[Federal Register: May 20, 2008 (Volume 73, Number 98)]
[Proposed Rules]
[Page 29183-29291]
[DOCID:fr20my08-24]

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Part II

Environmental Protection Agency

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40 CFR Parts 50, 51, 53 et al.

National Ambient Air Quality Standards for Lead; Proposed Rule

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Parts 50, 51, 53 and 58

[EPA-HQ-OAR-2006-0735; FRL-8563-9]
RIN 2060-AN83

National Ambient Air Quality Standards for Lead

AGENCY: Environmental Protection Agency (EPA).

ACTION: Proposed rule.

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SUMMARY: Based on its review of the air quality criteria and national
ambient air quality standards (NAAQS) for lead (Pb), EPA proposes to
make revisions to the primary and secondary NAAQS for Pb to provide
requisite protection of public health and welfare, respectively. EPA
proposes to revise various elements of the primary standard to provide
increased protection for children and other at-risk populations against
an array of adverse health effects, most notably including neurological
effects, particularly neurocognitive and neurobehavioral effects, in
children. With regard to the level and indicator of the standard, EPA
proposes to revise the level to within the range of 0.10 to 0.30 [mu]g/
m\3\ in conjunction with retaining the current indicator of Pb in total
suspended particles (Pb-TSP) but with allowance for the use of Pb-
PM10 data, and solicits comment on alternative levels up to
0.50 [mu]g/m\3\ and down below 0.10 [mu]g/m\3\. With regard to the
averaging time and form of the standard, EPA proposes two options: To
retain the current averaging time of a calendar quarter and the current
not-to-be-exceeded form, revised to apply across a 3-year span; and to
revise the averaging time to a calendar month and the form to the
second-highest monthly average across a 3-year span. EPA also solicits
comment on revising the indicator to Pb-PM10 and on the same
broad range of levels on which EPA is soliciting comment for the Pb-TSP
indicator (up to 0.50 [mu]g/m\3\). EPA also invites comment on when, if
ever, it would be appropriate to set a NAAQS for Pb at a level of zero.
EPA proposes to make the secondary standard identical in all respects
to the proposed primary standard.
    EPA is also proposing corresponding changes to data handling
procedures, including the treatment of exceptional events, and to
ambient air monitoring and reporting requirements for Pb including
those related to sampling and analysis methods, network design,
sampling schedule, and data reporting. Finally, EPA is providing
guidance on its proposed approach for implementing the proposed revised
primary and secondary standards for Pb.
    Consistent with the terms of a court order, by September 15, 2008
the Administrator will sign a notice of final rulemaking for
publication in the Federal Register.

DATES: Comments must be received by July 21, 2008. Under the Paperwork
Reduction Act, comments on the information collection provisions must
be received by OMB on or before June 19, 2008.
    Public Hearings: EPA intends to hold public hearings on this
proposed rule in June 2008 in St. Louis, Missouri and Baltimore,
Maryland. These will be announced in a separate Federal Register notice
that provides details, including specific times and addresses, for
these hearings.

ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-
OAR-2006-0735 by one of the following methods:
     http://www.regulations.gov: Follow the online instructions
for submitting comments.
     E-mail<EMAIL_ADDRESS>     Fax:<PHONE_NUMBER>.
     Mail: Docket No. EPA-HQ-OAR-2006-0735, Environmental
Protection Agency, Mail code 6102T, 1200 Pennsylvania Ave., NW.,
Washington, DC 20460. Please include a total of two copies.
     Hand Delivery: Docket No. EPA-HQ-OAR-2006-0735,
Environmental Protection Agency, EPA West, 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-
2006-0735. 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 http://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 http://
www.regulations.gov or e-mail. The http://www.regulations.gov Web site
is an ``anonymous access'' system, which means EPA will not know your
identity or contact information unless you provide it in the body of
your comment. If you send an e-mail comment directly to EPA without
going through http://www.regulations.gov, your e-mail 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, 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 EPA cannot read your comment due to
technical difficulties and cannot contact you for clarification, 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 EPA's public
docket, visit the EPA Docket Center homepage at http://www.epa.gov/
epahome/dockets.htm.
    Docket: All documents in the docket are listed in the http://
www.regulations.gov index. 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, will be publicly available only in hard copy.
Publicly available docket materials are available either electronically
in http://www.regulations.gov or in hard copy at the Air and Radiation
Docket and Information Center, EPA/DC, EPA West, 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 and
Information Center is<PHONE_NUMBER>.

FOR FURTHER INFORMATION CONTACT: For further information in general or
specifically with regard to sections I through III or VII, contact Dr.
Deirdre 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:<PHONE_NUMBER>; e-mail<EMAIL_ADDRESS>With
regard to Section IV, contact Mr. Mark Schmidt, Air Quality Analysis
Division, Office of Air Quality Planning and Standards, U.S.
Environmental Protection Agency, Mail code C304-04, Research Triangle
Park, NC 27711; telephone:<PHONE_NUMBER>; fax:<PHONE_NUMBER>; e-mail:
<EMAIL_ADDRESS>With regard to Section V, contact Mr. Kevin
Cavender,

Air Quality Analysis Division, Office of Air Quality Planning and
Standards, U.S. Environmental Protection Agency, Mail code C304-06,
Research Triangle Park, NC 27711; telephone:<PHONE_NUMBER>; fax: 919-
541-1903; e-mail<EMAIL_ADDRESS>With regard to Section VI,
contact Mr. Larry Wallace, Ph.D., Air Quality Policy Division, Office
of Air Quality Planning and Standards, U.S. Environmental Protection
Agency, Mail code C539-01, Research Triangle Park, NC 27711; telephone:
919-541-0906; fax:<PHONE_NUMBER>; e-mail<EMAIL_ADDRESS>
SUPPLEMENTARY INFORMATION:

General Information

What Should I Consider as I Prepare My Comments for EPA?

    1. Submitting CBI. Do not submit this information to EPA through
http://www.regulations.gov or e-mail. 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 EPA, mark the outside of the disk or CD-ROM
as CBI and then identify electronically within the disk or CD-ROM the
specific information that is claimed as CBI. In addition to one
complete version of the comment that includes information claimed as
CBI, a copy of the comment that does not contain the information
claimed as CBI must be submitted for inclusion in the public docket.
Information so marked will not be disclosed except in accordance with
procedures set forth in 40 CFR part 2.
    2. Tips for Preparing Your Comments. When submitting comments,
remember to:
     Identify the rulemaking by docket number and other
identifying information (subject heading, Federal Register date and
page number).
     Follow directions--the agency may ask you to respond to
specific questions or organize comments by referencing a Code of
Federal Regulations (CFR) part or section number.
     Explain why you agree or disagree, suggest alternatives,
and substitute language for your requested changes.
     Describe any assumptions and provide any technical
information and/or data that you used.
     If you estimate potential costs or burdens, explain how
you arrived at your estimate in sufficient detail to allow for it to be
reproduced.
     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 Related Information

    A number of documents relevant to this rulemaking, including the
advance notice of proposed rulemaking (72 FR 71488), the Air Quality
Criteria for Lead (Criteria Document) (USEPA, 2006a), the Staff Paper,
related risk assessment reports, and other related technical documents
are available on 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 and other
related documents are also available for inspection and copying in the
EPA docket identified above.

Table of Contents

    The following topics are discussed in this preamble:

I. Background
    A. Legislative Requirements
    B. History of Lead NAAQS Reviews
    C. Current Related Lead Control Programs
    D. Current Lead NAAQS Review
II. Rationale for Proposed Decision on the Primary Standard
    A. Multimedia, Multipathway Considerations and Background
    1. Atmospheric Emissions and Distribution of Lead
    2. Air-Related Human Exposure Pathways
    3. Nonair-Related and Air-Related Background Human Exposure
Pathways
    4. Contributions to Children's Lead Exposures
    B. Health Effects Information
    1. Blood Lead
    a. Internal Disposition of Lead
    b. Use of Blood Lead as Dose Metric
    c. Air-to-Blood Relationships
    2. Nature of Effects
    a. Broad Array of Effects
    b. Neurological Effects in Children
    3. Lead-Related Impacts on Public Health
    a. At-Risk Subpopulations
    b. Potential Public Health Impacts
    4. Key Observations
    C. Human Exposure and Health Risk Assessments
    1. Overview of Risk Assessment From Last Review
    2. Design Aspects of Exposure and Risk Assessments
    a. CASAC Advice
    b. Health Endpoint, Risk Metric and Concentration-response
Functions
    c. Case Study Approach
    d. Air Quality Scenarios
    e. Categorization of Policy-Relevant Exposure Pathways
    f. Analytical Steps
    g. Generating Multiple Sets of Risk Results
    h. Key Limitations and Uncertainties
    3. Summary of Estimates and Key Observations
    a. Blood Pb Estimates
    b. IQ Loss Estimates
    D. Conclusions on Adequacy of the Current Primary Standard
    1. Background
    a. The Current Standard
    b. Policy Options Considered in the Last Review
    2. Considerations in the Current Review
    a. Evidence-Based Considerations
    b. Exposure- and Risk-Based Considerations
    3. CASAC Advice and Recommendations
    4. Administrator's Proposed Conclusions Concerning Adequacy
    E. Conclusions on the Elements of the Standard
    1. Indicator
    2. Averaging Time and Form
    3. Level for a Pb NAAQS With Pb-TSP Indicator
    a. Evidence-Based Considerations
    b. Exposure- and Risk-Based Considerations
    c. CASAC Advice and Recommendations
    d. Administrator's Proposed Conclusion Concerning Level
    4. Level for a Pb NAAQS With Pb-PM10 Indicator
    a. Considerations With Regard to Particles Not Captured by
PM10
    b. CASAC Advice
    c. Approaches for Levels for a PM10-Based Standard
    F. Proposed Decision on the Primary Standard
III. Rationale for Proposed Decision on the Secondary Standard
    A. Welfare Effects Information
    B. Screening Level Ecological Risk Assessment
    1. Design Aspects of the Assessment and Associated Uncertainties
    2. Summary of Results
    C. The Secondary Standard
    1. Background on the Current Standard
    2. Approach for Current Review
    3. Conclusions on Adequacy of the Current Standard
    a. Evidence-Based Considerations
    b. Risk-Based Considerations
    c. CASAC Advice and Recommendations
    d. Administrator's Proposed Conclusions on Adequacy of Current
Standard
    4. Conclusions and Proposed Decision on the Elements of the
Secondary Standard
IV. Proposed Appendix R on Interpretation of the NAAQS for Lead and
Proposed Revisions to the Exceptional Events Rule
    A. Background
    B. Interpretation of the NAAQS for Lead
    1. Interpretation of a Standard Based on Pb-TSP
    2. Interpretation of Alternative Elements
    C. Exceptional Events Information Submission Schedule
V. Proposed Amendments to Ambient Monitoring Requirements
    A. Sampling and Analysis Methods
    1. Background
    2. Proposed Changes
    a. Pb-TSP Sampling Method
    b. Pb-PM10 Sampling Method
    c. Analysis Method
    d. FEM Criteria
    e. Quality Assurance

    B. Network Design
    1. Background
    2. Proposed Changes
    C. Sampling Schedule
    1. Background
    2. Proposed Changes
    D. Monitoring for the Secondary NAAQS
    1. Background
    2. Proposed Changes
    E. Other Monitoring Regulation Changes
    1. Reporting of Average Pressure and Temperature
    2. Special Purpose Monitoring Exemption
VI. Implementation Considerations
    A. Designations for the Lead NAAQS
    1. Potential Schedule for Designations of A Revised Lead NAAQS
    B. Lead Nonattainment Area Boundaries
    1. County-Based Boundaries
    2. MSA-Based Boundaries
    C. Classifications
    D. Section 110(a)(2) Lead NAAQS Infrastructure Requirements
    E. Attainment Dates
    F. Attainment Planning Requirements
    1. Schedule for Attaining a Revised Pb NAAQS
    2. RACM for Lead Nonattainment Areas
    3. Demonstration of Attainment for Lead Nonattainment Areas
    4. Reasonable Further Progress (RFP)
    5. Contingency Measures
    6. Nonattainment New Source Review (NSR) and Prevention of
Significant Deterioration (PSD) Requirements
    7. Emissions Inventories
    8. Modeling
    G. General Conformity
    H. Transition From the Current NAAQS to a Revised NAAQS for Lead
VII. Statutory and Executive Order Reviews
    References

