[Federal Register: November 12, 2008 (Volume 73, Number 219)]
[Rules and Regulations]
[Page 66963-67062]
[DOCID:fr12no08-21]

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Part II

Environmental Protection Agency

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40 CFR Parts 50, 51, 53, and 58

National Ambient Air Quality Standards for Lead; Final Rule

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Parts 50, 51, 53 and 58

[EPA-HQ-OAR-2006-0735; FRL-8732-9]
RIN 2060-AN83

National Ambient Air Quality Standards for Lead

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final 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 is making
revisions to the primary and secondary NAAQS for Pb to provide
requisite protection of public health and welfare, respectively. With
regard to the primary standard, EPA is revising the level to 0.15
[mu]g/m3. EPA is retaining the current indicator of Pb in
total suspended particles (Pb-TSP). EPA is revising the averaging time
to a rolling 3-month period with a maximum (not-to-be-exceeded) form,
evaluated over a 3-year period. EPA is revising the secondary standard
to be identical in all respects to the revised primary standard.
    EPA is also revising data handling procedures, including allowance
for the use of Pb-PM10 data in certain circumstances, and
the treatment of exceptional events, and 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 revising emissions inventory reporting
requirements and providing guidance on its approach for implementing
the revised primary and secondary standards for Pb.

DATES: This final rule is effective on January 12, 2009.

ADDRESSES: EPA has established a docket for this action under Docket ID
No. EPA-HQ-OAR-2006-0735. All documents in the docket are listed on the
www.regulations.gov Web site. Although listed in the index, some
information is not publicly available, e.g., confidential business
information or other information whose disclosure is restricted by
statute. Certain other material, such as copyrighted material, will be
publicly available only in hard copy form. Publicly available docket
materials are available either electronically through
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<PHONE_NUMBER> 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 VIII, 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>With
regard to section VII, contact Mr. Tom Link, Air Quality Policy
Division, Office of Air Quality Planning and Standards, U.S.
Environmental Protection Agency, Mail code C539-04, Research Triangle
Park, NC 27711; telephone:<PHONE_NUMBER>; e-mail<EMAIL_ADDRESS>
SUPPLEMENTARY INFORMATION:

Table of Contents

    The following topics are discussed in this preamble:
I. Summary and Background
    A. Summary of Revisions to the Lead NAAQS
    B. Legislative Requirements
    C. Review of Air Quality Criteria and Standards for Lead
    D. Current Related Control Requirements
    E. Summary of Proposed Revisions to the Lead NAAQS
    F. Organization and Approach to Final Lead NAAQS Decisions
II. Rationale for Final Decisions on the Primary Lead Standard
    A. Introduction
    1. Overview of Multimedia, Multipathway Considerations and
Background
    2. Overview of Health Effects Information
    a. Blood Lead
    b. Array of Health Effects and At-risk Subpopulations
    c. Neurological Effects in Children
    3. Overview of Human Exposure and Health Risk Assessments
    B. Need for Revision of the Current Primary Lead Standard
    1. Introduction
    2. Comments on the Need for Revision
    3. Conclusions Regarding the Need for Revision
    C. Conclusions on the Elements of the Primary Lead Standard
    1. Indicator
    a. Basis for Proposed Decision
    b. Comments on Indicator
    c. Conclusions on Indicator
    2. Averaging Time and Form
    a. Basis for Proposed Decision
    b. Comments on Averaging Time and Form
    c. Conclusions on Averaging Time and Form
    3. Level
    a. Basis for Proposed Range
    b. Comments on Level
    c. Conclusions on Level
    D. Final Decision on the Primary Lead Standard
III. Secondary Lead Standard
    A. Introduction
    1. Overview of Welfare Effects Evidence
    2. Overview of Screening Level Ecological Risk Assessment
    B. Conclusions on the Secondary Lead Standard
    1. Basis for Proposed Decision
    2. Comments on the Proposed Secondary Standard
    3. Administrator's Conclusions
    C. Final Decision on the Secondary Lead Standard
IV. Appendix R--Interpretation of the NAAQS for Lead
    A. Ambient Data Requirements
    1. Proposed Provisions
    2. Comments on Ambient Data Requirements
    3. Conclusions on Ambient Data Requirements
    B. Averaging Time and Procedure
    1. Proposed Provisions
    2. Comments on Averaging Time and Procedure
    3. Conclusions on Averaging Time and Procedure
    C. Data Completeness
    1. Proposed Provisions
    2. Comments on Data Completeness
    3. Conclusions on Data Completeness
    D. Scaling Factors to Relate Pb-TSP and Pb-PM10
    1. Proposed Provisions
    2. Comments on Scaling Factors
    3. Conclusions on Scaling Factors
    E. Use of Pb-TSP and Pb-PM10 Data
    1. Proposed Provisions
    2. Comments on Use of Pb-TSP and Pb-PM10 Data
    3. Conclusions on Use of Pb-TSP and Pb-PM10 Data

