[Federal Register Volume 81, Number 201 (Tuesday, October 18, 2016)]
[Rules and Regulations]
[Pages 71906-71943]
[FR Doc No: 2016-23153]

Vol. 81

Tuesday,

No. 201

October 18, 2016

Part V

Environmental Protection Agency

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40 CFR Part 50

Review of the National Ambient Air Quality Standards for Lead; Final
Rule

Federal Register / Vol. 81 , No. 201 / Tuesday, October 18, 2016 /
Rules and Regulations

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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.

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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<PHONE_NUMBER>.

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:<PHONE_NUMBER>; fax: (919)
541-0237; email<EMAIL_ADDRESS>
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.'' \1\ A secondary standard, as defined in section 109(b)(2),
must ``specify a level of air quality the attainment and maintenance of
which, in the judgment of the Administrator, based on such criteria, is
requisite to protect the public welfare from any known or anticipated
adverse effects associated with the presence of [the] pollutant in the
ambient air.''
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    \1\ The legislative history of section 109 indicates that a
primary standard is to be set at ``the maximum permissible ambient
air level . . . which will protect the health of any [sensitive]
group of the population,'' and that for this purpose ``reference
should be made to a representative sample of persons comprising the
sensitive group rather than to a single person in such a group.''
See S. Rep. No. 91-1196, 91st Cong., 2d Sess. 10 (1970).
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    The requirement that primary standards provide an adequate margin
of safety was intended to address uncertainties associated with
inconclusive scientific and technical information available at the time
of standard setting. It was also intended to provide a reasonable
degree of protection against hazards that research has not yet
identified. See Lead Industries Association v. EPA, 647 F.2d 1130, 1154
(D.C. Cir. 1980), cert. denied, 449 U.S. 1042 (1980); American
Petroleum Institute v. Costle, 665 F.2d 1176, 1186 (D.C. Cir. 1981),
cert. denied, 455 U.S. 1034 (1982); American Farm Bureau Federation v.
EPA, 559 F. 3d 512, 533 (D.C. Cir. 2009); Association of Battery
Recyclers v. EPA, 604 F. 3d 613, 617-18 (D.C. Cir. 2010). Both kinds of
uncertainties are components of the risk associated with pollution at
levels below those at which human health effects can be said to occur
with reasonable scientific certainty. Thus, in selecting primary
standards that provide an adequate margin of safety, the Administrator
is seeking not only to prevent pollution levels that have been
demonstrated to be harmful but also to prevent lower pollutant levels
that may pose an unacceptable risk of harm, even if the risk is not
precisely identified as to nature or degree. The CAA does not require
the Administrator to establish a primary NAAQS at a zero-risk level or
at background concentration levels, see Lead Industries v. EPA, 647
F.2d at 1156 n.51, but rather at a level that reduces risk sufficiently
so as to protect public health with an adequate margin of safety.
    In addressing the requirement for an adequate margin of safety, the
EPA considers such factors as the nature and severity of the health
effects involved, the size of sensitive population(s) at risk,\2\ and
the kind and degree of the uncertainties that must be addressed. The
selection of any particular approach to providing an adequate margin of
safety is a policy choice left specifically to the Administrator's
judgment. See Lead Industries Association v. EPA, 647 F.2d at 1161-62.
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    \2\ 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.
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    In setting primary and secondary standards that are ``requisite''
to protect public health and welfare, respectively, as provided in
section 109(b), the EPA's task is to establish standards that are
neither more nor less stringent than necessary for these purposes. In
so doing, the EPA may not consider the

