[Federal Register Volume 80, Number 2 (Monday, January 5, 2015)]
[Proposed Rules]
[Pages 277-324]
[FR Doc No: 2014-30681]

Vol. 80

Monday,

No. 2

January 5, 2015

Part II

Environmental Protection Agency

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40 CFR Part 50

 National Ambient Air Quality Standards for Lead; Proposed Rule

Federal Register / Vol. 80 , No. 2 / Monday, January 5, 2015 /
Proposed Rules

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 50

[EPA-HQ-OAR-2010-0108; FRL-9915-57-OAR]
RIN 2060-AQ44

National Ambient Air Quality Standards for Lead

AGENCY: Environmental Protection Agency.

ACTION: Proposed rule.

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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 proposing to retain the
current standards, without revision.

DATES: Comments must be received on or before April 6, 2015.
    Public Hearings: If, by January 26, 2015, the EPA receives a
request from a member of the public to speak at a public hearing
concerning the proposed decision, we will hold a public hearing, with
information about the hearing provided in a subsequent notice in the
Federal Register.

ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-
OAR-2010-0108 by one of the following methods:
     Federal eRulemaking Portal: http://www.regulations.gov:
Follow the on-line instructions for submitting comments.
     Email<EMAIL_ADDRESS>Include docket ID No. EPA-
HQ-OAR-2010-0108 in the subject line of the message.
     Fax:<PHONE_NUMBER>.
     Mail: Docket No. EPA-HQ-OAR-2010-0108, Environmental
Protection Agency, Mail Code 28221T, 1200 Pennsylvania Ave. NW.,
Washington, DC 20460.
     Hand Delivery: Docket No. EPA-HQ-OAR-2010-0108,
Environmental Protection Agency, EPA WJC West Building, Room 3334, 1301
Constitution Ave. NW., Washington, DC. Such deliveries are only
accepted during the Docket's normal hours of operation, and special
arrangements should be made for deliveries of boxed information.
    Instructions: Direct your comments to Docket ID No. EPA-HQ-OAR-
2010-0108. The EPA's policy is that all comments received will be
included in the public docket without change and may be made available
online at www.regulations.gov, including any personal information
provided, unless the comment includes information claimed to be
Confidential Business Information (CBI) or other information whose
disclosure is restricted by statute. Do not submit information that you
consider to be CBI or otherwise protected through www.regulations.gov
or email. The www.regulations.gov Web site is an ``anonymous access''
system, which means the EPA will not know your identity or contact
information unless you provide it in the body of your comment. If you
send an email comment directly to the EPA without going through
www.regulations.gov, your email address will be automatically captured
and included as part of the comment that is placed in the public docket
and made available on the Internet. If you submit an electronic
comment, the EPA recommends that you include your name and other
contact information in the body of your comment and with any disk or
CD-ROM you submit. If the EPA cannot read your comment due to technical
difficulties and cannot contact you for clarification, the EPA may not
be able to consider your comment. Electronic files should avoid the use
of special characters, any form of encryption, and be free of any
defects or viruses. For additional information about the EPA's public
docket, visit the EPA Docket Center homepage at http://www.epa.gov/epahome/dockets.htm.
    Public Hearing: To request a public hearing or information
pertaining to a public hearing on this document, contact Ms. Eloise
Shepherd, Health and Environmental Impacts Division, Office of Air
Quality Planning and Standards (C504-02), U.S. Environmental Protection
Agency, Research Triangle Park, NC 27711; telephone number (919) 541-
5507; fax number<PHONE_NUMBER>; email address:
<EMAIL_ADDRESS>See the SUPPLEMENTARY INFORMATION for further
information about a possible public hearing.
    Docket: All documents in the docket are listed on the
www.regulations.gov Web site. This includes documents in the rulemaking
docket (Docket ID No. EPA-HQ-OAR-2010-0108) and a separate docket,
established for the Integrated Science Assessment for this review
(Docket ID No. EPA-HQ-ORD-2011-0051) that has been incorporated by
reference into the rulemaking docket. All documents in these dockets
are listed on the www.regulations.gov Web site. Although listed in the
index, some information is not publicly available, e.g., CBI or other
information whose disclosure is restricted by statute. Certain other
material, such as copyrighted material, is not placed on the Internet
and may be viewed, with prior arrangement, at the EPA Docket Center.
Publicly available docket materials are available either electronically
in www.regulations.gov or in hard copy at the Air and Radiation Docket
Information Center, EPA/DC, WJC West Building, Room 3334, 1301
Constitution Ave. NW., Washington, DC. The Public Reading Room is open
from 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding legal
holidays. The telephone number for the Public Reading Room is (202)
566-1744 and the telephone number for the Air and Radiation Docket
Information Center is<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>To request a public hearing or
information pertaining to a public hearing on this document, contact
Ms. Eloise Shepherd, Health and Environmental Impacts Division, Office
of Air Quality Planning and Standards (C504-02), U.S. Environmental
Protection Agency, Research Triangle Park, NC 27711; telephone number
(919) 541-5507; fax number<PHONE_NUMBER>; email address:
<EMAIL_ADDRESS>
SUPPLEMENTARY INFORMATION:

General Information

Preparing Comments for the EPA

    1. Submitting CBI. Do not submit this information to the EPA
through www.regulations.gov or email. Clearly mark the part or all of
the information that you claim to be CBI. For CBI information in a disk
or CD-ROM that you mail to the EPA, mark the outside of the disk or CD-
ROM as CBI and then identify electronically within the disk or CD-ROM
the specific information that is claimed as CBI. In addition to one
complete version of the comment that includes information claimed as
CBI, a copy of the comment that does not contain the information
claimed as CBI must be submitted for inclusion in the public docket.
Information so marked will not be disclosed except in accordance with
procedures set forth in 40 CFR part 2.
    2. Tips for Preparing Your Comments. When submitting comments,
remember to:
     Identify the rulemaking by docket number and other
identifying information (subject heading, Federal Register date and
page number).
     Follow directions--the agency may ask you to respond to
specific questions or organize comments by referencing a

Code of Federal Regulations (CFR) part or section number.
     Explain why you agree or disagree, suggest alternatives,
and substitute language for your requested changes.
     Describe any assumptions and provide any technical
information and/or data that you used.
     Provide specific examples to illustrate your concerns, and
suggest alternatives.
     Explain your views as clearly as possible, avoiding the
use of profanity or personal threats.
     Make sure to submit your comments by the comment period
deadline identified.

Availability of Information Related to This Action

    A number of the documents that are relevant to this action are
available through the EPA's Office of Air Quality Planning and
Standards (OAQPS) Technology Transfer Network (TTN) Web site at http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html. These documents
include the Plan for Review of the National Ambient Air Quality
Standards for Lead (USEPA, 2011a), available at http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_pd.html, the Integrated Science Assessment
for Lead (USEPA, 2013a), available at http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_isa.html, the Review of the National Ambient Air
Quality Standards for Lead: Risk and Exposure Assessment Planning
Document (USEPA, 2011b), available at http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_pd.html, and the Policy Assessment for the
Review of the Lead National Ambient Air Quality Standards (USEPA,
2014), available at http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_pa.html. These and other related documents are also available
for inspection and copying in the EPA docket identified above.

Information About a Possible Public Hearing

    To request a public hearing or information pertaining to a public
hearing on this document, contact Ms. Eloise Shepherd, Health and
Environmental Impacts Division, Office of Air Quality Planning and
Standards (C504-02), U.S. Environmental Protection Agency, Research
Triangle Park, NC 27711; telephone number<PHONE_NUMBER>; fax number
(919) 541-0804; email address<EMAIL_ADDRESS>
Table of Contents

    The following topics are discussed in this preamble:

I. Background
    A. Legislative Requirements
    B. Related Lead Control Programs
    C. Review of the Air Quality Criteria and Standards for Lead
    D. Multimedia, Multipathway Aspects of Lead
    E. Air Quality Monitoring
II. Rationale for Proposed Decision on the Primary Standard
    A. General Approach
    1. Approach in the Last Review
    2. Approach for the Current Review
    B. Health Effects Information
    1. Array of Effects
    2. Critical Periods of Exposure
    3. Nervous System Effects in Children
    4. At-Risk Populations
    5. Potential Impacts on Public Health
    C. Blood Lead as a Biomarker of Exposure and Relationships With
Air Lead
    D. Summary of Risk and Exposure Assessment Information
    1. Overview
    2. Summary of Design Aspects
    3. Key Limitations and Uncertainties
    4. Summary of Risk Estimates and Key Observations
    E. Conclusions on Adequacy of the Current Primary Standard
    1. Evidence-Based Considerations in the Policy Assessment
    2. Exposure/Risk-Based Considerations in the Policy Assessment
    3. CASAC Advice
    4. Administrator's Proposed Conclusions on the Adequacy of the
Current Primary Standard
III. Rationale for Proposed Decision on the Secondary Standard
    A. General Approach
    1. Approach in the Last Review
    2. Approach for the Current Review
    B. Welfare Effects Information
    C. Summary of Risk Assessment Information
    D. Conclusions on Adequacy of the Current Secondary Standard
    1. Evidence- and Risk-Based Considerations in the Policy
Assessment
    2. CASAC Advice
    3. Administrator's Proposed Conclusions on the Adequacy of the
Current Standard
IV. Statutory and Executive Order Reviews
    A. Executive Order 12866: Regulatory Planning and Review and
Executive Order 13563: Improving Regulation and Regulatory Review
    B. Paperwork Reduction Act
    C. Regulatory Flexibility Act
    D. Unfunded Mandates Reform Act
    E. Executive Order 13132: Federalism
    F. Executive Order 13175: Consultation and Coordination With
Indian Tribal Governments
    G. Executive Order 13045: Protection of Children From
Environmental Health and Safety Risks
    H. Executive Order 13211: Actions That Significantly Affect
Energy Supply, Distribution, or Use
    I. National Technology Transfer and Advancement Act
    J. Executive Order 12898: Federal Actions To Address
Environmental Justice in Minority Populations and Low-Income
Populations
    K. Determination Under Section 307(d)
References

