associations with blood Pb (

e.g.,

ISA, section 4.3.13) but note that, based on consideration of the full body of evidence for neurocognitive effects, the EPA has determined a causal relationship to exist between relevant blood Pb levels and neurocognitive impacts in children (ISA, section 4.3.15.1).

Based primarily on studies of FSIQ, the assessment of the currently available studies, as was the case in the last review, continues to recognize a nonlinear relationship between blood Pb levels and effects on cognitive function, with a greater incremental effect (greater slope) at lower relative to higher blood Pb levels within the range thus far studied, extending from well above 10 μg/dL to below 5 μg/dL (ISA, section 4.3.12). This was supported by the evidence available in the last review, including the analysis of the large pooled international dataset comprised of blood Pb measurements and IQ test results from seven prospective cohorts (Lanphear et al., 2005; Rothenberg and Rothenberg, 2005; ISA, section 4.3.12). The blood Pb measurements in this pooled dataset that were concurrent with the IQ tests ranged from 2.5 μg/dL to 33.2 μg/dL.

The study by Lanphear et al. (2005) additionally presented analyses that stratified the dataset based on peak blood Pb levels (

e.g.,

with cutpoints of 7.5 μg/dL and 10 μg/dL peak blood Pb) and found that the coefficients from linear models of the association for IQ with concurrent blood Pb levels were higher in the lower peak blood Pb level subsets than the higher groups (ISA, section 4.3.12; Lanphear et al., 2005).

In other publications, stratified analyses of several individual cohorts also observed higher coefficients for blood Pb relationships with measures of neurocognitive function in lower as compared to higher blood Pb subgroups (ISA, section 4.3.12; Canfield et al., 2003; Bellinger and Needleman, 2003; Kordas et al., 2006; Tellez-Rojo et al., 2006). Of these subgroup analyses, those involving the lowest mean blood Pb levels and closest to the current mean for U.S. preschool children are listed in Table 1 of the proposal (drawn from Table 3 of the 2008 preamble to the final rule [73 FR 67003, November 12, 2008], and Kirrane and Patel, 2014).

These analyses were important inputs for the air-related IQ loss evidence-based framework which informed decisions on a revised standard in the last review (73 FR 67005, November 12, 2008), discussed in section II.A.1 above. Specifically, the framework focused on the median of the four average linear slope estimates from the studies recognized in Table 3 of the 2008 decision (73 FR 67003, November 12, 2008). As shown in Table 1 of the proposal, the median is unchanged by

consideration of the information newly available in this review.

As described in the PA and noted in the proposal, since the completion of the ISA, two errors have been identified with the pooled dataset analyzed by Lanphear et al. (2005) (Kirrane and Patel, 2014). A recent publication and the EPA have separately recalculated the statistics and mathematical model parameters of Lanphear et al. (2005) using the corrected pooled dataset (see Kirrane and Patel, 2014). While the magnitude of the loglinear and linear regression coefficients are modified slightly based on the corrections, the conclusions drawn from these coefficients, including the finding of a steeper slope at lower (as compared to higher) blood Pb concentrations, are not affected (Kirrane and Patel, 2014).

One of these four subgroup analyses is the analysis of the lowest blood Pb subset of the pooled international study by Lanphear et al. (2005). The nonlinear model developed from the full pooled dataset is the basis of the C-R functions used in the 2007 REA, in which risk was estimated over a large range of blood Pb levels (PA, section 3.4.3.3). Given the narrower focus of the evidence-based framework on IQ response at the end of studied blood Pb levels (closer to U.S. mean level), the C-R functions in Table 1 are from linear analyses (each from separate publications) for the study group subsets with blood Pb levels closest to mean for children in the U.S. today.

As the framework focused on the median of the four slopes in Table 1, the change to the one from Lanphear et al. (2005) based on the recalculation described above has no impact on conclusions drawn from the framework.

