```

[Federal Register Volume 80, Number 2 (Monday, January 5, 2015)]
[Proposed Rules]
[Pages 277-324]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 2014-30681]

[[Page 277]]

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

[[Page 278]]

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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: a-and-r-Docket@epa.gov. Include docket ID No. EPA-
HQ-OAR-2010-0108 in the subject line of the message.
     Fax: 202-566-9744.
     Mail: Docket No. EPA-HQ-OAR-2010-0108, Environmental 
Protection Agency, Mail Code 28221T, 1200 Pennsylvania Ave. NW., 
Washington, DC 20460.
     Hand Delivery: Docket No. EPA-HQ-OAR-2010-0108, 
Environmental Protection Agency, EPA WJC West Building, Room 3334, 1301 
Constitution Ave. NW., Washington, DC. Such deliveries are only 
accepted during the Docket's normal hours of operation, and special 
arrangements should be made for deliveries of boxed information.
    Instructions: Direct your comments to Docket ID No. EPA-HQ-OAR-
2010-0108. The EPA's policy is that all comments received will be 
included in the public docket without change and may be made available 
online at www.regulations.gov, including any personal information 
provided, unless the comment includes information claimed to be 
Confidential Business Information (CBI) or other information whose 
disclosure is restricted by statute. Do not submit information that you 
consider to be CBI or otherwise protected through www.regulations.gov 
or email. The www.regulations.gov Web site is an ``anonymous access'' 
system, which means the EPA will not know your identity or contact 
information unless you provide it in the body of your comment. If you 
send an email comment directly to the EPA without going through 
www.regulations.gov, your email address will be automatically captured 
and included as part of the comment that is placed in the public docket 
and made available on the Internet. If you submit an electronic 
comment, the EPA recommends that you include your name and other 
contact information in the body of your comment and with any disk or 
CD-ROM you submit. If the EPA cannot read your comment due to technical 
difficulties and cannot contact you for clarification, the EPA may not 
be able to consider your comment. Electronic files should avoid the use 
of special characters, any form of encryption, and be free of any 
defects or viruses. For additional information about the EPA's public 
docket, visit the EPA Docket Center homepage at http://www.epa.gov/epahome/dockets.htm.
    Public Hearing: To request a public hearing or information 
pertaining to a public hearing on this document, contact Ms. Eloise 
Shepherd, Health and Environmental Impacts Division, Office of Air 
Quality Planning and Standards (C504-02), U.S. Environmental Protection 
Agency, Research Triangle Park, NC 27711; telephone number (919) 541-
5507; fax number (919) 541-0804; email address: 
shepherd.eloise@epa.gov. See the SUPPLEMENTARY INFORMATION for further 
information about a possible public hearing.
    Docket: All documents in the docket are listed on the 
www.regulations.gov Web site. This includes documents in the rulemaking 
docket (Docket ID No. EPA-HQ-OAR-2010-0108) and a separate docket, 
established for the Integrated Science Assessment for this review 
(Docket ID No. EPA-HQ-ORD-2011-0051) that has been incorporated by 
reference into the rulemaking docket. All documents in these dockets 
are listed on the www.regulations.gov Web site. Although listed in the 
index, some information is not publicly available, e.g., CBI or other 
information whose disclosure is restricted by statute. Certain other 
material, such as copyrighted material, is not placed on the Internet 
and may be viewed, with prior arrangement, at the EPA Docket Center. 
Publicly available docket materials are available either electronically 
in www.regulations.gov or in hard copy at the Air and Radiation Docket 
Information Center, EPA/DC, WJC West Building, Room 3334, 1301 
Constitution Ave. NW., Washington, DC. The Public Reading Room is open 
from 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding legal 
holidays. The telephone number for the Public Reading Room is (202) 
566-1744 and the telephone number for the Air and Radiation Docket 
Information Center is (202) 566-1742.

FOR FURTHER INFORMATION CONTACT: Dr. Deirdre L. Murphy, Health and 
Environmental Impacts Division, Office of Air Quality Planning and 
Standards, U.S. Environmental Protection Agency, Mail Code C504-06, 
Research Triangle Park, NC 27711; telephone: (919) 541-0729; fax: (919) 
541-0237; email: murphy.deirdre@epa.gov. To request a public hearing or 
information pertaining to a public hearing on this document, contact 
Ms. Eloise Shepherd, Health and Environmental Impacts Division, Office 
of Air Quality Planning and Standards (C504-02), U.S. Environmental 
Protection Agency, Research Triangle Park, NC 27711; telephone number 
(919) 541-5507; fax number (919) 541-0804; email address: 
shepherd.eloise@epa.gov.

SUPPLEMENTARY INFORMATION:

General Information

Preparing Comments for the EPA

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

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

Availability of Information Related to This Action

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

Information About a Possible Public Hearing

    To request a public hearing or information pertaining to a public 
hearing on this document, contact Ms. Eloise Shepherd, Health and 
Environmental Impacts Division, Office of Air Quality Planning and 
Standards (C504-02), U.S. Environmental Protection Agency, Research 
Triangle Park, NC 27711; telephone number (919) 541-5507; fax number 
(919) 541-0804; email address: shepherd.eloise@epa.gov.

Table of Contents

    The following topics are discussed in this preamble:

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

I. Background

A. Legislative Requirements

    Two sections of the Clean Air Act (CAA or the Act) govern the 
establishment and revision of the NAAQS. Section 108 (42 U.S.C. 7408) 
directs the Administrator to identify and list certain air pollutants 
and then to issue air quality criteria for those pollutants. The 
Administrator is to list those air pollutants that in her ``judgment, 
cause or contribute to air pollution which may reasonably be 
anticipated to endanger public health or welfare;'' ``the presence of 
which in the ambient air results from numerous or diverse mobile or 
stationary sources;'' and ``for which . . . [the Administrator] plans 
to issue air quality criteria . . .'' Air quality criteria are intended 
to ``accurately reflect the latest scientific knowledge useful in 
indicating the kind and extent of all identifiable effects on public 
health or welfare which may be expected from the presence of [a] 
pollutant in the ambient air . . .'' 42 U.S.C. 7408(b). Section 109 (42 
U.S.C. 7409) directs the Administrator to propose and promulgate 
``primary'' and ``secondary'' NAAQS for pollutants for which air 
quality criteria are issued. Section 109(b)(1) defines a primary 
standard as one ``the attainment and maintenance of which in the 
judgment of the Administrator, based on such criteria and allowing an 
adequate margin of safety, are requisite to protect the public 
health.'' \1\ A secondary standard, as defined in section 109(b)(2), 
must ``specify a level of air quality the attainment and maintenance of 
which, in the judgment of the Administrator, based on such criteria, is 
requisite to protect the public welfare from any known or anticipated 
adverse effects associated with the presence of [the] pollutant in the 
ambient air.'' \2\
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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

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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

[[Page 281]]

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

[[Page 282]]

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

    Unlike pollutants such as particulate matter and carbon monoxide, 
air quality criteria had not been issued for Pb as of the enactment of 
the CAA of 1970, which first set forth the requirement to set NAAQS 
based on air quality criteria. In the years just after enactment of the 
CAA, the EPA did not list Pb under Section 108 of the Act, having 
determined to control Pb air pollution through regulations to phase out 
the use of Pb additives in gasoline (See 41 FR 14921, April 8, 1976). 
However, the decision not to list Pb under Section 108 was challenged 
by environmental and public health groups, and the U.S. District Court 
for the Southern District of New York concluded that the EPA was 
required to list Pb under Section 108. Natural Resources Defense 
Council v. EPA, 411 F. Supp. 864 21 (S.D. N.Y. 1976), affirmed, 545 
F.2d 320 (2d Cir. 1978). Accordingly, on April 8, 1976, the EPA 
published a notice in the Federal Register that Pb had been listed 
under Section 108 as a criteria pollutant (41 FR 14921, April 8, 1976) 
and on October 5, 1978, the EPA promulgated primary and secondary NAAQS 
for Pb under Section 109 of the Act (43 FR 46246, October 5, 1978). 
Both primary and secondary standards were set at a level of 1.5 
micrograms per cubic meter ([mu]g/m\3\), measured as Pb in total 
suspended particles (Pb-TSP), not to be exceeded by the maximum 
arithmetic mean concentration averaged over a calendar quarter. These 
standards were based on the 1977 Air Quality Criteria for Lead (USEPA, 
1977).
    The first review of the Pb standards was initiated in the mid-
1980s. The scientific assessment for that review is described in the 
1986 Air Quality Criteria for Lead (USEPA, 1986a; henceforth referred 
to as the 1986 CD), the associated Addendum (USEPA, 1986b) and the 1990 
Supplement (USEPA, 1990a). As part of the review, the agency designed 
and performed human exposure and health risk analyses (USEPA, 1989), 
the results of which were presented in a 1990 Staff Paper (USEPA, 
1990b). Based on the scientific assessment and the human exposure and 
health risk analyses, the 1990 Staff Paper presented recommendations 
for consideration by the Administrator (USEPA, 1990b). After 
consideration of the documents developed during the review and the 
significantly changed circumstances since Pb was listed in 1976, the 
agency did not propose any revisions to the 1978 Pb NAAQS. In a 
parallel effort, the agency developed the broad, multi-program, 
multimedia, integrated U.S. Strategy for Reducing Lead Exposure (USEPA, 
1991). As part of implementing this strategy, the agency focused 
efforts primarily on regulatory and remedial clean-up actions aimed at 
reducing Pb exposures from a variety of nonair sources judged to pose 
more extensive public health risks to U.S. populations, as well as on 
actions to reduce Pb emissions to air, such as bringing more areas into 
compliance with the existing Pb NAAQS (USEPA, 1991). The EPA continues 
this broad, multi-program, multimedia approach to reducing Pb exposures 
today, as described in section I.B above.
    The last review of the 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).
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    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

[[Page 283]]

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).
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    \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

[[Page 284]]

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

D. Multimedia, Multipathway Aspects of Lead

    Since Pb distributes from air to other media and is persistent, our 
review of the NAAQS for Pb considers the protection provided against 
such effects associated both with exposures to Pb in ambient air and 
with exposures to Pb that makes its way into other media from ambient 
air. Additionally, in assessing the adequacy of protection afforded by 
the current NAAQS, we are mindful of the long history of greater and 
more widespread atmospheric emissions that occurred in previous years 
(both before and after establishment of the 1978 NAAQS) and that 
contributed to the Pb that exists in human populations and ecosystems 
today. Likewise, we also recognize the role of other, nonair sources of 
Pb now and in the past that also contribute to the Pb that exists in 
human populations and ecosystems today.
    Lead emitted to ambient air is transported through the air and is 
also distributed from air to other media. This multimedia distribution 
of Pb emitted into ambient air (air-related Pb) contributes to multiple 
air-related pathways of human and ecosystem exposure (ISA, sections 
3.1.1 and 3.7.1). Air-related pathways may also involve media other 
than air, including indoor and outdoor dust, soil, surface water and 
sediments, vegetation and biota. Air-related Pb exposure pathways for 
humans include inhalation of ambient air or ingestion of food, water or 
other materials, including dust and soil, that have been contaminated 
through a pathway involving Pb deposition from ambient air (ISA, 
section 3.1.1.1). Ambient air inhalation pathways include both 
inhalation of air outdoors and inhalation of ambient air that has 
infiltrated into indoor environments. The air-related ingestion 
pathways occur as a result of Pb passing through the ambient air, being 
distributed to other environmental media and contributing to human 
exposures via contact with and ingestion of indoor and outdoor dusts, 
outdoor soil, food and drinking water.
    Lead exposures via the various inhalation and ingestion air-related 
pathways may vary with regard to the time in which they respond to 
changes in air Pb concentrations. For example, exposures resulting from 
human exposure pathways most directly involving Pb in ambient air and 
exchanges of ambient air with indoor air (e.g., inhalation) can respond 
most quickly, while those for pathways involving exposure to Pb 
deposited from ambient air into the environment (e.g., diet) may be 
expected to respond more slowly. The extent of this will be influenced 
by the magnitude of change, as well as--for deposition-related 
pathways--the extent of prior deposition and environment 
characteristics influencing availability of prior deposited Pb.
    Lead currently occurring in nonair media may also derive from 
sources other than ambient air (nonair Pb sources) (ISA, sections 2.3 
and 3.7.1). For example, Pb in dust inside some houses or outdoors in 
some urban areas may derive from the common past usage of leaded paint, 
while Pb in drinking water may derive from the use of leaded pipe or 
solder in drinking water distribution systems (ISA, section 3.1.3.3). 
We also recognize the history of much greater air emissions of Pb in 
the past, such as that associated with leaded gasoline usage and higher 
industrial emissions which have left a legacy of Pb in other (nonair) 
media.
    The relative importance of different pathways of human exposure to 
Pb, as well as the relative contributions from Pb resulting from recent 
and historic air emissions and from nonair sources, vary across the 
U.S. population as a result of both extrinsic factors, such as a home's 
proximity to industrial Pb sources or its history of leaded paint 
usage, and intrinsic factors, such as a person's age and nutritional 
status (ISA, sections 5.1, 5.2, 5.2.1, 5.2.5 and 5.2.6). Thus, the 
relative contributions from specific pathways is situation specific 
(ISA, p. 1-11), although a predominant Pb exposure pathway for very 
young children is the incidental ingestion of indoor dust by hand-to-
mouth activity (ISA, section 3.1.1.1). For adults, however, diet may be 
the primary Pb exposure pathway (2006 CD, section 3.4). Similarly, the 
relative importance of air-related and nonair-related Pb also varies 
with the relative magnitudes of exposure by those pathways, which may 
vary with different circumstances.
    The distribution of Pb from ambient air to other environmental 
media also influences the exposure pathways for organisms in 
terrestrial and aquatic ecosystems. Exposure of terrestrial animals and 
vegetation to air-related Pb can occur by contact with ambient air or 
by contact with soil, water or food items that have been contaminated 
by Pb from ambient air (ISA, section 6.2). Transport of Pb into aquatic 
systems similarly provides for exposure of biota in those systems, and 
exposures may vary among systems as a result of differences in sources 
and levels of contamination, as well as characteristics of the systems 
themselves, such as salinity, pH and turbidity (ISA, section 2.3.2). In 
addition to Pb contributed by current atmospheric deposition, Pb may 
occur in aquatic systems as a result of nonair sources such as 
industrial discharges or mine-related drainage, of historical air Pb 
emissions (e.g., contributing to deposition to a water body or via 
runoff from soils near historical air sources) or combinations of 
different types of sources (e.g., resuspension of sediments 
contaminated by urban runoff and surface water discharges).
    The persistence of Pb contributes an important temporal aspect to 
lead's environmental pathways, and the time (or lag) associated with 
realization of the impact of air Pb concentrations on concentrations in 
other media can vary with the media (e.g., ISA, section 6.2.2). For 
example, exposure pathways most directly involving Pb in ambient air or 
surface waters can respond more quickly to changes in ambient air Pb 
concentrations while pathways involving exposure to Pb in soil or 
sediments generally respond more slowly. An additional influence on the 
response time for nonair media is the environmental presence of Pb 
associated with past, generally higher, air concentrations. For 
example, after a reduction in air Pb concentrations, the time needed 
for sediment or surface soil concentrations to indicate a response to 
reduced air Pb concentrations might be expected to be longer in areas 
of more substantial past contamination than in areas with lesser past 
contamination. Thus, considering the Pb concentrations occurring in 
nonair environmental media as a result of air quality conditions that 
meet the current NAAQS is a complexity of this review, as it also was, 
although to a lesser degree, with regard to the prior standard in the 
last review.

E. Air Quality Monitoring

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

[[Page 285]]

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.
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    \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 2.10.1.2. 
These conditions include where Pb concentrations are not expected to 
equal or exceed 0.10 [mu]g/m\3\ as an arithmetic 3-month mean and 
where the source of Pb emissions is expected to emit a substantial 
majority of its Pb in the size fraction captured by PM10 
monitors.
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    Since the phase-out of Pb in on-road gasoline, Pb is widely 
recognized as a 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.
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    \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.
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    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).

[[Page 286]]

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.
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    \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).
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    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.
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    \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.
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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

[[Page 287]]

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

[[Page 288]]

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

[[Page 289]]

of the framework and in the resultant estimates (73 FR 67000, November 
12, 2008).
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    \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

[[Page 290]]

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).
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    \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

[[Page 291]]

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

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

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

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

    As in prior reviews of the Pb NAAQS, this review is focused on 
those effects most pertinent to ambient air Pb exposures. Given the 
reductions in ambient air Pb concentrations over the past decades, 
these effects are generally those associated with the lowest levels of 
Pb exposure that have been evaluated. Additionally, we recognize the 
limitations on our ability to draw conclusions regarding the exposure 
conditions contributing to the findings from epidemiological analyses 
of blood Pb levels in populations of older children and adults, 
particularly in light of their history of higher Pb exposures. Evidence 
available in future reviews may better inform this issue. In the last 
review, while recognizing the range of health effects in variously aged 
populations related to Pb exposure, we focused on the health effects 
for which the evidence was strongest with regard to relationships with 
the lowest exposure levels, neurocognitive effects in young children.
    As is the case for studies of nervous system effects in children 
(discussed in more detail in section II.B.3 below), newly available 
studies of other effects in child and adult cohorts include cohorts 
with similar or somewhat lower mean blood Pb levels than in previously 
available studies. Categories of effects for which a causal 
relationship has been concluded in the ISA and for which there are a 
few newly available epidemiological studies indicating blood Pb 
associations with effects in study groups with somewhat lower blood Pb 
levels than previously available for these effects include effects on 
development (delayed puberty onset) and reproduction (male reproductive 
function) and on the cardiovascular system (hypertension) (ISA, 
sections 4.4 and 4.8; 2006 CD, sections 6.5 and 6.6). With regard to 
the former category, study groups in the newly available studies 
include groups composed of older children ranging up to age 18 years, 
for which there is increased uncertainty regarding historical exposures 
and their role in the observed effects.\26\ An additional factor that 
handicaps our consideration of exposure levels associated with these 
findings is the appreciable uncertainty associated with our 
understanding of Pb biokinetics during this lifestage (ISA, sections 
3.2, 3.3, and 4.8.6). The evidence newly available for Pb relationships 
with cardiovascular effects in adults include some studies with 
somewhat lower blood Pb levels than in the last review. The long 
exposure histories of these cohorts, as well as the generally higher Pb 
exposures of the past, complicate conclusions regarding exposure levels 
that may be eliciting observed effects (ISA, sections 4.4.2.4 and 
4.4.7).\27\ Accordingly, as discussed further below, we focus in this 
review, as in the last, on neurocognitive effects in young children.
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    \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).
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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

[[Page 292]]

evidence base for purposes of drawing causal conclusions with regard to 
Pb generally. The complexity of Pb exposure pathways and internal 
dosimetry, however, tends to limit the extent to which these types of 
studies inform our more specific understanding of the Pb exposure 
circumstances (e.g., timing within lifetime, duration, frequency and 
magnitude) eliciting the various effects.
    As at the time of the last review (and discussed more fully in 
section II.B.3 below), assessment of the full evidence base, including 
evidence newly available in this review, demonstrates that Pb exposure 
prenatally and also in early childhood can contribute to neurocognitive 
impacts in childhood, with evidence also indicating the potential for 
effects persisting into adulthood (ISA, sections 1.9.4, 1.9.5, and 
1.10). In addition to the observed associations of prenatal and 
childhood blood Pb with effects at various ages in childhood, there is 
also evidence of Pb-related cognitive function effects in non-
occupationally exposed adults (ISA, section 4.3.11). This includes 
evidence of associations of such effects in adulthood with childhood 
blood Pb levels and in other cohorts, with concurrent (adult) blood Pb 
levels (ISA, sections 4.3.2.1, 4.3.2.7 and 4.3.11). As the studies 
finding associations of adult effects with childhood blood Pb levels 
did not examine adult blood Pb levels, the relative influence of adult 
Pb exposure cannot be ascertained, and a corresponding lack of early 
life exposure or biomarker measurements for the latter studies limits 
our ability to draw conclusions regarding specific Pb exposure 
circumstances eliciting the observed effects (4.3.11). Findings of 
stronger associations for adult neurocognitive effects with bone Pb, 
however, indicate the role of historical or cumulative exposures for 
those effects (ISA, section 4.3).
    A critical aspect of much of the epidemiological evidence, 
particularly studies focused on adults (and older children) in the U.S. 
today, is the backdrop of generally declining environmental Pb exposure 
(from higher exposures during their younger years) that is common 
across many study populations (ISA, p. 4-2).\28\ An additional factor 
complicating the interpretation of health effect associations with 
blood Pb measurements in older children and younger adults is the 
common behaviors of younger children (e.g., hand-to-mouth contact) that 
generally contribute to relatively greater exposures earlier in life 
(ISA, sections 3.1.1, 4.2.1). Such exposure histories for adults and 
older children complicate our ability to draw conclusions regarding 
critical time periods and lifestages for Pb exposures eliciting the 
effects for which associations with Pb biomarkers have been observed in 
these populations (e.g., ISA, section 1.9.6).\29\ Thus, our confidence 
is greatest in the role of early childhood exposure in contributing to 
Pb-related neurocognitive effects that have been associated with blood 
Pb levels in young children. This is due, in part, to the relatively 
short exposure histories of young children (ISA, sections 1.9.4, 1.9.6 
and 4.3.11).
---------------------------------------------------------------------------

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

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

    \30\ In the collective body of evidence of nervous system 
effects in children, it is difficult to distinguish exposure in 
later lifestages (e.g., school age) and its associated risk from 
risks resulting from exposure in prenatal and early childhood (ISA, 
section 4.3.11). While early childhood is recognized as a time of 
increased susceptibility, a difficulty in identifying a discrete 
period of susceptibility from epidemiological studies has been that 
the period of peak exposure, reflected in peak blood Pb levels, is 
around 18-27 months when hand-to-mouth activity is at its maximum 
(ISA, section 3.4.1 and 5.2.1.1; 2006 CD, p. 6-60). The task is 
additionally complicated by the role of maternal exposure history in 
contributing Pb to the developing fetus (ISA, section 3.2.2.4.).
---------------------------------------------------------------------------

    As in the last review, there is also substantial evidence of other 
neurobehavioral effects in children, including effects on externalizing 
behaviors (reduced attention span, increased impulsivity, 
hyperactivity, and conduct disorders) and on internalizing behaviors. 
The evidence for many of these endpoints, as with neurocognitive 
effects, also includes associations of effects at various ages in 
childhood and for some effects, into adulthood, with blood Pb levels 
reflective of several different lifestages (e.g., prenatal and several 
different ages in childhood) (ISA, sections 4.3.3 and 4.3.4). There is 
similar or relatively less extensive evidence to inform our 
understanding of such effects associated with specific time periods of 
exposure at specific lifestages than is the case for effects on 
cognitive function.
    Across the range of Pb effects on physiological systems and 
processes other than the nervous system, the evidence base for blood 
pressure and hypertension is somewhat more informative with regard to 
the circumstances of Pb exposure eliciting the observed effects than 
are the evidence bases for many other effects. In the case of Pb-
induced increases in blood pressure, the evidence indicates an 
importance of long-term exposure (ISA, sections 1.6.2 and 4.4.7.1). The 
greater uncertainties regarding the time, duration and magnitude of 
exposure contributing to these observed health effects complicate 
identification of sensitive lifestages and associated exposure patterns 
that might be compared with our understanding of the sensitivity of 
young children to neurocognitive impacts of Pb. Thus, while augmenting 
the evidence base on these additional endpoints, the newly available 
evidence does not lead us to identify a health endpoint expected to be 
more sensitive to Pb exposure than neurocognitive endpoints in 
children, leading us to continue to conclude that the appropriate 
primary focus for our review is on neurocognitive endpoints in 
children.

[[Page 293]]

    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 4.3.2.1 and 4.3.2.2; Bellinger and Needleman, 2003; 
Canfield et al., 2003; Lanphear et al., 2005; Tellez-Rojo et al., 2006; 
Bellinger, 2008; Canfield, 2008; Tellez-Rojo, 2008; Kirrane and Patel, 
2014).\32\ Newly 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 
4.3.2.5; Chandramouli et al., 2009; Miranda et al., 2009). One of these 
two studies, which represented integer blood Pb levels as categorical 
variables, indicated a small effect on end-of-grade reading score of 
blood Pb levels as low as 2 [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 
levels in this study, we note that blood Pb levels in children aged 8-
11 are generally lower than those in pre-school children, for reasons 
related to behavioral and other factors (ISA, sections 3.3.5, 3.4.1 and 
5.2.1.1). It is likely that the blood Pb levels of this study group at 
earlier ages, e.g., prior to school entry, were higher and the 
available information does not provide a basis to judge whether the 
blood Pb levels in this study represent lower exposure levels than 
those experienced by the younger study groups. In still older children, 
a large cross-sectional investigation of blood Pb association with 
effects on memory and learning that was available in the last review 
was focused on children aged 6-16 years, born during 1972-1988, with a 
mean blood Pb of 1.9 [mu]g/dL (Lanphear et al., 2000). A study newly 
available in this review, focused on a subset of the earlier study 
cohort (ages 12-16, born during 1975-1982), also reports a significant 
negative association of blood Pb with learning and memory test results 
with mean blood Pb levels of approximately 2 [mu]g/dL (ISA, section 
4.3.2.3; Lanphear et al., 2000; Krieg et al., 2010). In considering 
these study findings with regard to the question of exposure levels 
eliciting effects, we recognize, however, that blood Pb levels are, in 
general, lower among teenagers than young children and also that, for 
these subjects specifically, the magnitude of blood Pb levels during 
the earlier childhood (e.g., pre-school ages) was much higher. For 
example, the mean blood Pb levels for the 1-5 year old age group in the 
NHANES 1976-80 sample was 15 [mu]g/dL, declining to 3.6 [mu]g/dL in the 
NHANES 1988-1991 sample (Pirkle et al., 1994; ISA, section 3.4.1). In 
summary, the available information is for population groups of ages for 
which the NHANES samples indicate exposure levels were higher earlier 
in childhood. Thus, in light of the NHANES information, although the

[[Page 294]]

blood Pb levels in the studies of cognitive effects in older child 
population groups are lower (at the time of the study) than the younger 
child study levels, the studies of older children do not provide a 
basis for concluding a role for lower Pb exposure levels than those 
experienced by the younger study groups.