I. Background

A. Legislative Requirements

    Two sections of the Clean Air Act (CAA or the Act) govern the
establishment and revision of the NAAQS. Section 108 (42 U.S.C. 7408)
directs the Administrator to identify and list certain air pollutants
and then to issue air quality criteria for those pollutants. The
Administrator is to list those air pollutants that in her ``judgment,
cause or contribute to air pollution which may reasonably be
anticipated to endanger public health or welfare;'' ``the presence of
which in the ambient air results from numerous or diverse mobile or
stationary sources;'' and ``for which . . . [the Administrator] plans
to issue air quality criteria . . .'' Air quality criteria are intended
to ``accurately reflect the latest scientific knowledge useful in
indicating the kind and extent of all identifiable effects on public
health or welfare which may be expected from the presence of [a]
pollutant in the ambient air . . .'' 42 U.S.C. 7408(b). Section 109 (42
U.S.C. 7409) directs the Administrator to propose and promulgate
``primary'' and ``secondary'' NAAQS for pollutants for which air
quality criteria are issued. Section 109(b)(1) defines a primary
standard as one ``the attainment and maintenance of which in the
judgment of the Administrator, based on such criteria and allowing an
adequate margin of safety, are requisite to protect the public
health.'' \1\ A secondary standard, as defined in section 109(b)(2),
must ``specify a level of air quality the attainment and maintenance of
which, in the judgment of the Administrator, based on such criteria, is
requisite to protect the public welfare from any known or anticipated
adverse effects associated with the presence of [the] pollutant in the
ambient air.'' \2\
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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).
    \2\ Welfare effects as defined in section 302(h) (42 U.S.C.
7602(h)) include, but are not limited to, ``effects on soils, water,
crops, vegetation, man-made materials, animals, wildlife, weather,
visibility and climate, damage to and deterioration of property, and
hazards to transportation, as well as effects on economic values and
on personal comfort and well-being.''
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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,\3\ and
the kind and degree of the uncertainties that must be addressed. The
selection of any particular approach to providing an adequate margin of
safety is a policy choice left specifically to the Administrator's
judgment. See Lead Industries Association v. EPA, 647 F.2d at 1161-62.
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    \3\ As used here and similarly throughout this notice, the term
population (or group) refers to persons having a quality or
characteristic in common, such as a specific pre-existing illness or
a specific age or life stage. As discussed more fully in section
II.B.4 below, the identification of sensitive groups (called at-risk
groups or at-risk populations) involves consideration of
susceptibility and vulnerability.
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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).\4\
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    \4\ Lists of CASAC members and of members of the CASAC Lead
Review Panel are available at: http://yosemite.epa.gov/sab/sabproduct.nsf/WebCASAC/CommitteesandMembership?OpenDocument.
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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 (SIPs) that provide for the attainment and
maintenance of such standards through control programs directed to
sources of the pollutants involved. The states, in conjunction with the
EPA, also administer the Prevention of Significant Deterioration
program (42 U.S.C. 7470-7479) for these pollutants.
    The NAAQS is only one component of the EPA's programs to address Pb
in the environment. Federal programs additionally provide for
nationwide reductions in air emissions of these and other air
pollutants through the Federal Motor Vehicle Control program under
Title II of the Act (42 U.S.C. 7521-7574), which involves controls for
automobile, truck, bus, motorcycle, nonroad engine, and aircraft
emissions; the new source performance standards under section 111 of
the Act (42 U.S.C. 7411); emissions standards for solid waste
incineration units and the national emission standards for hazardous
air pollutants (NESHAP) under sections 129 (42 U.S.C. 7429) and 112 (42
U.S.C. 7412) of the Act, respectively.
    The EPA has taken a number of actions associated with these air
pollution control programs since the last review of the Pb NAAQS,
including completion of several regulations which will result in
reduced Pb emissions from stationary sources regulated under the CAA
sections 112 and 129. For example, in January 2012, the EPA updated the
NESHAP for the secondary lead smelting source category (77 FR 555,
January 5, 2012). These amendments to the original maximum achievable
control technology standards apply to facilities nationwide that use
furnaces to recover Pb from Pb-bearing scrap, mainly from automobile
batteries (15 existing facilities, one under construction). By the
effective date in 2014, this action is estimated to result in a Pb
emissions reduction of 13.6 tons per year (tpy) across the category (a
68% reduction). Somewhat lesser Pb emissions reductions are also
expected from regulations completed in 2013 for commercial and
industrial solid waste incineration units (78 FR 9112, February 7,
2013), as well as several other regulations since 2007 (72 FR 73179,
December 26, 2007; 72 FR 74088, December 28, 2007; 73 FR 225, November
20, 2008; 78 FR 10006, February 12, 2013; 76 FR 15372, March 21, 2011;
78 FR 7138, January 31, 2013; 74 FR 51368, October 6, 2009; Policy
Assessment, Appendix 2A).
    The presentation below briefly summarizes additional ongoing
activities that, although not directly pertinent to the review of the
NAAQS, are associated with controlling environmental Pb levels and
human Pb exposures more broadly. Among those identified are the EPA
programs intended to encourage exposure reduction programs in other
countries.
    Reducing Pb exposures has long been recognized as a federal
priority as environmental and public health agencies continue to
grapple with soil and dust Pb levels from the historical use of Pb in
paint and gasoline and from other sources (Alliance to End Childhood
Lead Poisoning, 1991; 62 FR 19885, April 23, 1997; 66 FR 52013, October
11, 2001; 68 FR 19931, April 23, 2003). A broad range of federal
programs beyond those that focus on air pollution control provide for
nationwide reductions in environmental releases and human exposures.
For example, pursuant to section 1412 of the Safe Drinking Water Act
(SDWA), the EPA regulates Pb in public drinking water systems through
corrosion control

and other utility actions which work together to minimize Pb levels at
the tap (40 CFR 141.80-141.91). Under section 1417 of the SDWA, pipes,
fittings and fixtures for potable water applications may not be used or
introduced into commerce unless they are considered ``lead free'' as
defined by that Act (40 CFR 141.43).\5\ Additionally, federal Pb
abatement programs provide for the reduction in human exposures and
environmental releases from in-place materials containing Pb (e.g., Pb-
based paint, urban soil and dust, and contaminated waste sites).
Federal regulations on disposal of Pb-based paint waste help facilitate
the removal of Pb-based paint from residences (68 FR 36487, June 18,
2003).
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    \5\ Effective in January 2014, the amount of Pb permitted in
pipes, fittings, and fixtures was lowered (see ``Summary of the
Reduction of Lead in Drinking Water Act and Frequently Asked
Questions'' at http://water.epa.gov/drink/info/lead/index.cfm).
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    Federal programs to reduce exposure to Pb in paint, dust, and soil
are specified under the comprehensive federal regulatory framework
developed under the Residential Lead-Based Paint Hazard Reduction Act
(Title X). Under Title X (codified as Title IV of the Toxic Substances
Control Act [TSCA]), the EPA has established regulations and associated
programs in six categories: (1) Training, certification and work
practice requirements for persons engaged in Pb-based paint activities
(abatement, inspection and risk assessment); accreditation of training
providers; and authorization of state and tribal Pb-based paint
programs; (2) training, certification, and work practice requirements
for persons engaged in home renovation, repair and painting (RRP)
activities; accreditation of RRP training providers; and authorization
of state and tribal RRP programs; (3) ensuring that, for most housing
constructed before 1978, information about Pb-based paint and Pb-based
paint hazards flows from sellers to purchasers, from landlords to
tenants, and from renovators to owners and occupants; (4) establishing
standards for identifying dangerous levels of Pb in paint, dust and
soil; (5) providing grant funding to establish and maintain state and
tribal Pb-based paint programs; and (6) providing information on Pb
hazards to the public, including steps that people can take to protect
themselves and their families from Pb-based paint hazards. The most
recent rule issued under Title IV of TSCA is for the Lead Renovation,
Repair and Painting Program (73 FR 21692, April 22, 2008), which became
fully effective in April 2010 and which applies to compensated
renovators and maintenance professionals who perform RRP activities in
housing and child-care facilities built prior to 1978. To foster
adoption of the rule's measures, the EPA has been conducting an
extensive education and outreach campaign to promote awareness of these
new requirements among both the regulated entities and the consumers
who hire them (http://www2.epa.gov/lead/renovation-repair-and-painting-program). In addition, the EPA is investigating whether Pb hazards are
also created by RRP activities in public and commercial buildings, in
which case the EPA plans to issue RRP requirements, where appropriate,
for this class of buildings (79 FR 31072, May 30, 2014).
    Programs associated with the Comprehensive Environmental Response,
Compensation, and Liability Act (CERCLA or Superfund) and Resource
Conservation Recovery Act (RCRA) also implement abatement programs,
reducing exposures to Pb and other pollutants. For example, the EPA
determines and implements protective levels for Pb in soil at Superfund
sites and RCRA corrective action facilities. Federal programs,
including those implementing RCRA, provide for management of hazardous
substances in hazardous and municipal solid waste (e.g., 66 FR 58258,
November 20, 2001). Federal regulations concerning batteries in
municipal solid waste facilitate the collection and recycling or proper
disposal of batteries containing Pb.\6\ Similarly, federal programs
provide for the reduction in environmental releases of hazardous
substances such as Pb in the management of wastewater (http://www.epa.gov/owm/).
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    \6\ See, e.g., ``Implementation of the Mercury-Containing and
Rechargeable Battery Management Act'' at http://www.epa.gov/epawaste/hazard/recycling/battery.pdf and ``Municipal Solid Waste
Generation, Recycling, and Disposal in the United States: Facts and
Figures for 2005 http://www.epa.gov/epawaste/nonhaz/municipal/pubs/msw-2005.pdf.
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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 ``Resource Conservation
Challenge'' (http://www.epa.gov/epaoswer/osw/conserve/index.htm), the
``National Waste Minimization Program'' (http://www.epa.gov/epaoswer/hazwaste/minimize/leadtire.htm), ``Plug in to eCycling'' (a partnership
between the EPA and consumer electronics manufacturers and retailers;
http://www.epa.gov/epaoswer/hazwaste/recycle/electron/crt.htm#crts),
and activities to reduce the practice of backyard trash burning (http://www.epa.gov/msw/backyard/pubs.htm).
    The EPA's research program identifies, encourages and conducts
research needed to locate and assess serious risks and to develop
methods and tools to characterize and help reduce risks related to Pb
exposure. For example, the EPA's Integrated Exposure Uptake Biokinetic
Model for Lead in Children (IEUBK model) is widely used and accepted as
a tool that informs the evaluation of site-specific data. More
recently, in recognition of the need for a single model that predicts
Pb concentrations in tissues for children and adults, the EPA has been
developing the All Ages Lead Model (AALM) to provide researchers and
risk assessors with a pharmacokinetic model capable of estimating
blood, tissue, and bone concentrations of Pb based on estimates of
exposure over the lifetime of the individual (USEPA, 2006a, sections
4.4.5 and 4.4.8; USEPA, 2013a, section 3.6). The EPA's research
activities on substances including Pb, such as those identified here,
focus on improving our characterization of health and environmental
effects, exposure, and control or management of environmental releases
(see http://www.epa.gov/research/).
    Other federal agencies also participate in programs intended to
reduce Pb exposures. For example, programs of the Centers for Disease
Control and Prevention (CDC) provide for the tracking of children's
blood Pb levels in the U.S. and provide guidance on levels at which
medical and environmental case management activities should be
implemented (CDC, 2012; ACCLPP, 2012). As a result of coordinated,
intensive efforts at the national, state and local levels, including
those programs described above, blood Pb levels in all segments of the
population have continued to decline from levels observed in the past.
For example, blood Pb levels for the general population of children 1
to 5 years of age have dropped to a geometric mean level of 1.17 [mu]g/
dL in the 2009-2010 National Health and Nutrition Examination Survey
(NHANES) 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, blood Pb levels in non-Hispanic
black, Mexican American and lower socioeconomic groups, which are
generally higher than those for the general population, have