Several studies newly available in the current review have, in all but one instance, also found a nonlinear blood Pb-cognitive function relationship in nonparametric regression analyses of the cohort blood Pb levels analyzed (ISA, section 4.3.12). These studies, however, used statistical approaches that did not produce quantitative results for each blood Pb group (ISA, section 4.3.12). Thus, newly available studies have not extended the range of observation for quantitative estimates of this relationship to lower blood Pb levels than those of the previous review. The ISA further notes that the potential for nonlinearity has not been examined in detail within a lower, narrower range of blood Pb levels than those of the full cohorts thus far studied in the currently available evidence base (ISA, section 4.3.12). Such an observation in the last review supported the consideration of linear slopes with regard to blood Pb levels at and below those represented in Table 1 of the proposal. In summary, the newly available evidence does not substantively alter our understanding of the C-R relationship (including quantitative aspects) for neurocognitive impact, such as IQ, with blood Pb in young children.

d. At-Risk Populations

In this section, as elsewhere, we use the term “at-risk populations”

to recognize populations that have a greater likelihood of experiencing Pb-related health effects,

i.e.,

groups with characteristics that contribute to an increased risk of Pb-related health effects. These populations are also referred to as sensitive groups (as in section I.A above). In identifying factors that increase risk of Pb-related health effects, we have considered evidence regarding factors contributing to increased susceptibility, generally including physiological or intrinsic factors contributing to a greater response for the same exposure and those contributing to increased exposure, including that resulting from behavior leading to increased contact with contaminated media (ISA, Chapter 5). Physiological risk factors include both conditions contributing to a group's increased risk of effects at a given blood Pb level and those that contribute to blood Pb levels higher than those otherwise associated with a given Pb exposure (

e.g.,

ISA, sections 5.3 and 5.1, respectively).

In the context of “at-risk populations,” the term “population” refers to persons having one or more qualities or characteristics including, for example, a specific pre-existing illness or a specific age or lifestage, with lifestage referring to a distinguishable time frame in an individual's life characterized by unique and relatively stable behavioral and/or physiological characteristics that are associated with development and growth.

In considering factors that increase risk by contributing to increased exposure or to increased blood Pb levels over those otherwise associated with a given Pb exposure, we note that the currently available evidence continues to support a nonlinear relationship between neurocognitive effects and blood Pb that indicates incrementally greater impacts at lower as compared to higher blood Pb levels (ISA, section 4.3.12), as described in section II.B.3 of the proposal and briefly noted in section II.A.2.c above. An important implication of this finding is that while children with higher blood Pb levels are at greater risk of Pb-related effects than children with lower blood Pb levels, on an incremental basis (

e.g.,

per μg/dL) the risk is greater for children at lower blood Pb levels. This was given particular attention in the last review of the Pb NAAQS, in which the standard was revised with consideration of the incremental impact of air-related Pb on young children in the U.S. and the recognition of greater incremental impact for those children with lower absolute blood Pb levels (73 FR 67002, November 12, 2008). Such consideration included a focus on those C-R studies involving the lowest blood Pb levels, as described in section II.A.1 above.

The information newly available in this review has not appreciably altered our previous understanding of at-risk populations for Pb in ambient air. As in the last review, the factor most prominently recognized to contribute to increased risk of Pb effects is childhood (ISA, section 1.9.6). As discussed in section II.B.2 of the proposal and briefly noted in section II.A.2.b above, 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). Thus, in the current review, as at the time of the last review of the Pb NAAQS, we recognize young children as an important at-risk population, with sensitivity extending to prenatal exposures and into childhood development.

An additional physiological risk factor that contributes to increased blood Pb levels is nutritional status, which can play a role in Pb absorption from the gastrointestinal tract, with iron-, calcium- and zinc-deficient diets contributing to increased Pb absorption and associated blood Pb levels (ISA, sections 3.2.1.2, 5.1, 5.3.10 and 5.4). Risk factors based on increased exposure include spending time in proximity to sources of Pb to ambient air or other environmental media, such as large active metals industries or locations of historical Pb contamination (ISA, sections 1.9.6, 3.7.1, 5.2.5 and 5.4). Residential factors associated with other sources of Pb exposure (

e.g.,

leaded paint or plumbing with Pb pipes or solder) are another exposure-related risk factor (ISA, sections 3.7.1, 5.2.6 and 5.4). Additionally, some races or ethnicities have been associated with higher blood Pb levels, with differential exposure indicated in some cases as the cause (ISA, sections 5.2.3 and 5.4).