I. Background

A. Legislative Requirements

    Two sections of the Clean Air Act (Act) govern the establishment
and revision of the NAAQS. Section 108 (42 U.S.C. 7408) directs the
Administrator to identify and list each air pollutant that ``in his
judgment, cause or contribute to air pollution which may reasonably be
anticipated to endanger public health and welfare'' and whose
``presence * * * in the ambient air results from numerous or diverse
mobile or stationary sources'' and to issue air quality criteria for
those that are listed. Air quality criteria are 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 ambient air * *
*''. Section 109 (42 U.S.C. 7409) directs the Administrator to propose
and promulgate ``primary'' and ``secondary'' NAAQS for pollutants
listed under section 108. Section 109(b)(1) defines a primary standard
as one ``the attainment and maintenance of which in the judgment of the
Administrator, based on [air quality] 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 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.'' 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 include an adequate margin
of safety was intended to address uncertainties associated with
inconclusive scientific and technical information available at the time
of standard setting. It was also intended to provide a reasonable
degree of protection against hazards that research has not yet
identified. 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). 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 include
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 Association 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.
    The selection of any particular approach to providing an adequate
margin of safety is a policy choice left specifically to the
Administrator's judgment. Lead Industries Association v. EPA, 647 F.2d
at 1161-62. In addressing the requirement for an adequate margin of
safety, EPA considers such factors as the nature and severity of the
health effects involved, the size of the population(s) at risk, and the
kind and degree of the uncertainties that must be addressed.
    In setting standards that are ``requisite'' to protect public
health and welfare, as provided in section 109(b), EPA's task is to
establish standards that are neither more nor less stringent than
necessary for these purposes. Whitman v. American Trucking
Associations, 531 U.S. 457, 473. Further the Supreme Court ruled that
``[t]he text of Sec.  109(b), interpreted in its statutory and
historical context and with appreciation for its importance to the CAA
as a whole, unambiguously bars cost considerations from the NAAQS-
setting process * * *'' Id. at 472.\3\ Section 109(d)(1) of the Act
requires that ``[n]ot 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 promulgated under this section and shall
make such revisions in such criteria and standards and promulgate such
new standards as may be appropriate in accordance with section 108 and
subsection (b) of this section.'' Section 109(d)(2)(A) requires that
``The Administrator shall appoint an independent scientific review
committee composed of seven members including at least one member of
the National Academy of Sciences, one physician, and one person
representing State air pollution control agencies.'' Section
109(d)(2)(B) requires that, ``[n]ot later than January 1, 1980, and at
five-year intervals thereafter, the committee referred to in
subparagraph (A) shall complete a review of the criteria published
under section 108 and the national primary and secondary ambient air
quality standards promulgated under this section and shall recommend to
the Administrator any new national ambient air quality standards and
revisions of existing criteria and standards as may be appropriate
under section 108 and subsection (b) of this

section.'' Since the early 1980's, this independent review function has
been performed by the Clean Air Scientific Advisory Committee (CASAC)
of EPA's Science Advisory Board.
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    \3\ In considering whether the CAA allowed for economic
considerations to play a role in the promulgation of the NAAQS, the
Supreme Court rejected arguments that because many more factors than
air pollution might affect public health, EPA should consider
compliance costs that produce health losses in setting the NAAQS.
531 U.S. at 466. Thus, EPA may not take into account possible public
health impacts from the economic cost of implementation. Id.
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B. History of Lead NAAQS Reviews

    On October 5, 1978 EPA promulgated primary and secondary NAAQS for
Pb under section 109 of the Act (43 FR 46246). 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 particulate
matter (Pb-TSP), not to be exceeded by the maximum arithmetic mean
concentration averaged over a calendar quarter. This standard was based
on the 1977 Air Quality Criteria for Lead (USEPA, 1977).
    A 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), 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 options for the Pb NAAQS level in the range of 0.5 to 1.5
[mu]g/m3, and suggested the second highest monthly average
in three years for the form and averaging time of the standard (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).

C. Current Related Lead Control Programs

    States are primarily responsible for ensuring attainment and
maintenance of national ambient air quality standards once EPA has
established them. 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
EPA, also administer the prevention of significant deterioration
program (42 U.S.C. 7470-7479) for these pollutants. In addition,
Federal programs provide for nationwide reductions in 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); and the national
emission standards for hazardous air pollutants under section 112 of
the Act (42 U.S.C. 7412).
    As Pb is a multimedia pollutant, a broad range of Federal programs
beyond those that focus on air pollution control provide for nationwide
reductions in environmental releases and human exposures. In addition,
the Centers for Disease Control and Prevention (CDC) programs provide
for the tracking of children's blood Pb levels nationally and provide
guidance on levels at which medical and environmental case management
activities should be implemented (CDC, 2005a; ACCLPP, 2007).\4\ In
1991, the Secretary of the Health and Human Services (HHS)
characterized Pb poisoning as the ``number one environmental threat to
the health of children in the United States'' (Alliance to End
Childhood Lead Poisoning, 1991). In 1997, President Clinton created, by
Executive Order 13045, the President's Task Force on Environmental
Health Risks and Safety Risks to Children in response to increased
awareness that children face disproportionate risks from environmental
health and safety hazards (62 FR 19885).\5\ By Executive Orders issued
in October 2001 and April 2003, President Bush extended the work for
the Task Force for an additional three and a half years beyond its
original charter (66 FR 52013 and 68 FR 19931). The Task Force set a
Federal goal of eliminating childhood Pb poisoning by the year 2010 and
reducing Pb poisoning in children was the Task Force's top priority.
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    \4\ As described in Section III below the CDC stated in 2005
that no ``safe'' threshold for blood Pb levels in young children has
been identified (CDC, 2005a).
    \5\ Co-chaired by the Secretary of the HHS and the Administrator
of the EPA, the Task Force consisted of representatives from 16
Federal departments and agencies.
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    Federal 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.\6\ Further,
in 1991, EPA lowered the maximum levels of Pb permitted in public water
systems from 50 parts per billion (ppb) to 15 ppb (56 FR 26460).
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    \6\ See ``Criteria for Classification of Solid Waste Disposal
Facilities and Practices and Criteria for Municipal Solid Waste
Landfills: Disposal of Residential Lead-Based Paint Waste; Final
Rule'' EPA-HQ-RCRA-2001-0017.
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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 and Title IV of the Toxic Substances Control
Act, EPA has established regulations and associated programs in the
following five categories: (1) Training and certification requirements
for persons engaged in lead-based paint activities; accreditation of
training providers; authorization of State and Tribal lead-based paint
programs; and work practice standards for the safe, reliable, and
effective identification and elimination of lead-based paint hazards;
(2) ensuring that, for most housing constructed before 1978, lead-based
paint information flows from sellers to purchasers, from landlords to
tenants, and from renovators to owners and occupants; (3) establishing
standards for identifying dangerous levels of Pb in paint, dust and
soil; (4) providing grant funding to establish and maintain State and
Tribal lead-based paint programs, and to address childhood lead
poisoning in the highest-risk communities; and (5) providing
information on Pb hazards to the public, including steps that people
can take to protect themselves and their families from lead-based paint
hazards.
    Under Title IV of TSCA, EPA established standards identifying
hazardous levels of lead in residential paint, dust, and soil in 2001.
This regulation supports the implementation of other regulations which
deal with worker training and certification, Pb hazard disclosure in
real estate transactions, Pb hazard evaluation and control in
Federally-owned housing prior to sale and housing receiving Federal
assistance, and U.S. Department of Housing and Urban Development grants
to local jurisdictions to perform

Pb hazard control. The TSCA Title IV term ``lead-based paint hazard''
implemented through this regulation identifies lead-based paint and all
residential lead-containing dust and soil regardless of the source of
Pb, which, due to their condition and location, would result in adverse
human health effects. One of the underlying principles of Title X is to
move the focus of public and private decision makers away from the mere
presence of lead-based paint, to the presence of lead-based paint
hazards, for which more substantive action should be undertaken to
control exposures, especially to young children. In addition the
success of the program will rely on the voluntary participation of
states and tribes as well as counties and cities to implement the
programs and on property owners to follow the standards and EPA's
recommendations. If EPA were to set unreasonable standards (e.g.,
standards that would recommend removal of all Pb from paint, dust, and
soil), States and Tribes may choose to opt out of the Title X Pb
program and property owners may choose to ignore EPA's advice believing
it lacks credibility and practical value. Consequently, EPA needed to
develop standards that would not waste resources by chasing risks of
negligible importance and that would be accepted by States, Tribes,
local governments and property owners. In addition, a separate
regulation establishes, among other things, under authority of TSCA
section 402, residential Pb dust cleanup levels and amendments to dust
and soil sampling requirements (66 FR 1206).
    On March 31, 2008, the Agency issued a new rule (Lead: Renovation,
Repair and Painting [RRP] Program) to protect children from lead-based
paint hazards. This rule applies to renovators and maintenance
professionals who perform renovation, repair, or painting in housing,
child-care facilities, and schools built prior to 1978. It requires
that contractors and maintenance professionals be certified; that their
employees be trained; and that they follow protective work practice
standards. These standards prohibit certain dangerous practices, such
as open flame burning or torching of lead-based paint. The required
work practices also include posting warning signs, restricting
occupants from work areas, containing work areas to prevent dust and
debris from spreading, conducting a thorough cleanup, and verifying
that cleanup was effective. The rule will be fully effective by April
2010. States and tribes may become authorized to implement this rule,
and the rule contains procedures for the authorization of states,
territories, and tribes to administer and enforce these standards and
regulations in lieu of a federal program. In announcing this rule, EPA
noted that almost 38 million homes in the United States contain some
lead-based paint, and that this rule's requirements were key components
of a comprehensive effort to eliminate childhood Pb poisoning. To
foster adoption of the rule's measures, EPA also intends to conduct an
extensive education and outreach campaign to promote awareness of these
new requirements.
    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, 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.\7\ For example,
Federal regulations concerning batteries in municipal solid waste
facilitate the collection and recycling or proper disposal of batteries
containing Pb.\8\ 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/).
---------------------------------------------------------------------------

    \7\ See, e.g., ``Hazardous Waste Management System;
Identification and Listing of Hazardous Waste: Inorganic Chemical
Manufacturing Wastes; Land Disposal Restrictions for Newly
Identified Wastes and CERCLA Hazardous Substance Designation and
Reportable Quantities; Final Rule'', http://www.epa.gov/epaoswer/
hazwaste/state/revision/frs/fr195.pdf and http://www.epa.gov/
epaoswer/hazwaste/ldr/basic.htm.
    \8\ See, e.g., ``Implementation of the Mercury-Containing and
Rechargeable Battery Management Act'' http://www.epa.gov/epaoswer/
hazwaste/recycle/battery.pdf and ``Municipal Solid Waste Generation,
Recycling, and Disposal in the United States: Facts and Figures for
2005'' http://www.epa.gov/epaoswer/osw/conserve/resources/msw-
2005.pdf.
---------------------------------------------------------------------------

    A variety of federal nonregulatory programs also provide for
reduced environmental release of Pb containing materials through more
general encouragement of 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 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).
    Efforts such as those programs described above have been successful
in that blood Pb levels in all segments of the population have dropped
significantly from levels observed around 1990. In particular, blood Pb
levels for the general population of children 1 to 5 years of age have
dropped to a median level of 1.6 [mu]g/dL and a level of 3.9 [mu]g/dL
for the 90th percentile child in the 2003-2004 National Health and
Nutrition Examination Survey (NHANES) as compared to median and 90th
percentile levels in 1988-1991 of 3.5 [mu]g/dL and 9.4 [mu]g/dL,
respectively (http://www.epa.gov/envirohealth/children/body_burdens/
b1-table.htm). These levels (median and 90th percentile) for the
general population of young children \9\ are at the low end of the
historic range of blood Pb levels for general population of children
aged 1-5 years. However, as discussed in Section II.B.1.b, levels have
been found to vary among children of different socioeconomic status and
other demographic characteristics (CD, p. 4-21) and racial/ethnic and
income disparities in blood Pb levels in children persist. The decline
in blood Pb levels in the United States has resulted from coordinated,
intensive efforts at the national, state, and local levels. The Agency
has continued to grapple with soil and dust Pb levels from the
historical use of Pb in paint and gasoline and other sources.
---------------------------------------------------------------------------

    \9\ The 95th percentile value for the 2003-2004 NHANES is 5.1
[mu]g/dL (Axelrad, 2008).
---------------------------------------------------------------------------

    EPA's research program, with other Federal agencies, defines,
encourages and conducts research needed to locate and assess serious
risks and to develop methods and tools to characterize and help reduce
risks. For example, EPA's Integrated Exposure Uptake Biokinetic Model
for Lead in Children (IEUBK model) for Pb in children and the Adult
Lead Methodology are widely used and accepted as tools that provide
guidance in evaluating site specific data. More recently, in
recognition of the need for a single model that predicts Pb
concentrations in tissues for children and adults, EPA is 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. EPA research activities on substances including Pb
focus on better characterizing aspects of health and environmental
effects, exposure, and control or management of environmental releases
(see http://www.epa.gov/ord/researchaccomplishments/index.html).