---------------------------------------------------------------------------

    \33\ Limitations of this study included a lack of consideration 
of potential confounding by parental caregiving quality or IQ (ISA, 
Table 4-3).
---------------------------------------------------------------------------

    With regard to other nervous system effects in children, the 
evidence base at lower blood Pb levels is somewhat extended since the 
last review with regard to the evidence on Pb and effects on 
externalizing behaviors, such as attention, impulsivity, hyperactivity 
and conduct disorders (ISA, section 4.3.3 and Table 4-17). Several 
newly available studies investigating the role of blood Pb levels in 
older children (primary school age and older) have reported significant 
associations for these effects with concurrent blood Pb levels, with 
mean levels generally on the order of 5 [mu]g/dL or higher (ISA, 
section 4.3.3). One exception is the newly available cross-sectional, 
categorical analysis of the NHANES 2001-2004 sample of children aged 8-
15 years, which found higher prevalence of conduct disorder in the 
subgroup with concurrent blood Pb levels of 0.8-1.0 [mu]g/dL as 
compared to the dL group (ISA, section 4.3.4 and Table 4-
12). As noted above, we recognize that many of these children, born 
between 1986 and 1996, are likely to have had much higher Pb exposures 
(and associated blood Pb levels) in their earlier years than those 
commonly experienced by young children today, thus making this study 
relatively uninformative with regard to evidence of effects associated 
with lower exposure levels than provided by evidence previously 
available.
    In summary, our conclusions regarding exposure levels at which Pb 
health effects occur, particularly with regard to such levels that 
might be common in the U.S. today, are complicated now, as in the last 
review, by several factors. These factors include the scarcity of 
information in epidemiological studies on cohort exposure histories, as 
well as by the backdrop of higher past exposure levels which frame the 
history of most, if not all, older study cohorts. Recognizing the 
complexity, as well as the potential role of higher exposure levels in 
the past, we continue to focus our consideration of this question on 
the evidence of effects in young children for which our understanding 
of exposure history is less uncertain.\34\ Within this evidence base, 
we recognize the lowest study group blood Pb levels to be associated 
with effects on cognitive function measures, indicating that to be the 
most sensitive endpoint. As described above, the evidence available in 
this review is generally consistent with that available in the last 
review with regard to blood Pb levels at which such effects had been 
reported (ISA, section 4.3.2; 2006 CD, section 8.4.2.1; 73 FR 66976-
66979, November 12, 2008). As blood Pb levels are a reflection of 
exposure history, particularly in early childhood (ISA, section 3.3.2), 
we conclude, by extension, that the currently available evidence does 
not indicate Pb effects at exposure levels appreciably lower than 
recognized in the last review.
---------------------------------------------------------------------------

    \34\ In focusing on effects associated with blood Pb levels in 
early childhood, however, we additionally recognize the evidence 
across categories of effects that relate to blood Pb levels in older 
child study groups (for which early childhood exposure may have had 
an influence) which provides additional support to an emphasis on 
nervous system effects (ISA, sections 4.3, 4.4, 4.5, 4.6, 4.7, 4.8).
---------------------------------------------------------------------------

    We additionally note that, as in the last review, a threshold blood 
Pb level with which nervous system effects, and specifically cognitive 
effects, occur in young children cannot be discerned from the currently 
available studies (ISA, sections 1.9.3 and 4.3.12). Epidemiological 
analyses have reported blood Pb associations with cognitive effects 
(FSIQ or BSID MDI \35\) for young child population subgroups (age 5 
years or younger) with individual blood Pb measurements as low as 
approximately 1 [mu]g/dL and mean concentrations as low as 2.9 to 3.8 
[mu]g/dL (ISA, section 4.3.12; Bellinger and Needleman, 2003; 
Bellinger, 2008; Canfield et al., 2003; Canfield, 2008; Tellez-Rojo et 
al., 2006; Tellez-Rojo, 2008). As concluded in the ISA, however, ``the 
current evidence does not preclude the possibility of a threshold for 
neurodevelopmental effects in children existing with lower blood levels 
than those currently examined'' (ISA, section 4.3.13).
---------------------------------------------------------------------------

    \35\ The Bayley Scales of Infant Development, Mental Development 
Index is a well-standardized and widely used assessment measure of 
infant cognitive development. Scores earlier than 24 months are not 
necessarily strongly correlated with later FSIQ scores in children 
with normal development (ISA, section 4.3.15.1).
---------------------------------------------------------------------------

    Important uncertainties associated with the evidence of effects at 
low exposure levels are similar to those recognized in the last review, 
including the shape of the concentration-response relationship for 
effects on neurocognitive function at low blood Pb levels in today's 
young children. Also of note is our interpretation of associations 
between blood Pb levels and effects in epidemiological studies, with 
which we recognize uncertainty with regard to the specific exposure 
circumstances (timing, duration, magnitude and frequency) that have 
elicited the observed effects, as well as uncertainties in relating 
ambient air concentrations (and associated air-related exposures) to 
blood Pb levels in early childhood, as discussed in section II.B.2 
above. We additionally recognize uncertainties associated with 
conclusions drawn with regard to the nature of the epidemiological 
associations with blood Pb (e.g., ISA, section 4.3.13), but note that, 
based on consideration of the full body of evidence for neurocognitive 
effects, the EPA has determined a causal relationship to exist between 
relevant blood Pb levels and neurocognitive impacts in children (ISA, 
section 4.3.15.1).
    Based primarily on studies of FSIQ, the assessment of the currently 
available studies, as was the case in the last review, continues to 
recognize a nonlinear relationship between blood Pb and effects on 
cognitive function, with a greater incremental effect (greater slope) 
at lower relative to higher blood Pb levels within the range thus far 
studied, extending from well above 10 [mu]g/dL to below 5 [mu]g/dL 
(ISA, section 4.3.12). This was supported by the evidence available in 
the last review, including the analysis of the large pooled 
international dataset comprised of blood Pb measurements and IQ test 
results from seven prospective cohorts (Lanphear et al., 2005; 
Rothenberg and Rothenberg, 2005; ISA, section 4.3.12). The blood Pb 
measurements in this pooled dataset that were concurrent with the IQ 
tests ranged from 2.5 [mu]g/dL to 33.2 [mu]g/dL. The study by Lanphear 
et al. (2005) additionally presented analyses that stratified the 
dataset based on peak blood Pb levels (e.g., with cutpoints of 7.5 
[mu]g/dL and 10 [mu]g/dL peak blood Pb) and found that the coefficients 
from linear models of the association for IQ with concurrent blood Pb 
were higher in the lower peak blood Pb level subsets than the higher 
groups (ISA, section 4.3.12; Lanphear et al., 2005).
    We note that since the completion of the ISA, two errors have been 
identified with the pooled dataset analyzed by Lanphear et al. (2005) 
(Kirrane and Patel, 2014). A recent publication and the EPA have 
separately recalculated the statistics and mathematical model 
parameters of Lanphear et al. (2005) using the corrected pooled dataset 
(see Kirrane and Patel, 2014). While the magnitude of the loglinear and 
linear regression coefficients are modified slightly based on the 
corrections, the conclusions drawn from these coefficients, including 
the finding of a steeper slope at lower (as compared to

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higher) blood Pb concentrations, are not affected (Kirrane and Patel, 
2014).
    In other publications, stratified analyses of several individual 
cohorts also observed higher coefficients for blood Pb relationships 
with measures of neurocognitive function in lower as compared to higher 
blood Pb subgroups (ISA, section 4.3.12; Canfield et al., 2003; 
Bellinger and Needleman, 2003; Kordas et al., 2006; Tellez-Rojo et al., 
2006). Of these subgroup analyses, those involving the lowest mean 
blood Pb levels and closest to the current mean for U.S. preschool 
children are listed in Table 1 (drawn from Table 3 of the 2008 final 
rulemaking notice [73 FR 67003, November 12, 2008], and Kirrane and 
Patel, 2014).\36\ These analyses were important inputs for the 
evidence-based, air-related IQ loss framework which informed decisions 
on a revised standard in the last review (73 FR 67005, November 12, 
2008), discussed in section II.A.1 above. As the framework focused on 
the median of the four slopes in Table 1, the change to the one from 
Lanphear et al. (2005) based on the recent recalculation described 
above has no impact on conclusions drawn from the framework.
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    \36\ One of these four is from the analysis of the lowest blood 
Pb subset of the pooled international study by Lanphear et al. 
(2005). The nonlinear model developed from the full pooled dataset 
is the basis of the C-R functions used in the 2007 REA, in which 
risk was estimated over a large range of blood Pb levels (PA, 
section 3.4.3.3). Given the narrower focus of the evidence-based 
framework on IQ response at the end of studied blood Pb levels 
(closer to U.S. mean level), the C-R functions in Table 1 are from 
linear analyses (each from separate publications) for the study 
group subsets with blood Pb levels closest to mean for children in 
the U.S. today.

 Table 1--Summary of Quantitative Relationships of IQ and Blood Pb for Analyses With Blood Pb Levels Closest to
                                    Those of Young Children in the U.S. Today
----------------------------------------------------------------------------------------------------------------
                  Blood Pb levels ([mu]g/dL)                                                      Average linear
---------------------------------------------------------------                                    slope \A\ (IQ
                                                  Range (min-            Study/analysis           \B\ points per
                Geometric mean                       max)                                            [mu]g/dL)
----------------------------------------------------------------------------------------------------------------
2.9...........................................         0.8-4.9  Tellez-Rojo et al. (2006)\B\,              -1.71
                                                                 subgroup w. concurrent blood Pb
                                                                 dL.
3.3...........................................         0.9-7.4  Lanphear et al. (2005)\C\,                 -2.53
                                                                 subgroup w. peak blood Pb dL.
3.32..........................................         0.5-8.4  Canfield et al. (2003) \C\ \D\,            -1.79
                                                                 subgroup w. peak blood Pb dL.
3.8...........................................           1-9.3  Bellinger and Needleman (2003)             -1.56
                                                                 \C\ \E\, subgroup w. peak blood
                                                                 Pb dL.
    Median value..............................  ..............  ................................           -1.75
----------------------------------------------------------------------------------------------------------------
A--Average linear slope estimates here are generally for relationship with IQ assessed concurrently with blood
  Pb measurement. As exceptions, Bellinger & Needleman (2003) slope is relationship for 10 year old IQ with
  blood Pb levels at 24 months, and the data for Boston cohort included in Lanphear et al. (2005) slope are
  relationship for 10 year old IQ with blood Pb levels at 5 years.
B--The slope for Tellez-Rojo et al. (2006) is for BSID (MDI), a measure of cognitive development appropriate to
  study population age (24-mos). The blood Pb levels for this subgroup are from Tellez-Rojo (2008).
C--The Lanphear et al. (2005) pooled international study also includes blood Pb data from the Rochester and
  Boston cohorts, although for different ages (6 and 5 years, respectively) than the ages analyzed in Canfield
  et al. (2003) and Bellinger and Needleman (2003). Thus, the ages at the blood Pb measurements used in
  derivation of the linear slope for the Lanphear et al. (2005) subgroup shown here are 5 to 7 years. The blood
  Pb levels and coefficient presented here for Lanphear et al. (2005) study group reflect the recalculation
  using the corrected pooled dataset (Kirrane and Patel, 2014).
D--Blood Pb levels for this subgroup are from Canfield (2008).
E--Blood Pb levels for this subgroup are from Bellinger (2008).

    Several studies newly available in the current review have, in all 
but one instance, also found a nonlinear blood Pb-cognitive function 
relationship in nonparametric regression analyses of the cohort blood 
Pb levels analyzed (ISA, section 4.3.12). These studies, however, used 
statistical approaches that did not produce quantitative results for 
each blood Pb group (ISA, section 4.3.12). Thus, newly available 
studies have not extended the range of observation for quantitative 
estimates of this relationship to lower blood Pb levels than those of 
the previous review. The ISA further notes that the potential for 
nonlinearity has not been examined in detail within a lower, narrower 
range of blood Pb levels than those of the full cohorts thus far 
studied in the currently available evidence base (ISA, section 4.3.12). 
Such an observation in the last review supported the consideration of 
linear slopes with regard to blood Pb levels at and below those 
represented in Table 1. In summary, the newly available evidence does 
not substantively alter our understanding of the C-R relationship 
(including quantitative aspects) for neurocognitive impact, such as IQ 
with blood Pb in young children.
4. At-Risk Populations
    In this section, we use the term ``at-risk populations'' \37\ to 
recognize populations that have a greater likelihood of experiencing 
Pb-related health effects, i.e., groups with characteristics that 
contribute to an increased risk of Pb-related health effects. These 
populations are also sometimes referred to as sensitive groups (as in 
section I.A above). In identifying factors that increase risk of Pb-
related health effects, the EPA has considered evidence regarding 
factors contributing to increased susceptibility, generally including 
physiological or intrinsic factors contributing to a greater response 
for the same exposure, and those contributing to increased exposure, 
including that resulting from behavior leading to increased contact 
with contaminated media (ISA, Chapter 5). Physiological risk factors 
include both conditions contributing to a group's increased risk of 
effects at a given blood Pb level, and those that contribute to blood 
Pb levels higher than those otherwise associated with a

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given Pb exposure (e.g., ISA, sections 5.3 and 5.1, respectively).
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    \37\ In the context of ``at-risk populations,'' the term 
``population'' refers to persons having one or more qualities or 
characteristics including, for example, a specific pre-existing 
illness or a specific age or lifestage, with lifestage referring to 
a distinguishable time frame in an individual's life characterized 
by unique and relatively stable behavioral and/or physiological 
characteristics that are associated with development and growth.
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    The information newly available in this review has not 
substantially altered our previous understanding of at-risk populations 
for Pb in ambient air. As in the last review, the factor most 
prominently recognized to contribute to increased risk of Pb effects is 
childhood (ISA, section 1.9.6). As noted in section II.B.2 above, 
although the specific ages or lifestages of greatest susceptibility 
\38\ or risk have not been established (e.g., ISA, section 4.3.11), the 
at-risk status of young children to the neurodevelopmental effects of 
Pb is well recognized (e.g., ISA, sections 1.9.6, 4.3, 5.2.1, 5.3.1, 
and 5.4). The evidence indicates that prenatal blood Pb levels are 
associated with nervous system effects, including mental development in 
very young children and can also be associated with cognitive 
decrements in older children (ISA, section 4.3). Additionally, the 
coincidence during early childhood of behaviors that increase exposure, 
such as hand-to-mouth contact by which children transfer Pb in settled 
particles to their mouths, and the development of the nervous system 
also contributes increased risk during this time (ISA, sections 3.7.1, 
4.3.2.6, 5.2.1.1, 5.3.1.1 and 5.4). Collectively, however, the evidence 
indicates both the susceptibility of the developing fetus and early 
postnatal years, as well as the potential for continued susceptibility 
through childhood as the human central nervous system continues to 
mature and be vulnerable to neurotoxicants (ISA, sections 1.9.5 and 
4.3.15; 2006 CD, section 6.2.12). As discussed in section II.B.2 above, 
while uncertainties remain with regard to the role of Pb exposures 
during a particular age of life in eliciting nervous system effects, 
such as cognitive function decrements, the full evidence base continues 
to indicate prenatal and early childhood lifestages as periods of 
increased Pb-related risk (ISA, sections 4.3.11 and 4.3.15).
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    \38\ As noted in the ISA, ``in most instances, `susceptibility' 
refers to biological or intrinsic factors (e.g., age and sex) while 
`vulnerability' refers to nonbiological or extrinsic factors (e.g., 
socioeconomic status [SES])'' and the terms ``at-risk'' and 
``sensitive'' populations have in various instances been used to 
encompass these concepts more generally (ISA, p. 5-1). In providing 
detail regarding factors contributing to an ``at-risk'' status in 
this section, we have used the other terms in particular instances, 
with our usage consistent with these common definitions.
---------------------------------------------------------------------------

    Several physiological factors increase the risk of Pb-related 
health effects by contributing to increased blood Pb levels over those 
otherwise associated with a given Pb exposure (ISA, sections 3.2, 3.3 
and 5.1). These include nutritional status, which plays a role in Pb 
absorption from the gastrointestinal tract (ISA, sections 3.2.1.2, 5.1, 
5.3.10 and 5.4). For example, diets deficient in iron, calcium or zinc 
can contribute to increased Pb absorption and associated higher blood 
Pb levels (ISA, sections 3.2.1.2, and 5.1). Evidence is suggestive of 
some genetic characteristics as potential risk factors, such as 
presence of the [delta]-aminolevulinic acid dehydratase-2 (ALAD-2) 
allele which has been indicated to increase blood Pb levels or Pb-
related risk of health effects in some studies (ISA, sections 3.3.2 and 
5.1).
    Risk factors based on increased exposure include spending time in 
proximity to sources of Pb to ambient air or other environmental media 
(e.g., large active metals industries or locations of historical Pb 
contamination) (ISA, sections 1.9.6, 3.7.1, 5.2.5 and 5.4). Residential 
factors associated with other sources of Pb exposure (e.g., leaded 
paint or plumbing with Pb pipes or solder) are another exposure-related 
risk factor (ISA, sections 3.7.1, 5.2.6 and 5.4). Additionally, some 
races or ethnicities have been associated with higher blood Pb levels, 
with differential exposure indicated in some cases as the cause (ISA, 
sections 5.2.3 and 5.4). Lower socioeconomic status (SES) has been 
associated with higher Pb exposure and higher blood Pb concentration, 
leading the ISA to conclude the evidence is suggestive for low SES as a 
risk factor (ISA, sections 5.3.16, 5.2.4 and 5.4). Although the 
differences in blood Pb levels between children of lower and higher 
income levels (as well as among some races or ethnicities) have 
lessened, blood Pb levels continue to be higher among lower-income 
children indicating higher exposure and/or greater influence of factors 
independent of exposure, such as nutritional factors (ISA, sections 
1.9.6, 5.2.1.1 and 5.4).
    In considering risk factors associated with increased Pb exposure 
or increased blood Pb levels, we note that the currently available 
evidence continues to support a nonlinear relationship between 
neurocognitive effects and blood Pb that indicates incrementally 
greater impacts at lower as compared to higher blood Pb levels (ISA, 
section 4.3.12), as described in section II.B.3 above. An important 
implication of this finding is that while children with higher blood Pb 
levels are at greater risk of Pb-related effects than children with 
lower blood Pb levels, on an incremental basis (e.g., per [micro]g/dL), 
the risk is greater for children at lower blood Pb levels. This was 
given particular attention in the last review of the Pb NAAQS, in which 
the standard was revised with consideration of the incremental impact 
of air-related Pb on young children in the U.S. and the recognition of 
greater impact for those children with lower absolute blood Pb levels 
(73 FR 67002, November 12, 2008). Such consideration included a focus 
on those C-R studies involving the lowest blood Pb levels, as described 
in section II.A.1 above.
    In summary, the information newly available in this review has not 
appreciably altered our understanding of human populations that are 
particularly sensitive to Pb exposures. In the current review, as at 
the time of the last review of the Pb NAAQS, we recognize young 
children as an important at-risk population, with sensitivity extending 
to prenatal exposures and into childhood development. Additional risk 
factors for increased blood Pb levels include deficiencies in dietary 
minerals (iron, calcium and zinc), some racial or ethnic 
backgrounds,\39\ and spending time in proximity to environmental 
sources of Pb or residing in older houses with Pb exposure related to 
paint or plumbing.\40\ The currently available evidence continues to 
additionally suggest a potential for increased risk associated with 
several other factors, including older adulthood,\41\ pre-existing 
disease

[[Page 297]]

(e.g., hypertension), variants for certain genes and increased stress 
(ISA, section 5.3.4). As discussed above, we recognize the sensitivity 
of the prenatal period and several lifestages of childhood to an array 
of neurocognitive and behavioral effects, and we particularly recognize 
young children as an important at-risk population in light of current 
environmental exposure levels. Age or lifestage was used to distinguish 
potential groups on which to focus in the last review in recognition of 
its role in exposure and susceptibility, and young children were the 
focus of the REA in consideration of the health effects evidence 
regarding endpoints of greatest public health concern and in 
recognition of effects on the developing nervous system as a sentinel 
endpoint for public health impacts of Pb. This identification continues 
to be supported by the evidence available in the current review.
---------------------------------------------------------------------------

    \39\ The ISA concludes that studies of race/ethnicity provide 
adequate evidence that race/ethnicity is an at-risk factor based on 
the higher exposure observed among non-white populations and some 
modification observed in studies of associations between Pb levels 
and some health effects, such as hypertension (ISA, section 6.4).
    \40\ The evidence for SES continues to indicate increased blood 
Pb levels in lower income children, although its role with regard to 
an increased health risk for the same blood Pb level is unclear and 
its role generally with regard to Pb-related risk is somewhat 
complicated. SES often serves as a marker term for one or a 
combination of unspecified or unknown environmental or behavioral 
variables. Further, it is independently associated with an adverse 
impact on neurocognitive development, and a few studies have 
examined SES as a potential modifier of the association of childhood 
Pb exposure with cognitive function with inconsistent findings 
regarding low SES as a potential risk factor. The ISA concludes the 
evidence for SES as a Pb risk factor is suggestive, based on the 
greater exposures or blood Pb levels in some low SES groups (ISA, 
section 5.4).
    \41\ The ISA identifies older adulthood as a lifestage of 
potentially greater risk of Pb-related health effects based 
primarily on the evidence of increases in blood Pb levels during 
this lifestage (ISA, sections 5.2.1.2, 5.3.1.2, and 5.4), as well as 
observed associations of some cardiovascular and nervous system 
effects with bone and blood Pb in older populations, with biological 
plausibility for the role of Pb provided by experimental animal 
studies (ISA, sections 4.3.5, 4.3.7 and 4.4). Exposure histories of 
older adult study populations, which included younger years during 
the time of leaded gasoline usage and other sources of Pb exposures 
which were more prevalent in the past than today, are likely 
contributors to their blood Pb levels (ISA, pp. lx-lxi; Figure 2-1 
and sections 2.5.2, 3.3.5 and 5.2.1.2).
---------------------------------------------------------------------------

5. Potential Impacts on Public Health
    There are several potential public health impacts associated with 
Pb exposure in the current U.S. population. In recognition of effects 
causally related to blood Pb levels somewhat near those most recently 
reported for today's population and for which the weight of the 
evidence is greatest, the potential public health impacts most 
prominently recognized in the ISA are population IQ impacts associated 
with childhood Pb exposure and prevalence of cardiovascular effects in 
adults (ISA, section 1.9.1). With regard to the latter category, as 
discussed above, the full body of evidence indicates a role of long-
term cumulative exposure, with uncertainty regarding the specific 
exposure circumstances contributing to the effects in the 
epidemiological studies of adult populations, for whom historical Pb 
exposures were likely much higher than exposures that commonly occur 
today (ISA, section 4.4). There is less uncertainty regarding the 
exposure patterns contributing to the blood Pb levels reported in 
studies of younger populations (ISA, sections 1.9.4 and 1.10). 
Accordingly, the discussion of public health implications relevant to 
this review is focused predominantly on nervous system effects, 
including IQ decrements, in children.
    The magnitude of a public health impact is dependent upon the type 
or severity of the effect, as well as the size of populations affected. 
Intelligence quotient is a well-established, widely recognized and 
rigorously standardized measure of neurocognitive function, as well as 
a global measure reflecting the integration of numerous processes (ISA, 
section 4.3.2; 2006 CD, sections 6.2.2 and 8.4.2). Examples of other 
measures of cognitive function negatively associated with Pb exposure 
include other measures of intelligence and cognitive development and 
measures of other cognitive abilities, such as learning, memory, and 
executive functions, as well as academic performance and achievement 
(ISA, section 4.3.2). Although some neurocognitive effects of Pb in 
children may be transient, some may persist into adulthood (ISA, 
section 1.9.5).\42\ We also note that deficits in neurodevelopment 
early in life may have lifetime consequences as ``[n]eurodevelopmental 
deficits measured in childhood may set affected children on 
trajectories more prone toward lower educational attainment and 
financial well-being'' (ISA, section 4.3.14). Thus, population groups 
for which neurodevelopment is affected by Pb exposure in early 
childhood are at risk of related impacts on their success later in 
life. Further, in considering population risk, the ISA notes that 
``[s]mall shifts in the population mean IQ can be highly significant 
from a public health perspective'' (ISA, p. xciii). For example, if Pb-
related decrements are manifested uniformly across the range of IQ 
scores in a population, ``a small shift in the population mean IQ may 
be significant from a public health perspective because such a shift 
could yield a larger proportion of individuals functioning in the low 
range of the IQ distribution, which is associated with increased risk 
of educational, vocational, and social failure'' as well as a decrease 
in the proportion with high IQ scores (ISA, section 1.9.1).