costs of implementing the standards. See generally, Whitman v. American
Trucking Associations, 531 U.S. 457, 465-472, 475-76 (2001). Likewise,
``[a]ttainability and technological feasibility are not relevant
considerations in the promulgation of national ambient air quality
standards.'' American Petroleum Institute v. Costle, 665 F. 2d at 1185.
    Section 109(d)(1) requires that ``not later than December 31, 1980,
and at 5-year intervals thereafter, the Administrator shall complete a
thorough review of the criteria published under section 108 and the
national ambient air quality standards . . . and shall make such
revisions in such criteria and standards and promulgate such new
standards as may be appropriate. . . .'' Section 109(d)(2) requires
that an independent scientific review committee ``shall complete a
review of the criteria . . . and the national primary and secondary
ambient air quality standards . . . and shall recommend to the
Administrator any new . . . standards and revisions of existing
criteria and standards as may be appropriate . . .'' Since the early
1980s, this independent review function has been performed by the Clean
Air Scientific Advisory Committee (CASAC).\3\
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    \3\ 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.
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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.\4\
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    \4\ 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).
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    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.\5\ 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/).
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    \5\ 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.
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    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 [mu]g/
dL in the 2009-2010 National Health and Nutrition Examination Survey
(NHANES) \6\ as compared to the geometric mean in 1999-2000 of 2.23
[micro]g/dL and in 1988-1991 of 3.6 [mu]g/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).
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    \6\ 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
[mu]g/dL in the 2011-2012 survey (CDC, 2015).
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    The EPA also participates in a broad range of international
programs focused on reducing environmental releases and human exposures
in other countries. For example, the Partnership for Clean Fuels and
Vehicles program engages governments and stakeholders in developing
countries to eliminate Pb in gasoline globally.\7\ From 2007 to 2011,
the number of countries known to still be using leaded gasoline was
reduced from just over 20 to six (USEPA, 2011c). As of January, leaded
gasoline for on-road use is known to be available (along with unleaded
gasoline) in three countries.\8\
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    \7\ 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.
    \8\ UNEP. ``Leaded Petrol Phase-out: Global Status as at January
2016'' map downloaded from http://www.unep.org/transport/new/pcfv/.
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    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).\9\
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    \9\ 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.
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C. Review of the Air Quality Criteria and Standards for Lead

    Unlike pollutants such as particulate matter and carbon monoxide,
air quality criteria had not been issued for Pb as of the enactment of
the CAA of 1970, which first set forth the requirement to set NAAQS
based on air quality criteria. In the years just after enactment of the
CAA, the EPA did not list Pb under section 108 of the Act, having
determined to control Pb air pollution through regulations to phase out
the use of Pb additives in gasoline (see 41 FR 14921, April 8, 1976).
However, the decision not to list Pb under section 108 was challenged
by environmental and public health groups, and the U.S. District Court
for the Southern District of New York concluded that the EPA was
required to list Pb under section 108. Natural Resources Defense
Council v. EPA, 411 F. Supp. 864 21 (S.D. N.Y. 1976), affirmed, 545
F.2d 320 (2d Cir. 1978). Accordingly, on April 8, 1976, the EPA
published a notice in the Federal Register that Pb had been listed
under section 108 as a criteria pollutant (41 FR 14921, April 8, 1976),
and on October 5, 1978, the EPA promulgated primary and secondary NAAQS
for Pb under section 109 of the Act (43 FR 46246, October 5, 1978).
Both primary and secondary standards were set at a level of 1.5
micrograms per cubic meter ([mu]g/m\3\), measured as Pb in total
suspended particles (Pb-TSP), not to be exceeded by the maximum
arithmetic mean concentration averaged over a calendar quarter. These
standards were based on the 1977 Air Quality Criteria for Lead (USEPA,
1977).
    The first review of the Pb standards was initiated in the mid-
1980s. The scientific assessment for that review is described in the
1986 Air Quality Criteria for Lead (USEPA, 1986a; henceforth referred
to as the 1986 CD), the associated Addendum (USEPA, 1986b) and the 1990
Supplement (USEPA, 1990a). As part of the review, the agency designed
and performed human exposure and health risk analyses (USEPA, 1989),
the results of which were presented in a 1990 Staff Paper (USEPA,
1990b). Based on the scientific assessment and the human exposure and
health risk analyses, the 1990 Staff Paper presented recommendations
for consideration by the Administrator (USEPA, 1990b). After
consideration of the documents developed during the review and the
significantly changed circumstances since Pb was listed in 1976, the
agency did not propose any revisions to the 1978 Pb NAAQS. In a
parallel effort, the agency developed the broad, multi-program,
multimedia, integrated U.S. Strategy for Reducing Lead Exposure (USEPA,
1991). As part of implementing this strategy, the agency focused
efforts primarily on regulatory and remedial clean-up actions aimed at
reducing Pb exposures from a variety of nonair sources judged to pose
more extensive public health risks to U.S. populations, as well as on
actions to reduce Pb emissions to air, such as bringing more areas into
compliance with the existing Pb NAAQS (USEPA, 1991). The EPA continues
this broad, multi-program, multimedia approach to reducing Pb exposures
today, as described in section I.B above.
    The last review of the 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).\10\ The
schedule for completion of the review was governed by a judicial order
in Missouri Coalition for the Environment v. EPA (No. 4:04CV00660 ERW,
September 14, 2005; and amended on April 29, 2008 and July 1, 2008).
---------------------------------------------------------------------------