D. Current Lead NAAQS Review

    EPA initiated the current review of the air quality criteria for Pb
on November 9, 2004, with a general call for information (69 FR 64926).
A project work plan (USEPA, 2005a) for the preparation of the Criteria
Document was released in January 2005 for CASAC and public review. EPA
held a series of workshops in August 2005, inviting recognized
scientific experts to discuss initial draft materials that dealt with
various lead-related issues being addressed in the Pb air quality
criteria document. The first draft of the Criteria Document (USEPA,
2005b) was released for CASAC and public review in December 2005 and
discussed at a CASAC meeting held on February 28-March 1, 2006.
    A second draft Criteria Document (USEPA, 2006b) was released for
CASAC and public review in May 2006, and discussed at the CASAC meeting
on June 28, 2006. A subsequent draft of Chapter 7--Integrative
Synthesis (Chapter 8 in the final Criteria Document), released on July
31, 2006, was discussed at an August 15, 2006, CASAC teleconference.
The final Criteria Document was released on September 30, 2006 (USEPA,
2006a; cited throughout this preamble as CD). While the Criteria
Document focuses on new scientific information available since the last
review, it integrates that information with scientific criteria from
previous reviews.
    In February 2006, EPA released the Plan for Review of the National
Ambient Air Quality Standards for Lead (USEPA, 2006c) that described
Agency plans and a timeline for reviewing the air quality criteria,
developing human exposure and risk assessments and an ecological risk
assessment, preparing a policy assessment, and developing the proposed
and final rulemakings.
    In May 2006, EPA released for CASAC and public review a draft
Analysis Plan for Human Health and Ecological Risk Assessment for the
Review of the Lead National Ambient Air Quality Standards (USEPA,
2006d), which was discussed at a June 29, 2006, CASAC meeting
(Henderson, 2006). The May 2006 assessment plan discussed two
assessment phases: A pilot phase and a full-scale phase. The pilot
phase of both the human health and ecological risk assessments was
presented in the draft Lead Human Exposure and Health Risk Assessments
and Ecological Risk Assessment for Selected Areas (ICF, 2006;
henceforth referred to as the first draft Risk Assessment Report) which
was released for CASAC and public review in December 2006. The first
draft Staff Paper, also released in December 2006, discussed the pilot
assessments and the most policy-relevant science from the Criteria
Document. These documents were reviewed by CASAC and the public at a
public meeting on February 6-7, 2007 (Henderson, 2007a).
    Subsequent to that meeting, EPA conducted full-scale human exposure
and health risk assessments, although no further work was done on the
ecological assessment due to resource limitations. A second draft Risk
Assessment Report (USEPA, 2007a), containing the full-scale human
exposure and health risk assessments, was released in July 2007 for
review by CASAC at a meeting held on August 28-29, 2007. Taking into
consideration CASAC comments (Henderson, 2007b) and public comments on
that document, we conducted additional human exposure and health risk
assessments. A final Risk Assessment Report (USEPA, 2007b) and final
Staff Paper (USEPA, 2007c) were released on November 1, 2007.
    The final Staff Paper presents OAQPS staff's evaluation of the
public health and welfare policy implications of the key studies and
scientific information contained in the Criteria Document and presents
and interprets results from the quantitative risk/exposure analyses
conducted for this review. Further, the Staff Paper presents OAQPS
staff recommendations on a range of policy options for the
Administrator to consider concerning whether, and if so how, to revise
the primary and secondary Pb NAAQS. Such an evaluation of policy
implications is intended to help ``bridge the gap'' between the
scientific assessment contained in the Criteria Document and the
judgments required of the EPA Administrator in determining whether it
is appropriate to retain or revise the NAAQS for Pb. In evaluating the
adequacy of the current standard and a range of alternatives, the Staff
Paper considered the available scientific evidence and quantitative
risk-based analyses, together with related limitations and
uncertainties, and focused on the information that is most pertinent to
evaluating the basic elements of national ambient air quality
standards: indicator,\10\ averaging time, form,\11\ and level. These
elements, which together serve to define each standard, must be
considered collectively in evaluating the public health and welfare
protection afforded by the Pb standards. The information, conclusions,
and OAQPS staff recommendations presented in the Staff Paper were
informed by comments and advice received from CASAC in its reviews of
the earlier draft Staff Paper and drafts of related risk/exposure
assessment reports, as well as comments on these earlier draft
documents submitted by public commenters.
---------------------------------------------------------------------------

    \10\ The ``indicator'' of a standard defines the chemical
species or mixture that is to be measured in determining whether an
area attains the standard.
    \11\ The ``form'' of a standard defines the air quality
statistic that is to be compared to the level of the standard in
determining whether an area attains the standard.
---------------------------------------------------------------------------

    Subsequent to completion of the Staff Paper, EPA issued an advance
notice of proposed rulemaking (ANPR) that was signed by the
Administrator on December 5, 2007 (72 FR 71488-71544). The ANPR is one
of the key features of the new NAAQS review process that EPA has
instituted over the past two years to help to improve the efficiency of
the process the Agency uses in reviewing the NAAQS while ensuring that
the Agency's decisions are informed by the best available science and
broad participation among experts in the scientific community and the
public. The ANPR provided the public an opportunity to comment on a
wide range of policy options that could be considered by the
Administrator. The substantial number of comments we received on the Pb
NAAQS ANPR helped inform the narrower range of options we are proposing
and taking comment on today. The new process (described at http://
www.epa.gov/ttn/naaqs/.) is being incorporated into the various ongoing
NAAQS reviews being conducted by the Agency, including the current
review of the Pb NAAQS.
    A public meeting of the CASAC was held on December 12-13, 2007 to
provide advice and recommendations to the Administrator based on its
review of the ANPR and the previously released final Staff Paper and
Risk Assessment Report. Information about this meeting was published in
the Federal Register on November 20, 2007 (72 FR 65335-65336),
transcripts of the meeting are in the Docket for this review and
CASAC's letter to the Administrator (Henderson, 2008) is also available
on the EPA Web site (http://www.epa.gov/sab).

    A public comment period for the ANPR extended from December 17,
2007 through January 16, 2008 and comments received are in the Docket
for this review. Comments were received from nearly 9000 private
citizens (roughly 200 of them were not part of one of several mass
comment campaign), 13 state and local agencies, one federal agency,
three regional or national associations of government agencies or
officials, 15 nongovernmental environmental or public health
organizations (including one submission on behalf of a coalition of 23
organizations) and five industries or industry organizations. Although
the Agency has not developed formal responses to comments received on
the ANPR, these comments have been considered in the development of
this notice and are generally described in subsequent sections on
proposed conclusions with regard to the adequacy of the standards and
with regard to the Administrator's proposed decisions on revisions to
the standards.
    The schedule for completion of this review is governed by a
judicial order in Missouri Coalition for the Environment, v. EPA (No.
4:04CV00660 ERW, Sept. 14, 2005). The order governing this review,
entered by the court on September 14, 2005 and amended on April 29,
2008, specifies that EPA sign, for publication, notices of proposed and
final rulemaking concerning its review of the Pb NAAQS no later than
May 1, 2008 and September 15, 2008, respectively. In light of the
compressed schedule ordered by the court for issuing the final rule,
EPA may be able to respond only to those comments submitted during the
public comment period on this proposal. EPA has considered all of the
comments submitted to date in preparing this proposal, but if
commenters believe that comments submitted on the ANPR are fully
applicable to the proposal and wish to ensure that those comments are
addressed by EPA as part of the final rulemaking, the earlier comments
should be resubmitted during the comment period on this proposal.
    This action presents the Administrator's proposed decisions on the
review of the current primary and secondary Pb standards. Throughout
this preamble a number of judgments, conclusions, findings, and
determinations proposed by the Administrator are noted. While they
identify the reasoning that supports this proposal, they are not
intended to be final or conclusive in nature. The EPA invites general,
specific, and/or technical comments on all issues involved with this
proposal, including all such proposed judgments, conclusions, findings,
and determinations.

II. Rationale for Proposed Decision on the Primary Standard

    This section presents the rationale for the Administrator's
proposed decision that the current primary standard is not requisite to
protect public health with an adequate margin of safety, and that the
existing Pb primary standard should be revised. With regard to the
primary standard for Pb, EPA is proposing options for the revision of
the various elements of the standard to provide increased protection
for children and other at-risk populations against an array of adverse
health effects, most notably including neurological effects in
children, particularly neurocognitive and neurobehavioral effects. With
regard to the level and indicator of the standard, EPA proposes to
revise the level of the standard to a level within the range of 0.10 to
0.30 [mu]g/m\3\ in conjunction with retaining the current indicator of
Pb in total suspended particles (Pb-TSP) but with allowance for the use
of Pb-PM10 data. With regard to the form and averaging time of the
standard, EPA proposes the following options: (1) To retain the current
averaging time of a calendar quarter and the current not-to-be-exceeded
form, revised so as to apply across a 3-year span, and (2) to revise
the averaging time to a calendar month and the form to be the second-
highest monthly average across a 3-year span. EPA also solicits comment
on revising the indicator to Pb-PM10.
    As discussed more fully below, this proposal is based on a thorough
review, in the Criteria Document, of the latest scientific information
on human health effects associated with the presence of Pb in the
ambient air. This proposal also takes into account: (1) Staff
assessments of the most policy-relevant information in the Criteria
Document and staff analyses of air quality, human exposure, and health
risks presented in the Staff Paper, upon which staff recommendations
for revisions to the primary Pb standard are based; (2) CASAC advice
and recommendations, as reflected in discussions of the ANPR and drafts
of the Criteria Document and Staff Paper 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.
    In developing this proposal, EPA has drawn upon an integrative
synthesis of the entire body of evidence, published through late 2006,
on human health effects associated with Pb exposure. Some 6000 newly
available studies were considered in this review. As discussed below in
section II.B, this body of evidence addresses a broad range of health
endpoints associated with exposure to Pb (EPA, 2006a, chapter 8), and
includes hundreds of epidemiologic studies conducted in the U.S.,
Canada, and many countries around the world since the time of the last
review (EPA, 2006a, chapter 6). This proposal also draws upon the
results of the quantitative exposure and risk assessments, discussed
below in section II.C. Evidence- and exposure/risk-based considerations
that form the basis for the Administrator's proposed decisions on the
adequacy of the current standard and on the elements of the proposed
alternative standards are discussed below in section II.D.2 and II.D.3,
respectively.