---------------------------------------------------------------------------

    \42\ The ISA states that the ``persistence of effects appears to 
depend on the duration and window of exposure as well as other 
factors that may affect an individual's ability to recover from an 
insult,'' with some evidence of greater recovery in children reared 
in households with more optimal caregiving characteristics and low 
concurrent blood Pb levels (ISA, p. 1-77; Bellinger et al., 1990).
---------------------------------------------------------------------------

    As summarized above, young children are the at-risk population that 
may be most at risk of health effects associated with exposure to Pb 
and children at greatest risk from air-related Pb are those children 
with highest air-related Pb exposure which we consider to be those 
living in areas of higher ambient air Pb concentrations. To inform our 
understanding of the extent of this population potentially at risk from 
air-related Pb, the PA includes two analyses. The first analysis is 
based on consideration of the available air Pb monitoring information. 
As the air quality data set available for the first analysis may not be 
inclusive of all of the newly sited monitors (as discussed in section 
2.2.1 of the PA) and there may be other areas with elevated Pb 
concentrations, a second analysis was performed in consideration of 
emissions estimates from the National Emissions Inventory (NEI), 
although with recognition of uncertainties associated with inferences 
drawn from such estimates with regard to ambient air Pb concentrations 
and exposures (PA, pp. 3-36 to 3-38).\43\
---------------------------------------------------------------------------

    \43\ Such uncertainties include those with regard to specific 
source characteristics and meteorology, not explicitly considered in 
the analysis. In light of such uncertainties, the PA interprets the 
emissions-based analysis to provide a bounding estimate below which 
the true value is expected to fall (PA, p. 3-37).
---------------------------------------------------------------------------

    The first PA analysis indicates that approximately one hundredth of 
one percent of the full population of children aged 5 or under in the 
U.S. reside within 0.5 km of monitors exceeding or within 10 percent of 
the level of the current standard (PA, section 2.2.2.2, pp. 3-36 to 3-
37, 4-25 and Table 3-4). In the second analysis, the size of young 
child populations residing in areas near large Pb sources was 
approximately four hundredths of one percent of the full U.S. 
population of children aged 5 years or younger (PA, pp. 3-37 to 3-38, 
4-25). The PA recognized uncertainties and potential limitations 
associated with the use of the emissions estimates in the second 
analysis to make inferences regarding ambient air Pb exposures, 
uncertainties both with regard to the accuracy of such estimates and 
also with regard to the role of specific source characteristics and 
meteorology, not explicitly considered here, in influencing ambient air 
Pb concentrations and contributing to substantial variation in air Pb 
concentrations at source locations (e.g., PA, Figure 2-11). 
Accordingly, while the second analysis is considered informative with 
regard to the potential prevalence of airborne Pb emissions and 
potential exposure of human populations, it is limited with regard to 
its ability to identify populations living in areas of elevated ambient 
air Pb concentrations. The PA interprets the two analyses together to 
indicate that well below one tenth of one percent of the full 
population of children aged 5 years or younger in the U.S. today live 
in areas with air Pb concentrations near or above the current standard, 
with the current monitoring data indicating the size of this population 
to be approximately one hundredth of a percent of the full population 
of children aged 5 or younger (PA, pp. 3-36 to 3-38, 4-25, 4-32).

[[Page 298]]

C. Blood Lead as a Biomarker of Exposure and Relationships With Air 
Lead

    Blood Pb is well established as a biomarker of Pb exposure and of 
internal dose, with relationships between air Pb concentrations and 
blood Pb concentrations informing consideration of the NAAQS for Pb 
since its initial establishment in 1978. Lead associated with inhaled 
particles may, depending on particle size and Pb solubility, be 
absorbed into the systemic circulation or transported with particles to 
the gastrointestinal tract (ISA, section 3.2.1.1), where its absorption 
is influenced by a range of factors (ISA, section 3.2.1.2). Lead in the 
blood stream is quickly distributed throughout the body (e.g., within 
days), available for exchange with the soft and skeletal tissues, the 
latter of which serves as the largest storage compartment (ISA, section 
3.2.2.2). Given the association with exposure and the relative ease of 
collection, blood Pb levels are extensively used as an index or 
biomarker of exposure by national and international health agencies, as 
well as in epidemiological and toxicological studies of Pb health 
effects and dose-response relationships (ISA, sections 3.3.2, 3.4.1, 
4.3, 4.4, 4.5, 4.6, 4.7, and 4.8). While bone Pb measurements are also 
used in epidemiological studies as an indicator of cumulative Pb 
exposure, blood Pb measurements remain the predominant, well-
established and well-characterized exposure approach.
    Since 1976, the CDC has been monitoring blood Pb levels nationally 
through the NHANES. This survey has documented the dramatic decline in 
mean blood Pb levels in all ages of the U.S. population that has 
occurred since the 1970s (PA, Figure 3-1), and that coincides with 
actions on leaded fuels, leaded paint, Pb in food packaging, and Pb-
containing plumbing materials that have reduced Pb exposure in the U.S. 
(ISA, section 3.4.1; Pirkle et al., 1994; Schwemberger et al., 2005). 
This decline has continued over the more recent past. For example, the 
2009-2010 geometric mean blood Pb level in U.S. children aged 1-5 years 
is 1.17 [mu]g/dL, as compared to 1.51 [mu]g/dL in 2007-2008 (ISA, 
section 3.4.1) and 1.8 [mu]g/dL in 2003-2004, the most recent data 
available at the time of the last review (73 FR 67002, November 12, 
2008). Somewhat less dramatic declines have been reported in the upper 
tails of the distribution and in different groups with higher blood Pb 
levels than the general child population (ISA, Figures 3-17 and 3-19).
    The blood Pb concentration in childhood (particularly early 
childhood) can more quickly (than in adulthood) reflect changes in 
total body burden (associated with the shorter exposure history) and 
can also reflect changes in recent exposures (ISA, section 3.3.5). The 
relationship of children's blood Pb to recent exposure may reflect 
their labile bone pool, with their rapid bone turnover in response to 
rapid childhood growth rates (ISA, section 3.3.5). The relatively 
smaller skeletal compartment of Pb in children (particularly very young 
children) compared to adults is subject to more rapid turnover. The 
distribution of Pb in the body is dynamic throughout life, with Pb in 
the body being exchanged between blood and bone and between blood and 
soft tissues (ISA, sections 3.3.5 and 3.2.2; 2006 CD, section 4.3.2). 
The rates of these exchanges vary with age, exposure and various 
physiological variables. For example, resorption of bone, which results 
in the mobilization of Pb from bone into the blood, is a somewhat rapid 
and ongoing process during childhood and a more gradual process in 
later adulthood (ISA, sections 3.2.2.2, 3.3.5 and 3.7.2; PA, pp. 3-2 to 
3-3).
    Lead in ambient air contributes to Pb in blood by multiple exposure 
pathways by both inhalation and ingestion exposure routes (ISA, section 
3.1.1). Multiple studies have demonstrated young children's blood Pb 
levels to reflect Pb exposures, including exposures to Pb in surface 
dust (e.g., Lanphear and Roghmann, 1997; Lanphear et al., 1998). These 
and studies of child populations near sources of air Pb emissions, such 
as metal smelters, have further demonstrated the effect of airborne Pb 
on interior dust and on blood Pb (ISA, sections 3.4.1, 3.5.1 and 3.5.3; 
Hilts, 2003; Gulson et al., 2004).
    As blood Pb is an integrated marker of aggregate Pb exposure across 
all pathways, the blood Pb C-R relationships described in 
epidemiological studies of Pb-exposed populations do not distinguish 
among different sources of Pb or pathways of Pb exposure (e.g., 
inhalation, ingestion of indoor dust, ingestion of dust containing 
leaded paint). Thus, our interpretation of the health effects evidence 
for purposes of this review necessitates characterization of the 
relationships between Pb from those sources and pathways of interest in 
this review (i.e., those related to Pb emitted into the air) and blood 
Pb.
    The evidence for air-to-blood relationships derives from analyses 
of datasets for populations residing in areas with differing air Pb 
concentrations, including datasets for circumstances in which blood Pb 
levels have changed in response to changes in air Pb. The control for 
variables other than air Pb that can affect blood Pb varies across 
these analyses. At the conclusion of the last review in 2008, the EPA 
interpreted the evidence as providing support for use (in informing the 
Administrator's decision on standard level) of a range of air-to-blood 
ratios \44\ ``inclusive at the upper end of estimates on the order of 
1:10 and at the lower end on the order of 1:5'' (73 FR 67002, November 
12, 2008). This conclusion reflected consideration of the air-to-blood 
ratios presented in the 1986 CD \45\ and associated observations 
regarding factors contributing to variation in such ratios, ratios 
reported subsequently and ratios estimated based on modeling performed 
in the REA, as well as advice from CASAC (73 FR 66973-66975, 67001-
67002, November 12, 2008). The information available in this review, 
which is assessed in the ISA and largely, although not completely, 
comprises studies that were available in the last review, does not 
alter the primary scientific conclusions drawn in the last review 
regarding the relationships between Pb in ambient air and Pb in 
children's blood. The ratios summarized in the ISA in this review span 
a range generally consistent with the range concluded in 2008 (ISA, 
section 3.5.1).
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    \44\ The quantitative relationship between ambient air Pb and 
blood Pb, often termed a slope or ratio, describes the increase in 
blood Pb (in [mu]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 [mu]g/m\3\) and x 
representing blood Pb (in [mu]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). Slopes are presented as simply the value of x.
    \45\ The 2006 CD did not include an assessment of then-current 
evidence on air-to-blood ratios.
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    The evidence pertaining to the quantitative relationship between 
air Pb and children's blood Pb is now, as in the past, limited by the 
circumstances in which the data are collected. These estimates are 
generally developed from studies of populations in a variety of Pb 
exposure circumstances. Accordingly, there is significant variability 
in air-to-blood ratios among the different study populations exposed to 
Pb through different air-related exposure pathways and at different 
exposure levels. This variability in air-to-blood estimates can relate 
to the representation of air-related pathways and study populations, 
including, for example, relatively narrow age ranges for the population 
in order to reduce age-related variability in blood Pb, or including 
populations with narrowly specified dietary sources. It

[[Page 299]]

can relate to the study population exposure and blood Pb levels (ISA, 
section 3.7.4). It can also relate to the precision of air and blood 
measurements and of the study circumstances, such as with regard to 
spatial and temporal aspects. Additionally, in situations where 
exposure to nonair sources covaries with air-related exposures that are 
not accounted for in deriving ratio estimates, uncertainties may relate 
to the potential for confounding by nonair exposure covariance (ISA, 
section 3.5). Most of the studies assessed in the ISA and PA have 
reported ratios for which the relationship is linear, while a subset 
are derived from nonlinear models (PA, Table 3-1; ISA, section 3.7.4).
    As was noted in the last review, age is an important influence on 
the magnitude of air-to-blood ratio estimates derived. Ratios for 
children are generally higher than those for adults, and higher for 
young children than older children, perhaps due to behavioral 
differences between the age groups, as well as their shorter exposure 
history. Similarly, given the common pattern of higher blood Pb levels 
in pre-school-aged children than during the rest of childhood, related 
to behaviors that increase environmental exposures (e.g., hand-to-mouth 
activity), ratios would be expected to be highest in earlier childhood. 
Additionally, estimates of air-to-blood ratios that include air-related 
ingestion pathways in addition to the inhalation pathway are 
``necessarily higher,'' in terms of blood Pb response, than those 
estimates based on inhalation alone (1986 CD, p. 11-106). Thus, the 
extent to which studies account for the full set of air-related 
inhalation and ingestion exposure pathways affects the magnitude of the 
resultant air-to-blood estimates, such that including fewer pathways as 
``air-related'' yields lower ratios. Estimates of air-to-blood ratios 
can also be influenced by population characteristics that may influence 
blood Pb; accordingly, some analyses include adjustments.
    Given the recognition of young children as a key at-risk population 
in this review, as in the last (as discussed in section II.B.3 above), 
as well as the influence of age on blood Pb levels, we have considered 
the available studies in groups based on the extent of their inclusion 
of children younger than or barely school age (less than or equal to 5 
years of age). Among the first group of studies, focused exclusively on 
young children, only one study dates from the end of or after the 
phase-out of leaded gasoline usage (Hilts, 2003). This study reports 
changes in children's blood Pb levels associated with reduced Pb 
emissions and associated air concentrations near a Pb smelter in Canada 
(for children through age 5). Given the timing of this study, after the 
leaded gasoline phase-out, and its setting near a smelter, the ambient 
air Pb in this study may be somewhat more comparable to that near 
sources in the U.S. today than other studies discussed herein. The 
study authors report an air-to-blood ratio of 1:6.\46\ An EPA analysis 
of the air and blood data reported for 1996, 1999 and 2001 results in a 
ratio of 1:6.5, and an analysis focused only on the 1996 and 1999 data 
(pre- and post- the new technology) yields a ratio of 1:7 (ISA, section 
3.5.1; Hilts, 2003).\47\ The two other studies that focused on children 
of age 5 or younger analyzed variations in air Pb as a result of 
variations in leaded gasoline usage in Chicago, Illinois and reported 
somewhat higher ratios of 1:8 and 1:8.6 (Hayes et al., 1994; Schwartz 
and Pitcher, 1989). We note, however, the blood Pb concentrations in 
the two leaded gasoline studies are appreciably higher (a factor of two 
or more) than those in the study near the smelter (Hilts, 2003), and 
also than those commonly reported in the U.S. today.
---------------------------------------------------------------------------

    \46\ Sources of uncertainty include the role of factors other 
than ambient air Pb reduction in influencing decreases in blood Pb 
(ISA, section 3.5.1). The author cited remedial programs (e.g., 
community and home-based dust control and education) as potentially 
responsible for some of the blood Pb reduction seen during the study 
period (1997 to 2001), although the author notes that these programs 
were in place in 1992, suggesting they are unlikely to have 
contributed to the sudden drop in blood Pb levels occurring after 
1997 (Hilts, 2003). Other aspects with potential implications for 
ratios include the potential for children with lower blood Pb levels 
not to return for subsequent testing, and the age range of 6 to 36 
months in the 2001 blood screening compared to ages up to 60 months 
in earlier years of the study (Hilts, 2003).
    \47\ This study considered changes in ambient air Pb levels and 
associated blood Pb levels over a 5-year period which included 
closure of an older Pb smelter and subsequent opening of a newer 
facility in 1997 and a temporary (3-month) shutdown of all smelting 
activity in the summer of 2001. The author observed that the air-to-
blood ratio for children in the area over the full period was 
approximately 1:6. The author noted limitations in the dataset 
associated with exposures in the second time period, after the 
temporary shutdown of the facility in 2001, including sampling of a 
different age group at that time and a shorter time period (3 
months) at these lower ambient air Pb levels prior to collection of 
blood Pb levels. Consequently, the EPA calculated an alternate air-
to-blood Pb ratio based on ambient air Pb and blood Pb reductions in 
the first time period, after opening of the new facility in 1997 
(ISA, section 3.5.1).
---------------------------------------------------------------------------

    The second group of studies includes but is not limited to children 
less than or equal to 5 years of age. This group includes a complex 
statistical analysis and associated dataset for a cohort of children 
born in Mexico City from 1987 through 1992 (Schnaas et al., 2004). 
Although this study, which was not assessed in the last review, 
encompasses the period of leaded gasoline usage, it further informs our 
understanding of factors influencing the quantitative relationship 
between air Pb and children's blood Pb. Air-to-blood ratios developed 
from this study are influenced by a number of factors and appear to 
range from roughly 1:2 to 1:6, in addition to an estimate of 1:9 (ISA, 
section 3.5.1), although the latter is derived from a data set 
restricted to the latter years of the study when little change in air 
Pb concentration occurred, such that the role of air Pb may be more 
uncertain. Estimates associated with the developmental period of 
highest exposure (e.g., age 2 years) range up to approximately 1:6, 
illustrating the influence of age on the ratio (ISA, section 3.5.1). 
Also in the second group of studies are two much older studies of 
populations with age ranges extending well beyond 6 years. The first is 
the review and meta-analysis by Brunekreef (1984) using datasets 
available at the time for variously aged children as old as 18 years 
with identified air monitoring methods and reliable blood Pb data for 
18 locations in the U.S. and internationally.\48\ Two air-to-blood 
ratio estimates derived from this study based on log-log models both 
round to 1:5 (for air concentrations corresponding to the geometric 
means of the two sets of data pairs [1.5 and 0.54 [mu]g/m\3\]). A ratio 
on the order of 1:9 was derived based on the study by Schwartz and 
Pitcher (1989) of the relationship between U.S. NHANES II blood Pb 
levels for white subjects, aged 
dL) indicate blood Pb distributions in this age group much higher than 
those pertinent to similarly aged children in the U.S. today and the 
air-to-blood ratio

[[Page 300]]

estimate reported was 1:3.6 (Tripathi et al., 2001). The more recent 
German study by Ranft et al. (2008) analyzed data from a nearly 20-year 
period associated with the leaded gasoline phase-out, during which 
average blood Pb levels declined from 9 [micro]g/dL in 1983 (345 
children, average age of 9 years) to 3 [micro]g/dL in 2000 (162 
children, average of 6 years).\49\ Average air Pb concentration 
declined from 0.45 [micro]g/m\3\ to 0.06 [micro]g/m\3\ over the same 
period, with the largest reduction occurring between the first study 
year (derived from two monitoring sites for full study area) and the 
second study year, 1991, for which air concentrations were derived from 
a combination of dispersion modeling and the two monitoring sites.\50\ 
For a mean air Pb concentration of 0.1 [micro]g/m\3\, the study's 
multivariate loglinear regression model predicted air-to-blood ratios 
of 3.2 and 6.4 for ``background'' blood Pb concentrations of 1.5 and 3 
[micro]g/dL, respectively. In this study, background referred to Pb in 
blood from other sources; the blood Pb distribution over the study 
period, including levels when air Pb concentrations are lowest, 
indicates 3 [micro]g/dL may be the better estimate of background for 
this study population. Inclusion of soil Pb as a variable in the model 
may have contributed to an underestimation of the blood Pb-air Pb 
ratios for this study because some of the Pb in soil likely originated 
in air and the blood Pb-air Pb slope does not include the portion of 
the soil/dust Pb ingestion pathway that derives from air Pb. Using 
univariate linear, log-log and loglinear models on the median air and 
blood Pb concentrations reported for the 5 years included in this 
study, the ISA also derived air-to-blood ratio estimates for data from 
this study ranging from 9 to 17 (ISA, p. 3-126; Ranft et al., 2008, 
Table 2). Uncertainties related to this study's estimates include those 
related to the bulk of air concentration reduction occurring between 
the first two time points (1983 and 1991) and the difference among the 
year's air datasets (e.g., two data sources [air monitors] in 1983 and 
multiple geographical points from a combination of the monitors and 
modeling in subsequent years).
---------------------------------------------------------------------------

    \49\ Blood Pb measurements were available on a total of 843 
children across five time periods, in the first of which the average 
child age was 9 years while it was approximately 6 years in each of 
the latter years: 1983 (n=356), 1991 (n=147), 1994 (n=122), 1997 
(n=56), and 2000 (n=162) (Ranft et al., 2008).
    \50\ The 1983 air Pb concentrations were based on two monitoring 
stations, while a combination of dispersion modeling and monitoring 
data was used in the later years. Surface soil Pb measurements were 
from 2000-2001, but geo-matched to blood Pb measurements across full 
study period (Ranft et al., 2008).
---------------------------------------------------------------------------

    In this review, as in the 2008 Pb NAAQS review, in addition to 
considering the evidence presented in the published literature and that 
reviewed in the 1986 CD, we also consider air-to-blood ratios derived 
from the exposure assessment (PA, p. 3-14; 73 FR 66974, November 12, 
2008; 2007 REA, section 5.2.5.2). In the exposure assessment 
(summarized in section II.D below), current modeling tools and 
information on children's activity patterns, behavior and physiology 
were used to estimate blood Pb levels associated with multimedia and 
multipathway Pb exposure. The results from the various case studies 
assessed, with consideration of the context in which they were derived 
(e.g., the extent to which the range of air-related pathways was 
simulated, and the limitations associated with those simulations), and 
the multiple sources of uncertainty are also informative to our 
understanding of air-to-blood ratios. Estimates of air-to-blood ratios 
for the two REA case studies that represent localized population 
exposures exhibited an increasing trend across air quality scenarios 
representing decreasing air concentrations. For example, across the 
alternative standard levels assessed, which ranged from a calendar 
quarter average of 1.5 [micro]g/m\3\ down to a monthly average of 0.02 
[micro]g/m\3\, the ratios ranged from 1:2 to 1:9 for the generalized 
(local) urban case study, with a similar trend, although of generally 
higher ratio, for the primary smelter case study subarea. This pattern 
of model-derived ratios is generally consistent with the range of 
ratios obtained from the literature, briefly discussed above. We 
continue to recognize a number of sources of uncertainty associated 
with these model-derived ratios which may contribute to high or low 
biases (as discussed further in section 3.1 of the PA).
    The evidence on the quantitative relationship between air Pb and 
air-related Pb in blood is now, as in the past, limited by the 
circumstances (such as those related to Pb exposure) in which the data 
were collected. Previous reviews have recognized the significant 
variability in air-to-blood ratios for different populations exposed to 
Pb through different air-related exposure pathways and at different air 
and blood levels, with the 1986 CD noting that ratios derived from 
studies involving the higher blood and air Pb levels pertaining to 
occupationally exposed workers are generally smaller than ratios from 
studies involving lower blood and air Pb levels (ISA, p. 3-132; 1986 
CD, p. 11-99). Consistent with this observation, slopes in the range of 
3 to 5 were estimated for child population datasets assessed in the 
1986 CD (ISA, p. 3-132; 1986 CD p. 11-100; Brunekreef, 1984). 
Additional studies considered in the last review and those assessed in 
the ISA provide evidence of ratios above this older range (ISA, p. 3-
133). For example, a ratio of 1:6.5-1:7 is indicated by the study by 
Hilts (2003), one of the few studies that evaluate the air Pb-blood Pb 
relationship in conditions that are closer to the current state in the 
U.S. (ISA, p. 3-132). We additionally note the variety of factors 
identified in the ISA that may potentially affect estimates of various 
ratios (including potentially coincident reductions in nonair Pb 
sources during the course of the studies), and for which a lack of 
complete information may preclude any adjustment of estimates to 
account for their role (ISA, section 3.5).
    In summary, as at the time of the last review of the NAAQS for Pb, 
the currently available evidence includes estimates of air-to-blood 
ratios, both empirical and model-derived, with associated limitations 
and related uncertainties. These limitations and uncertainties, which 
are summarized here and also noted in the ISA, usually include 
uncertainty associated with reductions in other Pb sources during the 
study period. The limited amount of new information available in this 
review has not appreciably altered the scientific conclusions reached 
in the last review regarding relationships between Pb in ambient air 
and Pb in children's blood or with regard to the range of ratios. The 
currently available evidence continues to indicate ratios relevant to 
the population of young children in the U.S. today, reflecting multiple 
air-related pathways in addition to inhalation, to be generally 
consistent with the approximate range of 1:5 to 1:10 given particular 
attention in the 2008 NAAQS decision, including the ``generally central 
estimate'' of 1:7 (73 FR 67002, 67004, November 12, 2008; ISA, pp. 3-
132 to 3-133).

D. Summary of Risk and Exposure Assessment Information

    The risk information available for this review and summarized here 
is based primarily on the exposure and risk assessment developed in the 
last review of the Pb NAAQS, described in the 2007 REA, the 2007 Staff 
Paper and the 2008 notice of final decision (USEPA, 2007a; USEPA, 
2007b; 73 FR 66964, November 12, 2008), as considered in the context of 
the evidence newly available in this review (PA, section 3.4). As 
described in

[[Page 301]]

the REA Planning Document, careful consideration of the information 
newly available in this review, with regard to designing and 
implementing a full REA for this review, led to the conclusion that 
performance of a new REA for this review was not warranted. We did not 
find the information newly available in this review to provide the 
means by which to develop an updated or enhanced risk model that would 
substantially improve the utility of risk estimates in informing the 
current Pb NAAQS review (REA Planning Document, section 2.3). Based on 
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).\51\ Accordingly, the risk/
exposure information considered in this review is drawn primarily from 
the 2007 REA, augmented by a limited new computation for one case study 
focused on risk associated with the current standard, as described 
below (PA, section 3.4 and Appendix 3A).
---------------------------------------------------------------------------

    \51\ In their review of the draft PA, the CASAC Pb Review Panel 
reinforced their concurrence with the EPA's decision not to develop 
a new REA (Frey, 2013).
---------------------------------------------------------------------------

1. Overview
    The focus for the risk assessment and associated estimates is on Pb 
derived from sources emitting Pb to ambient air. As discussed in 
section I.D above, the multimedia and persistent nature of Pb, the role 
of multiple exposure pathways, and the contributions of nonair sources 
of Pb to human exposure media all present challenges and contribute 
significant additional complexity to the health risk assessment that 
goes far beyond the situation for similar assessments typically 
performed for other NAAQS pollutants (e.g., that focus only on the 
inhalation pathway). The conceptual model that informed planning for 
the 2007 REA identified sources, pathways, routes, exposed populations, 
and health endpoints, focusing on those aspects of Pb exposure most 
relevant to the review, while also recognizing the role of Pb exposure 
pathways unrelated to Pb in ambient air (2007 REA, section 2.1). 