Lower socioeconomic status (SES) has been associated with higher Pb exposure and higher blood Pb concentration in some study groups, leading the ISA to conclude the evidence is suggestive for low SES as a risk factor (ISA, sections 5.3.16, 5.2.4 and 5.4).

Although the differences in blood Pb levels, nationally, between children of lower and higher income levels (as well as among some races or ethnicities) have lessened, blood Pb levels continue to be higher among lower-income children indicating higher exposure and/or greater influence of factors independent of exposure, such as nutritional factors (ISA, sections 1.9.6, 5.2.1.1 and 5.4).

The evidence is also suggestive of increased risk associated with several other factors: older adulthood,

pre-

existing disease (

e.g.,

hypertension), variants for certain genes and increased stress (ISA, section 5.3.4).

The approach used by the EPA in evaluating the evidence regarding factors that may influence the risk of Pb-related health effects is described in chapter 5 of the ISA.

Although the evidence for SES continues to indicate increased blood Pb levels in lower income children, its role with regard to an increased health risk for the same blood Pb level is unclear and its role generally with regard to Pb-related risk is somewhat complicated. SES often serves as a marker term for one or a combination of unspecified or unknown environmental or behavioral variables. Further, it is independently associated with an adverse impact on neurocognitive development, and a few studies have examined SES as a potential modifier of the association of childhood Pb exposure with cognitive function with inconsistent findings regarding low SES as a potential risk factor.

The ISA identifies older adulthood as a lifestage of potentially greater risk of Pb-related health effects based primarily on the evidence of increases in blood Pb levels during this lifestage (ISA, sections 5.2.1.2, 5.3.1.2, and 5.4), as well as observed associations of some cardiovascular and nervous system effects with bone and blood Pb in older populations, with biological plausibility for the role of Pb provided by experimental animal studies (ISA, sections 4.3.5, 4.3.7 and 4.4). Exposure

histories of older adult study populations, which included younger years during the time of leaded gasoline usage and other sources of Pb exposures which were more prevalent in the past than today, are likely contributors to their blood Pb levels (ISA, pp. lx-lxi; Figure 2-1 and sections 2.5.2, 3.3.5 and 5.2.1.2).

In summary, we recognize the sensitivity of the prenatal period and several stages of childhood to an array of neurocognitive and behavioral effects, and we particularly recognize young children as an important at-risk population in light of current environmental exposure levels. Age or lifestage was used to distinguish potential groups on which to focus in the last review in recognition of its role in exposure and susceptibility, and young children were the focus of the REA in consideration of the health effects evidence regarding endpoints of greatest public health concern and in recognition of effects on the developing nervous system as a sentinel endpoint for public health impacts of Pb. This identification continues to be supported by the evidence available in the current review.

e. Potential Impacts on Public Health

There are several potential public health impacts associated with Pb exposure in the current U.S. population. In recognition of effects causally related to blood Pb levels somewhat near those most recently reported for today's population and for which the weight of the evidence is greatest, the potential public health impacts most prominently recognized in the ISA are population IQ impacts associated with childhood Pb exposure and prevalence of cardiovascular effects in adults (ISA, section 1.9.1). With regard to the latter category, as discussed above, the full body of evidence indicates a role of long-term cumulative exposure, with uncertainty regarding the specific exposure circumstances contributing to the effects in the epidemiological studies of adult populations, for whom historical Pb exposures were likely much higher than exposures that commonly occur today (ISA, section 4.4). There is less uncertainty regarding the exposure patterns contributing to the blood Pb levels reported in studies of younger populations (ISA, sections 1.9.4 and 1.10). Accordingly, the discussion of public health implications relevant to this review is focused predominantly on nervous system effects, including IQ decrements, in children.

The magnitude of a public health impact is dependent upon the type or severity of the effect, as well as the size of populations affected. Intelligence quotient is a well-established, widely recognized and rigorously standardized measure of neurocognitive function, as well as a global measure reflecting the integration of numerous processes (ISA, section 4.3.2; 2006 CD, sections 6.2.2 and 8.4.2). In considering population risk, the distribution of effects across members of the population is important. For example, if Pb-related decrements are manifested uniformly across the range of IQ scores in a population, “a small shift in the population mean IQ may be significant from a public health perspective because such a shift could yield a larger proportion of individuals functioning in the low range of the IQ distribution, which is associated with increased risk of educational, vocational, and social failure” as well as a decrease in the proportion with high IQ scores (ISA, section 1.9.1). Examples of other measures of cognitive function negatively associated with Pb exposure include other measures of intelligence and cognitive development and measures of other cognitive abilities, such as learning, memory, and executive functions, as well as academic performance and achievement (ISA, section 4.3.2). Although some neurocognitive effects of Pb in children may be transient, some may persist into adulthood (ISA, section 1.9.5).