    F. Data Reporting and Rounding
    1. Proposed Provisions
    2. Comments on Data Reporting and Rounding
    3. Conclusions on Data Reporting and Rounding
    G. Other Aspects of Data Interpretation
V. Ambient Monitoring Related to Revised Lead Standards
    A. Sampling and Analysis Methods
    1. Pb-TSP Method
    a. Proposed Changes
    b. Comments on Pb-TSP Method
    c. Decisions on Pb-TSP Method
    2. Pb-PM10 Method
    a. Proposed FRM for Pb-PM10 Monitoring
    b. Comments on Proposed Pb-PM10 FRM
    c. Decisions on Pb-PM10 FRM
    3. FEM Requirements
    a. Proposed FEM Requirements
    b. Comments
    c. Decisions on FEM Requirements
    4. Quality Assurance Requirements
    a. Proposed Changes
    b. Comments
    c. Decisions on Quality Assurance Requirements
    B. Network Design
    1. Proposed Changes
    2. Comments on Network Design
    a. Source-oriented monitoring
    b. Non-source-oriented monitoring
    c. Roadway Monitoring
    d. Use of Pb-PM10 Monitors
    e. Required timeline for monitor installation and operation
    3. Decisions on Network Design Requirements
    C. Sampling Frequency
    D. Monitoring for the Secondary Standard
    E. Other Monitoring Regulation Changes
    1. Reporting of Average Pressure and Temperature
    2. Special Purpose Monitoring
    3. Reporting of Pb-TSP Concentrations
VI. Implementation Considerations
    A. Designations for the Lead NAAQS
    1. Proposal
    2. Comments and Responses
    3. Final
    B. Lead Nonattainment Area Boundaries
    1. Proposal
    2. Comments and Responses
    3. Final
    C. Classifications
    1. Proposal
    2. Comments and Responses
    3. Final
    D. Section 110(a)(2) Lead NAAQS Infrastructure Requirements
    1. Proposal
    2. Final
    E. Attainment Dates
    1. Proposal
    2. Comments and Responses
    3. Final
    F. Attainment Planning Requirements
    1. RACM/RACT for Lead Nonattainment Areas
    a. Proposal
    b. Comments and Responses
    c. Final
    2. Demonstration of Attainment for Lead Nonattainment Areas
    a. Proposal
    b. Final
    3. Reasonable Further Progress (RFP)
    a. Proposal
    b. Comments and Responses
    c. Final
    4. Contingency Measures
    a. Proposal
    b. Comments and Responses
    c. Final
    5. Nonattainment New Source Review (NSR) and Prevention of
Significant Deterioration (PSD) Requirements
    a. Proposal
    b. Comments and Responses
    c. Final
    6. Emissions Inventories
    a. Proposal
    b. Comments and Responses
    c. Final
    7. Modeling
    a. Proposal
    b. Comments and Responses
    c. Final
    G. General Conformity
    1. Proposal
    2. Final
    H. Transition From the Current NAAQS to a Revised NAAQS for Lead
    1. Proposal
    2. Final
VII. Exceptional Events Information Submission Schedule for Lead
NAAQS
    A. Proposal
    B. Comments and Responses
    C. Final
VIII. Statutory and Executive Order Reviews
    A. Executive Order 12866: Regulatory Planning and Review
    B. Paperwork Reduction Act
    C. Regulatory Flexibility Act
    D. Unfunded Mandates Reform Act
    E. Executive Order 13132: Federalism
    F. Executive Order 13175: Consultation and Coordination With
Indian Tribal Governments
    G. Executive Order 13045: Protection of Children From
Environmental Health & Safety Risks
    H. Executive Order 13211: Actions That Significantly Affect
Energy Supply, Distribution or Use
    I. National Technology Transfer and Advancement Act
    J. Executive Order 12898: Federal Actions to Address
Environmental Justice in Minority Populations and Low-Income
Populations
    K. Congressional Review Act
References