Limitations in the available data and models affected our 
characterization of the various complexities associated with exposure 
to ambient air Pb. As a result, the assessment included a number of 
simplifying assumptions in a number of areas and the estimates of air-
related Pb risk produced are approximate and are characterized by upper 
and lower bounds.
    As recognized in I.D above, sources of human Pb exposure include 
current and historical air emissions sources, as well as miscellaneous 
nonair sources, which can contribute to multiple exposure media and 
associated pathways (e.g., inhalation of ambient air, ingestion of 
indoor dust, outdoor soil/dust and diet or drinking water). In addition 
to airborne emissions (recent or those in the past), sources of Pb to 
these pathways also include old leaded paint, including Pb mobilized 
indoors during renovation/repair activities, and contaminated soils. 
Lead in diet and drinking water may have air pathway-related 
contributions as well as contributions from nonair sources (e.g., Pb 
solder on water distribution pipes and Pb in materials used in food 
processing). Limitations in our data and modeling tools handicapped our 
ability to fully separate the nonair contributions to Pb exposure from 
estimates of air-related Pb exposure and risk. As a result, we have 
developed bounds within which we estimate air-related Pb risk to fall. 
The lower bound is based on a combination of pathway-specific estimates 
that do not completely represent all air-related pathways, while the 
upper bound is based on a combination of pathway-specific estimates 
that includes pathways that are not air-related but the separating out 
of which is precluded by modeling and data limitations.
    Inclusion of exposure populations, exposure/dose metric, health 
effects endpoint and risk metric in the 2007 REA were based on 
consideration of the then-currently available evidence as assessed in 
detail in the 2006 CD. As discussed in the REA Planning Document 
(USEPA, 2011b), these selections continue to be supported by the 
evidence now available in this review as described in the ISA. The REA 
focused on risk to the central nervous system in childhood as the most 
sensitive effect that could be quantitatively assessed, with decrement 
in IQ used as the risk metric. Exposure and biokinetic modeling was 
used to estimate blood Pb concentrations in children exposed to Pb up 
to age 7 years.\52\ This focus reflected the evidence for young 
children with regard to air-related exposure pathways and 
susceptibility to Pb health impacts (e.g., ISA, sections 3.1.1, 4.3, 
5.2.1.1, 5.3.1.1, and 5.4). For example, the hand-to-mouth activity of 
young children contributes to their Pb exposure (i.e., incidental soil 
and indoor dust ingestion) and ambient air-related Pb has been shown to 
contribute to Pb in outdoor soil and indoor house dust (ISA, sections 
3.1.1 and 3.4.1; 2006 CD, section 3.2.3).
---------------------------------------------------------------------------

    \52\ The pathways represented in this modeling included 
childhood inhalation and ingestion pathways, as well as maternal 
contributions to newborn body burden (2007 REA, Appendix H, Exhibit 
H-6).
---------------------------------------------------------------------------

    The 2007 REA relied on a case study approach to provide estimates 
that inform our understanding of air-related exposure and risk in 
different types of air Pb exposure situations. Lead exposure and 
associated risk were estimated for multiple case studies that generally 
represent two types of residential population exposures to air-related 
Pb: (1) Location-specific urban populations of children with a broad 
range of air-related exposures, reflecting existence of urban 
concentration gradients; and (2) children residing in localized areas 
with air-related exposures representing air concentrations specifically 
reflecting the standard level being evaluated (see PA, Table 3-6). 
Thus, the two types of case studies differed with regard to the extent 
to which they represented population variability in air-related Pb 
exposure.
    In drawing on the 2007 REA for our purposes in this review, we 
focused on two case studies, one from each of these two categories: (1) 
The location-specific urban case study for Chicago and (2) the 
generalized (local) urban case study (PA, Table 3-6). Accordingly, our 
summary of analysis details below focuses on details particular to 
these two case studies. The generalized (local) urban case study (also 
referred to as general urban case study) was not based on a specific 
geographic location and reflected several simplifying assumptions in 
representing exposure including uniform ambient air Pb levels 
associated with the standard of interest across the hypothetical study 
area and a uniform study population. Based on the nature of the 
population exposures represented by the two categories of case study, 
the generalized (local) urban case study includes populations that are 
relatively more highly exposed by way of air pathways to air Pb 
concentrations near the standard level evaluated, compared with the 
populations in the location-specific urban case. The location-specific 
urban case studies provided representations of urban populations with a 
broad range of air-related exposures due to spatial gradients in both 
ambient air Pb levels and population density. For example, the highest 
air concentrations in these case studies (i.e., those closest to the 
standard being assessed) were found in very small parts of the study 
areas, while a large majority of the case study

[[Page 302]]

populations resided in areas with much lower air concentrations.
2. Summary of Design Aspects
    The approach to assessing exposure and risk for the two categories 
of case studies was comprised of four main analytical steps: (1) 
Estimation of ambient air Pb concentrations, (2) estimation of Pb 
concentrations in other key exposure media, including outdoor soil and 
indoor dust, (3) use of exposure media Pb concentrations, with other 
pathway Pb intake rates (e.g., diet), to estimate blood Pb levels in 
children using biokinetic modeling, and (4) use of C-R functions 
derived from epidemiological studies to estimate IQ loss associated 
with the blood Pb levels.
    Concentrations of Pb were estimated in ambient media and indoor 
dust using a combination of empirical data and modeling projections. 
The use of empirical data brings with it uncertainty related to the 
potential inclusion of nonair source signals in these measurements 
(e.g., house paint contributions to indoor dust and outdoor soil Pb). 
Conversely, the use of modeling tools introduces other uncertainties 
(e.g., model and parameter uncertainties).
    Characterization of Pb in ambient air relied on (1) the use of 
ambient monitor data for the location-specific urban case studies and 
(2) an assumption of uniform ambient air Pb levels (matching the 
standard level being considered) for the generalized (local) urban case 
study. For the location-specific urban case studies, we used Pb 
monitors within each study area to characterize spatial gradients. By 
contrast, the generalized (local) urban case study is designed to 
assess exposure and risk for a smaller group of residents (e.g., 
neighborhood) exposed at the level of the standard and, therefore, did 
not rely on monitor data; rather, ambient air Pb concentration was 
fixed at the standard being assessed. For the generalized (local) urban 
case study, which has a single exposure zone in which air Pb 
concentrations do not vary spatially, we derived a single air Pb 
concentration estimate to meet the standard assessed. Concentrations in 
the location-specific urban study areas, which relied on empirical 
(monitor-based) data to define ambient air Pb concentrations, reflected 
contributions from all sources affecting the concentrations in those 
locations, be they currently active stationary or mobile sources, 
resuspension of previously deposited Pb or other.\53\
---------------------------------------------------------------------------

    \53\ Additional detail on estimation of ambient (outdoor) and 
indoor air concentrations is presented in section 5.2.2 and 
Appendices A through D of the 2007 REA.
---------------------------------------------------------------------------

    The air quality scenarios assessed in the 2007 REA included 
conditions just meeting the NAAQS that was current at the time of the 
last review (1.5 [micro]g/m\3\, as a calendar quarter average), 
conditions meeting several alternative, lower standards,\54\ and 
current conditions in the three location-specific urban case studies 
(PA, section 3.4.3.2). The full impact of changes in air Pb conditions 
associated with attainment of lower standards was not simulated, 
however, due to limitations in the available data and modeling tools 
that precluded simulation of linkages between some media and air Pb. 
Specifically, while Pb concentrations in indoor dust were simulated to 
change with the different air quality scenarios for which there were 
differing ambient air Pb concentrations (outdoors and indoors), dietary 
and drinking water Pb concentrations, as well as soil Pb 
concentrations, were not varied across the air quality scenarios in any 
case study (see PA, Table 3-7).\55\
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    \54\ The alternatives lower than the NAAQS at the time of the 
last review for which air quality scenarios were assessed were a 
maximum calendar quarter average of 0.2 [micro]g/m\3\ and maximum 
monthly averages of 0.5, 0.2, 0.05 and 0.02 [micro]g/m\3\ (PA, Table 
3-8).
    \55\ Characterization of Pb concentrations in outdoor surface 
soil/dust for the generalized (local) and location-specific urban 
cases studies was based on the use of nationally representative 
residential soil measurements obtained from the literature (2007 
REA, sections 3.1.3 and 5.2.2.2 and Appendix F). Diet and drinking 
water intake and concentrations, as well as other model inputs, were 
based on the most current information (2007 REA, Appendix H).
---------------------------------------------------------------------------

    In estimating blood Pb levels using the IEUBK model, Pb 
concentrations in exposure media (e.g., ambient air, diet, water, 
indoor dust) were held constant throughout the 7-year simulation 
period, while behavioral and physiological variables were changed with 
age of child (2007 REA, sections 3.2.1.1 and 5.2.4). Detail on methods 
used to characterize media Pb concentrations and all IEUBK inputs for 
each case study are in the 2007 REA, sections 3.1, 3.2, 5.2.3 and 
5.2.4, and appendices C through H. Population variability in Pb intake 
and uptake was simulated through use of the IEUBK model to first 
generate a central-tendency estimate of the blood Pb levels for the 
group of children within a given exposure zone of a study area, coupled 
with use of a geometric standard deviation (GSD) and for the location-
specific case studies, Monte Carlo-based population sampling (PA, 
section 3.4; 2007 REA, Appendix H). The risk characterization step 
employed in the 2007 REA generated a distribution of IQ loss estimates 
for the set of children simulated in the assessment.
    Specifically, blood Pb estimates for the concurrent blood Pb metric 
\56\ were combined with four C-R functions for blood Pb concentration 
with IQ loss based on the analysis by Lanphear et al. (2005) of a 
pooled international dataset of blood Pb and IQ (see the 2007 REA, 
section 5.3.1.1). We used the four different C-R functions to provide 
different characterizations of behavior at low exposures in recognition 
of uncertainty related to modeling this endpoint, particularly at lower 
blood Pb levels for which there is limited representation in the 
Lanphear et al. (2005) pooled dataset.\57\ In considering the risk 
estimates here (as in the last review), we focus on estimates for one 
of the four functions (referred to as the loglinear with low-exposure 
linearization C-R function [PA, section 3.4.3.3]). The range of risk 
estimates reflecting all four C-R functions provide perspective on the 
impact of uncertainty in this key modeling step. Additional detail on 
the C-R functions is provided in the PA and the 2007 Pb Staff Paper 
(PA, section 3.4.3.3; USEPA, 2007b, section 4.2.1).\58\ We focus on the 
median IQ loss estimates, as in the last review, due to increased 
confidence in these estimates relative to the higher percentile 
estimates, for which we recognize significant uncertainty (PA,

[[Page 303]]

sections 3.4.5, 3.4.6 and 3.4.7; 2007 Staff Paper, p. 4-20).
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    \56\ As in the last review, we give primary emphasis to 
estimates based on the concurrent blood Pb metric, consistent with 
CASAC advice in the last review (Henderson, 2007b).
    \57\ The 5th percentile for the concurrent blood Pb measurements 
in that dataset is 2.5 [micro]g/dL, and the median is 9.7 [micro]g/
dL (Lanphear et al., 2005).
    \58\ As noted in section II.B.3 above, since the completion of 
the ISA in the current review, two errors have been identified with 
the pooled dataset analyzed by Lanphear et al., (2005) (Kirrane and 
Patel, 2014). The EPA and a recent publication have separately 
recalculated the statistics and mathematical models of Lanphear et 
al., (2005) using the corrected pooled dataset (Kirrane and Patel, 
2014). While the conclusions drawn from these coefficients, 
including the finding of a steeper slope at lower (as compared to 
higher) blood Pb concentrations, are unaffected, the magnitude of 
the loglinear and linear regression coefficients are somewhat lower 
based on the corrections. For example, the loglinear model 
coefficient used for the C-R function, on which the EPA focused in 
the last review and also focuses on here, changed only negligibly 
from -2.7 to -2.65 when recalculated using the corrected pooled 
dataset (Kirrane and Patel, 2014). As a result, the risk estimates 
for this function would be expected to be very similar although 
slightly lower if derived using the recalculated loglinear model 
coefficient for the corrected dataset. Since the loglinear model 
coefficient calculated from the corrected dataset is unchanged at 
two significant figures from that original reported, any change to 
the risk estimates would be very small and, particularly in light of 
other uncertainties in the analysis, does not materially affect 
staff's consideration of the results.
---------------------------------------------------------------------------

    As the 2007 REA did not include an air quality scenario simulated 
to just meet the standard selected by the 2008 decision,\59\ we 
employed two different approaches to estimate risk pertaining to 
conditions just meeting the current Pb standard (set in 2008) for our 
purposes in this review. First, given the similarity to the current 
standard of the then-current conditions scenario for the Chicago case 
study (among all the 2007 REA scenarios), we consider the risk 
estimates for that scenario as informative with regard to risk 
associated with the current standard.\60\ To augment the risk 
information available in this current review and in recognition of the 
variation among specific locations and urban areas with regard to air 
quality patterns and exposed population, we have also newly developed 
estimates for an air quality scenario just meeting the current Pb NAAQS 
in the context of the generalized (local) urban case study. These 
estimates were derived based on interpolation from the risk estimates 
available for scenarios previously assessed for the generalized (local) 
urban case study. Such interpolated estimates were only developed for 
the generalized urban case study due to its use of a single exposure 
zone which greatly simplified the method employed.\61\
---------------------------------------------------------------------------

    \59\ The 2008 decision on the level for the revised NAAQS was 
based primarily on consideration of the evidence-based air-related 
IQ loss framework; risk estimates available for scenarios simulated 
in the 2007 REA were concluded to be roughly consistent with and 
generally supportive of the evidence-based air-related IQ loss 
estimates (see section II.A.1 above).
    \60\ In the Chicago urban case study, the maximum monthly 
average concentration was 0.31 [micro]g/m\3\, and the maximum 
calendar quarter average concentration was 0.14 [micro]g/m\3\ (2003-
2005 data; 2007 REA, Appendix O).
    \61\ We did not interpolate risk estimates for the current 
standard for the other case studies (i.e., the primary Pb smelter 
and location-specific urban case studies) because those case studies 
utilized a more complex, spatially-differentiated and population-
based approach (see 2007 REA) which precludes application of the 
simple linear interpolation approach described, without introduction 
of substantial added uncertainty (relative to the other estimates 
for the same case study). The simplicity of the generalized (local) 
urban study area, however, with its single exposure zone, is 
amenable to the linear interpolation of risk described here.
---------------------------------------------------------------------------

    The general approach we followed to newly develop estimates for the 
current standard in the generalized (local) urban case study was to 
identify the two alternative standard scenarios simulated in the 2007 
REA which represented air quality conditions bracketing those for the 
current standard and then linearly interpolate an estimate of risk for 
the current standard based on the slope created from the two bracketing 
estimates (PA, section 3.4.3.3.2 and Appendix 3A). By this method, the 
air quality scenario for the current standard (0.15 [micro]g/m\3\, as a 
not-to-be-exceeded 3-month average) was found to be bracketed by the 
scenarios for alternative standards of 0.20 [micro]g/m\3\ (maximum 
calendar quarter average) and 0.20 [micro]g/m\3\ (maximum monthly 
average). Using interpolation between the risk estimates for these two 
scenarios, we developed median risk estimates for the current standard 
(PA, Appendix 3A).
3. Key Limitations and Uncertainties
    In characterizing risk associated with Pb from air-related exposure 
pathways, we faced a variety of challenges and employed a number of 
methods. The challenges related to significant data and modeling 
limitations which affected our ability to parse out the portion of 
total (all-pathway) blood Pb and IQ loss attributable to air-related 
pathways, as well as our representation of key sources of variability 
and characterization of uncertainty. Although we separated total 
estimates into risk estimates for diet/drinking water and two air-
related categories (``recent air'' and ``past air''), significant 
limitations in our modeling tools and data resulted in an inability to 
parse risk estimates specific to the air-related pathways. For example, 
we recognize that Pb in diet and drinking water sources may include 
some Pb derived from Pb in the ambient air, as well as Pb from nonair 
sources, but limitations precluded explicit modeling of the 
contribution from air pathways to these exposure pathways, such that 
the air-related component of these exposures was not estimated. Rather, 
we focused on estimates from the two air-related categories, which we 
considered to under- and over-estimate air-related risk, respectively, 
to create bounds within which we consider air-related risk to fall.
    The first air-related category (``recent'') included Pb exposure 
pathways tied most directly to ambient air, which consequently have the 
potential to respond relatively more quickly to changes in air Pb 
(i.e., inhalation and ingestion of indoor dust Pb derived from the 
infiltration of ambient air Pb indoors). Importantly, media 
concentrations associated with the pathways in this category were 
simulated to change in response to air concentrations (as noted in 
section II.D.2 above and described in section 3.4.3.1 of the PA). The 
air-related Pb exposure pathways in the second air-related category 
(``past air''), all of which are associated with atmospheric 
deposition, included ingestion of Pb in outdoor dust/soil and ingestion 
of the portion of Pb in indoor dust that after deposition from ambient 
air outdoors is carried indoors with humans. While there is the 
potential for these other air-related exposures to be affected (over 
some time frame) by changes in air Pb concentrations (associated with 
an adjustment to the Pb standard), limitations in our data and tools 
precluded simulation of that relationship. Consequently, risk estimated 
for this category reflects media measurements available for the 2007 
REA and is identical for all air quality scenarios. Further, although 
paint is not an air-related source of Pb exposure, it may be reflected 
somewhat in estimates developed for the ``past air'' category, due to 
modeling constraints (2007 Staff Paper, section 4.2.4). Thus, as 
exposures included in the first air-related category (``recent'') do 
not completely capture all air-related pathways, we consider risk for 
this category an underestimate of air-related risk. Yet, as exposures 
included in the second air-related category include pathways that are 
not air-related, we consider the summed risk across both categories to 
include a slight over-estimate of air-related risk.
    In summary, because of limitations in the assessment design, data 
and modeling tools, we consider our estimates of risk attributable to 
air-related exposure pathways to be approximate and to be bounded on 
the low end by the risk estimated for the ``recent air'' category and 
on the upper end by the risk estimated for the ``recent air'' plus 
``past air'' categories. With regard to the latter, we are additionally 
cognizant of the modeling and data limitations which reduce the extent 
to which the upper end of these bounds reflects impacts of alternative 
air quality conditions simulated. We note that this limitation will 
tend to contribute to estimates for the ``past air'' category 
representing relatively greater overestimates with relatively lower air 
Pb air quality scenarios.
    We recognize several important sources of variability in air-
related Pb exposures and associated risk, for which the approaches by 
which they were addressed in the 2007 REA are summarized here (PA, 
section 3.4.6).
     Variation in distributions of potential urban residential 
exposure and risk across U.S. urban residential areas is addressed by 
the inclusion of location-specific urban study areas that reflect a 
diverse set of urban areas in the U.S.

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     Representation of a more highly exposed subset of urban 
residents potentially exposed at the level of the standard is addressed 
by the inclusion of the generalized (local) urban study area.
     Variation in residential exposure to ambient air Pb within 
an urban area of the location-specific case studies is addressed 
through the partitioning of these study areas into exposure zones to 
provide some representation of spatial gradients in ambient air Pb and 
their interaction with population distribution and demographics.
     Inter-individual variability in blood Pb levels is 
addressed through the use of empirically derived GSDs to develop blood 
Pb distribution for the child population in each exposure zone, with 
GSDs selected particular to each case study population.
     Inter-individual variability in IQ response to blood Pb is 
addressed through the use of C-R functions for IQ loss based on a 
pooled analysis reflecting studies of diverse populations.
    With regard to uncertainties, we recognize one overarching area 
concerning the precision of our estimation of the neurocognitive risk 
(as represented by IQ loss) associated with ambient air Pb. For reasons 
related to the evidence of nonlinear responses of blood Pb to Pb 
exposure and of Pb-associated IQ response to blood Pb, the 2007 REA 
first estimated blood Pb levels and associated risk for total Pb 
exposure (i.e., including Pb from air-related and nonair exposure 
pathways) and then separated out estimates for pathways of interest 
(PA, section 3.4.4). However, as described above, significant 
limitations in our modeling tools affected our ability to develop 
precise estimates for air-related exposure pathways. We believe these 
limitations led to a slight overestimation of the risks for the ``past 
air'' category and to an under-representation of air-related pathways 
for the ``recent air'' category. Thus, we characterized the risk 
attributable to air-related exposure pathways to be bounded by the 
estimates developed for the ``past air'' category and the sum of 
estimates for the ``recent air'' and ``past air'' categories. For air 
quality scenarios other than those for the previous NAAQS, this upper 
bound is recognized as having a potential upward bias with regard to 
its reflection of the simulated air quality conditions because modeling 
and data limitations precluded simulation of the influence of lower air 
Pb concentrations on the outdoor dust and soil exposure pathways (PA, 
section 3.4.4).
    We recognize a range of additional uncertainties, limitations, and 
assumptions that are reflected in various ways in the 2007 REA and 
associated results (PA, section 3.4.7), which include the following.
     Temporal Aspects: During the 7-year exposure period, media 
concentrations remain fixed and the simulated child resides at the same 
residence (although exposure factors, including behavioral and 
physiological parameters, are adjusted to match the aging of the 
child). These aspects introduce uncertainty into the risk estimates, 
although the existence of a directional bias is unclear.
     Generalized (local) Urban Case Study: The design for this 
case study employs assumptions regarding uniformity that are reasonable 
in the context of a general description of a small neighborhood 
population but would contribute significant uncertainty to 
extrapolation of these estimates to a specific urban location, 
particularly a relatively large one. An additional area of uncertainty 
concerns the representation of variability in air quality. Given the 
relatively greater variability common in areas of high Pb 
concentrations, the approach used to reflect variability may bias the 
estimates high.
     Location-specific Urban Case Studies: Limitations in the 
spatial density of ambient air monitors in the simulated areas limit 
our characterization of spatial gradients of ambient air Pb levels in 
these case studies. This factor introduces uncertainty into the risk 
estimates for this category of case study; the existence of a 
directional bias is unclear.
     Air Quality Simulation: Focus on only then-current 
conditions (2003-2005) scenario for the Chicago urban case study in 
this review precludes uncertainty associated with simulations of 
alternative air quality scenarios in the 2007 REA.
     Outdoor Soil/Dust Pb Concentrations: Limitations in 
datasets on Pb levels in surface soil/dust Pb in urban areas and in our 
ability to simulate the impact of reduced air Pb levels related to 
lowering the NAAQS in the 2007 REA contribute uncertainty to air-
related risk estimates for the current standard in the generalized 
(local) urban case study. The likely impact is a high bias on these 
risk estimates (related to low bias on estimating risk reduction for 
lower standard levels in the 2007 REA) given lack of simulated changes 
in soil Pb related to changes in ambient air Pb.
     Indoor Dust Pb Concentrations: Limitations and uncertainty 
in modeling of indoor dust Pb levels, including the impact of 
reductions in ambient air Pb levels, contributes uncertainty to air-
related risk estimates. Although the indoor dust modeling does link 
changes in ambient air Pb to changes in indoor dust Pb, it does not 
include a link between ambient air Pb, outdoor soil Pb and subsequent 
changes in the level of Pb carried (or ``tracked'') into the house. 
This could introduce low bias into the total estimates of air-related 
Pb exposure and risk.
     Interindividual Variability in Blood Pb Levels: 
Uncertainty related to population variability in blood Pb levels 
related to interindividual variability in factors other than media 
concentration and limitations in modeling of this introduces 
significant uncertainty into blood Pb and IQ loss estimates for the 
95th percentile of the population. The extent of any systematic bias 
from this source of uncertainty is unknown.
     Pathway Apportionment for Higher Percentile Blood Pb and 
Risks: Limitations, primarily in data, prevented us from characterizing 
the degree of correlation among high-end Pb exposures for the various 
pathways (e.g., the degree to which an individual experiencing high 
drinking water Pb exposure would also experience high Pb paint exposure 
and high ambient air-related Pb exposure). Our inability to 
characterize potential correlations between exposure pathways 
(particularly at the higher percentile exposure levels) limited our 
ability to (1) effectively model high-end Pb risk and (2) apportion 
that risk between different exposure pathways, including ambient air-
related pathways.
     IQ Loss C-R Functions: Specification of the quantitative 
relationship between blood Pb level and IQ loss is subject to greater 
uncertainty at lower blood Pb levels. The use of four C-R functions 
models (which each treat the response at low blood Pb levels in a 
different manner) is considered to provide a reasonable 
characterization of this source of uncertainty and its impact on risk 
estimates. Comparison of risk estimates from the four models indicates 
this source of uncertainty to have a potentially significant impact on 
risk.
4. Summary of Risk Estimates and Key Observations
    In this summary of risk estimates, drawn from the PA, we focus on 
the estimates of air-related IQ loss derived using the C-R function in 
which we have greatest confidence (see PA, sections 3.4.3.3.1 and 
3.4.7) for the median child in a given case study (exposure modeled 
through age 7 years), given the substantially greater uncertainty 
associated with air-related

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risk estimates for extremes of the risk distribution, such as the 95th 
percentile (PA, section 3.4). Estimates for other risk metrics and the 
full range of case studies and air quality scenarios are described 
elsewhere in detail (e.g., 2007 REA, sections 4.2 and 5.3.2 and 
appendices; 2007 Staff Paper, chapter 4; 73 FR 66964, November 12, 
2008). Based on results from the 2007 REA for a location-specific urban 
study area (Chicago case study) and on those newly derived in this 
review based on interpolation from the 2007 REA results (for the 
generalized [local] urban case study), median air-related IQ loss for 
the current standard is estimated, with rounding, to generally fall 
near or somewhat above a rough lower bound of 1 point IQ loss and below 
a rough upper bound of 3 points IQ loss. As would be expected by the 
use of interpolation, the newly derived estimates are consistent with 
the estimates for similar air quality scenarios that were available in 
the last review (PA, section 3.4.5). For example, the generalized 
(local) urban case study current standard scenario estimates for median 
air-related IQ loss are identical to those for the scenario of just 
meeting a potential alternative of 0.2 [mu]g/m\3\ maximum calendar 
quarter average for that case study (PA, Table 3-11). Further, the 
upper bound below which the median IQ loss is estimated to fall is also 
approximately 3 IQ points in the generalized (local) urban case study 
scenarios for just meeting potential alternatives of 0.2 [mu]g/m\3\, 
0.05 and 0.02 [mu]g/m\3\ maximum monthly average, providing an 
indication of the limitations associated with estimating air-related Pb 
exposures and risk for lower air Pb scenarios (PA, sections 3.4.4 and 
3.4.5).