also declined (USEPA, 2013a, sections 3.4.1, 5.2.3 and 5.2.4; Jones et
al., 2009).
    The EPA also participates in a broad range of international
programs focused on reducing environmental releases and human exposures
in other countries. For example, the Partnership for Clean Fuels and
Vehicles program engages governments and stakeholders in developing
countries to eliminate Pb in gasoline globally.\7\ From 2007 to 2011,
the number of countries known to still be using leaded gasoline was
reduced from just over 20 to six, with three of the six also offering
unleaded fuel. All six were expected to eliminate Pb from fuel in the
near future (USEPA, 2011c). The EPA is a contributor to the Global
Alliance to Eliminate Lead Paint, a cooperative initiative jointly led
by the World Health Organization and the United Nations Environment
Programme (UNEP) to focus and catalyze the efforts to achieve
international goals to prevent children's Pb exposure from paints
containing Pb and to minimize occupational exposures to Pb paint. This
alliance has the broad objective of promoting a phase-out of the
manufacture and sale of paints containing Pb and eventually to
eliminate the risks that such paints pose. The UNEP is also engaged on
the problem of managing wastes containing Pb, including Pb-containing
batteries. The Governing Council of the UNEP, of which the U.S. is a
member, has adopted decisions focused on promoting the environmentally
sound management of products, wastes and contaminated sites containing
Pb and reducing risks to human health and the environment from Pb and
cadmium throughout the life cycles of those substances (UNEP Governing
Council, 2011, 2013). The EPA is also engaged in the issue of
environmental impacts of spent Pb-acid batteries internationally
through the Commission for Environmental Cooperation (CEC), where the
EPA Administrator along with the cabinet-level or equivalent
representatives of Mexico and Canada comprise the CEC's senior
governing body (CEC Council).\8\
---------------------------------------------------------------------------

    \7\ International programs in which the U.S. participates,
including those identified here, are described at: http://epa.gov/international/air/pcfv.html, http://www.unep.org/transport/pcfv/,
http://www.unep.org/hazardoussubstances/Home/tabid/197/hazardoussubstances/LeadCadmium/PrioritiesforAction/GAELP/tabid/6176/Default.aspx.
    \8\ The CEC was established to support cooperation among the
North American Free Trade Agreement partners to address
environmental issues of continental concern, including the
environmental challenges and opportunities presented by continent-
wide free trade.
---------------------------------------------------------------------------

C. Review of the Air Quality Criteria and Standards for Lead

    Unlike pollutants such as particulate matter and carbon monoxide,
air quality criteria had not been issued for Pb as of the enactment of
the CAA of 1970, which first set forth the requirement to set NAAQS
based on air quality criteria. In the years just after enactment of the
CAA, the EPA did not list Pb under Section 108 of the Act, having
determined to control Pb air pollution through regulations to phase out
the use of Pb additives in gasoline (See 41 FR 14921, April 8, 1976).
However, the decision not to list Pb under Section 108 was challenged
by environmental and public health groups, and the U.S. District Court
for the Southern District of New York concluded that the EPA was
required to list Pb under Section 108. Natural Resources Defense
Council v. EPA, 411 F. Supp. 864 21 (S.D. N.Y. 1976), affirmed, 545
F.2d 320 (2d Cir. 1978). Accordingly, on April 8, 1976, the EPA
published a notice in the Federal Register that Pb had been listed
under Section 108 as a criteria pollutant (41 FR 14921, April 8, 1976)
and on October 5, 1978, the EPA promulgated primary and secondary NAAQS
for Pb under Section 109 of the Act (43 FR 46246, October 5, 1978).
Both primary and secondary standards were set at a level of 1.5
micrograms per cubic meter ([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 Pb air quality criteria and standards was
initiated in November 2004 (69 FR 64926, November 9, 2004); the
agency's plans for preparation of the Air Quality Criteria Document and
conduct of the NAAQS review were presented in documents completed in
2005 and early 2006 (USEPA, 2005a; USEPA 2006b).\9\ The schedule for
completion of the review was governed by a judicial order in Missouri
Coalition for the Environment v. EPA (No. 4:04CV00660 ERW, September
14, 2005; and amended on April 29, 2008 and July 1, 2008).
---------------------------------------------------------------------------

    \9\ In the current review, these two documents have been
combined in the Integrated Review Plan for the National Ambient Air
Quality Standards for Lead (USEPA, 2011a).
---------------------------------------------------------------------------

    The scientific assessment for the review is described in the 2006
Air Quality Criteria for Lead (USEPA, 2006a; henceforth referred to as
the 2006 CD), multiple drafts of which received review by CASAC and the
public. The EPA also conducted human exposure and health risk
assessments and a pilot ecological risk assessment for the review,
after consultation with CASAC and receiving public comment on a draft
analysis plan (USEPA, 2006c). Drafts of these quantitative assessments
were reviewed by CASAC and the public. The pilot ecological risk
assessment was released in December 2006 (ICF International, 2006), and
the final health risk assessment report was released in November 2007
(USEPA, 2007a). The policy assessment, based on both of these
assessments, air quality analyses and key evidence from the 2006 CD,
was presented in the Staff Paper (USEPA, 2007b), a draft of which also
received CASAC and public review. The final Staff Paper presented OAQPS
staff's evaluation of the public health and welfare policy implications
of the key studies and scientific information contained in the 2006 CD
and presented and interpreted results from the quantitative risk/
exposure analyses

conducted for this review. Based on this evaluation, the Staff Paper
presented OAQPS staff recommendations that the Administrator give
consideration to substantially revising the primary and secondary
standards to a range of levels at or below 0.2 [mu]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).\10\ CASAC provided advice and recommendations to the
Administrator with regard to the Pb NAAQS based on its review of the
ANPR and the previously released final Staff Paper and risk assessment
reports. In 2008, the proposed decision on revisions to the Pb NAAQS
was signed on May 1 and published in the Federal Register on May 20 (73
FR 29184, May 20, 2008). Members of the public provided comments and
the CASAC Pb Panel also provided advice and recommendations to the
Administrator based on its review of the proposal notice. The final
decision on revisions to the Pb NAAQS was signed on October 15, 2008,
and published in the Federal Register on November 12, 2008 (73 FR
66964, November 12, 2008).
---------------------------------------------------------------------------

    \10\ The ANPR, one of the features of the revised NAAQS review
process that EPA instituted in 2006, was replaced by reinstatement
of the Policy Assessment prepared by OAQPS staff (previously termed
the OAQPS Staff Paper) in 2009 (Jackson, 2009).
---------------------------------------------------------------------------

    The November 2008 notice described the EPA's decision to revise the
primary and secondary NAAQS for Pb, as discussed more fully in section
II.A.1 below. In consideration of the much-expanded health effects
evidence on neurocognitive effects of Pb in children, the EPA
substantially revised the primary standard from a level of 1.5 [mu]g/
m\3\ to a level of 0.15 [mu]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 Federal Register notices for
the proposed and final rules (73 FR 29184, May 20, 2008; 73 FR 66964,
November 12, 2008).
    On February 26, 2010, the EPA formally initiated its current review
of the air quality criteria and standards for Pb, requesting the
submission of recent scientific information on specified topics (75 FR
8934, February 26, 2010). Soon after this, the EPA held a workshop to
discuss the policy-relevant science, which informed identification of
key policy issues and questions to frame the review of the Pb NAAQS (75
FR 20843, April 21, 2010). Drawing from the workshop discussions, the
EPA developed the draft Integrated Review Plan (draft IRP, USEPA,
2011d). The draft IRP was made available in late March 2011 for
consultation with the CASAC Pb Review Panel and for public comment (76
FR 20347, April 12, 2011). This document was discussed by the Panel via
a publicly accessible teleconference consultation on May 5, 2011 (76 FR
21346, April 15, 2011; Frey, 2011a). The final Integrated Review Plan
for the National Ambient Air Quality Standards for Lead (IRP),
developed in consideration of the CASAC consultation and public
comment, was released in November 2011 (USEPA, 2011a; 76 FR 76972,
December 9, 2011).
    In developing the Integrated Science Assessment (ISA) for this
review, the EPA held a workshop in December 2010 to discuss with
invited scientific experts preliminary draft materials and released the
first external review draft of the document for CASAC review and public
comment in May 2011 (USEPA, 2011e; 76 FR 26284, May 6, 2011; 76 FR
36120, June 21, 2011). The CASAC Pb Review Panel met at a public
meeting on July 20, 2011, to review the draft ISA (76 FR 36120, June
21, 2011). The CASAC provided comments in a December 9, 2011, letter to
the EPA Administrator (Frey and Samet, 2011). The second external
review draft ISA was released for CASAC review and public comment in
February 2012 (USEPA, 2012a; 77 FR 5247, February 2, 2012) and was the
subject of a public meeting on April 10-11, 2012 (77 FR 14783, March
13, 2012). The CASAC provided comments in a July 20, 2012, letter
(Samet and Frey, 2012). The third external review draft was released
for CASAC review and public comment in November 2012 (USEPA, 2012b; 77
FR 70776, November 27, 2012) and was the subject of a public meeting on
February 5-6, 2013 (78 FR 938, January 7, 2013). The CASAC provided
comments in a June 4, 2013, letter (Frey, 2013a). The final ISA was
released in late June 2013 (USEPA, 2013a, henceforth referred to as the
ISA; 78 FR 38318, June 26, 2013).
    In June 2011, the EPA developed and released the Risk and Exposure
Assessment Planning Document (REA Planning Document) for consultation
with CASAC and public comment (USEPA, 2011b; 76 FR 58509). This
document presented a critical evaluation of the information related to
Pb human and ecological exposure and risk (e.g., data, modeling
approaches) newly available in this review, with a focus on
consideration of the extent to which new or substantially revised REAs
for health and ecological risk might be warranted by the newly
available evidence. Evaluation of the newly available information with
regard to designing and implementing health and ecological REAs for
this review led us to conclude that the currently available information
did not provide a basis for developing new quantitative risk and
exposure assessments that would have substantially improved utility for
informing the agency's consideration of health and welfare effects and
evaluation of the adequacy of the current primary and secondary
standards, respectively (REA Planning Document, sections 2.3 and 3.3,
respectively). The CASAC Pb Review Panel provided consultative advice
on that document and its conclusions at a public meeting on July 21,
2011 (76 FR 36120, June 21, 2011; Frey, 2011b). Based on their
consideration of the REA Planning Document analysis, the CASAC Pb
Review Panel generally concurred with the conclusion that a new REA was
not warranted in this review (Frey, 2011b; Frey, 2013b). In
consideration of the conclusions reached in the REA Planning Document
and CASAC's consultative advice, the EPA has not developed REAs for
health and ecological risk for this review. Accordingly, we consider
the risk assessment findings from the last review for human exposure
and health risk (USEPA, 2007a, henceforth referred to as the 2007 REA)
and ecological risk (ICF International, 2006; henceforth referred to as
the 2006 REA) with regard to any appropriate further interpretation in
light of the evidence newly available in this review.
    A draft of the Policy Assessment (PA) was released for public
comment and review by CASAC in January 2013 (USEPA, 2013b; 77 FR 70776,
November

27, 2012) and was the subject of a public meeting on February 5-6, 2013
(78 FR 938, January 7, 2013). Comments provided by the CASAC in a June
4, 2013 letter (Frey, 2013b), as well as public comments received on
the draft PA were considered in preparing the final PA, which was
released in May 2014 (USEPA, 2014; 79 FR 26751, May 9, 2014).