A. Multimedia, Multipathway Considerations and Background

1. Atmospheric Emissions and Distribution of Lead
    Lead is emitted into the air from many sources encompassing a wide
variety of source types (Staff Paper, Section 2.2). Further, once
deposited out of the air, Pb can subsequently be resuspended into the
air (CD, pp. 2-62 to 2-66). There are over 100 categories of sources of
Pb emissions included in the EPA's 2002 National Emissions Inventory
(NEI),\12 \ the top five of which include: Mobile sources (leaded
aviation gas) \13\; industrial, commercial, institutional and process
boilers; utility boilers; iron and steel foundries; and primary Pb
smelting (Staff Paper Section 2.2). Further, there are some 13,000
industrial, commercial or institutional point sources in the 2002 NEI,
each with one or more processes that emit Pb to the atmosphere. In
addition to these 13,000 sources, there are approximately 3,000
airports at which leaded gasoline is used (Staff Paper, p. 2-8). Among
these sources, more than one thousand are estimated to emit at least a
tenth of a ton of Pb per year (Staff Paper, Section 2.2.3). Because of
its persistence, Pb emissions contribute to media

concentrations for some time into the future.
---------------------------------------------------------------------------

    \12\ As noted in the Staff Paper, quantitative estimates of
emissions associated with resuspension of soil-bound Pb particles
and contaminated road dust are not included in the 2002 NEI.
    \13\ The emissions estimates identified as mobile sources in the
current NEI are currently limited to combustion of leaded aviation
gas in piston-engine aircraft. Lead emissions estimates for other
mobile source emissions of Pb (e.g., brake wear, tire wear, loss of
Pb wheel weights and others) are not included in the current NEI.
---------------------------------------------------------------------------

    Lead emitted to the air is predominantly in particulate form, with
the particles occurring in many sizes. Once emitted, Pb particles can
be transported long or short distances depending on their size, which
influences the amount of time spent in aerosol phase. In general,
larger particles tend to deposit more quickly, within shorter distances
from emissions points, while smaller particles will remain in aerosol
phase and travel longer distances before depositing. Additionally, once
deposited, Pb particles can be resuspended back into the air and
undergo a second dispersal. Thus, the atmospheric transport processes
of Pb contribute to its broad dispersal, with larger particles
generally occurring as a greater contribution to total airborne Pb at
locations closer to the point of emission than at more distant
locations where the relative contribution from smaller particles is
greater (CD, Section 2.3.1 and p. 3-3).
    Airborne concentrations of Pb in total suspended particulate matter
(Pb-TSP) in the United States have fallen substantially since the
current Pb NAAQS was set in 1978.\14\ Despite this decline, there have
still been a small number of areas, associated with large stationary
sources of Pb, that have not met the NAAQS over the past few years. The
average maximum quarterly mean concentration for the time period 2003-
2005 among source-oriented monitoring sites in the U.S. is 0.48 [mu]g/
m3, while the corresponding average for non-source-oriented
sites is 0.03 [mu]g/m3.\15\ The average and median among all
monitoring-site-specific maximum quarterly mean concentrations for this
time period are 0.17 [mu]g/m3 and 0.03 [mu]g/m3,
respectively. Coincident with the historical trend in reduction in Pb
levels, however, there has also been a substantial reduction in number
of Pb-TSP monitoring sites. As described below in section II.B.3.b,
many of the highest Pb emitting sources in the 2002 NEI do not have
nearby Pb-TSP monitors, which may lead to underestimates of the extent
of occurrences of relatively higher Pb concentrations (as recognized in
the Staff Paper, Section 2.3.2 and, with regard to more recent
analysis, in section II.B.3.b below).
---------------------------------------------------------------------------

    \14\ Air Pb concentrations nationally are estimated to have
declined more than 90% since the early 1980s, in locations not known
to be directly influenced by stationary sources (Staff Paper, pp. 2-
22 to 2-23).
    \15\ The data set included data for 189 monitor sites meeting
the data analysis screening criteria. Details with regard to the
data set and analyses supporting the values provided here are
presented in Section 2.3.2 of the Staff Paper.
---------------------------------------------------------------------------

2. Air-Related Human Exposure Pathways
    As when the standard was set in 1978, we recognize that exposure to
air Pb can occur directly by inhalation, or indirectly by ingestion of
Pb-contaminated food, water or nonfood materials including dust and
soil (43 FR 46247). This occurs as Pb emitted into the ambient air is
distributed to other environmental media and can contribute to human
exposures via indoor and outdoor dusts, outdoor soil, food and drinking
water, as well as inhalation of air (CD, pp. 3-1 to 3-2). Accordingly,
people are exposed to Pb emitted into ambient air by both inhalation
and ingestion pathways. In general, air-related pathways include those
pathways where Pb passes through ambient air on its path from a source
to human exposure. EPA considers risks to public health from exposure
to Pb that was emitted into the air as relevant to our consideration of
the primary standard. Therefore , we consider these air-related
pathways to be policy-relevant in this review. Air-related Pb exposure
pathways include: Inhalation of airborne Pb (that may include Pb
emitted into the air and deposited and then resuspended); and ingestion
of Pb that, once airborne, has made its way into indoor dust, outdoor
dust or soil, dietary items (e.g., crops and livestock), and drinking
water (e.g., CD, Figure 3-1).
    Ambient air Pb contributes to Pb in indoor dust through transport
of Pb suspended in ambient air that is then deposited indoors and
through transport of Pb that has deposited outdoors from ambient air
and is transported indoors in ways other than through ambient air (CD,
Section 3.2.3; Adgate et al., 1998). For example, infiltration of
ambient air into buildings brings airborne Pb indoors where deposition
of particles contributes to Pb in dust on indoor surfaces (CD, p. 3-28;
Caravanos et al., 2006a). Indoor dust may be ingested (e.g., via hand-
to-mouth activity by children; CD, p. 8-12) or may be resuspended
through household activities and inhaled (CD, p. 8-12). Ambient air Pb
can also deposit onto outdoor surfaces (including surface soil) with
which humans may come into contact (CD, Section 2.3.2; Farfel et al.,
2003; Caravanos et al., 2006a, b). Human contact with this deposited Pb
may result in incidental ingestion from this exposure pathway and may
also result in some of this Pb being carried indoors (e.g., on clothes
and shoes) adding to indoor dust Pb (CD, p. 3-28; von Lindern et al.,
2003a, b). Additionally, Pb from ambient air that deposits on outdoor
surfaces may also be resuspended and carried indoors in the air where
it can be inhaled. Thus, indoor dust receives air-related Pb directly
from ambient air coming indoors and also more indirectly, after
deposition from ambient air onto outdoor surfaces.
    As mentioned above, humans may contact Pb in dust on outdoor
surfaces, including surface soil and other materials, that has
deposited from ambient air (CD, Section 3.2; Caravanos et al., 2006a;
Mielke et al., 1991; Roels et al., 1980). Human exposure to this
deposited Pb can occur through incidental ingestion, and, when the
deposited Pb is resuspended, by inhalation. Atmospheric deposition of
Pb also contributes to Pb in vegetation, both as a result of contact
with above ground portions of the plant and through contributions to
soil and transport of Pb into roots (CD, pp. 7-9 and AXZ7-39; USEPA,
1986a, Sections 6.5.3 and <IP_ADDRESS>.1). Livestock may subsequently be
exposed to Pb in vegetation (e.g., grasses and silage) and in surface
soils via incidental ingestion of soil while grazing (USEPA 1986a,
Section <IP_ADDRESS>.2). Atmospheric deposition is estimated to comprise a
significant proportion of Pb in food (CD, p. 3-48; Flegel et al., 1990;
Juberg et al., 1997; Dudka and Miller, 1999). Atmospheric deposition
outdoors also contributes to Pb in surface waters, although given the
widespread use of settling or filtration in drinking water treatment,
air-related Pb is generally a small component of Pb in treated drinking
water (CD, Section 2.3.2 and p. 3-33).
    Air-related exposure pathways are affected by changes to air
quality, including changes in concentrations of Pb in air and/or
changes in atmospheric deposition of Pb. Further, because of its
persistence in the environment, Pb deposited from the air may
contribute to human and ecological exposures for years into the future
(CD, pp. 3-18 to 3-19, pp. 3-23 to 2-24). Thus, because of the roles in
human exposure pathways of both air concentration and air deposition,
and of the persistence of Pb, once deposited, some pathways respond
more quickly to changes in air quality than others. Pathways most
directly involving Pb in ambient air and exchanges of ambient air with
indoor air respond more quickly while pathways involving exposure to Pb
deposited from ambient air into the environment generally respond more
slowly (CD, pp. 3-18 to 3-19).

    Exposure pathways tied most directly to ambient air, and that
consequently have the potential to respond relatively more quickly to
changes in air Pb, include inhalation of ambient air, and ingestion of
Pb in indoor dust directly contaminated with Pb from ambient air.\16\
Lead from ambient air contaminates indoor dust directly when outdoor
air comes inside (through open doors or windows, for example) and Pb in
that air deposits to indoor surfaces (Caravanos et al., 2006a; CD, p.
8-22). This includes Pb that was previously deposited outdoors and is
then resuspended and transported indoors. Lead in dust on outdoor
surfaces also responds to air deposition (Caravanos et al., 2006).
Pathways in which the air quality impact is reflected over a somewhat
longer time frame generally are associated with outdoor atmospheric
deposition, and include ingestion pathways such as the following: (1)
Ingestion of Pb in outdoor soil; (2) ingestion of Pb in indoor dust
indirectly contaminated with Pb from the outdoor air (e.g, ``tracking
in'' of Pb deposited to outdoor surface soil, as compared to ambient
air transport of resuspended outdoor soil); (3) ingestion of Pb in diet
that is attributable to deposited air Pb, and; (4) ingestion of Pb in
drinking water that is attributable to deposited air Pb (e.g., Pb
entering water bodies used for drinking supply).
---------------------------------------------------------------------------

    \16\ We note that in the risk assessment, we only assessed
alternate standard impacts on the subset of air-related pathways
that respond relatively quickly to changes in air Pb.
---------------------------------------------------------------------------

3. Nonair-Related and Air-Related Background Human Exposure Pathways
    As when the standard was set in 1978, there continue to be multiple
sources of exposure, both air-related and others (nonair-related).
Human exposure pathways that are not air-related are those in which Pb
does not pass through ambient air. These pathways as well as air-
related human exposure pathways that involve natural sources of Pb to
air are considered policy-relevant background in this review. In the
context of NAAQS for other criteria pollutants which are not multimedia
in nature, such as ozone, the term policy-relevant background is used
to distinguish anthropogenic air emissions from naturally occurring
non-anthropogenic emissions to separate pollution levels that can be
controlled by U.S. regulations from levels that are generally
uncontrollable by the United States (USEPA, 2007d). In the case of Pb,
however, due to the multimedia, multipathway nature of human exposures
to Pb, policy-relevant background is defined more broadly to include
not only the ``quite low'' levels of naturally occurring Pb emissions
into the air from non-anthropogenic sources such as volcanoes, sea
salt, and windborne soil particles from areas free of anthropogenic
activity (see below), but also Pb from nonair sources. These are
collectively referred to as ``policy-relevant background.''
    The pathways of human exposure to Pb that are not air-related
include ingestion of Pb from indoor Pb paint \17\, Pb in diet as a
result of inadvertent additions during food processing, and Pb in
drinking water attributable to Pb in distribution systems (CD, Chapter
3). Other less prevalent, potential pathways of Pb exposure that are
not air-related include ingestion of some calcium supplements or of
food contaminated during storage in some Pb glazed glassware, and hand-
to-mouth contact with some imported vinyl miniblinds or with some hair
dyes containing Pb acetate, as well as some cosmetics and folk remedies
(CD, pp. 3-50 to 3-51).
---------------------------------------------------------------------------

    \17\ Weathering of outdoor Pb paint may also contribute to soil
Pb levels adjacent to the house.
---------------------------------------------------------------------------

    Some amount of Pb in the air derives from background sources, such
as volcanoes, sea salt, and windborne soil particles from areas free of
anthropogenic activity (CD, Section 2.2.1). The impact of these sources
on current air concentrations is expected to be quite low (relative to
current concentrations) and has been estimated to fall within the range
from 0.00002 [mu]g/m3 and 0.00007 [mu]g/m3 based
on mass balance calculations for global emissions (CD, Section 3.1 and
USEPA 1986, Section <IP_ADDRESS>.3). The midpoint in this range, 0.00005
[mu]g/m3, has been used in the past to represent the
contribution of naturally occurring air Pb to total human exposure
(USEPA 1986, Section <IP_ADDRESS>.3). The data available to derive such an
estimate are limited and such a value might be expected to vary
geographically with the natural distribution of Pb. Comparing this to
reported air Pb measurements is complicated by limitations of the
common analytical methods and by inconsistent reporting practices. This
value is one half the lowest reported nonzero value in AQS. Little
information is available regarding anthropogenic sources of airborne Pb
located outside of North America, which would also be considered
policy-relevant background. In considering contributions from policy-
relevant background to human exposures and associated health effects,
however, any credible estimate of policy-relevant background in air is
likely insignificant in comparison to the contributions from exposures
to nonair media.
4. Contributions to Children's Lead Exposures
    As when the standard was set in 1978, EPA recognizes that there
remain today contributions to blood Pb levels from nonair sources. The
relative contribution of Pb in different exposure media to human
exposure varies, particularly for different age groups. For example,
some studies have found that dietary intake of Pb may be a predominant
source of Pb exposure among adults, greater than consumption of water
and beverages or inhalation (CD, p. 3-43).\18\ For young children,
however, ingestion of indoor dust can be a significant Pb exposure
pathway, such that dust ingested via hand-to-mouth activity can be a
more important source of Pb exposure than inhalation, although indoor
dust can also be resuspended through household activities and pose an
inhalation risk as well (CD, p. 3-27 to 3-28; Melnyk et al. 2000).\19\
---------------------------------------------------------------------------