    As summarized in section II.D.3 above, a range of limitations and 
areas of uncertainty were associated with the information available in 
the last review (PA, sections 3.4.4, 3.4.6 and 3.4.7). In this review, 
the REA Planning Document concluded that none of the primary sources of 
uncertainty identified to have the greatest impact on risk estimates 
would be substantially reduced through the use of newly available 
information (USEPA, 2011b). Thus, the key observations regarding air-
related Pb risk modeled for the set of standard levels assessed in the 
2007 REA, as well as the risk estimates interpolated for the current 
standard, are not significantly affected by the new information. 
Further, our overall characterization of uncertainty and variability 
associated with those estimates (as summarized above and in sections 
3.4.6 and 3.4.7 of the PA) is not appreciably affected by new 
information. As recognized at the time of the last review, exposure and 
risk modeling conducted for this analysis was complex and subject to 
significant uncertainties due to limitations in the data and models, 
among other aspects. Of particular note, limitations in the assessment 
design, data and modeling tools handicapped us from sharply separating 
Pb linked to ambient air from Pb that is not air related.
    In summary, the estimates of risk attributable to air-related 
exposures, with which we recognize a variety of sources of uncertainty, 
are considered to be approximate, falling within upper and lower 
bounds. These bounds for scenarios just meeting the current standard 
are roughly estimated, with rounding, as 3 and 1 IQ points, which over- 
and underestimate risk, respectively. In characterizing the magnitude 
of air-related risk associated with the current standard, we focus on 
median estimates, for which we have appreciably greater confidence than 
estimates for outer ends of the risk distribution (see PA, section 
3.4.7) and on risks derived using the C-R function in which we have 
greatest confidence (see PA, sections 3.4.3.3.1 and 3.4.7). These risk 
results for the current standard, both those estimated in the last 
review for one of the location-specific urban study area populations 
and those newly derived in this review using interpolation of the 
estimates from the last review for the generalized (local) urban case 
study, which is recognized to reflect a generalized high end of air-
related exposure for localized populations, provide approximate bounds 
for air-related risk, with attendant uncertainties described above. 
Focusing on the results for the generalized (local) urban case study, 
the interpolated estimates for the scenario representing the current 
standard are very similar to estimates for the two 0.2 [mu]g/m\3\ 
scenarios (maximum monthly and calendar quarter averages) simulated in 
the 2007 REA \62\ and are appreciably lower than those associated with 
the previous standard. For this case study, across the two 0.2 [mu]g/
m\3\ scenarios, the current standard scenario and the more restrictive 
air quality scenarios, the upper bound below which air-related risk is 
estimated to fall rounds to the same value, reflecting the significant 
limitations associated with developing precise estimates of air-related 
risk, particularly for the lower air Pb scenarios (PA, sections 3.4.4, 
3.4.5, and 3.4.7).
---------------------------------------------------------------------------

    \62\ There is uncertainty associated with judging differences 
between the current standard and these potential alternative 
standards due to the difference in air quality datasets used to 
estimate air concentration variability of the 2007 REA estimates 
versus the interpolated risk estimate.
---------------------------------------------------------------------------

E. Conclusions on Adequacy of the Current Primary Standard

    In evaluating whether, in view of the advances in scientific 
knowledge and additional information now available, it is appropriate 
to retain or revise the current standard, the Administrator builds upon 
the last review and reflects upon the body of evidence and information 
now available. The Administrator has taken into account both evidence-
based and quantitative exposure- and risk-based considerations in 
developing conclusions on the adequacy of the current primary Pb 
standard. Evidence-based considerations draw upon the EPA's assessment 
and integrated synthesis of the scientific evidence from 
epidemiological studies and experimental animal studies evaluating 
health effects related to exposures to Pb, with a focus on policy-
relevant considerations as discussed in the PA. The exposure/risk-based 
considerations draw from the results of the quantitative analyses 
presented in the 2007 REA, augmented as described in the PA, and 
summarized in section II.D above, and consideration of those results in 
the PA. More specifically, estimates of the magnitude of ambient Pb-
related exposures for young children and associated impacts on IQ 
associated with just meeting the current primary Pb NAAQS have been 
considered. Together the evidence-based and risk-based considerations 
have informed the Administrator's proposed conclusions related to the 
adequacy of the current Pb standard in light of the currently available 
scientific evidence.
    As described in section II.A.2 above, consideration of the evidence 
and the exposure/risk information in the PA and by the Administrator is 
framed by consideration of a series of key policy-relevant questions. 
The following sections describe the consideration of these questions in 
the PA, the advice received from CASAC, as well as the comments 
received from various parties, and then present the Administrator's 
proposed conclusions regarding the adequacy of the current primary 
standard.
1. Evidence-Based Considerations in the Policy Assessment
    In considering the evidence with regard to the issue of adequacy of 
the current standard, the PA addresses several questions that build on 
the information summarized in sections II.B and II.C above (and 
sections 3.1 through

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3.3 of the PA) to more broadly address the extent to which the current 
evidence base supports the adequacy of the public health protection 
afforded by the current primary standard. The first question addresses 
the integrated consideration of the health effects evidence, in light 
of aspects described in sections II.A.1 and II.A.2 above. The second 
question focuses on consideration of associated areas of uncertainty. 
The third question then integrates consideration of the prior two 
questions with a focus on the standard, including each of the four 
elements. The PA considerations and conclusions with regard to these 
questions are summarized below.
    In considering the extent to which information newly available in 
this review may have altered scientific support for the occurrence of 
health effects associated with Pb in ambient air, the PA concludes that 
the current evidence continues to support the EPA's conclusions from 
the previous review regarding key aspects of the health effects 
evidence for Pb and the health effects of multimedia exposure 
associated with levels of Pb occurring in ambient air in the U.S. (PA, 
section 4.2.1). The conclusions in this regard are based on 
consideration of the assessment of the currently available evidence in 
the ISA, particularly with regard to key aspects summarized in Chapter 
3 of the PA, in light of the assessment of the evidence in the last 
review as described in the 2006 CD and summarized in the notice of 
final rulemaking (73 FR 66964, November 12, 2008). Key aspects of these 
conclusions are summarized below.
    As at the time of the last review, blood Pb continues to be the 
predominant biomarker employed to assess exposure and health risk of Pb 
(ISA, Chapters 3 and 4), as discussed in section II.C above. This 
widely accepted role of blood Pb in assessing exposure and risk is 
illustrated by its established use in programs to prevent both 
occupational Pb poisoning and childhood Pb poisoning, with the latter 
program, implemented by the CDC, recently issuing updated guidance on 
blood Pb measurement interpretation (CDC, 2012). As in the past, the 
current evidence continues to indicate the close linkage of blood Pb 
levels in young children to their body burden; this linkage is 
associated with the ongoing bone remodeling during that lifestage (ISA, 
section 3.3.5). This tight linkage plays a role in the somewhat rapid 
response of children's blood Pb to changes in exposure (particularly to 
exposure increases), which contributes to its usefulness as an exposure 
biomarker (ISA, sections 3.2.2, 3.3.5, and 3.3.5.1). Additionally, the 
weight of evidence documenting relationships between children's blood 
Pb and health effects, most particularly those on the nervous and 
hematological systems (e.g., ISA, sections 4.3 and 4.7), speaks to its 
usefulness in assessing health risk.
    As in the last review, the evidence on air-to-blood relationships 
available today continues to be composed of studies based on an array 
of circumstances and population groups (of different age ranges), 
analyzed by a variety of techniques, which together contribute to 
appreciable variability in the associated quantitative estimates and 
uncertainty with regard to the relationships existing in the U.S. 
today. Accordingly, interpretation of this evidence base, as discussed 
in section II.C above, also includes consideration of factors that may 
be influencing various study estimates. We consider the study estimates 
in light of such factors both with regard to the extent to which the 
factors affect the usefulness of specific study estimates for the 
general purpose here of quantitatively characterizing relationships 
between Pb in ambient air and air-related Pb in children's blood and 
also with regard to the pertinence of such factors more specifically to 
conditions and populations in the U.S. today. As noted in the PA, the 
current evidence, while including two additional studies not available 
at the time of the last review, is not appreciably changed from that 
available in the last review (PA, section 3.1). The range of estimates 
that can be derived from the full dataset is broad and not changed by 
the inclusion of the newly available estimates. Further, the PA 
recognizes significant uncertainties regarding the air Pb to air-
related blood Pb relationship for the current conditions where 
concentrations of Pb in both ambient air and children's blood are 
substantially lower than they have been in the past. In considering the 
strengths, limitations and uncertainties associated with the full 
dataset, the currently available evidence appears to continue to 
support a range of estimates for the purpose at hand that is generally 
consistent with the range given weight in the last review, 1:5 to 1:10 
(ISA, section 3.7.4 and Table 3-12; 73 FR 67001-2, 67004, November 12, 
2008). The PA additionally notes that the generally central estimate of 
1:7 identified for this range in the last review is consistent with the 
study involving blood Pb for pre-school children and air Pb conditions 
near a large source of Pb to ambient air with concentrations near (and/
or previously above) the level of the current Pb standard (ISA, section 
3.5.1; Hilts, 2003).\63\ In so noting, the PA also recognizes the 
general overlap of such circumstances with those represented by the 
evidence-based, air-related IQ loss framework,\64\ for which air-to-
blood ratio is a key input. In characterizing the range of air-to-blood 
ratio estimates, we recognize uncertainty inherent in such estimates as 
well as the variation in currently available estimates resulting from a 
variety of factors, including differences in the populations examined, 
as well as in the Pb sources or exposure pathways addressed in those 
study analyses (ISA, section 3.7.4).
---------------------------------------------------------------------------

    \63\ The older study by Hayes et al. (1994) during time of 
leaded gasoline indicated a generally similar ratio of 1:8, although 
the blood Pb levels in that study were much higher than those in the 
study by Hilts (2003). Among the studies focused on this age group, 
the latter study includes blood Pb levels closest to those in U.S. 
today.
    \64\ Concentrations near air sources are higher than those at 
more distant sites (as described in PA, section 2.2.2); it is near-
source locations where there is the potential for concentrations at 
or near the current standard.
---------------------------------------------------------------------------

    The scientific evidence continues to recognize a broad array of 
health effects on multiple organ systems or biological processes 
related to blood Pb, including Pb in blood prenatally (ISA, section 
1.6). The currently available evidence continues to support 
identification of neurocognitive effects in young children as the most 
sensitive endpoint associated with blood Pb concentrations (ISA, 
section 1.6.1), which as an integrated index of exposure reflects the 
aggregate exposure to all sources of Pb through multiple pathways 
(inhalation and ingestion). Evidence continues to indicate that some 
neurocognitive effects in young children may not be reversible and may 
have effects that persist into adulthood (ISA, section 1.9.5). Thus, as 
discussed in section II.B. above, the evidence of Pb effects at the low 
end of the studied blood Pb levels (closest to those common in the U.S. 
today) continues to be strongest and of greatest concern for effects on 
the nervous system, most particularly those on cognitive function in 
children.
    As in the last review, evidence on risk factors continues to 
support the identification of young children as an important at-risk 
population for Pb health effects (ISA, section 5.4). The current 
evidence also continues to indicate important roles as factors that 
increase risk of Pb-related health effects for the following: 
Nutritional factors, such as iron and calcium intake; elevated blood Pb 
levels; and proximity to sources of Pb exposure, such as industrial 
releases or buildings with old,

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deteriorating, leaded paint. Further, some races or ethnic groups 
continue to demonstrate increased blood Pb levels relative to others, 
which may be related to these and other factors (ISA, sections 5.1, 5.2 
and 5.4).
    With regard to our understanding of the relationship between 
exposure or blood Pb levels in young children and neurocognitive 
effects, the PA notes that the evidence in this review, as in the last, 
does not establish a threshold blood Pb level for neurocognitive 
effects in young children (ISA, sections 1.9.4 and 4.3.12). The lowest 
blood Pb levels at which associations with neurocognitive impacts have 
been observed in pre-school and school age children continue to range 
down below 5 [mu]g/dL, with the lowest group levels that have been 
associated with such effects ranging down to 2 [mu]g/dL (ISA, sections 
1.6.1 and 4.3.15.1). Additionally, as in the last review, there is 
evidence that the relationship of young children's blood Pb with 
neurocognitive impacts, such as IQ, is nonlinear across a wide range of 
blood Pb, with greater incremental impacts at lower versus higher blood 
Pb levels (ISA, sections 1.9.4 and 4.3.12). Accordingly, as in the last 
review, the PA focuses on C-R relationships from study groups with 
blood Pb levels closest to those in children in the U.S. today, which 
are generally lower than epidemiological study groups. The currently 
available evidence does not identify additional C-R slopes for study 
groups of young children (e.g., dL, 
as discussed in section II.B.3 above (ISA, section 4.3.12). Thus, the 
blood Pb concentration--IQ response functions or slopes identified in 
this review for epidemiological study groups of young children with 
mean blood Pb levels closest to that of children in the U.S. today 
include the same set recognized at the time of the last review (see 
Table 1 above), the median of which is 1.75 IQ points decrement per 
[mu]g/dL blood Pb (73 FR 67003, November 12, 2008).
    In considering the evidence with regard to the extent to which 
important uncertainties identified in the last review have been reduced 
or to which new uncertainties have emerged, as summarized in discussing 
the previous question and in section II.B above, the PA concludes that 
no new uncertainties were identified as emerging since the last review. 
However, the PA recognizes important uncertainties identified in the 
last review that remain today. Importantly, given our focus in this 
review, as in the last review, on neurocognitive impacts associated 
with Pb exposure in early childhood, the PA recognizes remaining 
uncertainties in our understanding of the C-R relationship of 
neurocognitive impacts, such as IQ decrements, with blood Pb level in 
young children, particularly across the range of blood Pb levels common 
in the U.S. today. With regard to C-R relationships for IQ, the 
evidence available in this review does not include studies that 
appreciably extend the range of blood Pb levels studied beyond those 
available in the last review. As in the last review, the early 
childhood (e.g., 2 to 7 years of age) blood Pb levels for which 
associations with IQ response have been reported continue to extend at 
the low end of the range to study group mean blood Pb levels of 2.9 to 
3.8 [mu]g/dL (e.g., 73 FR 67003, November 12, 2008, Table 3). The 
studies examining C-R relationships down to these blood Pb levels, as 
summarized in section II.B.3 above, continue to indicate higher C-R 
slopes in those groups with lower blood Pb levels than in study groups 
with higher blood Pb levels (ISA, section 4.3.12). The lack of studies 
considering C-R relationships for Pb effects on IQ at still lower blood 
Pb levels contributes to uncertainty regarding the quantitative 
relationship between blood Pb and IQ response in populations with mean 
blood Pb levels closer to the most recently available mean for children 
aged 1 to 5 years of age (e.g., 1.17 [mu]g/dL in 2009-2010 [ISA, p. 3-
85]).
    Further, the PA recognizes important uncertainties in our 
understanding of the relationship between ambient air Pb concentrations 
and air-related Pb in children's blood. The evidence newly available in 
this review has not reduced such key uncertainties. As in the last 
review, air-to-blood ratios based on the available evidence continue to 
vary, with our conclusions based on the current evidence generally 
consistent with the range of 1:5 to 1:10 given emphasis in the last 
review (73 FR 67002, November 12, 2008; ISA, section 3.7.4). There 
continues to be uncertainty regarding the extent to which this range 
represents the relationship between ambient air Pb and Pb in children's 
blood (derived from the full set of air-related exposure pathways) and 
with regard to its reflection of exposures associated with ambient air 
Pb levels common in the U.S. today and to circumstances reflecting just 
meeting the current Pb standard (ISA, section 3.7.4). The PA 
additionally notes the significant uncertainty remaining with regard to 
the temporal relationships of ambient Pb levels and associated exposure 
with occurrence of a health effect (73 FR 67005, November 12, 2008).
    In integrating consideration of the prior two questions with a 
focus on the standard, the PA then addresses the question regarding the 
extent to which newly available information supports or calls into 
question any of the basic elements of the current Pb standard. The PA 
addresses this question for each of the elements of the standard in 
light of the health effects evidence and other relevant information 
available in this review (and summarized in sections II.B and II.C 
above). As an initial matter, the PA recognizes the weight of the 
scientific evidence available in this review that continues to support 
our focus on effects on the nervous system of young children, 
specifically neurocognitive decrements, as the most sensitive endpoint. 
Consistent with the evidence available in the last review, the 
currently available evidence continues to indicate that a standard that 
provides requisite public health protection against the occurrence of 
such effects in at-risk populations would also provide the requisite 
public health protection against the full array of health effects of 
Pb. Accordingly, the discussion of the elements below is framed by that 
background.
Indicator
    The indicator for the current Pb standard is Pb-TSP. Key 
considerations in retaining this indicator in the last review are 
summarized in section II.A.1. Exposure to Pb in all sizes of particles 
passing through ambient air can contribute to Pb in blood and 
associated health effects by a wide array of exposure pathways (ISA, 
section 3.1). These pathways include the ingestion route, as well as 
inhalation (ISA, section 3.1), and a wide array of particle sizes play 
a role in these pathways (ISA, section 3.1.1.1). As at the time of the 
last review, the PA recognizes the variability of the Pb-TSP FRM in its 
capture of airborne Pb particles (as discussed in section 2.2.1.3.1 of 
the PA). As in the last review, the PA also notes that an alternative 
approach for collection of a conceptually comparable range of particle 
sizes, including ultra-coarse particles, is not yet available. 
Additionally, the limited available information regarding relationships 
between Pb-TSP and Pb in other size fractions indicates appreciable 
variation in this relationship, particularly near sources of Pb 
emissions where concentrations and potential exposures are greatest. 
Thus, the PA concludes that the information available in this review 
does not address previously

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identified limitations and uncertainties for the current indicator. Nor 
does the newly available information identify additional limitations or 
uncertainties.
    The PA notes that the evidence available in this review continues 
to indicate the role of a range of air Pb particle sizes in 
contributing to Pb exposure (e.g., ISA, section 3.1.1.1) that 
contributes to Pb in blood and associated health effects. For example, 
the evidence indicates larger particle sizes for Pb that occurs in soil 
and house dust and may be ingested as compared to Pb particles commonly 
occurring in the atmosphere and the size fraction of the latter that 
may be inhaled (ISA, section 3.1.1.1). Taken together, the PA concludes 
that the evidence currently available reinforces the appropriateness of 
an indicator for the Pb standard that reflects a wide range of airborne 
Pb particles.
Averaging Time and Form
    The averaging time and form of the standard were revised in the 
last Pb NAAQS review, based on considerations summarized in section 
II.A.1 above. The current standard is a not-to-be-exceeded rolling 3-
month average (40 CFR 50.16), derived from three monthly averages 
calculated in accordance with the current data handling procedures (40 
CFR part 50, Appendix R). The form is a maximum, evaluated within a 3-
year period (40 CFR 50.16). As at the time of the last review, the PA 
notes that evidence continues to support the importance of periods on 
the order of 3 months and the prominent role of deposition-related 
exposure pathways, with uncertainty associated with characterization of 
precise time periods associating ambient air Pb with air-related health 
effects. The PA concludes that relevant factors continue to be 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. The PA concludes that the 
newly available evidence in this review does not appreciably improve 
our understanding of the period of time in which air Pb concentrations 
would lead to the health effects most at issue in this review (PA, 
section 4.2.1). Newly available evidence accordingly also does not 
appreciably improve our understanding of the period of time for which 
control of air Pb concentrations would protect against exposures most 
pertinent to the health effects most at issue in this review. Thus, 
while there continue to be limitations in the evidence to inform our 
consideration of these elements of the standard and associated 
uncertainty, the available evidence continues to provide support for 
the decisions made in the last review regarding these elements of the 
current Pb standard.
Level
    The level of the current standard is 0.15 [mu]g/m\3\ (40 CFR 
50.16). As described in section II.A.1 above, this level was selected 
in 2008 with consideration of, among other factors, an evidence-based 
air-related IQ loss framework, for which there are two primary inputs: 
Air-to-blood ratios and C-R functions for blood Pb-IQ response in young 
children. Additionally taken into consideration were the uncertainties 
inherent in these inputs.\65\ Application of the framework also 
entailed consideration of a magnitude of air-related IQ loss, which as 
further described in section II.A.1 above, is used in conjunction with 
this specific framework in light of the framework context, limitations 
and uncertainties. Additionally, selection of a level for the standard 
in 2008 was made in conjunction with decisions on indicator, averaging 
time and form.
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    \65\ As discussed further below, the Administrator also 
considered the exposure/risk-based information, which he found to be 
roughly consistent and generally supportive of the framework 
estimates (73 FR 67004).
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    As an initial matter, the PA considers the extent to which the 
evidence-based, air-related IQ loss framework which informed the 
Administrator's decision in the last review is supported by the 
currently available evidence and information. In so doing, the PA 
recognizes the support provided by the currently available evidence for 
the key conclusions drawn in the last review with regard to health 
effects of greatest concern, at-risk populations, the influence of Pb 
in ambient air on Pb in children's blood and the association between 
children's blood Pb and decrements in neurocognitive function (e.g., 
IQ). The PA additionally notes the complexity associated with 
interpreting the scientific evidence with regard to specific levels of 
Pb in ambient air, given the focus of the evidence on blood Pb as the 
key biomarker of children's aggregate exposure. The need to make such 
interpretations in the face of the associated complexity supported use 
of the evidence-based framework in the last review. In considering the 
currently available evidence for the same purposes in this review, the 
PA concludes that the evidence-based framework continues to provide a 
useful tool for consideration of the evidence with regard to the level 
of the standard.
    The PA next turned to consideration of the primary inputs to the 
framework: Air-to-blood ratios and C-R functions for blood Pb-IQ 
response in young children. With regard to the former, the PA concludes 
the limited newly available information assessed in the ISA, and 
discussed in section II.C above, to be generally consistent with the 
information in this area that was available at the time of the last 
review. The PA additionally recognizes the variability and uncertainty 
associated with quantitative air-to-blood ratios based on this 
information, as also existed in the last review. As in the last review, 
factors contributing to the variability and uncertainty of these 
estimates are varied and include aspects of the study populations 
(e.g., age and Pb exposure pathways) and the study circumstances (e.g., 
length of study period and variations in sources of Pb exposure during 
the study period). The PA notes that the full range of estimates 
associated with the available evidence is wide and considers it 
appropriate to give emphasis to estimates pertaining to circumstances 
closest to those in the U.S. today with regard to ambient air Pb and 
children's blood Pb concentrations, while recognizing the limitations 
associated with the available information. With that in mind, the PA 
considers the currently available evidence to continue to support the 
range of estimates for air-to-blood ratios concluded in the last review 
to be most appropriate for the current population of young children in 
the U.S., in light of the multiple air-related exposure pathways by 
which children are exposed and of the levels of air and blood Pb common 
today. Identification of this range also included consideration of the 
limitations associated with the available information and inherent 
uncertainties. This range of air-to-blood ratios included 1:10 at the 
upper end and 1:5 at the lower end. The PA further recognizes that the 
limited evidence for air Pb and children's blood Pb concentrations 
closest to those in U.S. today continues to provide support for the 
Administrator's emphasis in the 2008 decision on the relatively central 
estimate of 1:7.
    With regard to the second input to the evidence-based framework, C-
R functions for the relationship of young children's blood Pb with 
neurocognitive impacts (e.g., IQ decrements), the PA considers several 
aspects of the evidence. First, as discussed in section II.B.3 above, 
the currently available information continues to provide evidence that 
this C-R relationship is nonlinear across the range of blood Pb levels 
from the higher concentrations

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more prevalent in the past to lower concentrations more common today. 
Thus, the PA continues to consider it particularly appropriate to focus 
on the evidence from studies with blood Pb levels closest to those of 
today's population which, as in the last review, includes studies with 
study group mean blood Pb levels ranging roughly from 3 to 4 [mu]g/dL 
in children aged 24 months to 7 years (PA, Table 3-3). As discussed in 
section II.B.3 above, this is also consistent with the evidence 
currently available for this age group of young children, which does 
not include additional C-R slopes for incremental neurocognitive 
decrement with blood Pb levels at or below this range. In considering 
whether this set of functions continues to be well supported by the 
evidence, as assessed in the ISA (ISA, section 4.3.2), the PA notes the 
somewhat wide range in slopes encompassed by these study groups, while 
also noting the stability of the median. For example, omission of any 
of the four slopes considered in the last review does not appreciably 
change the median (e.g., the median would change from -1.75 IQ points 
per [mu]g/dL blood Pb to -1.71 or -1.79). Thus, while differing 
judgments might be made with regard to inclusion of each of the four 
study groups, these estimates are generally supported by the current 
review of the evidence in the ISA. Further, the stability of the median 
to modifications to this limited dataset lead the PA to conclude that 
the currently available evidence continues to support consideration of 
-1.75 IQ points per [mu]g/dL blood Pb as a well-founded and stable 
estimate for purposes of describing the neurocognitive impact 
quantitatively on this age group of U.S. children.