I. Summary and Background

A. Summary of Revisions to the Lead NAAQS

    Based on its review of the air quality criteria and national
ambient air quality standards (NAAQS) for lead (Pb), EPA is making
revisions to the primary and secondary NAAQS for Pb to provide
requisite protection of public health and welfare, respectively. With
regard to the primary standard, EPA is revising 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, including neurocognitive
and neurobehavioral effects. EPA is revising the level to 0.15 [mu]g/
m\3\. EPA is retaining the current indicator of Pb in total suspended
particles (Pb-TSP). EPA is revising the averaging time to a rolling 3-
month period with a maximum (not-to-be-exceeded) form, evaluated over a
3-year period.
    EPA is revising the secondary standard to be identical in all
respects to the revised primary standard.
    EPA is also revising data handling procedures, including allowance
for the use of Pb-PM10 data in certain circumstances, and
the treatment of exceptional events, and ambient air monitoring and
reporting requirements for Pb, including those related to sampling and
analysis methods, network design, sampling schedule, and data
reporting.

B. 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, emissions of
which ``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 [the]
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 pollutant 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\
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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.
Whitman v. American Trucking Associations, 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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    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.

C. Review of Air Quality Criteria and Standards for Lead

    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/m\3\, 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).
    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. 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.
    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 information from
previous reviews.
    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,\4\ averaging time, form,\5\ 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.
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    \4\ The ``indicator'' of a standard defines the chemical species
or mixture that is to be measured in determining whether an area
attains the standard.
    \5\ 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.
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    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). 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.
    A public meeting of 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. Transcripts of the meeting and CASAC's letter
to the Administrator (Henderson, 2008a) are in the docket for this
review and CASAC's letter is also available on the EPA Web site (http:/
/www.epa.gov/sab).
    A public comment period for the ANPR extended 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 campaigns), 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 businesses or
industry organizations.
    The proposed decision (henceforth ``proposal'') on revisions to the
Pb NAAQS was signed on May 1, 2008 and published in the Federal
Register on May 20, 2008. Public teleconferences of the CASAC Pb Panel
were held on June 9 and July 8, 2008 to provide advice and
recommendations to the Administrator based on its review of the
proposal notice. CASAC's letter to the Administrator (Henderson, 2008b)
is in the docket for this review and also available on the EPA Web site
(http://www.epa.gov/sab).
    The EPA held two public hearings to provide direct opportunities
for oral testimony by the public on the proposal. The hearings were
held concurrently on June 12, 2008 in Baltimore, Maryland and St.
Louis, Missouri. At these public hearings, EPA heard testimony from 33
individuals representing themselves or specific interested
organizations. Transcripts from these hearings and written testimony
provided at the hearings are in the docket for this review.
Additionally, a large number of written comments were received from
various commenters during the public comment period on the proposal.
Comments were received from EPA's