    \10\ 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 [micro]g/
m\3\.
    Immediately subsequent to completion of the Staff Paper, the EPA
issued an advance notice of proposed rulemaking (ANPR) that was signed
by the Administrator on December 5, 2007 (72 FR 71488, December 17,
2007).\11\ 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).
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    \11\ 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 [micro]g/m\3\ to a level of 0.15
[micro]g/m\3\. The averaging time was revised to a rolling 3-month
period with a maximum (not-to-be-exceeded) form, evaluated over a 3-
year period. The indicator of Pb-TSP was retained, reflecting the
evidence that Pb particles of all sizes pose health risks. The
secondary standard was revised to be identical in all respects to the
revised primary standard (40 CFR 50.16). Revisions to the NAAQS were
accompanied by revisions to the data handling procedures, the treatment
of exceptional events and the ambient air monitoring and reporting
requirements, as well as emissions inventory reporting requirements.
One aspect of the revised data handling requirements is the allowance
for the use of monitoring for particulate matter with mean diameter
below 10 microns (Pb-PM10) 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) \12\ 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).
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    \12\ 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,\13\ which

have undergone CASAC and public review. The studies assessed in the ISA
\14\ 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.
---------------------------------------------------------------------------

    \13\ 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.
    \14\ 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 <IP_ADDRESS>). 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 <IP_ADDRESS>).
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 <IP_ADDRESS>). 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.\15\ 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.
---------------------------------------------------------------------------

    \15\ 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.
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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-
PM10 or Pb in particulate matter with mean aerodynamic
diameter less than or equal to 2.5 microns (Pb-PM2.5), 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,\16\ Pb-PM10 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).
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    \16\ The Pb-PM10 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 <IP_ADDRESS>.
These conditions include where Pb concentrations are not expected to
equal or exceed 0.10 [mu]g/m\3\ as an arithmetic 3-month mean and
where the source of Pb emissions is expected to emit a substantial
majority of its Pb in the size fraction captured by PM10
monitors.
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    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.\17\ 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\18\ 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.
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    \17\ 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)).
    \18\ 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).
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    Monitoring agencies may also conduct non-source-oriented Pb
monitoring at the NCore monitoring sites.\19\ In 2015, all NCore sites
with a population of 500,000 or more (as defined by the U.S. Census
Bureau) \20\ were measuring Pb concentrations, with a 2014 analysis
indicating generally similar numbers of sites measuring Pb in TSP and
Pb in PM10 (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-PM10 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 [micro]g/m\3\
(Cavender, 2014). Other monitoring networks that provide data on Pb in
PM10 or PM2.5 at non-source-oriented urban, and
some rural, sites include the National Air Toxics Trends Stations for
PM10 and the Chemical Speciation Network for
PM2.5. Data on Pb in PM2.5 are also provided at
the rural sites of the Interagency Monitoring of Protected Visual
Environments network (also known as the IMPROVE network).
---------------------------------------------------------------------------

    \19\ 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.
    \20\ 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 [micro]g/dL, extending from 8 down to 2 [micro]g/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 PM10 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-PM10-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).\21\
---------------------------------------------------------------------------

    \21\ However, in order to take advantage of the increased
precision of Pb-PM10 measurements and decreased spatial
variation of Pb-PM10 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-PM10),
a role was provided for Pb-PM10 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 \22\ 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 ([micro]g/m\3\), air-to-blood ratio (albeit in
terms of [micro]g/dL blood Pb per [micro]g/m\3\ air concentration), and
slope for the C-R function in terms of points of IQ decrement per
[micro]g/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).
---------------------------------------------------------------------------

    \22\ The term ``air-to-blood ratio'' describes the increase in
blood Pb (in [micro]g/dL) estimated to be associated with each unit
increase of air Pb (in [micro]g/m\3\). Ratios are presented in the
form of 1:x, with the 1 representing air Pb (in [micro]g/m\3\) and x
representing blood Pb (in [micro]g/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.,\23\ 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 [micro]g/dL blood Pb
was selected for use with the framework. With the framework, potential
alternative standard levels ([micro]g/m\3\) are multiplied by estimates
of air-to-blood ratio ([micro]g/dL blood Pb per [micro]g/m\3\ air Pb)
and the median slope for the C-R function (points IQ decrement per
[micro]g/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).
---------------------------------------------------------------------------