    In summary, in considering the evidence and information available 
in this review pertaining to the level of the current Pb standard, the 
PA notes that the evidence available in this review, as summarized in 
the ISA, continues to support the air-related IQ loss evidence-based 
framework, with the inputs that were used in the last review. These 
include estimates of air-to-blood ratios ranging from 1:5 to 1:10, with 
a generally central estimate of 1:7. Additionally, the C-R functions 
most relevant to blood Pb levels in U.S. children today continue to be 
provided by the set of four analyses considered in the last review for 
which the median estimate is -1.75 IQ points per [mu]g/dL Pb in young 
children's blood. Thus, the PA observed that the evidence available in 
this review has changed little if at all with regard to the aspects 
given weight in the conclusion on level for the new standard in the 
last review and would not appear to call into question any of the basic 
elements of the standard. In so doing, the PA additionally recognizes 
that the overall decision on adequacy of the current standard is a 
public health policy judgment by the Administrator.
2. Exposure/Risk-Based Considerations in the Policy Assessment
    In consideration of the issue of adequacy of public health 
protection provided by the current standard, the PA also considered the 
quantitative exposure/risk assessment completed in the last review, 
augmented as described in section II.C above. The PA recognizes 
substantial uncertainty inherent in the REA estimates of air-related 
risk associated with localized conditions just meeting the current 
standard, which we have characterized as approximate and falling within 
rough bounds.\66\ This approximate estimate of risk for children living 
in such areas is generally overlapping with and consistent with the 
evidence-based air-related IQ loss estimates described in section 
II.A.1 above. The PA discussion with regard to interpretation of the 
exposure/risk information for air quality conditions associated with 
just meeting the current standard is organized around two questions, as 
summarized here (PA, section 4.2.2).
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    \66\ We note that the value of the upper bound is influenced by 
risk associated with exposure pathways that were not varied with 
alternative standard levels, a modeling limitation with the 
potential to contribute to overestimation of the upper bound with 
air quality scenarios involving air Pb levels below current 
conditions for the study area (see sections 3.4.4 and 3.4.7 above).
---------------------------------------------------------------------------

    In considering the level of confidence associated with estimates of 
air-related risk generated for simulations just meeting the current Pb 
standard, the PA recognizes, as an initial matter, the significant 
limitations and complexity associated with the risk and exposure 
assessments for Pb that are far beyond those associated with similar 
assessments typically performed for other criteria pollutants. In 
completing the assessment, we were constrained by significant 
limitations with regard to data and tools particular to the problem at 
hand. Further, the multimedia and persistent nature of Pb and the role 
of multiple exposure pathways contribute significant additional 
complexity to the assessment as compared to other assessments that 
focus only on the inhalation pathway. As a result, the estimates of 
air-related exposure and risk are approximate, presented as upper and 
lower bounds within which we consider air-related risk likely to fall. 
The description of overall confidence in this characterization of air-
related risk is based on consideration of the overall design of the 
analysis (summarized in section II.D), the degree to which key sources 
of variability are reflected in the design of the analysis (summarized 
in section II.D.3), and our characterization of key sources of 
uncertainty (summarized in section II.D.3).
    With regard to key sources of uncertainty, the PA notes 
particularly those affecting the precision of the air-related risk 
estimates. Associated sources of uncertainty include the inability to 
simulate changes in air-related Pb as a function of changes in ambient 
air Pb in exposure pathways other than those involving inhalation of 
ambient air and ingestion of indoor dust. This contributes to the 
positive bias of the upper bound for the air-related risk estimates. 
The PA additionally recognizes the significant uncertainty associated 
with estimating upper percentiles of the distribution of air-related 
blood Pb concentration estimates (and associated IQ loss estimates) due 
to limitations in available information. Lastly, the PA recognizes the 
uncertainty associated with application of the C-R function at the 
lower blood Pb levels in the distribution; this relates to the limited 
representation of blood Pb levels of this magnitude in the dataset from 
which the C-R function is derived (PA, section 4.2.2).
    In the quantitative risk information available in this review, we 
have air-related risk estimates for simulations just meeting the 
current standard from one of the location-specific urban case studies 
(Chicago) and from the generalized (local) urban case study. With 
regard to the latter, the PA notes its simplified design that does not 
include multiple exposure zones; thus reducing the dimensions 
simulated. The PA concludes a reasonable degree of confidence in 
aspects of the generalized (local) urban case study for the specific 
situation we consider it to represent (i.e., a temporal pattern of air 
Pb concentrations that just meets the level of the standard), and when 
the associated estimates are characterized as approximate, within upper 
and lower bounds (as described above), while also recognizing 
considerable associated uncertainty.
    In considering the extent to which the estimated air-related risks 
remaining upon just meeting the current Pb standard are important from 
a public health perspective, the PA considers the nature and magnitude 
of such estimated risks (and attendant uncertainties), including such 
impacts on the affected

[[Page 310]]

population, and additionally considers the size of the affected 
population. In considering the quantitative risk estimates for 
decrements in IQ, we recognize that although some neurocognitive 
effects may be transient, some effects may persist into adulthood, 
affecting success later in life (ISA, sections 1.9.5 and 4.3.14). The 
PA additionally recognizes the potential population impacts of small 
changes in population mean values of metrics such as IQ, presuming a 
uniform manifestation of Pb-related decrement across the range of 
population IQ (ISA, section 1.9.1; PA, section 3.3).
    As summarized in sections II.D above, limitations in modeling tools 
and data affected our ability to develop precise risk estimates for 
air-related Pb exposure pathways and contributed uncertainties to the 
risk estimates. The results are approximate estimates which we describe 
through the use of rough upper and lower bounds within which we 
estimate air-related risk to fall. We have recognized a number of 
uncertainties in the underlying risk estimates from the 2007 REA and in 
the interpolation approach employed in the new analyses for this 
review. We have characterized the magnitude of air-related risk 
associated with the current standard with a focus on median estimates, 
for which we have appreciably greater confidence than estimates for 
outer ends of risk distribution (see section 3.4.7 of the PA) and on 
risks derived using the C-R function in which we have greatest 
confidence (see sections 3.4.3.3.1 and 3.4.7 of the PA). These risk 
estimates include estimates from the last review for one of the 
location-specific urban study area populations as well as estimates 
newly derived in this review based on interpolation from 2007 REA 
results for the generalized (local) urban case study, which is 
recognized to reflect a generalized high end of air-related exposure 
for localized populations. Taken together, these results for just 
meeting the current standard include a high-end localized risk estimate 
for air-related Pb of a magnitude falling within general rough bounds 
of 1 and 3 points IQ loss, with attendant uncertainties, and with 
appreciably lower risks with increasing distance from the highest 
exposure locations.
    In considering the importance of such risk from a public health 
perspective, the PA also considers the size of at-risk populations 
represented by the REA case studies. As summarized in section II.D.1 
above (and described more fully in the PA, section 3.4), the 
generalized (local) urban case study is considered to represent a 
localized urban population exposed near the level of the standard, such 
as a very small, compact neighborhood near a source contributing to air 
Pb concentrations just meeting the standard. This case study provides 
representation in the risk assessment for such small populations at the 
upper end of the gradient in ambient air concentrations expected to 
occur near sources; thus estimates for this case study reflect 
exposures nearest the standard being evaluated. While we do not have 
precise estimates of the number of young children living in such areas 
of the U.S. today, we have information that informs our understanding 
of their magnitude. For example, as summarized in section II.B.5 above, 
the PA estimates some 2,700 children, aged 5 years and younger, to be 
living in localized areas with elevated air Pb concentrations that are 
above or near the current standard. Based on the 2010 census estimates 
of approximately 24.3 million children in the U.S. aged 5 years or 
younger, this indicates the size of the population of young children of 
this age living in areas in close proximity to areas where air Pb 
concentrations may be above or near the current standard to be 
generally on the order of a hundredth of a percent of the full 
population of correspondingly aged children.67 68 While 
these estimates pertain to the age group of children aged 5 years and 
younger, the PA additionally notes that a focus on an alternative age 
range (e.g., through age 7), while increasing the number for children 
living in such locations, would not be expected to appreciably change 
the percentage of the full U.S. age group that the subset represents.
---------------------------------------------------------------------------

    \67\ The areas included in this estimate where the standard is 
currently exceeded are treated, for present purposes, as areas with 
air Pb concentrations just meeting the current standard and are 
included for purposes of this analysis (PA, pp. 3-36 to 3-38). This 
is in light of the requirement for areas not in attainment with the 
standard to attain the standard as expeditiously as practicable, but 
no later than 5 years after designation.
    \68\ A second PA analysis, performed in recognition of the 
potential for the first analysis to under-represent sites with 
elevated Pb concentrations, but with its own attendant 
uncertainties, indicates the potential for the population group in 
such areas to be only slightly larger, in terms of hundredths of a 
percent of the full population of children in this age group (PA, 
pp. 3-36 to 3-38, 4-25, 4-32).
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3. CASAC Advice
    In the current review of the primary standard for Pb, the CASAC has 
provided advice and recommendations in their review of drafts of the 
ISA, of the REA Planning Document, and of the draft PA. We have 
additionally received comments from the public on drafts of these 
documents.\69\
---------------------------------------------------------------------------

    \69\ As noted in section II.E.3 above, written comments 
submitted to the agency, as well as transcripts and minutes of the 
public meetings held in conjunction with CASAC's reviews of 
documents for the review will be available in the docket for this 
rulemaking.
---------------------------------------------------------------------------

    In their comments on the draft PA, the CASAC concurred with staff's 
overall preliminary conclusions that it is appropriate to consider 
retaining the current primary standard without revision, stating that 
``the current scientific literature does not support a revision to the 
Primary Lead (Pb) National Ambient Air Quality Standard (NAAQS)'' 
(Frey, 2013b). They further noted that ``[a]lthough the current review 
incorporates a substantial body of new scientific literature, the new 
literature does not justify a revision to the standards because it does 
not significantly reduce substantial data gaps and uncertainties (e.g., 
air-blood Pb relationship at low levels; sources contributing to 
current population blood Pb levels, especially in children; the 
relationship between Pb and childhood neurocognitive function at 
current population exposure levels; the relationship between ambient 
air Pb and outdoor dust and surface soil Pb concentrations).'' In 
recognition of these limitations in the available information, the 
CASAC provided recommendations on research to address these data gaps 
and uncertainties so as to inform future Pb NAAQS reviews (Frey, 
2013b).
    The CASAC comments indicated agreements with key aspects of staff's 
consideration of the exposure/risk information and currently available 
evidence in this review (Frey, 2013b, Consensus Response to Charge 
Questions, p. 7).

    The use of exposure/risk information from the previous Pb NAAQS 
review appears appropriate given the absence of significant new 
information that could fundamentally change the interpretation of 
the exposure/risk information. This interpretation is reasonable 
given that information supporting the current standard is largely 
unchanged since the current standard was issued.
    The CASAC agrees that the adverse impact of low levels of Pb 
exposure on neurocognitive function and development in children 
remains the most sensitive health endpoint, and that a primary Pb 
NAAQS designed to protect against that effect will offer 
satisfactory protection against the many other health impacts 
associated with Pb exposure.
    The CASAC concurs with the draft PA that the scientific findings 
pertaining to air-to-blood Pb ratios and the C-R relationships 
between blood Pb and childhood IQ decrements that formed the basis 
of the current Pb NAAQS remain valid and are consistent with current 
data.

[[Page 311]]

    The CASAC concurred with the appropriateness of the application of 
the evidence-based framework from the last Pb NAAQS review. With regard 
to the key inputs to that framework, CASAC concluded that ``[t]he new 
literature published since the previous review provides further support 
for the health effect conclusions presented in that review'' and that 
the studies newly available in this review ``do not fundamentally alter 
the uncertainties for air-to-blood ratios or C-R functions for IQ 
decrements in young children'' (Frey, 2013b, Consensus Response to 
Charge Questions, p. 6).
    The comments from CASAC also took note of the uncertainties that 
remain in this review, which contribute to the uncertainties associated 
with drawing conclusions regarding air-related exposures and associated 
health risk at or below the level of the current standard, stating 
their agreement with ``the EPA conclusion that `there is appreciable 
uncertainty associated with drawing conclusions regarding whether there 
would be reductions in blood Pb levels from alternative lower levels as 
compared to the level of the current standard' '' (Frey, 2013b, 
Consensus Response to Charge Questions, p. 6).
    Of the limited public comments received on this review to date that 
have addressed adequacy of the current primary Pb standard, all but one 
state support for retaining the current standard without revision, 
citing uncertainties in the available evidence and risk information. 
The other commenter expressed the view that the standard should be 
revised to be more restrictive given the evidence of Pb effects in 
populations with mean blood Pb levels below 10 [micro]g/dL.
4. Administrator's Proposed Conclusions on the Adequacy of the Current 
Primary Standard
    Based on the large body of evidence concerning the health effects 
and potential public health impacts of exposure to Pb emitted into 
ambient air, and taking into consideration the attendant uncertainties 
and limitations of the evidence, the Administrator proposes to conclude 
that the current primary standard provides the requisite protection of 
public health, with an adequate margin of safety and should be 
retained.
    In considering the adequacy of the current standard, the 
Administrator has carefully considered the assessment of the available 
evidence and conclusions contained in the ISA; the technical 
information, including exposure/risk information, staff conclusions, 
and associated rationale, presented in the PA; the advice and 
recommendations from CASAC; and public comments to date in this review. 
In the discussion below, the Administrator gives weight to the PA 
conclusions, with which CASAC has concurred, and takes note of key 
aspects of the rationale presented for those conclusions which 
contribute to her proposed decision.
    As an initial matter, the Administrator takes note of the PA 
discussion with regard to the complexity involved in considering the 
adequacy of protection in the case of the primary Pb standard, which 
differs substantially from that involved in consideration of the 
primary NAAQS for other pollutants, for which the limited focus on the 
inhalation pathway is a relatively simpler context. Additionally, while 
an important component of the evidence base for most other NAAQS 
pollutants is the availability of studies that have investigated an 
association between current concentrations of the pollutant in ambient 
air and the occurrence of health effects plausibly related to ambient 
air exposure to that pollutant, the evidence base that supports 
conclusions in this review of the Pb NAAQS includes most prominently 
epidemiological studies focused on associations of blood Pb levels in 
U.S. populations with health effects plausibly related to Pb exposures. 
Support for conclusions regarding the plausibility for ambient air Pb 
to play a role in such findings derives, in part, from studies linking 
Pb in ambient air with the occurrence of health effects. However, such 
studies (dating from the past or from other countries) involve ambient 
air Pb concentrations many times greater than those that would meet the 
current standard. Thus, in considering the adequacy of the current Pb 
standard, rather than considering studies that have directly 
investigated current concentrations of Pb in ambient air (including in 
locations where the current standard is met) and the occurrence of 
health effects, we primarily consider the evidence for, and risk 
estimated from, models, based upon key relationships, such as those 
among ambient air Pb, Pb exposure, blood Pb and health effects. This 
evidence, with its associated limitations and uncertainties, 
contributes to the EPA's conclusions regarding a relationship between 
ambient air Pb conditions under the current standard and health 
effects.
    With regard to the current evidence, the Administrator first takes 
note of the well-established body of evidence on the health effects of 
Pb, augmented in some aspects since the last review, which continues to 
support identification of neurocognitive effects in young children as 
the most sensitive endpoint associated with Pb exposure. The evidence, 
as summarized in the PA and discussed in detail in the ISA, continues 
to indicate that a standard that provides protection from 
neurocognitive effects in young children additionally provides 
protection for other health effects of Pb, such as those reported in 
adult populations. The Administrator takes note of the PA finding that 
application of the evidence-based, air-related IQ loss framework, 
developed in the last review, continues to provide a useful approach 
for considering and integrating the evidence on relationships between 
Pb in ambient air and Pb in children's blood and risks of 
neurocognitive effects (for which IQ loss is used as an indicator). She 
additionally takes note of the PA finding (described in section II.E.1 
above) that the currently available evidence base, while somewhat 
expanded since the last review, is not appreciably expanded or 
supportive of appreciably different conclusions with regard to air-to-
blood ratios or C-R functions for neurocognitive decrements in young 
children. She concurs with the PA findings, summarized in section 
II.E.1 above, that application of this framework, in light of the 
current evidence and exposure/risk information, continues to support a 
standard as protective as the current standard.
    In considering the nature and magnitude of the array of 
uncertainties that are inherent in the scientific evidence and 
analyses, the Administrator recognizes that our understanding of the 
relationships between the presence of a pollutant in ambient air and 
associated health effects is based on a broad body of information 
encompassing not only more established aspects of the evidence, but 
also aspects in which there may be substantial uncertainty. In the case 
of the Pb NAAQS review, she takes note of the recognition in the PA of 
increased uncertainty in characterizing the relationship of effects on 
IQ with blood Pb levels below those represented in the evidence base 
and in projecting the magnitude of blood Pb response to ambient air Pb 
concentrations at and below the level of the current standard. The PA 
recognizes this increased uncertainty, particularly in light of the 
multiple factors that play a role in such a projection (e.g., 
meteorology, atmospheric dispersion and deposition, human physiology 
and behavior), each of which carry attendant uncertainties. The 
Administrator recognizes that collectively, these aspects of the

[[Page 312]]

evidence and associated uncertainties contribute to a recognition that 
for Pb, as for other pollutants, 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.
    In making a judgment on the point at which health effects 
associated with Pb become important from a public health perspective, 
the Administrator has considered the public health significance of a 
decrement of a very small number of IQ points in the at-risk population 
of young children, in light of associated uncertainties. She notes that 
her judgment on this matter relates to her consideration of the IQ loss 
estimates yielded by the air-related IQ loss evidence-based framework 
for specific combinations of standard level, air-to-blood ratio and C-R 
function. In considering the public health significance of IQ loss 
estimates in young children, the Administrator gives weight to the 
comments of CASAC and some public commenters in the last review which 
recognized a population mean IQ loss of 1 to 2 points to be of public 
health significance and recommended that a very high percentage of the 
population be protected from such a magnitude of IQ loss (73 FR 67000, 
November 12, 2008). In so doing, the Administrator additionally notes 
that the EPA is aware of no new information or new commonly accepted 
guidelines or criteria within the public health community for 
interpreting public health significance of neurocognitive effects in 
the context of a decision on adequacy of the current Pb standard (PA, 
pp. 4-33 to 4-34).
    With the objective identified by CASAC in the 2008 review in mind, 
the Administrator considers the role of the air-related IQ loss 
evidence-based framework in informing consideration of standards that 
might be concluded to provide such a level of protection. In so doing, 
she first recognizes, like the Administrator at the time of the last 
review, that the IQ loss estimates produced with the evidence-based 
framework do not correspond to a specific quantitative public health 
policy goal for air-related IQ loss that would be acceptable or 
unacceptable for the entire population of children in the U.S. Rather, 
the conceptual context for the evidence-based framework is that it 
provides estimates for the mean air-related IQ loss of a subset of the 
population of U.S. children (i.e., the subset living in close proximity 
to air Pb sources that contributed to elevated air Pb concentrations 
that equal the current level of the standard). This is the subset 
expected to experience air-related Pb exposures at the high end of the 
national 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. Further, the Administrator recognizes uncertainties 
associated with those estimates, and notes the PA conclusion that the 
uncertainties increase with estimates associated with successively 
lower standard levels. The Administrator additionally takes note of the 
PA estimates for the size of such a population, drawn from information 
on numbers of young children (aged 5 years or younger) living near 
monitors registering ambient Pb concentrations above or within 10 
percent of the NAAQS, which indicate it to be on the order of one 
hundredth of one percent of the U.S. population of children of this 
age, with an upper bound of approximately four hundredths of one 
percent, drawn from similar demographic information based on proximity 
to large Pb sources, as identified using the NEI (PA, pp. 3-36 to 3-
38). In summary, the current evidence, as considered within the 
conceptual and quantitative context of the evidence-based framework, 
and current air monitoring information indicates that the current 
standard would be expected to satisfy the public health policy goal 
recommended by CASAC in the last Pb NAAQS review, and CASAC did not 
provide a different goal in the present review. Thus, the evidence 
indicates that the current standard provides protection for young 
children from neurocognitive impacts, including IQ loss, consistent 
with advice from CASAC regarding IQ loss of public health significance.
    In drawing conclusions from application of the evidence-based 
framework with regard to adequacy of the current standard, the 
Administrator further recognizes the degree to which IQ loss estimates 
drawn from the air-related IQ loss evidence-based framework reflect 
mean blood Pb levels that are below those represented in the currently 
available evidence for young children. For example, in the case of the 
current standard level of 0.15 [micro]g/m\3\, multiplication by the 
air-to-blood ratio of 1:7, the value that was the focus of the last 
review and which the evidence continues to support in this review, 
yields a mean air-related blood Pb level of 1.05 [micro]g/dL. This 
blood Pb level is half the level of the lowest blood Pb subgroup of 
pre-school children in which neurocognitive effects have been observed 
(PA, Table 3-2; Miranda et al., 2009) and well below the means of 
subgroups for which continuous C-R functions have been estimated (Table 
1 above). The Administrator views such an extension below the lowest 
studied levels to be reasonable given the lack of identified blood Pb 
level threshold in the current evidence base for neurocognitive effects 
and the need for the NAAQS to provide a margin of safety. She takes 
note, however, of the PA finding that the framework IQ loss estimates 
for standard levels lower than the current standard level represent 
still greater extrapolations from the current evidence base with 
corresponding increased uncertainty (PA, section 3.2, pp. 4-32 to 4-
33).
    In considering application of the evidence-based framework in this 
review with regard to the extent there is support within the evidence 
for a standard with greater protection, the Administrator additionally 
takes note of the uncertainties that remain in our understanding of 
important aspects of ambient air Pb exposure and associated health 
effects, as discussed in the PA (PA, Chapter 3) and summarized in 
sections II.B and II.C above. With regard to the air-to-blood ratios 
that reflect the relationship between concentrations of Pb in ambient 
air and air-related Pb in children's blood, she particularly notes the 
limitations and uncertainties identified in the ISA and PA with regard 
to the available studies and the gaps and uncertainties in the evidence 
base. These include gaps and uncertainties with regard to studies that 
have investigated such quantitative relationships under conditions 
pertaining to the current standard (e.g., in localized areas near air 
Pb sources where the standard is just met in the U.S. today), as well 
as with regard to evidence to inform our understanding of the 
quantitative aspects of relationships between ambient air Pb and 
outdoor soil/dust Pb and indoor dust Pb. These critical exposure 
pathways are also represented in the evidence-based air-related IQ loss 
framework within the estimates of air-to-blood ratios. In light of 
these uncertainties and limitations in the evidence base, the 
Administrator gives weight to the PA conclusion of greater uncertainty 
with regard to relationships between concentrations of Pb in ambient 
air and air-related Pb in children's blood, and with regard to 
estimates of the slope of the C-R function of neurocognitive impacts 
(IQ loss) for application of the framework to

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levels below the current standard, given the weaker linkage with 
existing evidence as discussed in the PA (PA, sections 3.1, 3.2 and 
4.2.1).
    With respect to exposure/risk-based considerations, as in the last 
review, the Administrator notes the complexity of the REA modeling 
analyses and the associated limitations and uncertainties. Based on 
consideration of the risk-related information for conditions just 
meeting the current standard, the Administrator takes note of the 
attendant uncertainties, discussed in detail in the PA (PA, sections 
3.4 and 4.2.2), while finding that the quantitative risk estimates, 
with a focus on those for the generalized (local) urban case study, are 
``roughly consistent with and generally supportive'' of estimates from 
the evidence-based air-related IQ loss framework. She further takes 
note of the PA finding of increasing uncertainty for air quality 
scenarios involving air Pb concentrations increasingly below the 
current conditions for each case study, due in part to modeling 
limitations that derive from uncertainty regarding relationships 
between ambient air Pb and outdoor soil/dust Pb and indoor dust Pb (PA, 
sections 3.4.3.1 and 3.4.7).
    Based on the above considerations and with consideration of advice 
from CASAC, the Administrator reaches the conclusion that the current 
body of evidence, in combination with the exposure/risk information, 
supports a primary standard as protective as the current standard. 
Based on consideration of the evidence and exposure/risk information 
available in this review with its attendant uncertainties and 
limitations and information that might inform public health policy 
judgments, as well as advice from CASAC, including their concurrence 
with the PA conclusions that revision of the primary Pb standard is not 
warranted at this time, the Administrator further concludes that it is 
appropriate to consider retaining the current standard without 
revision.
    The Administrator bases these proposed conclusions on consideration 
of the health effects evidence, including consideration of this 
evidence in the context of the evidence-based, air-related IQ loss 
framework, and with support from the exposure/risk information, 
recognizing the uncertainties attendant with both. In so doing, she 
takes note of the PA description of the complexities and limitations in 
the evidence base associated with reaching conclusions regarding the 
magnitude of risk associated with the current standard, as well as the 
increasing uncertainty of risk estimates for lower air Pb 
concentrations. Inherent in the Administrator's conclusions are public 
health policy judgments on the public health implications of the blood 
Pb levels and risk estimated for air-related Pb under the current 
standard, including the public health significance of the Pb effects 
being considered, as well as aspects of the use of the evidence-based 
framework that may be considered to contribute to the margin of safety. 