D. Multimedia, Multipathway Aspects of Lead

    Since Pb distributes from air to other media and is persistent, our
review of the NAAQS for Pb considers the protection provided against
such effects associated both with exposures to Pb in ambient air and
with exposures to Pb that makes its way into other media from ambient
air. Additionally, in assessing the adequacy of protection afforded by
the current NAAQS, we are mindful of the long history of greater and
more widespread atmospheric emissions that occurred in previous years
(both before and after establishment of the 1978 NAAQS) and that
contributed to the Pb that exists in human populations and ecosystems
today. Likewise, we also recognize the role of other, nonair sources of
Pb now and in the past that also contribute to the Pb that exists in
human populations and ecosystems today.
    Lead emitted to ambient air is transported through the air and is
also distributed from air to other media. This multimedia distribution
of Pb emitted into ambient air (air-related Pb) contributes to multiple
air-related pathways of human and ecosystem exposure (ISA, sections
3.1.1 and 3.7.1). Air-related pathways may also involve media other
than air, including indoor and outdoor dust, soil, surface water and
sediments, vegetation and biota. Air-related Pb exposure pathways for
humans include inhalation of ambient air or ingestion of food, water or
other materials, including dust and soil, that have been contaminated
through a pathway involving Pb deposition from ambient air (ISA,
section <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 exposures via the various inhalation and ingestion air-related
pathways may vary with regard to the time in which they respond to
changes in air Pb concentrations. For example, exposures resulting from
human exposure pathways most directly involving Pb in ambient air and
exchanges of ambient air with indoor air (e.g., inhalation) can respond
most quickly, while those for pathways involving exposure to Pb
deposited from ambient air into the environment (e.g., diet) may be
expected to respond more slowly. The extent of this will be influenced
by the magnitude of change, as well as--for deposition-related
pathways--the extent of prior deposition and environment
characteristics influencing availability of prior deposited Pb.
    Lead currently occurring in nonair media may also derive from
sources other than ambient air (nonair Pb sources) (ISA, sections 2.3
and 3.7.1). For example, Pb in dust inside some houses or outdoors in
some urban areas may derive from the common past usage of leaded paint,
while Pb in drinking water may derive from the use of leaded pipe or
solder in drinking water distribution systems (ISA, section <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 is situation specific
(ISA, p. 1-11), although a predominant Pb exposure pathway for very
young children is the incidental ingestion of indoor dust by hand-to-
mouth activity (ISA, section <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. An additional influence on the
response time for nonair media is the environmental presence of Pb
associated with past, generally higher, air concentrations. For
example, after a reduction in air Pb concentrations, the time needed
for sediment or surface soil concentrations to indicate a response to
reduced air Pb concentrations might be expected to be longer in areas
of more substantial past contamination than in areas with lesser past
contamination. Thus, considering the Pb concentrations occurring in
nonair environmental media as a result of air quality conditions that
meet the current NAAQS is a complexity of this review, as it also was,
although to a lesser degree, with regard to the prior standard in the
last review.

E. Air Quality Monitoring

    Lead emitted to the air is predominantly in particulate form. Once
emitted, particle-bound Pb can be transported long or short distances
depending on particle size, which influences the amount of time spent
in the aerosol phase. In general, larger particles tend to deposit more
quickly, within shorter distances from emissions points, while smaller
particles remain in aerosol phase and travel longer

distances before depositing (ISA, section 1.2.1). Accordingly, airborne
concentrations of Pb near sources are much higher (and the
representation of larger particles generally greater) than at sites not
directly influenced by sources (PA, Figure 2-11; ISA sections 2.3.1 and
2.5.3).
    Ambient air monitoring data for Pb, in terms of Pb-TSP, Pb-
PM10 or Pb in particulate matter with mean diameter smaller
than 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 CASAC's
Ambient Air Monitoring and Methods Subcommittee, the EPA adopted a new
FRM for Pb-TSP, based on inductively coupled plasma-mass spectrometry
(78 FR 40000, July 3, 2013). The previous FRM was retained as an FEM,
and existing FEMs were retained as well.
    The Pb monitoring network design requirements (40 CFR part 58,
Appendix D, paragraph 4.5) include two types of monitoring sites--
source-oriented monitoring sites and non-source-oriented monitoring
sites--as well as the collection of a year of Pb-TSP measurements at 15
specific airports. The indicator for the current Pb NAAQS is Pb-TSP,
although in some situations,\11\ ambient Pb-PM10
concentrations may be used in judging nonattainment. Currently,
approximately 260 Pb-TSP monitors are in operation; these are a mixture
of source- and non-source-oriented monitors.
---------------------------------------------------------------------------

    \11\ The Pb-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.
---------------------------------------------------------------------------

    Since the phase-out of Pb in on-road gasoline, Pb is widely
recognized as a source-oriented air pollutant. Variability in air Pb
concentrations is highest in areas including a Pb source, ``with high
concentrations downwind of the sources and low concentration at areas
far from sources'' (ISA, p. 2-92). The current requirements for source-
oriented monitoring include placement of monitor sites near sources of
air Pb emissions which are expected to or have been shown to contribute
to ambient air Pb concentrations in excess of the NAAQS. At a minimum,
there must be one source-oriented site located to measure the maximum
Pb concentration in ambient air resulting from each non-airport Pb
source which emits 0.50 or more tons of Pb per year and from each
airport which emits 1.0 or more tons of Pb per year.\12\ The EPA
Regional Administrators may require additional monitoring beyond the
minimum requirements where the likelihood of Pb air quality violations
is significant. Such locations may include those near additional
industrial Pb sources, recently closed industrial sources and other
sources of resuspended Pb dust, as well as airports where piston-engine
aircraft emit Pb associated with combustion of leaded aviation fuel (40
CFR part 58, Appendix D, section 4.5(c)). A single year of monitoring
was also required near 15 specific airports \13\ in order to gather
additional information on the likelihood of NAAQS exceedances due to
the combustion of leaded aviation gasoline (75 FR 81126, December 27,
2010; 40 CFR part 58, Appendix D, 4.5(a)(iii)). These airport
monitoring data along with other data gathering and analyses will
inform the EPA's ongoing investigation into the potential for Pb
emissions from piston-engine aircraft to cause or contribute to air
pollution that may reasonably be anticipated to endanger public health
or welfare. This investigation is occurring under section 231 of the
CAA, separate from the Pb NAAQS review. As a whole, the various data
gathering and analyses are expected to improve our understanding of Pb
concentrations in ambient air near airports and conditions influencing
these concentrations.
---------------------------------------------------------------------------

    \12\ The Regional Administrator may waive this requirement for
monitoring near Pb sources if the state or, where appropriate, local
agency can demonstrate the Pb source will not contribute to a
maximum 3-month average Pb concentration in ambient air in excess of
50 percent of the NAAQS level based on historical monitoring data,
modeling, or other means (40 CFR part 58, Appendix D, section
4.5(a)(ii)).
    \13\ These airports were selected based on three criteria:
annual Pb inventory between 0.5 ton/year and 1.0 ton/year, ambient
air within 150 meters of the location of maximum emissions (e.g.,
the end of the runway or run-up location), and airport configuration
and meteorological scenario that leads to a greater frequency of
operations from one runway. These criteria are expected,
collectively, to identify airports with the highest potential to
have ambient air Pb concentrations approaching or exceeding the Pb
NAAQS (75 FR 81126).
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    Monitoring agencies are also required, under 40 CFR part 58,
Appendix D, to conduct non-source-oriented Pb monitoring at the NCore
sites \14\ required in metropolitan areas with a population of 500,000
or more (as defined by the U.S. Census Bureau).\15\ Either Pb-TSP or
Pb-PM10 monitoring may be performed at these sites.
Currently, all 50 NCore Pb sites are operational and measuring Pb
concentrations, with 28 measuring Pb in TSP and 24 measuring Pb in
PM10 (2 sites are measuring both Pb in TSP and Pb in
PM10). In a separate action addressing a range of issues
related to monitoring requirements for criteria pollutants, the EPA is
proposing to remove the requirement for Pb monitoring at NCore sites
(79 FR 54395, September 11, 2014). This change is being proposed in
consideration of current information indicating concentrations at these
sites to be well below the Pb NAAQS and of the presence of other
monitoring networks that provide information on Pb concentrations in
urban areas not directly impacted by Pb sources. The data available for
these sites indicate maximum 3-month average concentrations (of Pb-
PM10 or Pb-TSP) well below the level of the Pb NAAQS, with
the vast majority of sites showing concentrations less than 0.01 [mu]g/
m\3\. Additionally, other monitoring networks provide data on Pb in
PM10 or PM2.5, at non-source-oriented urban, and
some rural, sites. These 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.
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    \14\ The NCore network, that formally began in January 2011, is
a subset of the state and local air monitoring stations network that
is intended to meet multiple monitoring objectives (e.g., long-term
trends analysis, model evaluation, health and ecosystem studies, as
well as NAAQS compliance). The complete NCore network consists of 63
urban and 15 rural stations, with each state containing at least one
NCore station; 46 of the states plus Washington, DC and Puerto Rico
have at least one urban station.
    \15\ http://www.census.gov/population/www/metroareas/metroarea.html.
---------------------------------------------------------------------------

    The long-term record of Pb monitoring data documents the dramatic
decline in atmospheric Pb concentrations that has occurred since the
1970s in response to reduced emissions (PA, Figures 2-1 and 2-7).
Currently, the highest concentrations occur near some metals industries
where some individual locations have concentrations that exceed the
NAAQS (PA, Figure 2-10). Concentrations at non-source-oriented
monitoring sites are much lower than those at source-oriented sites and
well below the standard (PA, Figure 2-11).