Children's Health Protection Advisory Committee, the American Academy
of Pediatrics, the American Medical Association, the American Thoracic
Society, two organizations of state and local air agencies (National
Association of Clean Air Agencies and Northeast States for Coordinated
Air Use Management), approximately 40 State, Tribal and local
government agencies, approximately 20 environmental or public health
organizations or coalitions, approximately 20 industry organizations or
companies, and approximately 6200 private citizens (roughly 150 of whom
were not part of one of several mass comment campaigns). Significant
issues raised in the public comments are discussed throughout the
preamble of this final action. A summary of all other significant
comments, along with EPA's responses (henceforth ``Response to
Comments''), can be found in the docket for this review.
    The schedule for completion of this review has been governed by a
judicial order in Missouri Coalition for the Environment v. EPA (No.
4:04CV00660 ERW, Sept. 14, 2005). The court-ordered schedule governing
this review, entered by the court on September 14, 2005 and amended on
April 29, 2008 and July 1, 2008, requires EPA to sign, for publication,
a notice of final rulemaking concerning its review of the Pb NAAQS no
later than October 15, 2008.
    Some commenters have referred to and discussed individual
scientific studies on the health effects of Pb that were not included
in the Criteria Document (EPA, 2006a) (`` `new' studies''). In
considering and responding to comments for which such ``new'' studies
were cited in support, EPA has provisionally considered the cited
studies in conjunction with other relevant ``new'' studies published
since the completion of the Criteria Document in the context of the
findings of the Criteria Document.
    As in prior NAAQS reviews, EPA is basing its decision in this
review on studies and related information included in the Criteria
Document and Staff Paper, which have undergone CASAC and public review.
In this Pb NAAQS review, EPA also prepared an ANPR, consistent with the
Agency's new NAAQS process. The ANPR discussed studies that were
included in the Criteria Document and Staff Paper. The studies assessed
in the Criteria Document and Staff Paper, and the integration of the
scientific evidence presented in them, have undergone extensive
critical review by EPA, CASAC, and the public. The rigor of that review
makes these studies, and their integrative assessment, the most
reliable source of scientific information on which to base decisions on
the NAAQS, decisions that all parties recognize as of great import.
NAAQS decisions can have profound impacts on public health and welfare,
and NAAQS decisions should be based on studies that have been
rigorously assessed in an integrative manner not only by EPA but also
by the statutorily mandated independent advisory committee, as well as
the public review that accompanies this process. EPA's provisional
consideration of these studies did not and could not provide that kind
of in-depth critical review.
    This decision is consistent with EPA's practice in prior NAAQS
reviews and its interpretation of the requirements of the CAA. Since
the 1970 amendments, the EPA has taken the view that NAAQS decisions
are to be based on scientific studies and related information that have
been assessed as a part of the pertinent air quality criteria, and has
consistently followed this approach. This longstanding interpretation
was strengthened by new legislative requirements enacted in 1977, which
added section 109(d)(2) of the Act concerning CASAC review of air
quality criteria. See 71 FR 61144, 61148 (October 17, 2006) (final
decision on review of PM NAAQS) for a detailed discussion of this issue
and EPA's past practice.
    As discussed in EPA's 1993 decision not to revise the NAAQS for
ozone, ``new'' studies may sometimes be of such significance that it is
appropriate to delay a decision on revision of a NAAQS and to
supplement the pertinent air quality criteria so the studies can be
taken into account (58 FR at 13013-13014, March 9, 1993). In the
present case, EPA's provisional consideration of ``new'' studies
concludes that, taken in context, the ``new'' information and findings
do not materially change any of the broad scientific conclusions
regarding the health effects and exposure pathways of ambient air Pb
made in the air quality criteria. For this reason, reopening the air
quality criteria review would not be warranted even if there were time
to do so under the court order governing the schedule for this
rulemaking.
    Accordingly, EPA is basing the final decisions in this review on
the studies and related information included in the Pb air quality
criteria that have undergone CASAC and public review. EPA will consider
the ``new'' studies for purposes of decision-making in the next
periodic review of the Pb NAAQS, which EPA expects to begin soon after
the conclusion of this review and which will provide the opportunity to
fully assess these studies through a more rigorous review process
involving EPA, CASAC, and the public. Further discussion of these
``new'' studies can be found in the Response to Comments document.

D. 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).\6\ 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).\7\ 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 identified as the
Task Force's top priority.
---------------------------------------------------------------------------

    \6\ As described in section II.A.2.a below the CDC stated in
2005 that no ``safe'' threshold for blood Pb levels in young
children has been identified (CDC, 2005a).
    \7\ 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.
---------------------------------------------------------------------------

    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 (68 FR 36487).
Further, in 1991, EPA lowered the maximum levels of Pb permitted in
public water systems from 50 parts per billion (ppb) to 15 ppb measured
at the consumer's tap (56 FR 26460).
    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 (TSCA), 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, 73 FR 21692) 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. 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 (see, e.g., 66 FR
58258). 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/).
---------------------------------------------------------------------------

    \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).
    As a result of coordinated, intensive efforts at the national,
state and local levels, including those programs described above, blood
Pb levels in all segments of the population have 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
recognized in section II.A.2.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 Agency has continued to
grapple with soil and dust Pb levels from the historical use of Pb in
paint and gasoline and from other sources.
---------------------------------------------------------------------------

    \9\ The 5th percentile, geometric mean, and 95th percentile
values for the 2003-2004 NHANES are 0.7, 1.8 and 5.1 [mu]g/dL,
respectively (Axelrad, 2008a,b).
---------------------------------------------------------------------------

    In addition to the Pb control programs summarized above, EPA's
research program, with other Federal agencies, identifies, 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).