We also note that deficits in neurodevelopment early in life may have lifetime consequences as “[n]eurodevelopmental deficits measured in childhood may set affected children on trajectories more prone toward lower educational attainment and financial well-being” (ISA, section 4.3.14). Thus, population groups for which neurodevelopment is affected by Pb exposure in early childhood are at risk of related impacts on their success later in life.

The ISA states that the “persistence of effects appears to depend on the duration and window of exposure as well as other factors that may affect an individual's ability to recover from an insult,” with some evidence of greater recovery in children reared in households with more optimal caregiving characteristics and low concurrent blood Pb levels (ISA, p. 1-77; Bellinger et al., 1990).

As indicated above, young children are the at-risk population that may be most at risk of health effects associated with exposure to Pb, and children at greatest risk from

air-related

Pb are those children with highest air-related Pb exposure, which we consider to be those living in areas of higher ambient air Pb concentrations (

e.g.,

concentrations near or above the current standard). Analyses in the PA indicate this group to be a very small subset of all young children in the U.S. Together the analyses indicate that well below one-tenth of one percent of the full population of children aged 5 years or younger in the U.S. today live in areas with air Pb concentrations near or above the current standard, with the current monitoring data indicating the size of this population to be approximately one-hundredth of a percent of the full population of children aged 5 or younger (PA, pp. 3-36 to 3-38, 4-25, 4-32). It is these children that were the Administrator's focus in revising the primary standard in 2008.

3. Overview of Information on Blood Lead Relationships With Air Lead

This section provides a brief overview of the information summarized in section II.C of the proposal on key aspects of the information available in this review on blood Pb as a biomarker and on relationships of blood Pb with air Pb (80 FR 298-300, January 5, 2015). Blood Pb is well established as a biomarker of Pb exposure and of internal dose, with relationships between air Pb concentrations and blood Pb concentrations informing consideration of the NAAQS for Pb since its initial establishment in 1978. The blood Pb concentration in childhood (particularly early childhood) can more quickly (than in adulthood) reflect changes in total body burden (associated with the shorter exposure history) and can also reflect changes in recent exposures (ISA, section 3.3.5). The relationship of children's blood Pb to recent exposure may reflect their labile bone pool, with their rapid bone turnover in response to rapid childhood growth rates (ISA, section 3.3.5). The relatively smaller skeletal compartment of Pb in children (particularly very young children) compared to adults is subject to more rapid turnover. Multiple studies have demonstrated young children's blood Pb levels to reflect Pb exposures, including exposures to Pb in surface dust (

e.g.,

Lanphear and Roghmann, 1997; Lanphear et al., 1998). These and studies of child populations near sources of air Pb emissions, such as metal smelters, have further demonstrated the effect of airborne Pb on interior dust and on blood Pb (ISA, sections 3.4.1, 3.5.1 and 3.5.3; Hilts, 2003; Gulson et al., 2004).

As blood Pb is an integrated marker of aggregate Pb exposure across all pathways, the blood Pb C-R relationships described in epidemiological studies of Pb-exposed populations do not distinguish among different sources of Pb or pathways of

Pb exposure (

e.g.,

inhalation, ingestion of indoor dust, ingestion of dust containing leaded paint). Thus, our interpretation of the health effects evidence for purposes of this review necessitates characterization of the relationships between Pb from those sources and pathways of interest in this review (

i.e.,

those related to Pb emitted into the air) and blood Pb.