    \18\ ``Some recent exposure studies have evaluated the relative
importance of diet to other routes of Pb exposure. In reports from
the NHEXAS, Pb concentrations measured in households throughout the
Midwest were significantly higher in solid food compared to
beverages and tap water (Clayton et al., 1999; Thomas et al., 1999).
However, beverages appeared to be the dominant dietary pathway for
Pb according to the statistical analysis (Clayton et al., 1999),
possibly indicating greater bodily absorption of Pb from liquid
sources (Thomas et al., 1999). Dietary intakes of Pb were greater
than those calculated for intake from home tap water or inhalation
on a [mu]g/day basis (Thomas et al., 1999). The NHEXAS study in
Arizona showed that, for adults, ingestion was a more important Pb
exposure route than inhalation (O'Rourke et al., 1999).'' (CD, p. 3-
43)
    \19\ For example, the Criteria Document states the following:
``Given the large amount of time people spend indoors, exposure to
Pb in dusts and indoor air can be significant. For children, dust
ingested via hand-to-mouth activity is often a more important source
of Pb exposure than inhalation. Dust can be resuspended through
household activities, thereby posing an inhalation risk as well.
House dust Pb can derive both from Pb-based paint and from other
sources outside the home. The latter include Pb-contaminated
airborne particles from currently operating industrial facilities or
resuspended soil particles contaminated by deposition of airborne Pb
from past emissions.'' (CD, p. E-6)
---------------------------------------------------------------------------

    Estimating contributions from nonair sources is complicated by the
existence of multiple and varied air-related pathways (as described in
section II.A.2 above), as well as the persistent nature of Pb. For
example, Pb that is a soil or dust contaminant today may have been
airborne yesterday or many years ago. The studies currently available
and reviewed in the Criteria Document that evaluate the multiple
pathways of Pb exposure, when considering exposure contributions from
outdoor dust/soil, do

not usually distinguish between outdoor soil/dust Pb resulting from
historical emissions and outdoor soil/dust Pb resulting from recent
emissions. Further, while indoor dust Pb has been identified as being a
predominant contributor to children's blood Pb, available studies do
not generally distinguish the different pathways (air-related and
other) contributing to indoor dust Pb. The exposure assessment for
children performed for this review has employed available data and
methods to develop estimates intended to inform a characterization of
these pathways (as described in section II.C below).
    Relative contributions to a child's total Pb exposure from air-
related exposure pathways (such as those identified in the sections
above) compared to other (nonair-related) Pb exposures depends on many
factors including ambient air concentrations and air deposition in the
area where the child resides (as well as in the area from which the
child's food derives), access to other sources of Pb exposure such as
Pb paint, tap water affected by plumbing containing Pb and access to
Pb-tainted products. Studies indicate that in the absence of paint-
related exposures, Pb from other sources such as stationary sources of
Pb emissions may dominate a child's Pb exposures (CD, section 3.2). In
other cases, such as children living in older housing with peeling
paint or where renovations have occurred, the dominant source may be
lead paint used in the house in the past (CD, pp. 3-50 and 3-51).
Depending on Pb levels in a home's tap water, drinking water can
sometimes be a significant source (CD, section 3.3). And in still other
cases, there may be more of a mixture of contributions from multiple
sources, with no one source dominating (CD, Chapter 3).
    As recognized in sections B.1.1 and II.B.3.a, blood Pb levels are
the commonly used index of exposure for Pb and they reflect external
sources of exposure, behavioral characteristics and physiological
factors. Lead derived from differing sources or taken into the body as
a result of differing exposure pathways (e.g., air- as compared to
nonair-related), is not easily distinguished. As mentioned above,
complications to consideration of estimates of air-related or
conversely, nonair, blood Pb levels are the roles of air Pb in human
exposure pathways and the persistence of Pb in the environment. As
described in section II.A.2, air-related pathways (those in which Pb
passes through the air on its path from source to human exposure) are
varied, including inhalation and ingestion, indoor dust, outdoor dust/
soil and diet, Pb suspended in and deposited from air, and encompassing
a range of time frames from more immediate to less so. Estimates of
blood Pb levels associated with air-related exposure pathways or only
with nonair exposure pathways will vary depending on how completely the
air-related pathways are characterized.
    Consistent with reductions in air Pb concentrations (as described
in section II.A.1 above) which contribute to blood Pb, nonair
contributions have also been reduced. For example, the use of Pb paint
in new houses has declined substantially over the 20th century, such
that according to the National Survey of Lead and Allergens in Housing
(USHUD, 2002) an estimated 24% of U.S. housing constructed between 1960
and 1978; 69% of the housing constructed between 1940 and 1959; and 87%
of the pre-1940 housing contains lead-based paint. Additionally, Pb
contributions to diet have been reported to have declined significantly
since 1978, perhaps as much as 70% or more between then and 1990 (WHO,
1995) and the 2006 Criteria Document identifies a drop in dietary Pb
intake by 2 to 5 year olds of 96% between the early 1980s and mid 1990s
(CD, Section 3.4 and p. 8-14).\20\ These reductions are generally
attributed to reductions in gasoline-related airborne Pb as well as the
reduction in use of Pb solder in canning food products (CD, Section
3.4).\21\ There have also been reductions in tap water Pb levels (CD,
section 3.3 and pp. 8-13 to 8-14). Contamination from the distribution/
plumbing system appears to remain the predominant source of Pb in the
drinking water (CD, section 3.3 and pp. 8-013 to 8-14).
---------------------------------------------------------------------------

    \20\ Additionally, the 1977 Criteria Document included a dietary
Pb intake estimate for the general population of 100 to 350 [mu]g
Pb/day, with estimates near and just below 100 [mu]g/day for young
children (USEPA 1977, pp. 1-2 and 12-32) and the 2006 Criteria
Document cites recent studies (for the mid-1990s) indicating a
dietary intake ranging from 2 to 10 [mu]g Pb/day for children (CD,
Section 3.4 and p. 8-14).
    \21\ Sources of Pb in food were identified in the 1986 Criteria
Document as including air-related sources, metals used in processing
raw foodstuffs, solder used in packaging and water used in cooking
(1986a, section 3.1.2).
---------------------------------------------------------------------------

    The availability of estimates of blood Pb levels resulting only
from air-related sources and exposures or only from those unrelated to
air is limited and, given the discussion above, would be expected to
vary for different populations. In addition to potential differences in
air-related and nonair-related blood Pb levels among populations with
different exposure circumstances (e.g., relatively more or lesser
exposure to air-related Pb), the absolute levels may also vary among
different age groups. As described in section II.B.1.b, average total
blood Pb levels in the U.S. differ among age groups, with levels being
highest in children aged one to five years old. We also note that
behavioral characteristics that influence Pb exposures vary among age
groups. For example as noted above, the predominant Pb exposure
pathways may differ between adults and children. The extent of any
quantitative impact of these differences on estimates of nonair blood
Pb levels is unknown.\22\
---------------------------------------------------------------------------

    \22\ As noted earlier in this section, for children, dust
ingestion by hand-to-mouth activity can be an important source of Pb
exposure, while for adults, dietary Pb can be predominant.
---------------------------------------------------------------------------

    In their advice to the Agency on levels for the standard, the CASAC
Pb Panel explored several approaches to deriving a level, one of which
required an estimate of the nonair component of blood Pb for the
average child. They recommended consideration of 1.0 to 1.4 [mu]g/dL or
lower for such an estimate for the average nonair blood Pb level for
young children (Henderson, 2007a, p. D-1). This range was developed
with consideration of simulations of the integrated exposure and uptake
biokinetic (IEUBK) model for lead for which the exposure concentration
inputs included zero air concentration and concentrations for soil and
dust of 50 ppm and 35 ppm, respectively (Henderson, 2007a, p. F-
60).\23\ \24\ \25\
---------------------------------------------------------------------------

    \23\ The soil and dust levels are described as ``typical
geochemical non-air input levels for dust and soil'' (Henderson,
2007a, p. F-60). The values used for these levels in this simulation
fall within the range of 1 to 200 ppm described in the Criteria
Document for soil not influenced by sources (CD, p. 3-18).
    \24\ The other IEUBK inputs (e.g., exposure and biokinetic
factors) were those used in the IEUBK modeling for the risk
assessment in this review (Henderson, 2007a, p. F-60).
    \25\ Individual CASAC member comments describing the IEUBK
simulations stated that the modeling produced a nonair blood Pb
level of ``1.4 [mu]g/dL as a geometric mean'' (Henderson, 2007a, p.
F-61).
---------------------------------------------------------------------------

    As is evident from the prior discussion, the many different
exposure pathways contributing to children's blood Pb levels, and other
factors, complicate our consideration of the available data with regard
to characterization of levels particular to specific pathways, air-
related or otherwise.

B. Health Effects Information

    The following summary focuses on health endpoints associated with
the range of exposures considered to be most relevant to current
exposure levels and makes note of several key aspects of the health
evidence for Pb. First (as