    \23\ 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 [micro]g/dL and the 5th and 95th percentiles
were 0.7 [micro]g/dL and 5.1 [micro]g/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 [micro]g/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 [micro]g/
m\3\, with the combination of the generally central estimate of air-to-
blood ratio of 1:7 and the median of the four C-R functions (-1.75 IQ
point decrement per [micro]g/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 [micro]g/m\3\, in combination with the
specified choice of indicator, averaging time and form, was requisite
to protect public health, including the health of sensitive groups,
with an adequate margin of safety (73 FR 67006, November 12, 2008). In
reaching decisions on level as well as the other elements of the
revised standard, the Administrator took note of the complexity
associated with consideration of health effects caused by different
ambient air concentrations of Pb and with uncertainties with regard to
the relationships between air concentrations, exposures, and health
effects. For example, selection of a maximum, not to be exceeded, form
in conjunction with a rolling 3-month averaging time over a 3-year span
was expected to have the effect that the at-risk population of children
would be exposed below the standard most of the time (73 FR 67005,
November 12, 2008). The Administrator additionally considered the
provision of an adequate margin of safety in making decisions on each
of the elements of the standard, including, for example ``selection of
TSP as the indicator and the rejection of the use of PM10
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 [mu]g/m\3\ as
the level of the standard'' (73 FR 67007, November 12, 2008).
    The Administrator additionally noted that a standard with this
level would reduce the risk of a variety of health effects associated
with exposure to Pb, including effects indicated in the epidemiological
studies at lower blood Pb levels, particularly including neurological
effects in children, and the potential for cardiovascular and renal
effects in adults (73 FR 67006, November 12, 2008). The Administrator
additionally considered higher and lower levels for the standard,
concluding that a level of 0.15 [micro]g/m\3\ provided for a standard
that was neither more or less stringent than necessary for this
purpose, recognizing that the Act does not require that primary
standards be set at a zero-risk level, but rather at a level that
reduces risk sufficiently so as to protect public health with an
adequate margin of safety (73 FR 67007, November 12, 2008). For
example, the Administrator additionally considered potential public
health protection provided by standard levels above 0.15 [micro]g/m\3\,
which he concluded were insufficient to protect public health with an
adequate margin of safety. The Administrator also noted that in light
of all of the evidence, including the evidence-based framework, the
degree of public health protection likely afforded by standard levels
below 0.15 [micro]g/m\3\ would be greater than what is necessary to
protect public safety with an adequate margin of safety.
    The Administrator concluded, based on review of all of the evidence
(including the evidence-based framework), that when taken as a whole
the selected standard, including the indicator, averaging time, form,
and level, would be ``sufficient but not more than necessary to protect
public health, including the health of sensitive subpopulations, with
an adequate margin of safety'' (73 FR 67007, November 12, 2008).
2. 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).\24\ Consistent with those conclusions, in the context of
pollutant exposures considered relevant to the Pb NAAQS review,\25\ the
ISA determines that causal relationships \26\ 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,\27\ as likely to be causal \28\ (ISA, Table 1-2, sections
1.6.4 and 1.6.7).
---------------------------------------------------------------------------

    \24\ 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).
    \25\ 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).
    \26\ 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).
    \27\ 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).
    \28\ 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).
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    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 <IP_ADDRESS> and
4.4.7).\29\ 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).

    \29\ Studies from the late 1960s and 1970s suggest that adult
blood Pb levels during that period ranged from roughly 13 to 16
[mu]g/dL and from 15 to 30 [micro]g/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).\30\ 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).\31\ 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).
---------------------------------------------------------------------------

    \30\ 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).
    \31\ 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).\32\ 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.
---------------------------------------------------------------------------

    \32\ 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 <IP_ADDRESS>; 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 <IP_ADDRESS>.).
---------------------------------------------------------------------------

    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 [micro]g/dL (e.g., ISA, p.
lxxxvii and section 4.3.2).\33\
---------------------------------------------------------------------------

    \33\ The value of 2 [mu]g/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
[mu]g/dL to 9 and >10 [mu]g/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
[mu]g/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 [mu]g/dL in children aged 24
months or ranging from 5 to 7 years (73 FR 66978-66979, November 12,
2008; ISA, sections <IP_ADDRESS> and <IP_ADDRESS>; 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).\34\ 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 [mu]g/dL (ISA, section
<IP_ADDRESS>; 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 [mu]g/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).
---------------------------------------------------------------------------

    \34\ 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,\35\ 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.\36\ 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 <IP_ADDRESS>; 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.
---------------------------------------------------------------------------

    \35\ 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.
    \36\ 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 \37\) for young child population subgroups (age 5
years or younger) with individual blood Pb measurements as low as
approximately 1 [mu]g/dL and mean concentrations as low as 2.9 to 3.8
[mu]g/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).
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    \37\ 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 <IP_ADDRESS>).
---------------------------------------------------------------------------

    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