The evidence for air-to-blood relationships derives from analyses of datasets for populations residing in areas with differing air Pb concentrations, including datasets for circumstances in which blood Pb levels have changed in response to changes in air Pb. The control for variables other than air Pb that can affect blood Pb varies across these analyses. At the conclusion of the last review in 2008, the EPA interpreted the evidence as providing support for use (in informing the Administrator's decision on standard level) of a range of air-to-blood ratios

“inclusive at the upper end of estimates on the order of 1:10 and at the lower end on the order of 1:5” (73 FR 67002, November 12, 2008). This conclusion reflected consideration of the air-to-blood ratios presented in the 1986 CD

and associated observations regarding factors contributing to variation in such ratios, ratios reported subsequently and ratios estimated based on modeling performed in the REA, as well as advice from CASAC (73 FR 66973-66975, 67001-67002, November 12, 2008). The information available in this review, which is assessed in the ISA and largely, although not completely, comprises studies that were available in the last review, does not alter the primary scientific conclusions drawn in the last review regarding the relationships between Pb in ambient air and Pb in children's blood. The ratios summarized in the ISA in this review span a range generally consistent with the range concluded in 2008 (ISA, section 3.5.1).

The quantitative relationship between ambient air Pb and blood Pb, often termed a slope or ratio, describes the increase in blood Pb (in μg/dL) estimated to be associated with each unit increase of air Pb (in μg/m

). Ratios are presented in the form of 1:x, with the 1 representing air Pb (in μg/m

) 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). Slopes are presented as simply the value of x.

The 2006 CD did not include an assessment of then-current evidence on air-to-blood ratios.

The evidence on the quantitative relationship between air Pb and air-related Pb in blood is now, as in the past, limited by the circumstances (such as those related to Pb exposure) in which the data were collected. Previous reviews have recognized the significant variability in air-to-blood ratios for different populations exposed to Pb through different air-related exposure pathways and at different air and blood levels, with the 1986 CD noting that ratios derived from studies involving the higher blood and air Pb levels pertaining to occupationally exposed workers are generally smaller than ratios from studies involving lower blood and air Pb levels (ISA, p. 3-132; 1986 CD, p. 11-99). Consistent with this observation, slopes in the range of 3 to 5 were estimated for child population datasets assessed in the 1986 CD (ISA, p. 3-132; 1986 CD p. 11-100; Brunekreef, 1984). Additional studies considered in the last review and those assessed in the ISA provide evidence of ratios above this older range (ISA, p. 3-133). For example, a ratio of 1:6.5 to 1:7 is indicated by the study by Hilts (2003), one of the few studies that evaluate the air Pb-blood Pb relationship in conditions that are closer to the current state in the U.S. (ISA, p. 3-132). We additionally note the variety of factors identified in the ISA that may potentially affect estimates of various ratios (including potentially coincident reductions in nonair Pb sources during the course of the studies) and for which a lack of complete information may preclude any adjustment of estimates to account for their role (ISA, section 3.5).

In summary, as at the time of the last review of the NAAQS for Pb, the currently available evidence includes estimates of air-to-blood ratios, both empirical and model-derived, with associated limitations and related uncertainties. These limitations and uncertainties, which are summarized here and also noted in the ISA, usually include uncertainty associated with reductions in other Pb sources during the study period. The limited amount of new information available in this review has not appreciably altered the scientific conclusions reached in the last review regarding relationships between Pb in ambient air and Pb in children's blood or with regard to the range of ratios. The currently available evidence continues to indicate ratios relevant to the population of young children in the U.S. today, reflecting multiple air-related pathways in addition to inhalation, to be generally consistent with the approximate range of 1:5 to 1:10 given particular attention in the 2008 NAAQS decision, including the “generally central estimate” of 1:7 (73 FR 67002, 67004, November 12, 2008; ISA, pp. 3-132 to 3-133).

4. Overview of Risk and Exposure Assessment Information

This section provides a brief overview of key aspects of the risk and exposure assessment information available in this review, which is based primarily on the exposure and risk assessment developed in the last review of the Pb NAAQS.

This overview is drawn from the summary presented in the proposal (80 FR 300-305, January 5, 2015). As described in the REA Planning Document, careful consideration of the information newly available in this review, with regard to designing and implementing a full REA for this review, led to the conclusion that performance of a new REA for this review was not warranted. We did not find the information newly available in this review to provide the means by which to develop an updated or enhanced risk model that would substantially improve the utility of risk estimates in informing the current Pb NAAQS review (REA Planning Document, section 2.3). Based on its 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).