described in Section II.A, above), because exposure to atmospheric Pb
particles occurs not only via direct inhalation of airborne particles,
but also via ingestion of deposited ambient Pb, the exposure considered
is multimedia and multipathway in nature, occurring via both the
inhalation and ingestion routes. Second, the exposure index or dose
metric most commonly used and associated with health effects
information is an internal biomarker (i.e., blood Pb). Additionally,
the exposure duration of interest (i.e., that influencing internal dose
pertinent to health effects of interest) may span months to potentially
years, as does the time scale of the environmental processes
influencing Pb deposition and fate. Lastly, the nature of the evidence
for the health effects of greatest interest for this review,
neurological effects, particularly neurocognitive and neurobehavioral
effects, in young children, are epidemiological data substantiated by
toxicological data that provide biological plausibility and insights on
mechanisms of action (CD, sections 5.3, 6.2 and 8.4.2).
    In recognition of the multi-pathway aspects of Pb, and the use of
an internal exposure metric in health risk assessment, the next section
describes the internal disposition or distribution of Pb, and the use
of blood Pb as an internal exposure or dose metric. This is followed by
a discussion of the nature of Pb-induced health effects that emphasizes
those with the strongest evidence. Potential impacts of Pb exposures on
public health, including recognition of potentially susceptible or
vulnerable subpopulations, are then discussed. Finally, key
observations about Pb-related health effects are summarized.
1. Blood Lead
    The health effects of Pb are remote from the portals of entry to
the body (i.e., the respiratory system and gastrointestinal tract).
Consequently, the internal disposition and distribution of Pb in the
blood is an integral aspect of the relationship between exposure and
effect. Additionally, the focus on blood Pb as the dose metric in
consideration of the Pb health effects evidence, while reducing our
uncertainty with regard to causality, leads to an additional
consideration with regard to contribution of air-related sources and
exposure pathways to blood Pb.
a. Internal Disposition of Lead
    This section briefly summarizes the current state of knowledge of
Pb disposition pertaining to both inhalation and ingestion routes of
exposure as described in the Criteria Document.
    Inhaled Pb particles deposit in the different regions of the
respiratory tract as a function of particle size (CD, pp. 4-3 to 4-4).
Lead associated with smaller particles, which are predominantly
deposited in the pulmonary region, may, depending on solubility, be
absorbed into the general circulation or transported to the
gastrointestinal tract (CD, pp. 4-3). Lead associated with larger
particles, which are predominantly deposited in the head and conducting
airways (e.g., nasal pharyngeal and tracheobronchial regions of
respiratory tract), may be transported into the esophagus and
swallowed, thus making its way to the gastrointestinal tract (CD, pp.
4-3 to 4-4), where it may be absorbed into the blood stream. Thus, Pb
can reach the gastrointestinal tract either directly through the
ingestion route or indirectly following inhalation.
    Once in the blood stream, where approximately 99% of the Pb
associates with red blood cells, the Pb is quickly distributed
throughout the body (e.g., within days) with the bone serving as a
large, long-term storage compartment, and soft tissues (e.g., kidney,
liver, brain, etc.) serving as smaller compartments, in which Pb may be
more mobile (CD, sections <IP_ADDRESS> and 8.3.1.). Additionally, the
epidemiologic evidence indicates that Pb freely crosses the placenta
resulting in continued fetal exposure throughout pregnancy, and that
exposure increases during the later half of pregnancy (CD, section
6.6.2).
    During childhood development, bone represents approximately 70% of
a child's body burden of Pb, and this accumulation continues through
adulthood, when more than 90% of the total Pb body burden is stored in
the bone (CD, section 4.2.2). Accordingly, levels of Pb in bone are
indicative of a person's long-term, cumulative exposure to Pb. In
contrast, blood Pb levels are usually indicative of recent exposures.
Depending on exposure dynamics, however, blood Pb may--through its
interaction with bone--be indicative of past exposure or of cumulative
body burden (CD, section <IP_ADDRESS>).
    Throughout life, Pb in the body is exchanged between blood and
bone, and between blood and soft tissues (CD, section 4.3.2), with
variation in these exchanges reflecting ``duration and intensity of the
exposure, age and various physiological variables'' (CD, p. 4-1). Past
exposures that contribute Pb to the bone, consequently, may influence
current levels of Pb in blood. Where past exposures were elevated in
comparison to recent exposures, this influence may complicate
interpretations with regard to recent exposure (CD, sections <IP_ADDRESS> to
<IP_ADDRESS>). That is, higher blood Pb concentrations may be indicative of
higher cumulative exposures or of a recent elevation in exposure (CD,
pp. 4-34 and 4-133).
    In several studies investigating the relationship between Pb
exposure and blood Pb in children (e.g., Lanphear and Roghmann 1997;
Lanphear et al., 1998), blood Pb levels have been shown to reflect Pb
exposures, with particular influence associated with exposures to Pb in
surface dust. Further, as stated in the Criteria Document ``these and
other studies of populations near active sources of air emissions
(e.g., smelters, etc.) substantiate the effect of airborne Pb and
resuspended soil Pb on interior dust and blood Pb'' (CD, p. 8-22).
b. Use of Blood Lead as Dose Metric
    Blood Pb levels are extensively used as an index or biomarker of
exposure by national and international health agencies, as well as in
epidemiological (CD, sections <IP_ADDRESS> and 8.3.2) and toxicological
studies of Pb health effects and dose-response relationships (CD,
Chapter 5). The prevalence of the use of blood Pb as an exposure index
or biomarker is related to both the ease of blood sample collection
(CD, p. 4-19; Section 4.3.1) and by findings of association with a
variety of health effects (CD, Section 8.3.2). For example, the U.S.
Centers for Disease Control and Prevention (CDC), and its predecessor
agencies, have for many years used blood Pb level as a metric for
identifying children at risk of adverse health effects and for
specifying particular public health recommendations (CDC, 1991; CDC,
2005a). In 1978, when the current Pb NAAQS was established, the CDC
recognized a blood Pb level of 30 [mu]g/dL as a level warranting
individual intervention (CDC, 1991). In 1985, the CDC recognized a
level of 25 [mu]g/dL for individual child intervention, and in 1991,
they recognized a level of 15 [mu]g/dL for individual intervention and
a level of 10 [mu]g/dL for implementing community-wide prevention
activities (CDC, 1991; CDCa, 2005). In 2005, with consideration of a
review of the evidence by their advisory committee, CDC revised their
statement on Preventing Lead Poisoning in Young Children, specifically
recognizing the evidence of adverse health effects in children with
blood Pb levels below 10 [mu]g/dL \26\ and the data demonstrating that

no ``safe'' threshold for blood Pb had been identified, and emphasizing
the importance of preventative measures (CDC, 2005a, ACCLPP, 2007).\27\
---------------------------------------------------------------------------

    \26\ As described by the Advisory Committee on Childhood Lead
Poisoning Prevention, ``In 1991, CDC defined the blood lead level
(BLL) that should prompt public health actions as 10 [mu]g/dL.
Concurrently, CDC also recognized that a BLL of 10 [mu]g/dL did not
define a threshold for the harmful effects of lead. Research
conducted since 1991 has strengthened the evidence that children's
physical and mental development can be affected at BLLS <10 [mu]g/
dL'' (ACCLPP, 2007).
    \27\ With the 2005 statement, CDC did not lower the 1991 level
of concern and identified a variety of reasons, reflecting both
scientific and practical considerations, for not doing so, including
a lack of effective clinical or public health interventions to
reliably and consistently reduce blood Pb levels that are already
below 10 [mu]g/dL, the lack of a demonstrated threshold for adverse
effects, and concerns for deflecting resources from children with
higher blood Pb levels (CDC, 2005a). CDC's Advisory Committee on
Childhood Lead Poisoning Prevention recently provided
recommendations regarding interpreting and managing blood Pb levels
below 10 [mu]g/dL in children and reducing childhood exposures to Pb
(ACCLPP, 2007).
---------------------------------------------------------------------------

    Since 1976, the CDC has been monitoring blood Pb levels nationally
through the National Health and Nutrition Examination Survey (NHANES).
This survey monitors blood Pb levels in multiple age groups in the U.S.
This information indicates variation in mean blood Pb levels across the
various age groups monitored. For example, mean values in 2001-2002 for
ages 1-5, 6-11, 12-19 and greater than or equal to 20 years of age, are
1.70, 1.25, 0.94, and 1.56, respectively (CD, p. 4-22).
    The NHANES information has documented the dramatic decline in mean
blood Pb levels in the U.S. population that has occurred since the
1970s and that coincides with regulations regarding leaded fuels,
leaded paint, and Pb-containing plumbing materials that have reduced Pb
exposure among the general population (CD, Sections <IP_ADDRESS> and 8.3.3;
Schwemberger et al., 2005). The Criteria Document summarizes related
information as follows (CD, p. E-6).

    In the United States, decreases in mobile sources of Pb,
resulting from the phasedown of Pb additives created a 98% decline
in emissions from 1970 to 2003. NHANES data show a consequent
parallel decline in blood-Pb levels in children aged 1 to 5 years
from a geometric mean of ~15 [mu]g/dL in 1976-1980 to ~1-2 [mu]g/dL
in the 2000-2004 period.

While levels in the U.S. general population, including geometric mean
levels in children aged 1-5, have declined significantly, levels have
been found to vary among children of different socioeconomic status
(SES) and other demographic characteristics (CD, p. 4-21). For example,
while the 2001-2004 median blood level for children aged 1-5 of all
races and ethnic groups is 1.6 [mu]g/dL, the median for the subset
living below the poverty level is 2.3 [mu]g/dL and 90th percentile
values for these two groups are 4.0 [mu]g/dL and 5.4 [mu]g/dL,
respectively. Similarly, the 2001-2004 median blood level for black,
non-Hispanic children aged 1-5 is 2.5 [mu]g/dL, while the median level
for the subset of that group living below the poverty level is 2.9
[mu]g/dL and the median level for the subset living in more well-off
households (i.e., with income more than 200% of the poverty level) is
1.9 [mu]g/dL. Associated 90th percentile values for 2001-2004 are 6.4
[mu]g/dL (for black, non-Hispanic children aged 1-5), 7.7 [mu]g/dL (for
the subset of that group living below the poverty level) and 4.1 [mu]g/
dL (for the subset living in a household with income more than 200% of
the poverty level).\28\ The recently released RRP rule (discussed above
in section I.C) is expected to contribute to further reductions in BLL
for children living in houses with Pb paint.
---------------------------------------------------------------------------

    \28\ This information is available at: http://www.epa.gov/
envirohealth/children/body_burdens/b1-table.htm (click on
``Download a universal spreadsheet file of the Body Burdens data
tables'').

    Bone measurements, as a result of the generally slower Pb turnover
in bone, are recognized as providing a better measure of cumulative Pb
exposure (CD, Section 8.3.2). The bone pool of Pb in children, however,
is thought to be much more labile than that in adults due to the more
rapid turnover of bone mineral as a result of growth (CD, p. 4-27). As
a result, changes in blood Pb concentration in children more closely
parallel changes in total body burden (CD, pp. 4-20 and 4-27). This is
in contrast to adults, whose bone has accumulated decades of Pb
exposures (with past exposures often greater than current ones), and
for whom the bone may be a significant source long after exposure has
ended (CD, Section <IP_ADDRESS>).
c. Air-to-Blood Relationships
    As described in Section II.A, Pb in ambient air contributes to Pb
in blood by multiple pathways, with the pertinent exposure routes
including both inhalation and ingestion (CD, Sections <IP_ADDRESS>, 4.2 and
4.4; Hilts, 2003). The quantitative relationship between ambient air Pb
and blood Pb, which is often termed a slope or ratio, describes the
increase in blood Pb (in [mu]g/dL) per unit of air Pb (in [mu]g/m
\3\).\29\
---------------------------------------------------------------------------

    \29\ 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.
---------------------------------------------------------------------------

    The evidence on this quantitative relationship 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
various Pb exposure circumstances. The 1986 Criteria Document discussed
the studies available at that time that addressed the relationship
between air Pb and blood Pb,\30\ recognizing that there is significant
variability in air-to-blood ratios for different populations exposed to
Pb through different air-related exposure pathways and at different
exposure levels.
---------------------------------------------------------------------------

    \30\ We note that the 2006 Criteria Document did not include a
discussion of more recent studies on air-to-blood ratios.
---------------------------------------------------------------------------

    In discussing the available evidence, the 1986 Criteria Document
observed that estimates of air-to-blood ratios that included 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 (USEPA 1986a, p. 11-106). Thus, the
extent to which studies account for the full set of air-related
exposure pathways affects the magnitude of the resultant air-to-blood
estimates, such that fewer pathways included as ``air-related'' yield
lower ratios. The 1986 Criteria Document also observed that ratios
derived from studies focused only on inhalation pathways (e.g., chamber
studies, occupational studies) have generally been on the order of 1:2
or lower, while ratios derived from studies including more air-related
pathways were generally higher (USEPA, 1986a, p. 11-106). Further, the
current evidence appears to indicate higher ratios for children as
compared to those for adults (USEPA, 1986a), perhaps due to behavioral
differences between the age groups.
    Reflecting these considerations, the 1986 Criteria Document
identified a range of air-to-blood ratios for children that reflected
both inhalation and ingestion-related air Pb contributions as generally
ranging from 1:3 to 1:5 based on the information available at that time
(USEPA 1986a, p. 11-106). Table 11-36 (p. 11-100) in the 1986 Criteria
Document (drawn from Table 1 in Brunekreef, 1984) presents air-to-blood
ratios from a number of studies in children (i.e., those with
identified air monitoring methods and reliable blood Pb data). For
example, air-to-blood ratios from the subset of those studies that used
quality control protocols and presented adjusted slopes \31\ include

adjusted ratios of 3.6 (Zielhuis et al., 1979), 5.2 (Billick et al.,
1979, 1980), 2.9 (Billick et al., 1983), and 8.5 (Brunekreef et al,
1983).
---------------------------------------------------------------------------

    \31\ Brunekreef et al. (1984) discusses potential confounders to
the relationship between air Pb and blood Pb, recognizing that
ideally all possible confounders should be taken into account in
deriving an adjusted air-to-blood relationship from a community
study. The studies cited here adjusted for parental education
(Zielhuis et al., 1979), age and race (Billick et al., 1979, 1980)
and additionally measuring height of air Pb (Billick et al., 1983);
Brunekreef et al. (1984) used multiple regression to control for
several confounders. The authors conclude that ``presentation of
both unadjusted and (stepwise) adjusted relationships is advisable,
to allow insight in the range of possible values for the
relationship'' (p. 83). Unadjusted ratios were presented for two of
these studies, including ratios of 4.0 (Zielhuis et al., 1979) and
18.5 (Brunekreef et al., 1983). Note, that the Brunekreef et al.,
1983 study is subject to a number of sources of uncertainty that
could result in air-to-blood Pb ratios that are biased high,
including the potential for underestimating ambient air Pb levels
due to the use of low volume British Smoke air monitors and the
potential for ongoing (higher historical) ambient air Pb levels to
have influenced blood Pb levels (see Section V.B.2 of the 1989 Pb
Staff Report for the Pb NAAQS review, EPA, 1989). In addition, the
1989 Staff Report notes that the higher air-to-blood ratios obtained
from this study could reflect the relatively lower blood Pb levels
seen across the study population (compared with blood Pb levels
reported in other studies from that period).
---------------------------------------------------------------------------