II. Rationale for Proposed Decision on the Primary Standard

    This section presents the rationale for the Administrator's
proposed decision to retain the existing Pb primary standard. As
discussed more fully below, this rationale is based on a thorough
review, in the ISA, of the latest scientific information, generally
published through September 2011,\16\ on human health effects
associated with Pb and pertaining to the presence of Pb in the ambient
air. This proposal also takes into account: (1) The PA's staff
assessments of the most policy-relevant information in the ISA and
staff analyses of air quality, human exposure and health risks, upon
which staff conclusions regarding appropriate considerations in this
review are based; (2) CASAC advice and recommendations, as reflected in
discussions of drafts of the ISA and PA at public meetings, in separate
written comments, and in CASAC's letters to the Administrator; and (3)
public comments received during the development of these documents,
either in connection with CASAC meetings or separately.
---------------------------------------------------------------------------

    \16\ In addition to the review's opening ``call for
information'' (75 FR 8934), ``literature searches were conducted
routinely to identify studies published since the last review,
focusing on studies published from 2006 (close of the previous
scientific assessment) through September 2011,'' and references
``that were considered for inclusion or actually cited in this ISA
can be found at http://hero.epa.gov/lead'' (ISA, p. 1-2).
---------------------------------------------------------------------------

    In presenting the rationale and its foundations, section II.A
provides background on the general approach for review of the primary
NAAQS for Pb, including a summary of the approach used in the last
review (section II.A.1) and the general approach for the current review
(section II.A.2). Sections II.B and II.C summarize the body of evidence
supporting this rationale, focusing on consideration of key policy-
relevant questions, and section II.D summarizes the exposure/risk
information for this review. Section II.E presents the Administrator's
proposed conclusions on adequacy of the current standard, drawing on
both evidence-based and exposure/risk-based considerations (sections
II.E.1 and II.E.2), and advice from CASAC (section II.E.3).

A. General Approach

    The past and current approaches described below are both based,
most fundamentally, on using the EPA's assessment of the current
scientific evidence and associated quantitative analyses to inform the
Administrator's judgment regarding a primary standard for Pb that
protects public health with an adequate margin of safety. We note that
in drawing conclusions with regard to the primary standard, the final
decision on the adequacy of the current standard is largely a public
health policy judgment to be made by the Administrator. The
Administrator's final decision must draw upon scientific information
and analyses about health effects, population exposure and risks, as
well as judgments about how to consider the range and magnitude of
uncertainties that are inherent in the scientific evidence and
analyses. Our approach to informing these judgments, discussed more
fully below, is based on the recognition that the available health
effects evidence generally reflects a continuum, consisting of levels
at which scientists generally agree that health effects are likely to
occur, through lower levels at which the likelihood and magnitude of
the response become increasingly uncertain. This approach is consistent
with the requirements of the NAAQS provisions of the Act and with how
the EPA and the courts have historically interpreted the Act. These
provisions require the Administrator to establish primary standards
that, in the judgment of the Administrator, are requisite to protect
public health with an adequate margin of safety. In so doing, the
Administrator seeks to establish standards that are neither more nor
less stringent than necessary for this purpose. The Act does not
require that primary standards be set at a zero-risk level, but rather
at a level that avoids unacceptable risks to public health including
the health of sensitive groups.\17\ The four basic elements of the
NAAQS (indicator, averaging time, level, and form) are considered
collectively in evaluating the health protection afforded by the
current standard.
---------------------------------------------------------------------------

    \17\ The at-risk population groups identified in a NAAQS review
may include low-income or minority groups. Where low-income/minority
groups are among the at-risk populations, the rulemaking decision
will be based on providing protection for these and other at-risk
populations and lifestages (e.g., children, older adults, persons
with pre-existing heart and lung disease). To the extent that low-
income/minority groups are not among the at-risk populations
identified in the ISA, a decision based on providing protection of
the at-risk lifestages and populations would be expected to provide
protection for the low-income/minority groups.
---------------------------------------------------------------------------

1. Approach in the Last Review
    The last review of the NAAQS for Pb was completed in 2008 (73 FR
66964, November 12, 2008). The 2008 decision to substantially revise
the primary standard was based on the extensive body of scientific
evidence published over almost three decades, from the time the
standard was originally set in 1978 through 2005-2006. In so doing, the
2008 decision considered the body of evidence as assessed in the 2006
CD (USEPA, 2006a), as well as the 2007 Staff Paper assessment of the
policy-relevant information contained in the CD and the quantitative
risk/exposure assessment (USEPA, 2007a, 2007b), the advice and
recommendations of CASAC (Henderson 2007a, 2007b, 2008a, 2008b), and
public comment. While recognizing that Pb has been demonstrated to
exert ``a broad array of deleterious effects on multiple organ
systems,'' the review focused on the effects most pertinent to ambient
air exposures, which given ambient air Pb reductions over the past 30
years, are those associated with relatively lower exposures and
associated blood Pb levels (73 FR 66975, November 12, 2008). In so
doing, the EPA recognized the general consensus that the developing
nervous system in children is among the most sensitive health endpoints
associated with Pb exposure, if not the most sensitive one. Thus,
primary attention was given to consideration of nervous system effects,
including neurocognitive and neurobehavioral effects, in children (73
FR 66976, November 12, 2008). The body of evidence included
associations of such effects in study populations of variously aged
children with mean blood Pb levels below 10 [micro]g/dL, extending from
8 down to 2 [micro]g/dL (73 FR 66976, November 12, 2008). The public
health implications of effects of air-related Pb on cognitive function
(e.g., IQ) in young children were given particular focus in the review.
    The conclusions reached by the Administrator in the last review
were based primarily on the scientific evidence, with the risk- and
exposure-based information providing support for various aspects of the
decision. In reaching his conclusion on the adequacy of the then-
current standard, which was set in 1978, the Administrator placed
primary consideration on the large body of scientific evidence
available in the review including significant new evidence concerning
effects at blood Pb concentrations substantially below those identified
when the standard was initially set (73 FR 66987, November 12, 2008; 43
FR 46246, October 5, 1978). Given particular attention was the robust
evidence of neurotoxic effects of Pb exposure in children, recognizing:
(1) That while blood Pb levels in U.S. children had decreased notably
since the late 1970s, newer epidemiological studies had investigated
and reported

associations of effects on the neurodevelopment of children with those
more recent lower blood Pb levels and (2) that the toxicological
evidence included extensive experimental laboratory animal evidence
substantiating well the plausibility of the epidemiological findings
observed in human children and expanding our understanding of likely
mechanisms underlying the neurotoxic effects (73 FR 66987, November 12,
2008). Additionally, within the range of blood Pb levels investigated
in the available evidence base, a threshold level for neurocognitive
effects was not identified (73 FR 66984, November 12, 2008; 2006 CD, p.
8-67). Further, the evidence indicated a steeper concentration-response
(C-R) relationship for effects on cognitive function at those lower
blood Pb levels than at higher blood Pb levels that were more common in
the past, ``indicating the potential for greater incremental impact
associated with exposure at these lower levels'' (73 FR 66987, November
12, 2008). As at the time when the standard was initially set in 1978,
the health effects evidence and exposure/risk assessment available in
the last review supported the conclusion that air-related Pb exposure
pathways contribute to blood Pb levels in young children by inhalation
and ingestion (73 FR 66987, November 12, 2008). The available
information in the last review also indicated, however, a likely
greater change in blood Pb per unit of air Pb than was estimated when
the standard was initially set (73 FR 66987, November 12, 2008).
    In the Administrator's decision on the adequacy of the 1978
standard, the Administrator considered the evidence using a very
specifically defined framework, referred to as an air-related IQ loss
evidence-based framework. This framework integrates evidence for the
relationship between Pb in air and Pb in young children's blood with
evidence for the relationship between Pb in young children's blood and
IQ loss (73 FR 66987, November 12, 2008). This evidence-based approach
considers air-related effects on neurocognitive function (using the
quantitative metric of IQ loss) associated with exposure in those areas
with elevated air concentrations equal to potential alternative levels
for the Pb standard. In simplest terms, the framework focuses on
children exposed to air-related Pb in those areas with elevated air Pb
concentrations equal to specific potential standard levels, providing
for estimation of a mean air-related IQ decrement for young children in
the high end of the national distribution of air-related exposures.
Thus, the conceptual context for the framework is that it provides
estimates of air-related IQ loss for the subset of U.S. children living
in close proximity to air Pb sources that contribute to such elevated
air Pb concentrations. In such cases, when a standard of a particular
level is just met at a monitor sited to record the highest source-
oriented concentration in an area, the large majority of children in
the larger surrounding area would likely experience exposures to
concentrations well below that level.
    The two primary inputs to the evidence-based air-related IQ loss
framework are air-to-blood ratios and C-R functions for the
relationship between blood Pb and IQ response in young children.
Additionally taken into consideration in applying and drawing
conclusions from the framework were the uncertainties inherent in these
inputs. Application of the framework also entailed consideration of an
appropriate level of protection from air-related IQ loss to be used in
conjunction with the framework. The framework estimates of mean air-
related IQ loss are derived through multiplication of the following
factors: standard level ([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 IQ decrement per
[micro]g/dL blood Pb.
    Based on the application of the air-related IQ loss framework to
the evidence, the Administrator concluded that, for exposures projected
for air Pb concentrations at the level of the 1978 standard, the
quantitative estimates of IQ loss associated with air-related Pb
indicated risk of a magnitude that, in his judgment, was significant
from a public health perspective, and that the evidence-based framework
supported a conclusion that the 1978 standard did not protect public
health with an adequate margin of safety (73 FR 66987, November 12,
2008). The Administrator further concluded that the evidence indicated
the need for a substantially lower standard level to provide increased
public health protection, especially for at-risk groups (most notably
children), against an array of effects, most importantly including
effects on the developing nervous system (73 FR 66987, November 12,
2008). In addition to giving primary consideration to the much expanded
evidence base since the standard was set, the Administrator also took
into consideration the exposure/risk assessments. In so doing, he
observed that, while taking into consideration their inherent
uncertainties and limitations, the quantitative estimates of IQ loss
associated with air-related Pb in air quality scenarios just meeting
the then-current standard also indicated risk of a magnitude that, in
his judgment, was significant from a public health perspective. Thus,
the Administrator concluded the exposure/risk estimates provided
additional support to the evidence-based conclusion that the standard
needed revision (73 FR 66987, November 12, 2008).
    In considering appropriate revisions to the prior standard in the
review completed in 2008, each of the four basic elements of the NAAQS
(indicator, averaging time, form and level) was evaluated. The
rationale for decisions on those elements is summarized below.
    With regard to indicator, consideration was given to replacing Pb-
TSP with Pb-PM10. The EPA recognized, however, that Pb in
all particle sizes contributes to Pb in blood and associated health
effects, additionally noting that the difference in particulate Pb
captured by TSP and PM10 monitors may be on the order of a
factor of two in some areas (73 FR 66991, November 12, 2008). Further,
the Administrator recognized uncertainty with regard to whether a Pb-
PM10-based standard would also effectively control ultra-
coarse \18\ Pb particles, which may have a greater presence in areas
near sources where Pb concentrations are highest (73 FR 66991, November
12, 2008). The Administrator decided to retain Pb-TSP as the indicator
to provide sufficient public health protection from the range of
particle sizes of ambient air Pb, including ultra-coarse particles (73
FR 66991, November 12, 2008). Additionally, a role was provided for Pb-
PM10 in the monitoring required for a Pb-TSP standard (73 FR
66991, November 12, 2008) based on the conclusion that use of Pb-
PM10 measurements at sites not influenced by sources of
ultra-coarse Pb, and where Pb concentrations are well below the
standard, would take advantage of the increased precision of these
measurements and decreased spatial variation of Pb-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) (73 FR 66991, November 12, 2008). Accordingly,
allowance was made for the use of Pb-PM10 monitoring for Pb
NAAQS attainment purposes in certain limited circumstances, at non-
source-oriented sites, where the Pb concentrations are expected to be
substantially below the standard and ultra-coarse particles are not
expected to be present (73 FR 66991, November 12, 2008).
---------------------------------------------------------------------------