These public health policy judgments include judgments related to the 
appropriate degree of public health protection that should be afforded 
to protect against risk of neurocognitive effects in at-risk 
populations, such as IQ loss in young children, as well as with regard 
to the appropriate weight to be given to differing aspects of the 
evidence and exposure/risk information, and how to consider their 
associated uncertainties. Based on these considerations and the 
judgments identified here, the Administrator concludes that the current 
standard provides the requisite protection of public health with an 
adequate margin of safety, including protection of at-risk populations, 
such as young children living near Pb emissions sources where ambient 
concentrations just meet the standard.
    In reaching this conclusion with regard to the adequacy of public 
health protection afforded by the existing primary standard, the 
Administrator recognizes that in establishing primary standards under 
the Act that are requisite to protect public health with an adequate 
margin of safety, she is seeking 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, even if the risk is not precisely identified as to nature or 
degree. The CAA 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, as described in section I.A above. This 
requirement was also intended to provide a reasonable degree of 
protection from hazards that research has not yet identified.
    In this context, the Administrator's proposed conclusion that the 
current standard provides the requisite protection and that a more 
restrictive standard would not be requisite additionally recognizes 
that the uncertainties and limitations associated with the many aspects 
of the estimated relationships between air Pb concentrations and blood 
Pb levels and associated health effects are amplified with 
consideration of increasingly lower air concentrations. In so doing, 
she takes note of the PA conclusion, with which CASAC has agreed, that 
based on the current evidence, there is appreciable uncertainty 
associated with drawing conclusions regarding whether there would be 
reductions in blood Pb levels and risk to public health from 
alternative lower levels of the standard as compared to the level of 
the current standard (PA, pp. 4-35 to 4-36; Frey, 2013b, p. 6). The 
Administrator judges this uncertainty to be too great for the current 
evidence and exposure/risk information to provide a basis for revising 
the current standard. Thus, based on the public health policy judgments 
described above, including the weight given to uncertainties in the 
evidence, the Administrator proposes to conclude that the current 
standard should be retained, without revision. The Administrator 
solicits comment on this conclusion.

III. Rationale for Proposed Decision on the Secondary Standard

    This section presents information relevant to the rationale for the 
Administrator's proposed decision to retain the existing secondary Pb 
standard, which as discussed more fully below, is based on a thorough 
review in the ISA of the latest scientific information, generally 
published through September 2011,\70\ on ecological or welfare 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 potential ecological exposures and risk, 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.
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    \70\ 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).

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[[Page 314]]

    Section III.A provides background on the general approach for 
review of the secondary NAAQS for Pb, including a summary of the 
approach used in the last review (section III.A.1) and the general 
approach for the current review (section III.A.2). Section III.B 
summarizes the body of evidence on ecological or welfare effects 
associated with Pb exposures, focusing on consideration of key policy-
relevant questions, and section III.C summarizes the exposure/risk 
information in this review. Section III.D presents the Administrator's 
proposed conclusions on adequacy of the current standard, drawing on 
both evidence-based and exposure/risk-based considerations (sections 
III.D.1), and advice from CASAC (section III.D.2).

A. General Approach

    The past and current approaches described below are all based most 
fundamentally on using the EPA's assessment of the current scientific 
evidence and previous quantitative analyses to inform the 
Administrator's judgment with regard to the secondary standard for Pb. 
In drawing conclusions for the Administrator's consideration with 
regard to the secondary standard, we note that the final decision on 
the adequacy of the current secondary Pb standard is largely a public 
welfare policy judgment to be made by the Administrator. The 
Administrator's final decision must draw upon scientific information 
and analyses about welfare effects, exposure and risks, as well as 
judgments about the appropriate response to the range of uncertainties 
that are inherent in the scientific evidence and analyses. This 
approach is consistent with the requirements of the NAAQS provisions of 
the Act. These provisions require the Administrator to establish a 
secondary standard that, in the judgment of the Administrator, 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.'' In so doing, the Administrator seeks to establish 
standards that are neither more nor less stringent than necessary for 
this purpose.
1. Approach in the Last Review
    In the last review, completed in 2008, the current secondary 
standard for Pb was set equal to the primary standard (73 FR 66964, 
November 12, 2008). As summarized in sections I.C and II.A.1 above, the 
primary standard was substantially revised in the last review. 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 2006 CD and the screening-
level ecological risk assessment (2006 REA; USEPA, 2007b), the advice 
and recommendations of CASAC (Henderson 2007a, 2007b, 2008a, 2008b), 
and public comment.
    In the previous review, the Staff Paper concluded, based on 
laboratory studies and current media concentrations in a wide range of 
locations, that it seemed likely that adverse effects were occurring 
from ambient air-related Pb, particularly near point sources, under the 
then-current standard (73 FR 67010, November 12, 2008). Given the 
limited data on Pb effects in ecosystems, and associated uncertainties, 
such as those with regard to factors such as the presence of multiple 
metals and historic environmental burdens, it was at the time, as it is 
now, necessary to look at evidence of Pb effects on organisms and 
extrapolate to ecosystem effects. Taking into account the available 
evidence and current media concentrations in a wide range of locations, 
the Administrator concluded that there was potential for adverse 
effects occurring under the then-current standard; however there were 
insufficient data to provide a quantitative basis for setting a 
secondary standard different from the primary (73 FR 67011, November 
12, 2008). Therefore, citing a general lack of data that would indicate 
the appropriate level of Pb in environmental media that may be 
associated with adverse effects, as well as the comments of the CASAC 
Pb panel that a significant change to current air concentrations (e.g., 
via a significant change to the standard) was likely to have 
significant beneficial effects on the magnitude of Pb exposures in the 
environment, the secondary standard was revised to be consistent with 
the revised primary standard (73 FR 67011, November 12, 2008).
2. Approach for the Current Review
    Our approach for reviewing the current secondary standard takes 
into consideration the approaches used in the last Pb NAAQS review and 
involves addressing key policy-relevant questions in light of currently 
available scientific and technical information. In evaluating whether 
it is appropriate to consider retaining the current secondary Pb 
standard, or whether consideration of revision is appropriate, we have 
adopted an approach in this review that builds on the general approach 
from the last review and reflects the body of evidence and information 
now available. As summarized above, the Administrator's decisions in 
the previous review were based on the conclusion that there was the 
potential for adverse ecological effects under the previous standard.
    In our approach here, we focus on consideration of the extent to 
which a broader body of scientific evidence is now available that would 
inform decisions on either the potential for adverse effects to 
ecosystems under the current standard or the ability to set a more 
ecologically relevant secondary standard than was feasible in the 
previous review. In considering the scientific and technical 
information in sections II.B and II.C below, as in the PA, we draw on 
the ecological effects evidence presented in detail in the ISA and 
aspects summarized in the PA, along with the information associated 
with the screening-level risk assessment also in the PA. In section 
III.D below, we have taken into account both evidence-based and risk-
based considerations framed by a series of policy-relevant questions 
presented in the PA. These questions generally discuss the extent to 
which we are able to better characterize effects and the likelihood of 
adverse effects in the environment under the current standard. Our 
approach to considering these issues recognizes that the available 
welfare effects evidence generally reflects laboratory-based evidence 
of toxicological effects on specific organisms exposed to 
concentrations of Pb. It is widely recognized, however, that 
environmental exposures from atmospherically derived Pb are likely to 
be lower than those commonly assessed in laboratory studies and that 
studies of exposures similar to those in the environment are often 
accompanied by significant confounding and modifying factors (e.g., 
other metals, acidification), increasing our uncertainty about the 
likelihood and magnitude of organism and ecosystem responses.

B. Welfare Effects Information

    Welfare effects addressed by the secondary NAAQS include, but are 
not limited to, effects on soils, water, crops, vegetation, manmade 
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 
wellbeing. This discussion presents key aspects of the current evidence 
of Pb-related welfare effects that are assessed in the ISA and the 2006 
CD, drawing from the summary of policy-relevant aspects in the PA (PA, 
section 5.1).
    Lead has been demonstrated to have harmful effects on reproduction 
and development, growth, and survival in

[[Page 315]]

many species as described in the assessment of the evidence available 
in this review and consistent with the conclusions drawn in the last 
review (ISA, section 1.7; 2006 CD, sections 7.1.5 and 7.2.5). A number 
of studies on ecological effects of Pb are newly available in this 
review and are critically assessed in the ISA as part of the full body 
of evidence. The full body of currently available evidence reaffirms 
conclusions on the array of effects recognized for Pb in the last 
review (ISA, section 1.7). In so doing, in the context of pollutant 
exposures considered relevant the ISA determines \71\ that causal \72\ 
or likely causal \73\ relationships exist in both freshwater and 
terrestrial ecosystems for Pb with effects on reproduction and 
development in vertebrates and invertebrates; growth in plants and 
invertebrates; and survival in vertebrates and invertebrates (ISA, 
Table 1-3). 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 ISA notes that 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 for health, ecological or welfare effects, 
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 to lxi).
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    \71\ 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).
    \72\ In determining that a causal relationship exists for Pb 
with specific ecological or welfare effects, the EPA has concluded 
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).
    \73\ In determining a likely causal relationship exists for Pb 
with specific ecological or welfare effects, the EPA has concluded 
that ``[e]vidence is sufficient to conclude that there is a likely 
causal association with relevant pollutant exposures . . . but 
uncertainties remain'' (ISA, p. lxii).
---------------------------------------------------------------------------

    Although considerable uncertainties are recognized in generalizing 
effects observed under particular, small-scale conditions, up to the 
ecosystem level of biological organization, the ISA determines that the 
cumulative evidence reported for Pb effects at such higher levels of 
biological organization and for endpoints in single species with direct 
relevance to population and ecosystem level effects (i.e., development 
and reproduction, growth, survival) is sufficient to conclude that a 
causal relationship is likely to exist between Pb exposures and 
community and ecosystem-level effects in freshwater and terrestrial 
systems (ISA, section 1.7.3.7).
    The ISA also presents evidence for saltwater ecosystems, concluding 
that current evidence is inadequate to make causality determinations 
for most population-level responses, as well as community and ecosystem 
effects, while finding the evidence to be suggestive linking Pb and 
effects on reproduction and development in marine invertebrates (ISA, 
Table 1-3, sections 6.3.12 and 6.4.21).
    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 about environmental 
exposures from ecological studies of organism-level effects, as most 
studies were conducted in laboratory settings which may not accurately 
represent field conditions or the multiple variables that govern 
exposure.
    The relationship between ambient air Pb and ecosystem response is 
important in making the connection between current emissions of Pb and 
the potential for adverse ecological effects. The limitations in the 
data available on this subject for the last review were significant. 
There is no new evidence since the last review that substantially 
improves our understanding of the relationship between ambient air Pb 
and measurable ecological effects. As stated in the last review, the 
role of ambient air Pb in contributing to ecosystem Pb has been 
declining over the past several decades. It remains difficult to 
apportion exposure between air and other sources to inform our 
understanding of the potential for ecosystem effects that might be 
associated with air emissions. As noted in the ISA, ``[t]he amount of 
Pb in ecosystems is a result of a number of inputs and it is not 
currently possible to determine the contribution of atmospherically-
derived Pb from total Pb in terrestrial, freshwater or saltwater 
systems'' (ISA, section 6.5). Further, considerable uncertainties also 
remain in drawing conclusions from effects evidence observed under 
laboratory conditions with regard to effects expected at the ecosystem 
level in the environment. In many cases it is difficult to characterize 
the nature and magnitude of effects and to quantify relationships 
between ambient concentrations of Pb and ecosystem response due to the 
existence of multiple stressors, variability in field conditions, and 
differences in Pb bioavailability at that level of organization (ISA, 
section 6.5). In summary, the ISA concludes that ``[r]ecent information 
available since the 2006 Pb AQCD, includes additional field studies in 
both terrestrial and aquatic ecosystems, but the connection between air 
concentration and ecosystem exposure continues to be poorly 
characterized for Pb and the contribution of atmospheric Pb to specific 
sites is not clear'' (ISA, section 6.5).
    It is also important to consider the fate and transport of both 
current Pb and Pb emitted in the past. It is this past legacy of Pb 
that was cited as a significant source of uncertainty in the last 
review. The extensive history of Pb uses in developed countries coupled 
with atmospheric transport processes has left a legacy of Pb in 
ecosystems globally (e.g., 2006 CD, sections 2.3.1 and 7.1; 1977 CD, 
section 6.3.1). Records of U.S. atmospheric emissions of Pb in the 
twentieth and late nineteenth centuries have been documented in 
sediment cores (PA, section 2.3; ISA, section 2.6.2; Landers et al., 
2010). Once deposited, Pb can be transported by stormwater runoff or 
resuspension to catchments and nearby water bodies or stored in soil 
layers in forested areas, its further movement influenced by soil or 
sediment composition and chemistry and physical processes. Some new 
studies are available that provide additional information, briefly 
summarized below, on Pb cycling, flux and retention within terrestrial 
and aquatic systems. This new information does not fundamentally change 
our understanding from the last review of Pb movement through or 
accumulation in ecosystems over time but rather improves our 
understanding of some of the underlying processes and

[[Page 316]]

mechanisms in soil, water and sediment. There is little new 
information, however, on fate and transport in ecosystems specifically 
related to air-derived Pb (ISA, section 2.3). There is limited newly 
available information with regard to the timing of ecosystem recovery 
from historic atmospheric deposition of Pb (ISA, sections 2.3.2.4 and 
2.3.3.3).
    Overall, recent studies in terrestrial ecosystems provide 
deposition data consistent with deposition fluxes reported in the 2006 
CD and demonstrate consistently that atmospheric deposition of Pb has 
decreased since the phase-out of leaded on-road gasoline (PA, section 
2.3.2.2; ISA, section 2.3.3). Follow-up studies in several locations at 
high elevation sites indicate little change in soil Pb concentrations 
since the phase-out of leaded onroad gasoline in surface soils, 
consistent with the high retention reportedly associated with reduced 
microbial activity at lower temperatures associated with high elevation 
sites. However, amounts of Pb in the surface soils at some lower 
altitude sites were reduced over the same time period in the same study 
(ISA, section 2.3.3). New studies in the ISA also enhance our 
understanding of Pb sequestration in forest soils by providing 
additional information on the role of leaf litter as a Pb reservoir in 
some situations and the effect of litter decomposition on Pb 
distribution (ISA, section 2.3.3).
    Recent research on Pb transport in aquatic systems has provided a 
large body of observations confirming that such transport is dominated 
by colloids rich in iron and organic material (ISA, section 2.3.2). 
Recent research on Pb flux in sediments provides greater detail on 
resuspension processes than was available in the 2006 CD, including 
research on resuspended Pb largely associated with organic material or 
iron and manganese particles and research on the important role played 
by anoxic or depleted oxygen environments in Pb cycling in aquatic 
systems. This newer research is consistent with prior evidence in 
indicating that appreciable resuspension and release from sediments 
largely occurs during discrete events related to storms. It has also 
confirmed that resuspension is an important process that strongly 
influences the lifetime of Pb in bodies of water. Finally, there have 
been advances in understanding and modeling of Pb partitioning between 
organic material and sediment in aquatic environments (ISA, section 
2.7.2).
    The bioavailability of Pb is also an important component of 
understanding the effects Pb is likely to have on organisms and 
ecosystems (ISA, section 6.3.3). It is the amount of Pb that can 
interact within the organism that leads to toxicity, and there are many 
factors which govern this interaction (ISA, sections 6.2.1 and 6.3.3). 
The bioavailability of metals varies widely depending on the physical, 
chemical, and biological conditions under which an organism is exposed 
(ISA, section 6.3.3). Studies newly available since the last Pb NAAQS 
review provide additional insight into factors that influence the 
bioavailability of Pb to specific organisms (ISA, section 6.3.3). In 
general, this evidence is supportive of previous conclusions and does 
not identify significant new variables from those identified 
previously. Section 6.3.3 of the ISA provides a detailed discussion of 
bioavailability in terrestrial systems. With regard to aquatic systems, 
a detailed discussion of bioavailability in freshwater systems is 
provided in sections 6.4.3 and 6.4.4 of the ISA, and section 6.4.14 of 
the ISA discusses bioavailability in saltwater systems.
    In terrestrial systems, the amount of bioavailable Pb present 
determines the impact of soil Pb to a much greater extent than does the 
total amount present (ISA, section 6.3.11). In such ecosystems, Pb is 
deposited either directly onto plant surfaces or onto soil where it can 
bind with organic matter or dissolve in pore water. The Pb dissolved in 
pore water is particularly bioavailable to organisms in the soil and, 
therefore, the impact of this Pb on the ecosystem is potentially 
greater than soil Pb that is not in pore water (ISA, section 6.3.11).
    In aquatic systems as in terrestrial systems, the amount of Pb 
bioavailable to organisms is a better predictor of effect on organisms 
than the overall amount of Pb in the system. Once atmospherically 
derived Pb enters surface water bodies through deposition or runoff, 
its fate and bioavailability are influenced by many water quality 
characteristics, such as pH, suspended solids levels and organic 
content (ISA, section 6.4.2). In sediments, bioavailability of Pb to 
sediment-dwelling organisms may be influenced by the presence of other 
metals, sulfides, iron oxides and manganese oxides and also by physical 
disturbance (ISA, section 2.6.2). For many aquatic organisms, Pb 
dissolved in the water column can be the primary exposure route, while 
for others sediment ingestion is significant (ISA, section 2.6.2). As 
recognized in the 2006 CD and further supported in the ISA, there is a 
body of evidence showing that uptake and elimination of Pb vary widely 
among aquatic species.
    There is a substantial amount of new evidence in this review 
regarding the ecological effects of Pb on individual terrestrial and 
aquatic species with less new information available on marine species 
and ecosystems. On the whole, this evidence supports previous 
conclusions that Pb has effects on growth, reproduction and survival, 
and that under some conditions these effects can be adverse to 
organisms and ecosystems. The ISA provides evidence of effects in 
additional species and in a few cases at lower exposures than reported 
in the previous review, but does not substantially alter our 
understanding of the ecological endpoints affected by Pb from the 
previous review. Looking beyond organism-level evidence, the evidence 
of adversity in natural systems remains sparse due to the difficulty in 
determining the effects of confounding factors such as co-occurring 
metals or system characteristics that influence bioavailability of Pb 
in field studies. The following paragraphs summarize the information 
presented in this review for terrestrial, aquatic and marine systems.
    With regard to terrestrial ecosystems, recent studies cited in this 
review support previous conclusions about the effects of Pb, namely 
that increasing soil Pb concentrations in areas of Pb contamination 
(e.g., mining sites and industrial sites) can cause decreases in 
microorganism abundance, diversity, and function. Previous reviews have 
also reported on effects on bird and plant communities (2006 CD, 
section AX7.1.3). The shifts in bacterial species and fungal diversity 
have been observed near long-established sources of Pb contamination 
(ISA, section 6.3.12.7). Most recent evidence for Pb toxicity to 
terrestrial plants, invertebrates and vertebrates is from single-
species assays in laboratory studies which do not capture the 
complexity of bioavailability and other modifiers of effect in natural 
systems (ISA, section 6.3.12.7). Further, models that might account for 
modifiers of bioavailability have proven difficult to develop (ISA, p. 
6-16).
    Evidence presented in the ISA and prior CDs demonstrates the 
toxicity of Pb in aquatic ecosystems and the role of many factors, 
including Pb speciation and various water chemistry properties, in 
modifying toxicity (ISA, section 1.7.2). Since the 2006 CD, additional 
evidence for community and ecosystem level effects of Pb is available, 
primarily in microcosm studies or field studies with other metals 
present (ISA, section 6.4.11). Such evidence described in

[[Page 317]]

previous CDs includes alteration of predator-prey dynamics, species 
richness, species composition, and biodiversity. New studies available 
in this review provide evidence in additional habitats for these 
community and ecological-scale effects, specifically in aquatic plant 
communities and sediment-associated communities at both acute and 
chronic exposures involving concentrations similar to those previously 
reported (ISA, section 6.4.7). In many cases, it is difficult to 
characterize the nature and magnitude of effects and to quantify 
relationships between ambient concentrations of Pb and ecosystem 
response due to existence of multiple ecosystem-level stressors, 
variability in field conditions, and differences in Pb bioavailability 
(ISA, sections 1.7.3.7 and 6.4.7). Additionally, the degree to which 
air concentrations have contributed to such effects in freshwater 
ecosystems is largely unknown.
    With regard to evidence in marine ecosystems, recently available 
evidence on the toxicity of Pb to marine algae augments the 2006 CD 
findings of variation in sensitivity across marine species. Recent 
studies on Pb exposure include reports of growth inhibition and 
oxidative stress in a few additional species of marine algae (ISA, 
section 6.4.15). Recent literature provides little new evidence of 
endpoints or effects in marine invertebrates beyond those reported in 
the 2006 CD. For example, some recent studies strengthen the evidence 
presented in the 2006 CD regarding negative effects of Pb exposure on 
marine invertebrates (ISA, section 6.4.15.2). Recent studies also 
identify several species exhibiting particularly low sensitivity to 
high acute exposures (ISA, section 6.4.15.2). Little new evidence is 
available of Pb effects on marine fish and mammals for reproductive, 
growth and survival endpoints that are particularly relevant to the 
population level of biological organization and higher (ISA, section 
6.4.15). New studies on organism-level effects from Pb in saltwater 
ecosystems (ISA, section 6.4.15) provide little evidence to inform our 
understanding of linkages among atmospheric concentrations, ambient 
exposures in saltwater systems and such effects or to inform our 
conclusions regarding the likelihood of adverse effects under 
conditions associated with the current NAAQS for Pb. Nor does the 
currently available evidence indicate significantly different exposure 
levels from the previous review at which ecological systems or 
receptors are expected to experience effects.
    During the last review, the 2006 CD assessed the available 
information on critical loads for Pb (2006 CD, section 7.3). This 
information included publications on methods and example applications, 
primarily in Europe, specific to the bedrock geology, soil types, 
vegetation, and historical deposition trends in each European country 
(2006 CD, p. E-24), with no analyses available for U.S. locations (2006 
CD, sections 7.3.4-7.3.6). As a result, the 2006 CD concluded that 
``[c]onsiderable research is necessary before critical load estimates 
can be formulated for ecosystems extant in the United States'' (2006 
CD, p. E-24).
    For this current review, newly available evidence pertaining to 
critical loads analysis includes limited recent research on 
consideration of bioavailability in characterizing Pb effect 
concentrations or indices and on modeling approaches to incorporate 
chemistry effects on Pb speciation and bioavailability (ISA, sections 
6.3.7 and 6.4.8). With consideration of this information and the four 
critical load analysis studies newly available in this review (none of 
which are for U.S. ecosystems), the ISA does not modify the conclusions 
noted above from the 2006 CD (ISA, sections 6.1.3, 6.3.7 and 6.4.8). In 
summary, the new information in this review does not appreciably change 
our evidence base or further inform our understanding of critical loads 
of Pb, including critical loads in sensitive U.S. ecosystems.
    There is no new evidence since the last review that substantially 
improves our understanding of the relationship between ambient air Pb 
and measurable ecological effects. As stated in the last review, the 
role of ambient air Pb in contributing to ecosystem Pb has been 
declining over the past several decades. It remains difficult to 
apportion exposure between air and other sources to better inform our 
understanding of the potential for ecosystem effects that might be 
associated with air emissions. As noted in the ISA, ``[t]he amount of 
Pb in ecosystems is a result of a number of inputs and it is not 
currently possible to determine the contribution of atmospherically-
derived Pb from total Pb in terrestrial, freshwater or saltwater 
systems'' (ISA, section 6.5). Further, considerable uncertainties also 
remain in drawing conclusions from evidence of effects observed under 
laboratory conditions with regard to effects expected at the ecosystem 
level in the environment. In many cases it is difficult to characterize 
the nature and magnitude of effects and to quantify relationships 
between ambient concentrations of Pb and ecosystem response due to the 
existence of multiple stressors, variability in field conditions, and 
differences in Pb bioavailability at that level of organization (ISA, 
section 6.5). In summary, the ISA concludes that ``[r]ecent information 
available since the 2006 Pb AQCD, includes additional field studies in 
both terrestrial and aquatic ecosystems, but the connection between air 
concentration and ecosystem exposure continues to be poorly 
characterized for Pb and the contribution of atmospheric Pb to specific 
sites is not clear'' (ISA, section 6.5).

C. Summary of Risk Assessment Information

    The risk assessment information available in this review and 
summarized here is based on the screening-level risk assessment 
performed for the last review, described in the 2006 REA, 2007 Staff 
Paper and 2008 notice of final decision (73 FR 66964, November 12, 
2008), as considered in the context of the evidence newly available in 
this review (PA, section 5.2). As described in the REA Planning 
Document, careful consideration of the information newly available in 
this review, with regard to designing and implementing a full REA for 
this review, led us to conclude that performance of a new REA for this 
review was not warranted (REA Planning Document, section 3.3). 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). Accordingly, the risk/
exposure information considered in this review is drawn primarily from 
the 2006 REA as summarized below (PA, section 5.2 and Appendix 5A; REA 
Planning Document, section 3.1).