    Additionally, the 1986 Criteria Document noted that ratios derived
from studies involving higher blood and air Pb levels are generally
smaller than ratios from studies involving lower blood and air Pb
levels (USEPA, 1986a. p. 11-99). In consideration of this factor, we
note that the range of 1:3 to 1:5 in air-to-blood ratios for children
noted in the 1986 Criteria Document generally reflected study
populations with blood Pb levels in the range of approximately 10-30
[mu]g/dL (USEPA 1986a, pp. 11-100; Brunekreef, 1984), much higher than
those common in today's population. This observation suggests that air-
to-blood ratios relevant for today's population of children would
likely extend higher than the 1:3 to 1:5 range identified in the 1986
Criteria Document.
    More recently, a study of 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 six years of age)
reports a ratio of 1:6 and additional analysis of the data by EPA for
the initial time period of the study resulted in a ratio of 1:7 (CD,
pp. 3-23 to 3-24; Hilts, 2003).\32\ Ambient air and blood Pb levels
associated with the Hilts (2003) study range from 1.1 to 0.03 [mu]g/
m\3\, and associated population mean blood Pb levels range from 11.5 to
4.7 [mu]g/dL, which are lower than levels associated with the older
studies cited in the 1986 Criteria Document (USEPA, 1986).
---------------------------------------------------------------------------

    \32\ This study considered changes in ambient air Pb levels and
associated blood Pb levels over a five-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, EPA calculated an alternate air-to-
blood Pb ratio based on consideration for ambient air Pb and blood
Pb reductions in the first time period (after opening of the new
facility in 1997).
---------------------------------------------------------------------------

    Sources of uncertainty related to air-to-blood ratios obtained from
Hilts (2003) study have been identified. One such area of uncertainty
relates to the pattern of changes in indoor Pb dustfall (presented in
Table 3 in the article) which suggests a potentially significant
decrease in Pb impacts to indoor dust prior to closure of an older Pb
smelter and start-up of a newer facility in 1997. Some have suggested
that this earlier reduction in indoor dustfall suggests that a
significant portion of the reduction in Pb exposure (and therefore, the
blood Pb reduction reflected in air-to-blood ratios) may have resulted
from efforts to increase public awareness of the Pb contamination issue
(e.g., through increased cleaning to reduce indoor dust levels) rather
than reductions in ambient air Pb and associated indoor dust Pb
contamination. In addition, notable fluctuations in blood Pb levels
observed prior to 1997 (as seen in Figure 2 of the article) have raised
questions as to whether factors other than ambient air Pb reduction
could be influencing decreases in blood Pb.\33\
---------------------------------------------------------------------------

    \33\ In the publication, the author acknowledges that remedial
programs (e.g., community and home-based dust control and education)
may have been responsible for some of the blood Pb reduction seen
during the study period (1997 to 2001). However, the author points
out that these programs were in place in 1992 and he suggests that
it is unlikely that they contributed to the sudden drop in blood Pb
levels occurring after 1997. In addition, the author describes a
number of aspects of the analysis, which could have implications for
air-to-blood ratios including a tendency over time for children with
lower blood Pb levels to not return for testing, and inclusion of
children aged 6 to 36 months in Pb screening in 2001 (in contrast to
the wider age range up to 60 months as was done in previous years).
---------------------------------------------------------------------------

    In addition to the study by Hilts (2003), we are aware of two other
studies published since the 1986 Criteria Document that report air-to-
blood ratios for children (Tripathi et al., 2001 and Hayes et al.,
1994). These studies were not cited in the 2006 Criteria Document, but
were referenced in public comments received by EPA during this
review.\34\ The study by Tripathi et al. (2001) reports an air-to-blood
ratio of approximately 1:3.6 for an analysis of children aged six
through ten in India. The ambient air and blood Pb levels in this study
(geometric mean blood Pb levels generally ranged from 10 to 15 [mu]g/
dL) are similar to levels reported in older studies reviewed in the
1986 Criteria Document and are much higher than current conditions in
the U.S. The study by Hayes (1994) compared patterns of ambient air Pb
reductions and blood Pb reductions for large numbers of children in
Chicago between 1971 and 1988, a period when significant reductions
occurred in both measures. The study reports an air-to-blood ratio of
1:5.6 associated with ambient air Pb levels near 1 [mu]g/m\3\ and a
ratio of 1:16 for ambient air Pb levels in the range of 0.25 [mu]g/
m\3\, indicating a pattern of higher ratios with lower ambient air Pb
and blood Pb levels consistent with conclusions in the 1986 Criteria
Document.\35\
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    \34\ EPA is not basing its proposed decisions on these two
studies, but notes that these estimates are consistent with other
studies that were included in the 1986 and 2006 Criteria Documents
and accordingly considered by CASAC and the public.
    \35\ As with all studies, we note that there are strengths and
limitations for these two studies which may affect the specific
magnitudes of the reported ratios, but that the studies' findings
and trends are generally consistent with the conclusions from the
1986 Criteria Document.
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    In their advice to the Agency, CASAC identified air-to-blood ratios
of 1:5, as used by the World Health Organization (2000), and 1:10, as
supported by an empirical analysis of changes in air Pb and changes in
blood Pb between 1976 and the time when the phase-out of Pb from
gasoline was completed (Henderson, 2007a).\36\
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    \36\ The CASAC Panel stated ``The Schwartz and Pitcher analysis
showed that in 1978, the midpoint of the National Health and
Nutrition Examination Survey (NHANES) II, gasoline Pb was
responsible for 9.1 [mu]g/dL of blood Pb in children. Their estimate
is based on their coefficient of 2.14 [mu]g/dL per 100 metric tons
(MT) per day of gasoline use, and usage of 426 MT/day in 1976.
Between 1976 and when the phase-out of Pb from gasoline was
completed, air Pb concentrations in U.S. cities fell a little less
than 1 [mu]g/m\3\ (24). These two facts imply a ratio of 9-10 [mu]g/
dL per [mu]g/m\3\ reduction in air Pb, taking all pathways into
account.'' (Henderson, 2007a, pp. D-2 to D-3).
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    Beyond considering the evidence presented in the published
literature and that reviewed in Pb Criteria Documents, we have also
considered air-to-blood ratios derived from the exposure assessment for
this review (discussed below in section II.C). In that assessment,
current modeling tools and information on children's activity patterns,
behavior and physiology (e.g., CD, Section 4.4) were used to estimate
blood Pb levels associated with

multimedia and multipathway Pb exposure. The results from the various
case studies included in this assessment, with consideration of the
context in which they were derived (e.g., the extent to which the range
of air-related pathways were simulated), are also informative to our
understanding of air-to-blood ratios.
    For the general urban case study, air-to-blood ratios ranged from
1:2 to 1:9 across the alternative standard levels assessed, which
ranged from the current standard of 1.5 [mu]g/m\3\ down to a level of
0.02 [mu]g/m\3\. This pattern of model-derived ratios generally
supports the range of ratios obtained from the literature and also
supports the observation that lower ambient air Pb levels are
associated with higher air-to-blood ratios. There are a number of
sources of uncertainty associated with these model-derived ratios. The
hybrid indoor dust Pb model, which is used in estimating indoor dust Pb
levels for the urban case studies, uses a HUD dataset reflecting
housing constructed before 1980 in establishing the relationship
between dust loading and concentration, which is a key component in the
hybrid dust model (see Section Attachment G-1 of the Risk Assessment,
Volume II). Given this application of the HUD dataset, there is the
potential that the non-linear relationship between indoor dust Pb
loading and concentration (which is reflected in the structure of the
hybrid dust model) could be driven more by the presence of indoor Pb
paint than contributions from outdoor ambient air Pb. We also note that
only recent air pathways were adjusted in modeling the impact of
ambient air Pb reductions on blood Pb levels in the urban case studies,
which could have implications for the air-to-blood ratios.
    For the primary Pb smelter (subarea) case study, air-to-blood
ratios ranged from 1:10 to 1:19 across the same range of alternative
standard levels, from 1.5 down to 0.02 [mu]g/m\3\.\37\ Because these
ratios are based on regression modeling developed using empirical data,
there is the potential for these ratios to capture more fully the
impact of ambient air on indoor dust Pb (and ultimately blood Pb),
including longer timeframe impacts resulting from changes in outdoor
deposition. Therefore, given that these ratios are higher than ratios
developed for the general urban case study using the hybrid indoor dust
Pb model (which only considers reductions in recent air), the ratios
estimated for the primary Pb smelter (subarea) support the evidence-
based observation discussed above that consideration of more of the
exposure pathways relating ambient air Pb to blood Pb, may result in
higher air-to-blood Pb ratios. In considering this case study, some
have suggested, however, that the regression modeling fails to
accurately reflect the temporal relationship between reductions in
ambient air Pb and indoor dust Pb, which could result in an over-
estimate of the degree of dust Pb reduction associated with a specified
degree of ambient air Pb reduction, which in turn could produce air-to-
blood Pb ratios that are biased high.
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    \37\ As noted below in section II.C.3.a, air-to-blood ratios for
the primary Pb smelter (full study area) range from 1:3 to 1:7
across the same range of alternative standard levels (from 1.5 down
to 0.02 [mu]g/m\3\).
---------------------------------------------------------------------------

    In summary, in EPA's view, the current evidence in conjunction with
the results and observations drawn from the exposure assessment,
including related uncertainties, supports consideration of a range of
air-to-blood ratios for children ranging from 1:3 to 1:7, reflecting
multiple air-related pathways beyond simply inhalation and the lower
air and blood Pb levels pertinent to this review. In light of the
uncertainties that remain in the available information on air-to-blood
ratios, EPA requests comment on this range and on the appropriate
weight to place on specific ratios within this range.
2. Nature of Effects
a. Broad Array of Effects
    Lead has been demonstrated to exert ``a broad array of deleterious
effects on multiple organ systems via widely diverse mechanisms of
action'' (CD, p. 8-24 and Section 8.4.1). This array of health effects
includes effects on heme biosynthesis and related functions;
neurological development and function; reproduction and physical
development; kidney function; cardiovascular function; and immune
function. The weight of evidence varies across this array of effects
and is comprehensively described in the Criteria Document. There is
also some evidence of Pb carcinogenicity, primarily from animal
studies, together with limited human evidence of suggestive
associations (CD, Sections 5.6.2, 6.7, and 8.4.10).\38\
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    \38\ Lead has 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 (CD,
Section 6.7.2). U.S. EPA considers Pb a probable carcinogen (http://
www.epa.gov/iris/subst/0277.htm; CD, p. 6-195).
---------------------------------------------------------------------------