    \18\ The term ``ultra-coarse'' refers to particles collected by
a TSP sampler but not by a PM10 sampler. This terminology
is consistent with the traditional usage of ``fine'' to refer to
particles collected by a PM2.5 sampler, and ``coarse'' to
refer to particles collected by a PM10 sampler but not by
a PM2.5 sampler, recognizing that there will be some
overlap in the particle sizes in the three types of collected
material.
---------------------------------------------------------------------------

    With regard to averaging time and form for the revised standard,
consideration was given to a monthly averaging time, with a form of
second maximum, and to 3-month and calendar quarter averaging times,
with not-to-be exceeded forms. While the Administrator recognized that
there were some factors that might imply support for a period as short
as a month for averaging time, he also noted other factors supporting
use of a longer time. He additionally took note of the complexity
inherent in this consideration for the primary Pb standard, which is
greater than in the case of other criteria pollutants due to the
multimedia nature of Pb and its multiple pathways of human exposure. In
this situation for Pb, the Administrator emphasized the importance of
considering all of the relevant factors, both those pertaining to the
human physiological response to changes in Pb exposures and those
pertaining to the response of air-related Pb exposure pathways to
changes in airborne Pb, in an integrated manner.
    As discussed further in the PA, the evidence on human physiological
response to changes in Pb exposure available in the last review
indicated that children's blood Pb levels respond quickly to increased
Pb exposure, particularly during the time of leaded gasoline usage but
likely with lessened immediacy since that time as children's exposure
pathways have changed (PA, section <IP_ADDRESS>). The Administrator also
recognized limitations and uncertainties in the evidence and
variability with regard to the information regarding the response time
of indoor dust Pb to ambient airborne Pb. In consideration of the
uncertainty associated with the evidence, the Administrator noted that
the two changes in form for the standard (to a rolling 3-month average
and to providing equal weighting to each month in deriving the 3-month
average) both afford greater weight to each individual month than did
the calendar quarter form of the 1978 standard, tending to control both
the likelihood that any month will exceed the level of the standard and
the magnitude of any such exceedance. Thus, based on an integrated
consideration of the range of relevant factors, the averaging time was
revised to a rolling 3-month period with a maximum (not-to-be-exceeded)
form, evaluated over a 3-year period. As compared to the previous
averaging time and form of calendar quarter (not-to-be exceeded), this
revision was considered to be more scientifically appropriate and more
health protective (73 FR 66996, November 12, 2008). The rolling average
gives equal weight to all 3-month periods, and the new calculation
method gives equal weight to each month within each 3-month period (73
FR 66996, November 12, 2008). Further, the rolling average yields
twelve 3-month averages each year to be compared to the NAAQS versus
four averages in each year for the block calendar quarters pertaining
to the previous standard (73 FR 66996, November 12, 2008).
    Lastly, based on the body of scientific evidence and information
available, as well as CASAC recommendations and public comment, the
Administrator decided on a standard level that, in combination with the
specified choice of indicator, averaging time, and form, he judged
requisite to protect public health, including the health of sensitive
groups, with an adequate margin of safety (73 FR 67006, November 12,
2008). In reaching the decision on level for the revised standard, the
Administrator considered as a useful guide the evidence-based framework
developed in that review. As described above, that framework integrates
evidence for the relationship between Pb in air and Pb in children's
blood and the relationship between Pb in children's blood and IQ loss.
Application of the air-related IQ loss evidence-based framework was
recognized, however, to provide ``no evidence- or risk-based bright
line that indicates a single appropriate level'' for the standard (73
FR 67006, November 12, 2008). Rather, the framework was seen as a
useful guide for consideration of health risks from exposure to ambient
levels of Pb in the air, in the context of a specified averaging time
and form, with regard to the Administrator's decision on a level for a
revised NAAQS that provides public health protection that is sufficient
but not more than necessary under the Act (73 FR 67004, November 12,
2008).
    As noted above, use of the evidence-based air-related IQ loss
framework to inform selection of a standard level involved
consideration of the evidence with regard to two input parameters. The
two input parameters are an air-to-blood ratio and a C-R function for
population IQ response associated with blood Pb level (73 FR 67004,
November 12, 2008). The evidence at the time of the last review
indicated a broad range of air-to-blood ratio estimates,\19\ each with
limitations and associated uncertainties. Based on the then-available
evidence, the Administrator concluded that 1:5 to 1:10 represented a
reasonable range to consider and identified 1:7 as a generally central
value on which to focus (73 FR 67004, November 12, 2008). With regard
to C-R functions, in light of the evidence of nonlinearity and of
steeper slopes at lower blood Pb levels, the Administrator concluded it
was appropriate to focus on C-R analyses based on blood Pb levels that
most closely reflected the then-current population of children in the
U.S.,\20\ recognizing the EPA's identification of four such analyses
and giving weight to the central estimate or median of the resultant C-
R functions (73 FR 67003, November 12, 2008, Table 3; 73 FR 67004,
November 12, 2008). The median estimate for the four C-R slopes of -
1.75 IQ points decrement per [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).
---------------------------------------------------------------------------

    \19\ 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).
    \20\ The geometric mean blood Pb level for U.S. children aged 5
years and below, reported for NHANES in 2003-04 (the most recent
years for which such an estimate was available at the time of the
2008 decision) was 1.8 [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).
---------------------------------------------------------------------------

    In considering the use of the evidence-based air-related IQ loss
framework to inform his judgment as to the appropriate degree of public
health protection that should be afforded by the NAAQS to provide
requisite protection against risk of neurocognitive effects in
sensitive populations, such as IQ loss in children, the Administrator
recognized in the 2008 review that there were no commonly accepted
guidelines or criteria within the public health community that would
provide a clear basis for such a judgment. During the 2008 review,
CASAC commented regarding the significance from a public health
perspective of a 1-2 point IQ loss in the entire population of children
and along with some commenters, emphasized that the NAAQS should
prevent air-related IQ loss of a significant magnitude, such as on the
order of 1-2 IQ points, in all but a small percentile of the
population. Similarly, the Administrator stated that ``ideally air-
related (as well as other) exposures to environmental Pb would be
reduced to the point that no IQ impact in children would occur'' (73 FR
66998, November 12, 2008). The Administrator further recognized that,
in the case of setting a NAAQS, he was required to make a judgment as
to what degree of protection is requisite to protect public health with
an adequate margin of safety (73 FR 66998, November 12, 2008). The
NAAQS must be sufficient but not more stringent than necessary to
achieve that result, and the Act does not require a zero-risk standard
(73 FR 66998, November 12, 2008). The Administrator additionally
recognized that the evidence-based air-related IQ loss framework did
not provide estimates pertaining to the U.S. population of children as
a whole. Rather, the framework provided estimates (with associated
uncertainties and limitations) for the mean of a subset of that
population, the subset of children assumed to be exposed to the level
of the standard. As described in the final decision ``[t]he framework
in effect focuses on the sensitive subpopulation that is the group of
children living near sources and more likely to be exposed at the level
of the standard'' (73 FR 67000, November 12, 2008). As further noted in
the final decision (73 FR 67000, November 12, 2008):

    EPA is unable to quantify the percentile of the U.S. population
of children that corresponds to the mean of this sensitive
subpopulation. Nor is EPA confident in its ability to develop
quantified estimates of air-related IQ loss for higher percentiles
than the mean of this subpopulation. EPA expects that the mean of
this subpopulation represents a high, but not quantifiable,
percentile of the U.S. population of children. As a result, EPA
expects that a standard based on consideration of this framework
would provide the same or greater protection from estimated air-
related IQ loss for a high, albeit unquantifiable, percentage of the
entire population of U.S. children.

    In reaching a judgment as to the appropriate degree of protection,
the Administrator considered advice and recommendations from CASAC and
public comments and recognized the uncertainties in the health effects
evidence and related information as well as the role of, and context
for, a selected air-related IQ loss in the application of the
framework, as described above. Based on these considerations, the
Administrator identified an air-related IQ loss of 2 points for use
with the framework, as a tool for considering the evidence with regard
to the level for the standard (73 FR 67005, November 12, 2008). In so
doing, the Administrator was not determining that such an IQ decrement
value was appropriate in other contexts (73 FR 67005, November 12,
2008). Given the various uncertainties associated with the framework
and the scientific evidence base, and the focus of the framework on the
sensitive subpopulation of children that are more highly exposed to
air-related Pb, a standard level selected in this way, in combination
with the selected averaging time and form, was expected to
significantly reduce and limit for a high percentage of U.S. children
the risk of experiencing an air-related IQ loss of that magnitude (73
FR 67005, November 12, 2008). At the standard level of 0.15 [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. Approach for the Current Review
    The approach in this review of the current primary standard takes
into consideration the approach used in the last Pb NAAQS review,
addressing key policy-relevant questions in light of currently
available scientific and technical information. To evaluate whether it
is appropriate to consider retaining the current primary Pb standard,
or whether consideration of revision is appropriate, the EPA has
adopted an approach in this review that builds upon the general
approach used in the last review and reflects the broader body of
evidence and information now available. As summarized above, the
Administrator's decisions in the prior review were based on an
integration of information on health effects associated with exposure
to Pb with that on relationships between ambient air Pb and blood Pb;
expert judgments on the adversity and public health significance of key
health effects; and policy judgments as to when the standard is
requisite to protect public health with an adequate margin of safety.
These considerations were informed by air quality and related analyses,
quantitative exposure and risk assessments, and qualitative assessment
of impacts that could not be quantified.
    Similarly in this review, as described in the PA, we draw on the
current evidence and quantitative assessments of exposure pertaining to
the public health risk of Pb in ambient air. In considering the
scientific and technical information here as in the PA, we consider
both the information available at the time of the last review and
information newly available since the last review, including most
particularly that which has been critically analyzed and characterized
in the current ISA. We additionally consider the quantitative exposure/
risk assessments from the last review that estimated Pb-related IQ
decrements associated with different air quality conditions in
simulated at-risk populations in multiple case studies (PA, section
3.4; 2007 REA). The evidence-based discussions presented below draw
upon evidence from epidemiological studies and experimental animal
studies evaluating health effects related to exposures to Pb, as
discussed in the ISA. The exposure/risk-based discussions have drawn
from the quantitative health risk analyses for Pb performed in the last
Pb NAAQS review in light of the currently available evidence (PA,
section 3.4; 2007 REA; REA Planning Document). Sections II.B through
II.D below summarize the current health effects and exposure/risk
information with a focus on the specific policy-relevant questions
identified for these categories of information in the PA (PA, chapter
3).