    The 2006 screening-level assessment focused on estimating the 
potential for ecological risks associated with ecosystem exposures to 
Pb emitted into ambient air (PA, section 5.2; 2006 REA, section 7). A 
national-scale screen was used to evaluate surface water and sediment 
monitoring locations across the U.S. for the potential for ecological 
impacts that might be associated with atmospheric deposition of Pb 
(2006 REA, section 7.1.2). In addition to the national-scale screen 
(2006 REA, section 3.6), the assessment involved a case study approach, 
with case studies for areas surrounding a primary Pb smelter (2006 REA, 
section 3.1) and a secondary Pb smelter (2006 REA, section 3.2), as 
well as a location near a non-urban roadway (2006 REA, section 3.4). An 
additional case study, focused on

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consideration of atmospherically derived Pb effects on an ecologically 
vulnerable ecosystem (Hubbard Brook Experimental Forest), was 
identified (2006 REA, section 3.5). The Hubbard Brook Experimental 
Forest (HBEF), in the White Mountain National Forest, near North 
Woodstock, New Hampshire, was selected as a fourth case study because 
of its location and its long record of available data on concentration 
trends of Pb in three media (air or deposition from air, soil, and 
surface water). The HBEF case study was a qualitative analysis focusing 
on a summary review of the literature, without new quantitative 
analyses (2006 REA, Appendix E). For the other three case studies, 
exposure concentrations of Pb in soil, surface water, and/or sediment 
concentrations were estimated from available monitoring data or 
modeling analysis and then compared to ecological screening benchmarks 
(2006 REA, section 7.1).
    In interpreting the results from the 2006 REA, the PA considers 
newly available evidence that may inform interpretation of risk under 
the now current standard (PA, section 5.2). Factors that could alter 
our interpretation of risk would include new evidence of harm at lower 
concentrations of Pb, new linkages that enable us to draw more explicit 
conclusions as to the air contribution of environmental exposures, and 
new methods of interpreting confounding factors that were largely 
uncontrolled in the previous risk assessment. In general, however, the 
key uncertainties identified in the last review remain today.
    The results for the ecological screening assessment for the three 
case studies and the national-scale screen for surface water and for 
sediment in the last review indicated a potential for adverse effects 
from ambient Pb to multiple ecological receptor groups in terrestrial 
and aquatic locations. Detailed descriptions of the location-specific 
case studies and the national screening assessment, key findings of the 
risk assessment for each, and an interpretation of the results with 
regard to past air conditions can be found in the 2006 REA. In 
considering the potential for adverse welfare effects to result from 
levels of air-related Pb that would meet the current standard, the 
findings of the 2006 REA, as summarized in the PA, are discussed below.
    While the contribution to Pb concentrations from air as compared to 
nonair sources is not quantified, air emissions from the primary Pb 
smelter case study facility were substantial (2006 REA, Appendix B). In 
addition, this facility, which closed in 2013, had been emitting Pb for 
many decades, including some seven decades prior to establishment of 
any Pb NAAQS, such that it is likely air concentrations associated with 
the facility were substantial relative to the 1978 NAAQS, which it 
exceeded at the time of the last review. At the time of the last review 
and also since the adoption of the current standard, concentrations 
monitored near this facility have exceeded the level of the applicable 
NAAQS (2007 Staff Paper, Appendix 2B-1; PA, Appendices 2D and 5A). 
Accordingly, this case study is not informative for considering the 
likelihood of adverse welfare effects related to Pb from air sources 
under air quality conditions associated with meeting the current Pb 
standard.
    The secondary Pb smelter case study location continues to emit Pb, 
and the county where this facility is located does not meet the current 
Pb standard (PA, Appendices 2D and 5A). Given the exceedances of the 
current standard, which likely extend back over 4 to 5 decades, this 
case study also is not informative for considering the likelihood of 
adverse welfare effects related to Pb from air sources under air 
quality conditions associated with meeting the current Pb standard.
    The locations for the near-roadway non-urban case study are highly 
impacted by past deposition of gasoline Pb. It is unknown whether 
current conditions at these sites exceed the current Pb standard, but, 
given evidence from the past of Pb concentrations near highways that 
ranged above the previous (1978) Pb standard (1986 CD, section 7.2.1), 
conditions at these locations during the time of leaded gasoline very 
likely exceeded the current standard. Similarly, those conditions 
likely resulted in Pb deposition associated with leaded gasoline that 
exceeds that being deposited under air quality conditions that would 
meet the current Pb standard. Given this legacy, consideration of the 
potential for environmental risks from levels of air-related Pb 
associated with meeting the current Pb standard in these locations is 
highly uncertain.
    The extent to which past air emissions of Pb have contributed to 
surface water or sediment Pb concentrations at the locations identified 
in the national scale surface water and sediment screen is unclear. For 
some of the surface water locations, nonair sources likely contributed 
significantly to the surface water Pb concentrations. For other 
locations, a lack of nearby nonair sources indicated a potential role 
for air sources to contribute to observed surface water Pb 
concentrations. Additionally, these concentrations may have been 
influenced by Pb in resuspended sediments and may reflect contribution 
of Pb from erosion of soils with Pb derived from historic as well as 
current air emissions.
    The most useful case study to the current review is that of the 
Vulnerable Ecosystem Case Study located in the HBEF. This case study 
was focused on consideration of information which included a long 
record (from 1976 through 2000) of available data on concentration 
trends of Pb in three media (air or deposition from air, soil, and 
surface water). While no quantitative analyses were performed, a 
summary review of literature published on HBEF was developed. This 
review indicated: (1) Atmospheric Pb inputs do not directly affect 
stream Pb levels at HBEF because deposited Pb is almost entirely 
retained in the soil profile; and (2) soil horizon analysis results 
showed Pb to have become more concentrated at lower soil depths over 
time, with the soil serving as a Pb sink, appreciably reducing Pb in 
pore water as it moves through the soil layers to streams (dissolved Pb 
concentrations were reduced from 5 [mu]g/L to about 5 ng/L from surface 
soil to streams). As a result, the HBEF studies concluded that the 
contribution of dissolved Pb from soils to streams was insignificant 
(2006 REA, Appendix E). Further, atmospheric input of Pb, based on bulk 
precipitation data, was estimated to decline substantially from the 
mid-1970s to 1989; forest floor soil Pb concentrations between 1976 and 
2000 were also estimated to decline appreciably (2006 REA, sections E.1 
and E.2). In considering HBEF and other terrestrial sites with Pb 
burdens derived primarily from long-range atmospheric transport, the 
2006 CD found that ``[d]espite years of elevated atmospheric Pb inputs 
and elevated concentrations in soils, there is little evidence that 
sites affected primarily by long-range Pb transport have experienced 
significant effects on ecosystem structure or function'' (2006 CD, p. 
AX7-98). The explanation suggested by the 2006 CD for this finding is 
``[l]ow concentrations of Pb in soil solutions, the result of strong 
complexation of Pb by soil organic matter'' (2006 CD, p. AZX7-98). 
While more recent soil or stream data on Pb concentrations are not 
available, we find it unlikely, given the general evidence for air Pb 
emissions and concentration

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declines over the past several decades (e.g., PA, Figures 2-1, 2-7 and 
2-8), that conditions would have worsened from those on which these 
conclusions were drawn (e.g., soil data through 2000). Therefore, this 
information suggests that the now-lower ambient air concentrations 
associated with meeting the current standard would not be expected to 
directly impact stream Pb levels.
    With regard to new evidence of Pb effects at lower concentrations, 
it is necessary to consider that the evidence of adversity due 
specifically to Pb in natural systems is limited, in no small part 
because of the difficulty in determining the effects of confounding 
factors such as multiple metals and modifying factors influencing 
bioavailability in field studies. Modeling of Pb-related exposure and 
risk to ecological receptors is subject to a wide array of sources of 
both variability and uncertainty. Variability is associated with 
geographic location, habitat types, physical and chemical 
characteristics of soils and water that influence Pb bioavailability 
and terrestrial and aquatic community composition. Lead uptake rates by 
invertebrates, fish, and plants may vary by species and season. For 
wildlife, variability also is associated with food ingestion rates by 
species and season, prey selection, and locations of home ranges for 
foraging relative to the Pb contamination levels (USEPA, 2005b).
    There are significant difficulties in quantifying the role of air 
emissions under the current standard, which is significantly lower than 
the previous standard. As recognized in the PA, Pb deposited before the 
standard was enacted remains in soils and sediments, complicating 
interpretations regarding the impact of the current standard; historic 
Pb emitted from leaded gasoline usage continues to move slowly through 
systems along with more recently deposited Pb and Pb derived from 
nonair sources (PA, section 1.3.2). The results from the location-
specific case studies and the surface and sediment screen performed in 
the last review are difficult to interpret in light of the current 
standard and are largely not useful in informing judgments of the 
potential for adverse effects at levels of deposition meeting the 
current standard.

D. Conclusions on Adequacy of the Current Secondary Standard

1. Evidence- and Risk-Based Considerations in the Policy Assessment
    The current evidence, as discussed more fully in the PA, continues 
to support the conclusions from the previous review regarding key 
aspects of the ecological effects evidence for Pb and the effects of 
exposure associated with levels of Pb occurring in ecological media in 
the U.S. The EPA's conclusions in this regard are based on 
consideration of the assessment of the currently available evidence in 
the ISA, particularly with regard to key aspects summarized in the PA.
    In considering the welfare effects evidence with respect to the 
adequacy of the current standard, the PA considers the array of 
evidence newly assessed in the ISA with regard to the degree to which 
this evidence supports conclusions about the effects of Pb in the 
environment that were drawn in the last review and the extent to which 
it reduces previously recognized areas of uncertainty. Further, the PA 
considers the current evidence and associated conclusions about the 
potential for effects to occur as a result of the much lower ambient Pb 
concentrations allowed by the current secondary standard (set in 2008) 
than those allowed by the prior standard, which was the focus of the 
last review. These considerations, as discussed below, inform the 
Administrator's conclusions regarding the extent to which the evidence 
supports or calls into question the adequacy of protection afforded by 
the current standard.
    The range of effects that Pb can exert on terrestrial and aquatic 
organisms indicated by information available in the current review is 
summarized in the ISA (ISA, sections 1.7, 6.3 and 6.4) and largely 
mirrors the findings of the previous review (PA, section 5.1). The 
integrated synthesis contained in the ISA conveys how effects of Pb can 
vary with species and life stage, duration of exposure, form of Pb, and 
media characteristics such as soil and water chemistry. A wide range of 
organism effects are recognized, including effects on growth, 
development (particularly of the nervous system) and reproductive 
success (ISA, sections 6.3 and 6.4). Lead is recognized to distribute 
from the air into multiple environmental media, as summarized in 
section I.D above, contributing to multiple exposure pathways for 
ecological receptors. As discussed in section 5.1 of the PA, many 
factors affect the bioavailability of Pb to receptors in terrestrial 
and aquatic ecosystems, contributing to differences between laboratory-
assessed toxicity and Pb toxicity in these ecosystems, and challenging 
our consideration of environmental impacts of Pb emitted to ambient 
air.
    In studies in a variety of ecosystems, adverse ecosystem-level 
effects (including decreases in species diversity, loss of vegetation, 
changes to community composition, primarily in soil microbes and 
plants, decreased growth of vegetation, and increased number of 
invasive species) have been demonstrated near smelters, mines and other 
industries that have released substantial amounts of Pb, among other 
materials, to the environment (ISA, sections 6.3.12 and 6.4.12). As 
noted in the PA, however, our ability to characterize the role of air 
emissions of Pb in contributing to these effects is complicated because 
of coincident releases to other media and of other pollutants. Co-
released pollutants include a variety of other heavy metals, in 
addition to sulfur dioxide, which may cause toxic effects in themselves 
and may interact with Pb in the environment, contributing uncertainty 
to characterization of the role of Pb from ambient air with regard to 
the reported effects (PA, section 5.1). These uncertainties limit our 
ability to draw conclusions regarding the extent to which Pb-related 
effects may be associated with ambient air conditions that would meet 
the current standard.
    The role of historically emitted Pb poses additional complications 
in addressing this question, as discussed in the PA (PA, section 
1.3.2). The vast majority of Pb in the U.S. environment today, 
particularly in terrestrial ecosystems, was deposited in the past 
during the use of Pb additives in gasoline (2006 CD, pp. 2-82, AX7-36 
to AX7-38, AX7-98; Johnson et al., 2004), although contributions from 
industrial activities, including metals industries, have also been 
documented (ISA, section 2.2.2.3, Jackson et al., 2004). The gasoline-
derived Pb was emitted in very large quantities (2006 CD, p. AX7-98 and 
ISA, Figure 2-8) and predominantly in small sized particles which were 
widely dispersed and transported across large distances, within and 
beyond the U.S. (ISA, section 2.2). As recognized in the PA, historical 
records provided by sediment cores in various environments document the 
substantially reduced Pb deposition (associated with reduced Pb 
emissions) in many locations (PA, sections 2.3.1 and 2.3.3.2; ISA, 
section 2.2.1). As Pb is persistent in the environment, these 
substantial past environmental releases are expected to generally 
dominate current nonair media concentrations.
    There is very limited evidence to relate specific ecosystem effects 
with current ambient air concentrations of Pb through deposition to 
terrestrial and aquatic ecosystems and subsequent movement of deposited 
Pb through the environment (e.g., soil, sediment, water,

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organisms). The potential for ecosystem effects of Pb from atmospheric 
sources under conditions meeting the current standard is difficult to 
assess due to limitations on the availability of information to fully 
characterize the distribution of Pb from the atmosphere into ecosystems 
over the long term, as well as limitations on information on the 
bioavailability of atmospherically deposited Pb (as affected by the 
specific characteristics of the receiving ecosystem). Therefore, while 
information available since the 2006 CD includes additional terrestrial 
and aquatic field studies, ``the connection between air concentration 
and ecosystem exposure and associated potential for welfare effects 
continues to be poorly characterized for Pb'' (ISA, section 6.5). Such 
a connection is even harder to characterize with respect to the current 
standard than it was in the last review with respect to the previous, 
much higher, standard.
    The current evidence also continues to support conclusions from the 
last review with regard to interpreting the risk and exposure results. 
These conclusions are based on consideration of the screening-level 
ecological risk assessment results from the last review as described in 
the 2006 REA and summarized in the notice of final rulemaking (73 FR 
67009, November 12, 2008) and in light of the currently available 
evidence in the ISA (PA, section 5.2). As noted in section III.C above, 
the results from three of the four case studies and from the national 
screens are largely not useful in informing judgments of the potential 
for adverse effects at levels of deposition associated with conditions 
that meet the current standard. The Vulnerable Ecosystem Case Study at 
the HBEF is more illustrative with regard to the current review and, 
accordingly, is given primary consideration. The EPA concluded that 
atmospheric Pb inputs of the past did not directly affect stream Pb 
levels at HBEF because deposited Pb is almost entirely retained in the 
soil profile and that there was ``little evidence that sites affected 
primarily by long-range Pb transport [such as this one] have 
experienced significant effects on ecosystem structure or function'' 
(2006 CD, p. AX-98). We further note here that, as conditions are 
unlikely to have worsened since those on which those conclusions were 
based, we find it likely that current ambient air concentrations do not 
directly impact stream Pb levels under air quality conditions 
associated with meeting the now-current standard.
    The available risk and exposure information continues to be 
sufficient to conclude that the 1978 standard was not providing 
adequate protection to ecosystems and, when considered with regard to 
air-related ecosystem exposures likely to occur with air Pb levels that 
just meet the now-current standard, additionally does not provide 
evidence of adverse effects under the current standard.
2. CASAC Advice
    In the current review of the secondary standard for Pb, the CASAC 
has provided advice and recommendations in their review of drafts of 
the ISA, of the REA Planning Document, and of the draft PA. We have 
additionally received comments from the public on drafts of these 
documents.\74\
---------------------------------------------------------------------------

    \74\ All written comments submitted to the agency will be 
available in the docket for this rulemaking, as will be transcripts 
and minutes of the public meetings held in conjunction with CASAC's 
review of drafts of the PA, the REA Planning Document and the ISA.
---------------------------------------------------------------------------

    In their advice and comments conveyed in the context of their 
review of the draft PA, the CASAC agreed with staff's preliminary 
conclusions that the available information since the last review is not 
sufficient to warrant revision to the secondary standard (Frey, 2013b). 
On this subject, the CASAC letter said that ``[o]verall, the CASAC 
concurs with the EPA that the current scientific literature does not 
support a revision to the Primary Lead (Pb) National Ambient Air 
quality Standard (NAAQS) nor the Secondary Pb NAAQS'' (Frey, 2013b, p. 
1). The CASAC also recognized the many uncertainties and data gaps in 
the new scientific literature and recommended that research be 
performed in the future to address these limitations (Frey, 2013b, p. 
2).

    Given the existing scientific data, the CASAC concurs with 
retaining the current secondary standard without revision. However, 
the CASAC also notes that important research gaps remain. For 
example questions remain regarding the relevance of the primary 
standard's indicator, level, averaging time, and form for the 
secondary standard. Other areas for additional research to address 
data gaps and uncertainty include developing a critical loads 
approach for U.S. conditions and a multi-media approach to account 
for legacy Pb and contributions from different sources. Addressing 
these gaps may require reconsideration of the secondary standard in 
future assessments.

    The very few public comments received on this review to date that 
have addressed adequacy of the current secondary Pb standard indicate 
support for retaining the current standard without revision, generally 
grouping the secondary standard with their similar view on the primary 
standard.
3. Administrator's Proposed Conclusions on the Adequacy of the Current 
Standard
    Based on the evidence and risk assessment information that is 
available in this review concerning the ecological effects and 
potential public welfare impacts of Pb emitted into ambient air, the 
Administrator proposes to conclude that the current secondary standard 
provides the requisite protection of public welfare from adverse 
effects and should be retained.
    In considering the adequacy of the current standard, the 
Administrator has considered the assessment of the available evidence 
and conclusions contained in the ISA; the staff assessment of and 
conclusions regarding the policy-relevant technical information, 
including screening-level risk information, presented in the PA; the 
advice and recommendations from CASAC; and public comments to date in 
this review. In the discussion below, the Administrator gives weight to 
the PA conclusions, with which CASAC has concurred, and takes note of 
key aspects of the rationale presented for those conclusions which 
contribute to her proposed decision.
    The Administrator notes the conclusion in the PA that the body of 
evidence on the ecological effects of Pb, expanded in some aspects 
since the last review, continues to support identification of 
ecological effects in organisms relating to growth, reproduction, and 
survival as the most relevant endpoints associated with Pb exposure. In 
consideration of the appreciable influence of site-specific 
environmental characteristics on the bioavailability and toxicity of 
environmental Pb in our assessment here, the PA noted the lack of 
studies conducted under conditions closely reflecting the natural 
environment. The currently available evidence, while somewhat expanded 
since the last review, does not include evidence of significant effects 
at lower concentrations or evidence of higher level ecosystem effects 
beyond those reported in the last review. There continue to be 
significant difficulties in interpreting effects evidence from 
laboratory studies to the natural environment and linking those effects 
to ambient air Pb concentrations. Further, the PA notes that the EPA is 
aware of no new critical loads information that would inform our 
interpretation of the public welfare significance of the effects of Pb 
in various U.S. ecosystems (PA, section 5.1). In summary, while new 
research has added to the understanding of Pb biogeochemistry and 
expanded the

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list of organisms for which Pb effects have been described, the PA 
notes there remains a significant lack of knowledge about the potential 
for adverse effects on public welfare from ambient air Pb in the 
environment and the exposures that occur from such air-derived Pb, 
particularly under conditions meeting the current standard (PA, section 
6.2.1). Thus, the scientific evidence presented in detail in the ISA, 
inclusive of that newly available in this review, is not substantively 
changed, most particularly with regard to the adequacy of the now 
current standard, from the information that was available in and 
supported the decision for revision in the last review (PA, section 
6.2.1).
    With respect to exposure/risk-based considerations, the PA 
recognizes the complexity of interpreting the previous risk assessment 
with regard to the ecological risk of ambient air Pb associated with 
conditions meeting the current standard and the associated limitations 
and uncertainties of such assessments. For example, the location-
specific case studies as well as the national screen conducted in the 
last review reflect both current air Pb deposition as well as past air 
and nonair source contributions (PA, section 6.3). The Administrator 
takes note of the PA conclusion that the previous assessment is 
consistent with and generally supportive of the evidence-based 
conclusions about Pb in the environment, yet the limitations on our 
ability to apportion Pb between past and present air contributions and 
between air and nonair sources remain significant.
    In the Administrator's consideration of the information available 
in this review of the Pb secondary standard, she gives weight to the PA 
conclusion that the currently available evidence and exposure/risk 
information do not call into question the adequacy of the current 
standard to provide the requisite protection for public welfare (PA, 
section 6.3). In so doing, she also notes the advice from CASAC in this 
review, including that ``[g]iven the existing scientific data, the 
CASAC concurs with retaining the current secondary standard without 
revision.'' In light of these and the above considerations, the 
Administrator finds that the currently available information does not 
call into question the adequacy of the current standard to provide the 
requisite protection for public welfare and, accordingly, reaches the 
conclusion that it is appropriate to retain the current secondary 
standard without revision. The Administrator solicits comment on this 
conclusion.

IV. Statutory and Executive Order Reviews

    Additional information about these statutes and Executive Orders 
can be found at http://www2.epa.gov/laws-regulations/laws-and-executive-orders.

A. Executive Order 12866: Regulatory Planning and Review and Executive 
Order 13563: Improving Regulation and Regulatory Review

    This action is not a significant regulatory action and was, 
therefore, not submitted to the Office of Management and Budget for 
review.

B. Paperwork Reduction Act

    This action does not impose an information collection burden under 
the Paperwork Reduction Act. There are no information collection 
requirements directly associated with revisions to a NAAQS under 
section 109 of the CAA and this action does not propose any revisions 
to the NAAQS.

C. Regulatory Flexibility Act

    I certify that this action will not have a significant economic 
impact on a substantial number of small entities under the Regulatory 
Flexibility Act. This action will not impose any requirements on small 
entities. Rather, this action proposes to retain, without revision, 
existing national standards for allowable concentrations of lead in 
ambient air as required by section 109 of the CAA. See also American 
Trucking Associations v. EPA. 175 F.3d at 1044-45 (NAAQS do not have 
significant impacts upon small entities because NAAQS themselves impose 
no regulations upon small entities).

D. Unfunded Mandates Reform Act

    This action does not contain any unfunded mandate as described in 
the Unfunded Mandates Reform Act, 2 U.S.C. 1531-1538 and does not 
significantly or uniquely affect small governments. This action imposes 
no enforceable duty on any state, local or tribal governments or the 
private sector.

E. Executive Order 13132: Federalism

    This action does not have federalism implications. It will not have 
substantial direct effects on the states, on the relationship between 
the national government and the states, or on the distribution of power 
and responsibilities among the various levels of government.

F. Executive Order 13175: Consultation and Coordination With Indian 
Tribal Governments

    This action does not have tribal implications, as specified in 
Executive Order 13175. This action does not change existing 
regulations. It does not have a substantial direct effect on one or 
more Indian Tribes, since Tribes are not obligated to adopt or 
implement any NAAQS. The Tribal Authority Rule gives Tribes the 
opportunity to develop and implement CAA programs such as the Pb NAAQS, 
but it leaves to the discretion of the Tribe whether to develop these 
programs and which programs, or appropriate elements of a program, they 
will adopt. Thus, Executive Order 13175 does not apply to this action.

G. Executive Order 13045: Protection of Children From Environmental 
Health and Safety Risks

    This action is not subject to Executive Order 13045 because it is 
not economically significant as defined in Executive Order 12866. The 
health effects evidence and risk assessment information for this 
action, which focuses on children in addressing the at-risk population, 
is summarized in sections II.B, II.C and II.D, and described in the ISA 
and PA, copies of which are in the public docket for this action.

H. Executive Order 13211: Actions That Significantly Affect Energy 
Supply, Distribution or Use

    This action is not subject to Executive Order 13211, because it is 
not a significant regulatory action under Executive Order 12866.

I. National Technology Transfer and Advancement Act

    This rulemaking does not involve technical standards.

J. Executive Order 12898: Federal Actions To Address Environmental 
Justice in Minority Populations and Low-Income Populations

    The EPA believes that this action will not have disproportionately 
high and adverse human health or environmental effects on minority, 
low-income or indigenous populations. The action proposed in this 
notice is to retain without revision the existing NAAQS for Pb based on 
the Administrator's conclusion that the existing standards protect 
public health, including the health of sensitive groups, with an 
adequate margin of safety. As discussed earlier in this preamble (see 
section II), the EPA expressly considered the available information 
regarding health effects among at-risk populations in reaching the 
proposed decision that the existing standards are requisite.

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K. Determination Under Section 307(d)

    Section 307(d)(1)(V) of the CAA provides that the provisions of 
section 307(d) apply to ``such other actions as the Administrator may 
determine.'' Pursuant to section 307(d)(1)(V), the Administrator 
determines that this action is subject to the provisions of section 
307(d).

References

Advisory Committee on Childhood Lead Poisoning Prevention (ACCLPP). 
(2012). Low Level Lead Exposure Harms Children: A Renewed Call for 
Primary Prevention. Report of the Advisory Committee on Childhood 
Lead Poisoning Prevention of the Centers for Disease Control and 
Prevention. January 4, 2012. Available at: http://www.cdc.gov/nceh/lead/ACCLPP/blood_lead_levels.htm.
Alliance to End Childhood Lead Poisoning. (1991). The First 
Comprehensive National Conference: Final Report. October 6,7,8, 
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List of Subjects in 40 CFR Part 50

    Environmental protection, Air pollution control, Carbon monoxide, 
Lead, Nitrogen dioxide, Ozone, Particulate matter, Sulfur oxides.

    Dated: December 19, 2014.
Gina McCarthy,
Administrator.
[FR Doc. 2014-30681 Filed 1-2-15; 8:45 am]
BILLING CODE 6560-50-P
```