Accordingly, the exposure/risk information considered in this review is drawn primarily from the 2007 REA, augmented by a limited new computation for one case study focused on risk associated with the current standard, as described in section II.D of the proposal and in section 3.4 and Appendix 3A of the PA.

The information in this review is based on the assessment from the last review, described in the 2007 REA, the 2007 Staff Paper and the 2008 notice of final decision (USEPA, 2007a; USEPA, 2007b; 73 FR 66964, November 12, 2008), as considered in the context of the evidence newly available in this review (PA, section 3.4; proposal, section II.D).

In its review of the draft PA, the CASAC Pb Review Panel reinforced its concurrence with the EPA's decision not to develop a new REA (Frey, 2013).

The focus for the risk assessment and associated estimates is on Pb derived from sources emitting Pb to ambient air. In order to characterize exposure and risk from these pathways, however, the assessment also recognized the role of Pb exposure pathways unrelated to Pb in ambient air (2007 REA, section 2.1). Sources of human Pb exposure include current and historical air emissions sources, as well as miscellaneous nonair sources, which can contribute to multiple exposure media and associated pathways, such as inhalation of ambient air, ingestion of indoor dust, outdoor soil/dust and diet or drinking water (as recognized in section I.D above). In addition to airborne emissions (recent or

those in the past), sources of Pb to these pathways also include old leaded paint, including Pb mobilized indoors during renovation/repair activities, and contaminated soils. Lead in diet and drinking water may have air pathway-related contributions as well as contributions from nonair sources (

e.g.,

Pb solder on older water distribution pipes and Pb in materials used in food processing).

Limitations in our data and modeling tools handicapped our ability to address the various complexities associated with exposure to ambient air Pb and to fully separate the nonair contributions to Pb exposure from estimates of air-related Pb exposure and risk. As a result, the assessment included a number of simplifying assumptions in a number of areas, and the estimates of air-related Pb risk produced are approximate, characterized by bounds within which air-related Pb risk is estimated to fall. The lower bound is based on a combination of pathway-specific estimates that do not completely represent all air-related pathways, while the upper bound is based on a combination of pathway-specific estimates that includes pathways that are not air-related but the separating out of which is precluded by modeling and data limitations (PA, section 3.4).

Key aspects of the 2007 REA, such as the exposure populations, exposure or dose metric, health effects endpoint and risk metric were based on consideration of the then-currently available evidence as assessed in detail in the 2006 CD. As discussed in the REA Planning Document (USEPA, 2011b), these selections continue to be supported by the evidence now available in this review as described in the ISA. The REA focused on risk to the central nervous system in childhood as the most sensitive effect that could be quantitatively assessed, with decrement in IQ used as the risk metric. Exposure and biokinetic modeling was used to estimate blood Pb concentrations in children exposed to Pb up to age 7 years.

This focus reflected the evidence for young children with regard to air-related exposure pathways and susceptibility to Pb health impacts (

e.g.,

ISA, sections 3.1.1, 4.3, 5.2.1.1, 5.3.1.1, and 5.4). For example, the hand-to-mouth activity of young children contributes to their Pb exposure (

i.e.,

incidental soil and indoor dust ingestion), and ambient air-related Pb has been shown to contribute to Pb in outdoor soil and indoor house dust (ISA, sections 3.1.1 and 3.4.1; 2006 CD, section 3.2.3).

The pathways represented in this modeling included childhood inhalation and ingestion pathways, as well as maternal contributions to newborn body burden (2007 REA, Appendix H, Exhibit H-6).

The 2007 REA relied on a case study approach to provide estimates that inform our understanding of air-related exposure and risk in different types of air Pb exposure situations. Lead exposure and associated risk were estimated for multiple case studies that generally represent two types of residential population exposures to air-related Pb: (1) Location-specific urban populations of children with a broad range of air-related exposures, reflecting existence of urban concentration gradients; and (2) children residing in localized areas with air-related exposures representing air concentrations specifically reflecting the standard level being evaluated (see PA, Table 3-6). Thus, the two types of case studies differed with regard to the extent to which they represented population variability in air-related Pb exposure.