B. Health Effects Information

1. Array of Effects
    Lead has been demonstrated to exert a broad array of deleterious
effects on multiple organ systems as described in the assessment of the
evidence available in this review and consistent with conclusions of
past CDs (ISA, section 1.6; 2006 CD, section 8.4.1). A sizeable number
of studies on Pb health effects are newly available in this review and
are critically assessed in the ISA as part of the full body of
evidence. The newly available evidence reaffirms conclusions on the
broad array of effects recognized for Pb in the last review (see ISA,
section 1.10).\21\ Consistent with those conclusions, in the context of
pollutant exposures considered relevant to the Pb NAAQS review,\22\ the
ISA determines that causal relationships \23\ exist for Pb with effects
on the nervous system in children (cognitive function decrements and
the group of externalizing behaviors comprising attention, impulsivity
and hyperactivity), the hematological system (altered heme synthesis
and decreased red blood cell survival and function), and the
cardiovascular system (hypertension and coronary heart disease), and on
reproduction and development (postnatal development and male
reproductive function) (ISA, Table 1-2). Additionally, the ISA
describes relationships between Pb and effects on the nervous system in
adults, on immune system function and with cancer \24\ as likely to be
causal \25\ (ISA, Table 1-2, sections 1.6.4 and 1.6.7).
---------------------------------------------------------------------------

    \21\ Since the last Pb NAAQS review, the ISAs which have
replaced CDs in documenting each review of the scientific evidence
(or air quality criteria) employ a systematic framework for weighing
the evidence and describing associated conclusions with regard to
causality using established descriptors: ``causal'' relationship
with relevant exposure, ``likely'' to be a causal relationship,
evidence is ``suggestive'' of a causal relationship, ``inadequate''
evidence to infer a causal relationship, and ``not likely'' to be a
causal relationship (ISA, Preamble).
    \22\ In drawing judgments regarding causality for the criteria
air pollutants, the ISA places emphasis ``on evidence of effects at
doses (e.g., blood Pb concentration) or exposures (e.g., air
concentrations) that are relevant to, or somewhat above, those
currently experienced by the population. The extent to which studies
of higher concentrations are considered varies . . . but generally
includes those with doses or exposures in the range of one to two
orders of magnitude above current or ambient conditions. Studies
that use higher doses or exposures may also be considered . . .
[t]hus, a causality determination is based on weight of evidence
evaluation . . ., focusing on the evidence from exposures or doses
generally ranging from current levels to one or two orders of
magnitude above current levels'' (ISA, pp. lx-lxi).
    \23\ In determining a causal relationship to exist for Pb with
specific health effects, the EPA concludes that ``[e]vidence is
sufficient to conclude that there is a causal relationship with
relevant pollutant exposures (i.e., doses or exposures generally
within one to two orders of magnitude of current levels)'' (ISA, p.
lxii).
    \24\ The EPA concludes that a causal relationship is likely to
exist between Pb exposure and cancer, based primarily on consistent,
strong evidence from experimental animal studies, but inconsistent
epidemiological evidence (ISA, section 4.10.5). Lead has also been
classified as a probable human carcinogen by the International
Agency for Research on Cancer, based mainly on sufficient animal
evidence, and as reasonably anticipated to be a human carcinogen by
the U.S. National Toxicology Program (ISA, section 4.10).
    \25\ In determining that there is likely to be a causal
relationship for Pb with specific health effects, the EPA has
concluded that ``[e]vidence is sufficient to conclude that a causal
relationship is likely to exist with relevant pollutant exposures,
but important uncertainties remain'' (ISA, p. lxii).
---------------------------------------------------------------------------

    In some categories of health effects, there is newly available
evidence regarding some aspects of the effects described in the last
review or that strengthens our conclusions regarding aspects of Pb
toxicity on a particular

physiological system. Among the nervous system effects of Pb, the newly
available evidence is consistent with conclusions in the previous
review which recognized that ``[t]he neurotoxic effects of Pb exposure
are among those most studied and most extensively documented among
human population groups'' (2006 CD, p. 8-25) and took note of the
diversity of studies in which such effects of Pb exposure early in
development (from fetal to postnatal childhood periods) have been
observed (2006 CD, p. E-9). Nervous system effects that receive
prominence in the current review, as in previous reviews, include those
affecting cognitive function and behavior in children (ISA, section
4.3), with conclusions that are consistent with findings of the last
review.
    Across the broad array of Pb effects for systems and processes
other than the nervous system, the evidence base has been augmented
with additional epidemiological investigations in a number of areas,
including developmental outcomes, such as puberty onset, and adult
outcomes related to cardiovascular function, for which several large
cohorts have been analyzed (ISA, Table 1-8 and sections 4.4 and 4.8).
Conclusions on these other systems and processes are generally
consistent with conclusions reached in the last review, while also
extending our conclusions on some aspects of these effects (ISA,
section 4.4 and Table 1-8).
    Based on the extensive assessment of the full body of evidence
available in this review, the major conclusions drawn by the ISA
regarding health effects of Pb in children include the following (ISA,
p. lxxxvii).

    Multiple epidemiologic studies conducted in diverse populations
of children consistently demonstrate the harmful effects of Pb
exposure on cognitive function (as measured by IQ decrements,
decreased academic performance and poorer performance on tests of
executive function). . . . Evidence suggests that some Pb-related
cognitive effects may be irreversible and that the
neurodevelopmental effects of Pb exposure may persist into adulthood
(Section 1.9.4). Epidemiologic studies also demonstrate that Pb
exposure is associated with decreased attention, and increased
impulsivity and hyperactivity in children (externalizing behaviors).
This is supported by findings in animal studies demonstrating both
analogous effects and biological plausibility at relevant exposure
levels. Pb exposure can also exert harmful effects on blood cells
and blood producing organs, and is likely to cause an increased risk
of symptoms of depression and anxiety and withdrawn behavior
(internalizing behaviors),decreases in auditory and motor function,
asthma and allergy, as well as conduct disorders in children and
young adults. There is some uncertainty about the Pb exposures
contributing to the effects and blood Pb levels observed in
epidemiologic studies; however, these uncertainties are greater in
studies of older children and adults than in studies of young
children (Section 1.9.5).

    Based on the extensive assessment of the full body of evidence
available in this review, the major conclusions drawn by the ISA
regarding health effects of Pb in adults include the following (ISA, p.
lxxxviii).

    A large body of evidence from both epidemiologic studies of
adults and experimental studies in animals demonstrates the effect
of long-term Pb exposure on increased blood pressure (BP) and
hypertension (Section 1.6.2). In addition to its effect on BP, Pb
exposure can also lead to coronary heart disease and death from
cardiovascular causes and is associated with cognitive function
decrements, symptoms of depression and anxiety, and immune effects
in adult humans. The extent to which the effects of Pb on the
cardiovascular system are reversible is not well-characterized.
Additionally, the frequency, timing, level, and duration of Pb
exposure causing the effects observed in adults has not been
pinpointed, and higher past exposures may contribute to the
development of health effects measured later in life.

    As in prior reviews of the Pb NAAQS, this review is focused on
those effects most pertinent to ambient air Pb exposures. Given the
reductions in ambient air Pb concentrations over the past decades,
these effects are generally those associated with the lowest levels of
Pb exposure that have been evaluated. Additionally, we recognize the
limitations on our ability to draw conclusions regarding the exposure
conditions contributing to the findings from epidemiological analyses
of blood Pb levels in populations of older children and adults,
particularly in light of their history of higher Pb exposures. Evidence
available in future reviews may better inform this issue. In the last
review, while recognizing the range of health effects in variously aged
populations related to Pb exposure, we focused on the health effects
for which the evidence was strongest with regard to relationships with
the lowest exposure levels, neurocognitive effects in young children.
    As is the case for studies of nervous system effects in children
(discussed in more detail in section II.B.3 below), newly available
studies of other effects in child and adult cohorts include cohorts
with similar or somewhat lower mean blood Pb levels than in previously
available studies. Categories of effects for which a causal
relationship has been concluded in the ISA and for which there are a
few newly available epidemiological studies indicating blood Pb
associations with effects in study groups with somewhat lower blood Pb
levels than previously available for these effects include effects on
development (delayed puberty onset) and reproduction (male reproductive
function) and on the cardiovascular system (hypertension) (ISA,
sections 4.4 and 4.8; 2006 CD, sections 6.5 and 6.6). With regard to
the former category, study groups in the newly available studies
include groups composed of older children ranging up to age 18 years,
for which there is increased uncertainty regarding historical exposures
and their role in the observed effects.\26\ An additional factor that
handicaps our consideration of exposure levels associated with these
findings is the appreciable uncertainty associated with our
understanding of Pb biokinetics during this lifestage (ISA, sections
3.2, 3.3, and 4.8.6). The evidence newly available for Pb relationships
with cardiovascular effects in adults include some studies with
somewhat lower blood Pb levels than in the last review. The long
exposure histories of these cohorts, as well as the generally higher Pb
exposures of the past, complicate conclusions regarding exposure levels
that may be eliciting observed effects (ISA, sections <IP_ADDRESS> and
4.4.7).\27\ Accordingly, as discussed further below, we focus in this
review, as in the last, on neurocognitive effects in young children.
---------------------------------------------------------------------------

    \26\ Several of these studies involve NHANES III cohorts for
which early childhood exposures were generally much higher than
those common in the U.S. today (ISA, section 4.8.5).
    \27\ Studies from the late 1960s and 1970s suggest that adult
blood Pb levels during that period ranged from roughly 13 to 16
[mu]g/dL and from 15 to 30 [mu]g/dL in children aged 6 and younger
(ISA, section 4.4.1).
---------------------------------------------------------------------------