    This review is focused on those effects most pertinent to ambient
exposures, which given the reductions in ambient Pb levels over the
past 30 years, are generally those associated with individual blood Pb
levels in children and adults in the range of 10 [mu]g/dL and lower.
Tables 8-5 and 8-6 in the Criteria Document highlight the key such
effects observed in children and adults, respectively (CD, pp. 8-60 to
8-62). The effects include neurological, hematological and immune
effects for children, and hematological, cardiovascular and renal
effects for adults. As evident from the discussions in Chapters 5, 6
and 8 of the Criteria Document, ``neurotoxic effects in children and
cardiovascular effects in adults are among those best substantiated as
occurring at blood Pb concentrations as low as 5 to 10 [mu]g/dL (or
possibly lower); and these categories are currently clearly of greatest
public health concern'' (CD, p. 8-60).\39\ The toxicological and
epidemiological information available since the time of the last review
``includes assessment of new evidence substantiating risks of
deleterious effects on certain health endpoints being induced by
distinctly lower than previously demonstrated Pb exposures indexed by
blood Pb levels extending well below 10 [mu]g/dL in children and/or
adults'' (CD, p. 8-25). Some health effects associated with individual
blood Pb levels extend below 5 [mu]g/dL, and some studies have observed
these effects at the lowest blood levels considered.
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    \39\ With regard to blood Pb levels in individual children
associated with particular neurological effects, the Criteria
Document states ``Collectively, the prospective cohort and cross-
sectional studies offer evidence that exposure to Pb affects the
intellectual attainment of preschool and school age children at
blood Pb levels <10 [mu]g/dL (most clearly in the 5 to 10 [mu]g/dL
range, but, less definitively, possibly lower).'' (p. 6-269)
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    With regard to population mean levels, the Criteria Document points
to studies reporting ``Pb effects on the intellectual attainment of
preschool and school age children at population mean concurrent blood-
Pb levels ranging down to as low as 2 to 8 [mu]g/dL'' (CD, p. E-9).
    We note that many studies over the past decade have, in
investigating effects at lower blood Pb levels, utilized the CDC
advisory level for individual children (10 [mu]g/dL) as a benchmark for
assessment, and this is reflected in the numerous references in the
Criteria Document to 10 [mu]g/dL. Individual study conclusions stated
with regard to effects observed below 10 [mu]g/dL are usually referring
to individual blood Pb levels. In fact, many such study groups have
been restricted to individual blood Pb levels below 10 [mu]g/dL or
below levels lower than 10 [mu]g/dL. We note that the

mean blood Pb level for these groups will necessarily be lower than the
blood Pb level they are restricted below.
    Threshold levels, in terms of blood Pb levels in individual
children, for neurological effects cannot be discerned from the
currently available studies (CD, pp. 8-60 to 8-63). The Criteria
Document states ``There is no level of Pb exposure that can yet be
identified, with confidence, as clearly not being associated with some
risk of deleterious health effects'' (CD, p. 8-63). As discussed in the
Criteria Document, ``a threshold for Pb neurotoxic effects may exist at
levels distinctly lower than the lowest exposures examined in these
epidemiologic studies'' (CD, p. 8-67).\40\
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    \40\ In consideration of the evidence from experimental animal
studies with regard to the issue of threshold for neurotoxic
effects, the CD notes that there is little evidence that allows for
clear delineation of a threshold, and that ``blood-Pb levels
associated with neurobehavioral effects appear to be reasonably
parallel between humans and animals at reasonably comparable blood-
Pb concentrations; and such effects appear likely to occur in humans
ranging down at least to 5-10 [mu]g/dL, or possibly lower (although
the possibility of a threshold for such neurotoxic effects cannot be
ruled out at lower blood-Pb concentrations)'' (CD, p. 8-38).
---------------------------------------------------------------------------

    In summary, the Agency has identified neurological, hematological
and immune effects in children and neurological, hematological,
cardiovascular and renal effects in adults as the effects observed at
blood Pb levels near or below 10 [mu]g/dL and further considers
neurological effects in children and cardiovascular effects in adults
to be categories of effects that ``are currently clearly of greatest
public health concern'' (CD, pp. 8-60 to 8-62). Neurological effects in
children are discussed further below.
b. Neurological Effects in Children
    Among the wide variety of health endpoints associated with Pb
exposures, there is general consensus that the developing nervous
system in young children is among, if not, the most sensitive. As
described in the Criteria Document, neurotoxic effects in children and
cardiovascular effects in adults are categories of effects that are
``currently clearly of greatest public health concern'' (CD, p. 8-
60).\41\ While also recognizing the occurrence of adult cardiovascular
effects at somewhat similarly low blood Pb levels \42\, neurological
effects in children are considered to be the sentinel effects in this
review and are the focus of the quantitative risk assessment conducted
for this review (discussed below in section III.C).
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    \41\ The Criteria Document states ``neurotoxic effects in
children and cardiovascular effects in adults are among those best
substantiated as occurring at blood-Pb concentrations as low as 5 to
10 [mu]g/dL (or possibly lower); and these categories of effects are
currently clearly of greatest public health concern (CD, p. 8-60).''
    \42\ For example, the Criteria Document describes associations
of blood Pb in adults with blood pressure in studies with population
mean blood Pb levels ranging from approximately 2 to 6 [mu]g/dL (CD,
section 6.5.2 and Table 6-2).
---------------------------------------------------------------------------

    The nervous system has long been recognized as a target of Pb
toxicity, with the developing nervous system affected at lower
exposures than the mature system (CD, Sections 5.3, 6.2.1, 6.2.2, and
8.4). While blood Pb levels in U.S. children ages one to five years
have decreased notably since the late 1970s, newer studies have
investigated and reported associations of effects on the
neurodevelopment of children with these more recent blood Pb levels
(CD, Chapter 6). Functional manifestations of Pb neurotoxicity during
childhood include sensory, motor, cognitive and behavioral impacts.
Numerous epidemiological studies have reported neurocognitive,
neurobehavioral, sensory, and motor function effects in children with
blood Pb levels below 10 [mu]g/dL (CD, Sections 6.2 and 8.4). \43\ As
discussed in the Criteria Document, ``extensive experimental laboratory
animal evidence has been generated that (a) substantiates well the
plausibility of the epidemiologic findings observed in human children
and adults and (b) expands our understanding of likely mechanisms
underlying the neurotoxic effects'' (CD, p. 8-25; Section 5.3).
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    \43\ Further, neurological effects in general include behavioral
effects, such as delinquent behavior (CD, sections 6.2.6 and
<IP_ADDRESS>), sensory effects, such as those related to hearing and
vision (CD, sections 6.2.7 and <IP_ADDRESS>), and deficits in neuromotor
function (CD, p. 8-36).
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    The evidence for neurotoxic effects in children is a robust
combination of epidemiological and toxicological evidence (CD, Sections
5.3, 6.2 and 8.5). The epidemiological evidence is supported by animal
studies that substantiate the biological plausibility of the
associations, and contributes to our understanding of mechanisms of
action for the effects (CD, Section 8.4.2).
    Cognitive effects associated with Pb exposures that have been
observed in epidemiological studies have included decrements in
intelligence test results, such as the widely used IQ score, and in
academic achievement as assessed by various standardized tests as well
as by class ranking and graduation rates (CD, Section 6.2.16 and pp 8-
29 to 8-30). As noted in the Criteria Document with regard to the
latter, ``Associations between Pb exposure and academic achievement
observed in the above-noted studies were significant even after
adjusting for IQ, suggesting that Pb-sensitive neuropsychological
processing and learning factors not reflected by global intelligence
indices might contribute to reduced performance on academic tasks''
(CD, pp 8-29 to 8-30).
    Other cognitive effects observed in studies of children have
included effects on attention, executive functions, language, memory,
learning and visuospatial processing (CD, Sections 5.3.5, 6.2.5 and
<IP_ADDRESS>), with attention and executive function effects associated with
Pb exposures indexed by blood Pb levels below 10 [mu]g/dL (CD, Section
6.2.5 and pp. 8-30 to 8-31). The evidence for the role of Pb in this
suite of effects includes experimental animal findings (discussed in
CD, Section <IP_ADDRESS>; p. 8-31), which provide strong biological
plausibility of Pb effects on learning ability, memory and attention
(CD, Section 5.3.5), as well as associated mechanistic findings. With
regard to persistence of effects the Criteria Document states the
following (CD, p. 8-67):

    Persistence or apparent ``irreversibility'' of effects can
result from two different scenarios: (1) Organic damage has occurred
without adequate repair or compensatory offsets, or (2) exposure
somehow persists. As Pb exposure can also derive from endogenous
sources (e.g., bone), a performance deficit that remains detectable
after external exposure has ended, rather than indicating
irreversibility, could reflect ongoing toxicity due to Pb remaining
at the critical target organ or Pb deposited at the organ post-
exposure as the result of redistribution of Pb among body pools. The
persistence of effect appears to depend on the duration of exposure
as well as other factors that may affect an individual's ability to
recover from an insult. The likelihood of reversibility also seems
to be related, at least for the adverse effects observed in certain
organ systems, to both the age-at-exposure and the age-at-
assessment.

The evidence with regard to persistence of Pb-induced deficits observed
in animal and epidemiological studies is described in discussion of
those studies in the Criteria Document (CD, Sections 5.3.5, 6.2.11, and
8.5.2). It is additionally important to note that there may be long-
term consequences of such deficits over a lifetime. Poor academic
skills and achievement can have ``enduring and important effects on
objective parameters of success in real life,'' as well as increased
risk of antisocial and delinquent behavior (CD, Section 6.2.16).

    As discussed in the Criteria Document, while there is no direct
animal test parallel to human IQ tests, ``in animals a wide variety of
tests that assess attention, learning, and memory suggest that Pb
exposure {of animals{time}  results in a global deficit in functioning,

just as it is indicated by decrements in IQ scores in children'' (CD,
p. 8-27). The animal and epidemiological evidence for this endpoint are
consistent and complementary (CD, p. 8-44). As stated in the Criteria
Document (p. 8-44):

    Findings from numerous experimental studies of rats and of
nonhuman primates, as discussed in Chapter 5, parallel the observed
human neurocognitive deficits and the processes responsible for
them. Learning and other higher order cognitive processes show the
greatest similarities in Pb-induced deficits between humans and
experimental animals. Deficits in cognition are due to the combined
and overlapping effects of Pb-induced perseveration, inability to
inhibit responding, inability to adapt to changing behavioral
requirements, aversion to delays, and distractibility. Higher level
neurocognitive functions are affected in both animals and humans at
very low exposure levels (<10 [mu]g/dL), more so than simple
cognitive functions.

    Epidemiologic studies of Pb and child development have demonstrated
inverse associations between blood Pb concentrations and children's IQ
and other cognitive-related outcomes at successively lower Pb exposure
levels over the past 30 years (CD, p. 6-64). This is supported by
multiple studies performed over the past 15 years (as discussed in the
CD, Section 6.2.13). For example, the overall weight of the available
evidence, described in the Criteria Document, provides clear
substantiation of neurocognitive decrements being associated in
children with mean blood Pb levels in the range of 5 to 10 [mu]g/dL,
and some analyses indicate Pb effects on intellectual attainment of
children for which population mean blood Pb levels in the analysis
ranged from 2 to 8 [mu]g/dL (CD, Sections 6.2, 8.4.2 and <IP_ADDRESS>).\44\
That is, while blood Pb levels in U.S. children have decreased notably
since the late 1970s, newer studies have investigated and reported
associations of effects on the neurodevelopment of children with blood
Pb levels similar to the more recent blood Pb levels (CD, Chapter 6).
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    \44\ ``The overall weight of the available evidence provides
clear substantiation of neurocognitive decrements being associated
in young children with blood-Pb concentrations in the range of 5-10
[mu]g/dL, and possibly somewhat lower. Some newly available analyses
appear to show Pb effects on the intellectual attainment of
preschool and school age children at population mean concurrent
blood-Pb levels ranging down to as low as 2 to 8 [mu]g/dL.'' (CD, p.
E-9)
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    The evidence described in the Criteria Document with regard to the
effect on children's cognitive function of blood Pb levels at the lower
concentration range includes the international pooled analysis by
Lanphear and others (2005), studies of individual cohorts such as the
Rochester, Boston, and Mexico City cohorts (Canfield et al., 2003a;
Canfield et al., 2003b; Bellinger and Needleman, 2003; Tellez-Rojo et
al., 2006), the study of African-American inner-city children from
Detroit (Chiodo et al., 2004), the cross-sectional study of young
children in three German cities (Walkowiak et al., 1998) and the cross-
sectional analysis of a nationally representative sample from the
NHANES III \45\ (Lanphear et al., 2000). These studies included
differing adjustments for different important potential confounders
(e.g., parental IQ or HOME score) or surrogates of these measures
(e.g., parental education and SES factors) through multivariate
analyses.46 47 Each of these studies has individual
strengths and limitations, however, a pattern of positive findings is
demonstrated across the studies. In these studies, statistically
significant associations of neurocognitive decrement \48\ with blood Pb
were found in the full study cohorts, as well as in some subgroups
restricted to children with lower blood Pb levels for which mean blood
Pb levels extended below 5 [mu]g/dL. More specifically, a statistically
significant association was reported for full-scale IQ with blood Pb at
age five in a subset analysis (n=71) of the Rochester cohort for which
the population mean blood Pb level was 3.32 [mu]g/dL, as well as in the
full study group (mean=5.8 [mu]g/dL, n=171) (Canfield et al., 2003a;