In drawing on the 2007 REA for our purposes in this review, we focused on two case studies, one from each of these two categories: (1) The location-specific urban case study for Chicago and (2) the generalized (local) urban case study (PA, Table 3-6). The generalized (local) urban case study (also referred to as

general urban case study

) was not based on a specific geographic location and reflected several simplifying assumptions in representing exposure including uniform ambient air Pb levels associated with the standard of interest across the hypothetical study area and a uniform study population. Based on the nature of the population exposures represented by the two categories of case study, the generalized (local) urban case study includes populations that are relatively more highly exposed by way of air pathways to air Pb concentrations near the standard level evaluated, compared with the populations in the location-specific urban case. The location-specific urban case studies provided representations of urban populations with a broad range of air-related exposures due to spatial gradients in both ambient air Pb levels and population density. For example, the highest air concentrations in these case studies (

i.e.,

those closest to the standard being assessed) were found in very small parts of the study areas, while a large majority of the case study populations resided in areas with much lower air concentrations.

Air-related risk estimates for the two case studies are accompanied by a number of uncertainties (summarized in section II.D.3 of the proposal and described in detail in section 3.4 of the PA). Exposure and risk modeling conducted for this analysis was complex and subject to significant uncertainties due to limitations in the data and models, among other aspects, as recognized at the time of the last review.

The multimedia and persistent nature of Pb, the role of multiple exposure pathways, and the contributions of nonair sources of Pb to human exposure media all present challenges and contribute significant additional complexity to the health risk assessment that goes far beyond the situation for similar assessments typically performed for other NAAQS pollutants (

e.g.,

that focus only on the inhalation pathway). Of particular note among the assessment limitations are limitations in the assessment design, data and modeling tools that handicapped us from sharply separating Pb linked to ambient air from Pb that is not air related. The resultant, approximate, air-related risk bounds, however, encompass estimates drawn from the air-related IQ loss evidence-based framework, providing a rough consistency and general support, as was the case in the last review (73 FR 67004, November 12, 2008).

As summarized in section II.D.3 of the proposal, a range of limitations and areas of uncertainty were associated with the information available in the last review (PA, sections 3.4.4, 3.4.6 and 3.4.7), and the newly available information in this review did not substantially reduce any of the primary sources of uncertainty identified to have the greatest impact on risk estimates (USEPA, 2011b). Thus, the key observations regarding air-related Pb risk modeled for the set of standard levels assessed in the 2007 REA, as well as the risk estimates interpolated for the current standard, are not significantly affected by the new information. Nor is our overall characterization of uncertainty and variability associated with those estimates (as summarized above and in sections 3.4.6 and 3.4.7 of the PA).

B. Conclusions on the Primary Standard

In drawing conclusions on the adequacy of the current primary Pb standard, in view of the advances in scientific knowledge and additional information now available, the Administrator considers the evidence base, information and policy judgments that were the foundation of the last review and reflects upon the body of evidence and information newly available in this review. The Administrator has taken into account both evidence-based and exposure- and risk-based considerations, advice from CASAC and public comment. Evidence-based considerations draw upon the EPA's assessment and integrated synthesis of the scientific evidence from epidemiological studies and experimental animal studies evaluating health effects related to exposures to Pb,

with a focus on policy-relevant considerations as discussed in the PA. The exposure- and risk-based considerations draw from the results of the quantitative analyses presented in the 2007 REA (augmented as described in the PA and summarized in section II.D of the proposal) and consideration of those results in the PA.

As described in section II.A.2 of the proposal, consideration of the evidence and exposure/risk information in the PA and by the Administrator is framed by consideration of a series of key policy-relevant questions. Section II.B.1 below summarizes the rationale for the Administrator's proposed decision, drawing from section II.E.4 of the proposal. A fuller presentation of PA considerations and conclusions, and advice from the CASAC, which were taken into account by the Administrator, is provided in sections II.E.1 through II.E.3 of the proposal. Advice received from CASAC in this review is briefly summarized in section II.B.2 below, and public comments on the proposed decision are addressed in section II.B.3. The Administrator's conclusions in this review regarding the adequacy of the current primary standard are described in section II.B.4.

1. Basis for the Proposed Decision

At the time of the proposal, the Administrator carefully considered the assessment of the current evidence and conclusions reached in the ISA; the currently available exposure/risk information, including associated limitations and uncertainties; considerations and staff conclusions and associated rationales presented in the PA; the ad

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