2. Critical Periods of Exposure
    As in the last review, we base our current understanding of health
effects associated with different Pb exposure circumstances at various
stages of life or in different populations on the full body of
available evidence and primarily on epidemiological studies of health
effects associated with population Pb biomarker levels (discussed
further in section II.B.3 below). The epidemiological evidence is
overwhelmingly composed of studies that rely on blood Pb for the
exposure metric, with the remainder largely including a focus on bone
Pb. Because these metrics reflect Pb in the body (e.g., as compared to
Pb exposure concentrations) and, in the case of blood Pb, reflect Pb
available for distribution to target sites, they strengthen the

evidence base for purposes of drawing causal conclusions with regard to
Pb generally. The complexity of Pb exposure pathways and internal
dosimetry, however, tends to limit the extent to which these types of
studies inform our more specific understanding of the Pb exposure
circumstances (e.g., timing within lifetime, duration, frequency and
magnitude) eliciting the various effects.
    As at the time of the last review (and discussed more fully in
section II.B.3 below), assessment of the full evidence base, including
evidence newly available in this review, demonstrates that Pb exposure
prenatally and also in early childhood can contribute to neurocognitive
impacts in childhood, with evidence also indicating the potential for
effects persisting into adulthood (ISA, sections 1.9.4, 1.9.5, and
1.10). In addition to the observed associations of prenatal and
childhood blood Pb with effects at various ages in childhood, there is
also evidence of Pb-related cognitive function effects in non-
occupationally exposed adults (ISA, section 4.3.11). This includes
evidence of associations of such effects in adulthood with childhood
blood Pb levels and in other cohorts, with concurrent (adult) blood Pb
levels (ISA, sections <IP_ADDRESS>, <IP_ADDRESS> and 4.3.11). As the studies
finding associations of adult effects with childhood blood Pb levels
did not examine adult blood Pb levels, the relative influence of adult
Pb exposure cannot be ascertained, and a corresponding lack of early
life exposure or biomarker measurements for the latter studies limits
our ability to draw conclusions regarding specific Pb exposure
circumstances eliciting the observed effects (4.3.11). Findings of
stronger associations for adult neurocognitive effects with bone Pb,
however, indicate the role of historical or cumulative exposures for
those effects (ISA, section 4.3).
    A critical aspect of much of the epidemiological evidence,
particularly studies focused on adults (and older children) in the U.S.
today, is the backdrop of generally declining environmental Pb exposure
(from higher exposures during their younger years) that is common
across many study populations (ISA, p. 4-2).\28\ An additional factor
complicating the interpretation of health effect associations with
blood Pb measurements in older children and younger adults is the
common behaviors of younger children (e.g., hand-to-mouth contact) that
generally contribute to relatively greater exposures earlier in life
(ISA, sections 3.1.1, 4.2.1). Such exposure histories for adults and
older children complicate our ability to draw conclusions regarding
critical time periods and lifestages for Pb exposures eliciting the
effects for which associations with Pb biomarkers have been observed in
these populations (e.g., ISA, section 1.9.6).\29\ Thus, our confidence
is greatest in the role of early childhood exposure in contributing to
Pb-related neurocognitive effects that have been associated with blood
Pb levels in young children. This is due, in part, to the relatively
short exposure histories of young children (ISA, sections 1.9.4, 1.9.6
and 4.3.11).
---------------------------------------------------------------------------

    \28\ The declines in Pb exposure concentrations occurring from
the 1970s through the early 1990s (and experienced by middle aged
and older adults of today), as indicated by NHANES blood Pb
information, were particularly dramatic (ISA, section 3.4.1).
    \29\ The evidence from experimental animal studies can be
informative with regard to key aspects of exposure circumstances in
eliciting specific effects, thus informing our interpretation of
epidemiological evidence. For example, the animal evidence base with
regard to Pb effects on blood pressure demonstrates the
etiologically-relevant role of long-term exposure (ISA, section
4.4.1). This finding then informs consideration of epidemiological
studies of adult populations for whom historical exposures were
likely more substantial than concurrent ones, suggesting that the
observed effects may be related to the past exposure (ISA, section
4.4.1). For other health effects, the animal evidence base may or
may not be informative in this manner.
---------------------------------------------------------------------------

    Epidemiological analyses evaluating risk of neurocognitive impacts
(e.g., reduced IQ) associated with different blood Pb metrics in
cohorts with differing exposure patterns (including those for which
blood Pb levels at different ages were not highly correlated) also
indicate associations with blood Pb measurements concurrent with full
scale IQ (FSIQ) tests at ages of approximately 6-7 years. The analyses
did not, however, conclusively demonstrate stronger findings for early
(e.g., age 2 years) or concurrent blood Pb (ISA, section 4.3.11).\30\
The experimental animal evidence additionally indicates early life
susceptibility (ISA, section 4.3.15 and p. 5-21). Thus, while
uncertainties remain with regard to the role of Pb exposures during a
particular age of life in eliciting nervous system effects, such as
cognitive function decrements, the full evidence base continues to
indicate prenatal and early childhood lifestages as periods of
increased Pb-related risk (ISA, sections 4.3.11 and 4.3.15). We
recognize increasing uncertainty, however, in our understanding of the
relative impact on neurocognitive function of additional Pb exposure of
children by school age or later that is associated with limitations of
the currently available evidence, including epidemiological cohorts
with generally similar temporal patterns of exposure.
---------------------------------------------------------------------------

    \30\ In the collective body of evidence of nervous system
effects in children, it is difficult to distinguish exposure in
later lifestages (e.g., school age) and its associated risk from
risks resulting from exposure in prenatal and early childhood (ISA,
section 4.3.11). While early childhood is recognized as a time of
increased susceptibility, a difficulty in identifying a discrete
period of susceptibility from epidemiological studies has been that
the period of peak exposure, reflected in peak blood Pb levels, is
around 18-27 months when hand-to-mouth activity is at its maximum
(ISA, section 3.4.1 and <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>.).
---------------------------------------------------------------------------

    As in the last review, there is also substantial evidence of other
neurobehavioral effects in children, including effects on externalizing
behaviors (reduced attention span, increased impulsivity,
hyperactivity, and conduct disorders) and on internalizing behaviors.
The evidence for many of these endpoints, as with neurocognitive
effects, also includes associations of effects at various ages in
childhood and for some effects, into adulthood, with blood Pb levels
reflective of several different lifestages (e.g., prenatal and several
different ages in childhood) (ISA, sections 4.3.3 and 4.3.4). There is
similar or relatively less extensive evidence to inform our
understanding of such effects associated with specific time periods of
exposure at specific lifestages than is the case for effects on
cognitive function.
    Across the range of Pb effects on physiological systems and
processes other than the nervous system, the evidence base for blood
pressure and hypertension is somewhat more informative with regard to
the circumstances of Pb exposure eliciting the observed effects than
are the evidence bases for many other effects. In the case of Pb-
induced increases in blood pressure, the evidence indicates an
importance of long-term exposure (ISA, sections 1.6.2 and <IP_ADDRESS>). The
greater uncertainties regarding the time, duration and magnitude of
exposure contributing to these observed health effects complicate
identification of sensitive lifestages and associated exposure patterns
that might be compared with our understanding of the sensitivity of
young children to neurocognitive impacts of Pb. Thus, while augmenting
the evidence base on these additional endpoints, the newly available
evidence does not lead us to identify a health endpoint expected to be
more sensitive to Pb exposure than neurocognitive endpoints in
children, leading us to continue to conclude that the appropriate
primary focus for our review is on neurocognitive endpoints in
children.

    In summary, as in the last review, we continue to recognize a
number of uncertainties regarding the circumstances of Pb exposure,
including timing or lifestages, eliciting specific health effects.
Consideration of the evidence newly available in this review has not
appreciably changed our understanding on this topic. The relationship
of long-term exposure to Pb with hypertension and increased blood
pressure in adults is substantiated despite some uncertainty regarding
the exposures circumstances (e.g., magnitude and timing) contributing
to blood Pb levels measured in epidemiological studies. Across the full
evidence base, the effects for which our understanding of relevant
exposure circumstances is greatest are neurocognitive effects in young
children. Moreover, available evidence does not suggest a more
sensitive endpoint. Thus, we continue to recognize and give particular
attention to the role of Pb exposures relatively early in childhood in
contributing to neurocognitive effects, some of which may persist into
adulthood.
3. Nervous System Effects in Children
    In considering the question of levels of Pb exposure at which
health effects occur, we recognize, as discussed in sections II.B.1 and
II.B.2 above, that the epidemiological evidence base for our
consideration in this review, as in the past, includes substantial
focus on internal biomarkers of exposure, such as blood Pb, with
relatively less information specific to exposure levels, including
those derived from air-related pathways. Given that blood and bone Pb
are integrated markers of aggregate exposure across all sources and
exposure pathways, our interpretation of studies relying on them is
informed by what is known regarding the historical context and exposure
circumstances of the study populations. For example, a critical aspect
of much of the epidemiological evidence is the backdrop of generally
declining Pb exposure over the past several decades (e.g., ISA,
sections 2.5 and 3.4.1; 2006 CD, section 3.4). Thus, as a generality,
recent epidemiological studies of populations with similar
characteristics as those studied in the past tend to involve lower
overall Pb exposures and accordingly lower blood Pb levels. This has
been of particular note in the evidence of blood Pb associations with
nervous system effects, particularly impacts on cognitive function in
children, for which we have seen associations with progressively lower
childhood blood Pb levels across past reviews (ISA, section 4.3.12;
1986 CD; USEPA, 1990a; 2006 CD; 73 FR 66976, November 12, 2008).
    The evidence currently available with regard to the magnitude of
blood Pb levels associated with neurocognitive effects in children is
generally consistent with that available in the review completed in
2008. Nervous system effects in children, specifically effects on
cognitive function, continue to be the effects that are best
substantiated as occurring at the lowest blood Pb concentrations (ISA,
pp. lxxxvii-lxxxviii). Associations of blood Pb with effects on
cognitive function measures in children have been reported in many
studies across a range of childhood blood Pb levels, including study
group (mean/median) levels ranging down to 2 [mu]g/dL (e.g., ISA, p.
lxxxvii and section 4.3.2).\31\
---------------------------------------------------------------------------

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

    \32\ 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.
---------------------------------------------------------------------------

    In a newly available study of blood Pb levels at primary school
age, a significant association of blood Pb in children aged 8-11 years
and concurrently measured FSIQ was reported for a cross-sectional
cohort in Korea with a mean blood Pb level of 1.7 [mu]g/dL and range of
0.43-4.91 [mu]g/dL (Kim et al., 2009).\33\ In considering the blood Pb