E. Summary of Proposed Revisions to the Lead NAAQS

    For reasons discussed in the proposal, the Administrator proposed
to revise the current primary and secondary Pb standards. With regard
to the primary Pb standard, the Administrator proposed to revise the
level of the Pb standard to a level within the range of 0.10 [mu]g/m\3\
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 averaging time and
form, the Administrator proposed 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. With regard to the secondary
standard for Pb, the Administrator proposed to revise the standard to
make it identical to the proposed primary standard.

F. Organization and Approach to Final Lead NAAQS Decisions

    This action presents the Administrator's final decisions regarding
the need to revise the current primary and secondary Pb standards.
Revisions to the primary standard for Pb are addressed below in section
II. The secondary Pb standard is addressed below in section III.
Related data completeness, data handling, data reporting and rounding
conventions are addressed in section IV, and related ambient monitoring
methods and network design are addressed below in section V.
Implementation of the revised NAAQS is discussed in section VI, and the
exceptional events information submission schedule is described in
section VII. A discussion of statutory and executive order reviews is
provided in section VIII.
    Today's final decisions are based on a thorough review in the
Criteria Document of scientific information on known and potential
human health and welfare effects associated with exposure to Pb in the
environment. These final decisions also take into account: (1)
Assessments in the Staff Paper and ANPR of the most policy-relevant
information in the Criteria Document as well as quantitative exposure
and risk assessments based on that information; (2) CASAC Panel advice
and recommendations, as reflected in its letters to the Administrator,
its discussions of drafts of the Criteria Document and Staff Paper, and
of the ANPR and the notice of proposed rulemaking at public meetings;
(3) public comments received during the development of these documents,
either in connection with CASAC Panel meetings or separately; and (4)
public comments received on the proposed rulemaking.

II. Rationale for Final Decision on the Primary Standard

A. Introduction

    This section presents the rationale for the Administrator's final
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. In developing this rationale,
EPA has drawn upon an integrative synthesis in the Criteria Document of
the entire body of evidence published through late 2006 on human health
effects associated with Pb exposure. Some 6000 studies were considered
in this review. 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).
    As discussed below, a significant amount of new research has been
conducted since the last review, with important new information coming
from epidemiological, toxicological, controlled human exposure, and
dosimetric studies. Moreover, the newly available research studies
evaluated in the Criteria Document have undergone intensive scrutiny
through multiple layers of peer review, with extended opportunities for
review and comment by the CASAC Panel and the public. As with virtually
any policy-relevant scientific research, there is uncertainty

in the characterization of health effects attributable to exposure to
ambient Pb. While important uncertainties remain, the review of the
health effects information has been extensive and deliberate. In the
judgment of the Administrator, this intensive evaluation of the
scientific evidence provides an adequate basis for regulatory decision
making at this time. This review also provides important input to EPA's
research plan for improving our future understanding of the
relationships between exposures to ambient Pb and health effects.
    The health effects information and quantitative exposure and health
risk assessment were summarized in sections II.B and II.C of the
proposal (73 FR at 29193-29220) and are only briefly outlined below in
sections II.A.2 and II.A.3. Responses to public comments specific to
the material presented in sections II.A.1 through II.A.3 below are
provided in the Response to Comments document.
    Subsequent sections of this preamble provide a more complete
discussion of the Administrator's rationale, in light of key issues
raised in public comments, for concluding that the current standard is
not requisite to protect public health with an adequate margin of
safety and that it is appropriate to revise the current primary Pb
standard to provide additional public health protection (section II.B),
as well as a more complete discussion of the Administrator's rationale
for retaining or revising the specific elements of the primary Pb
standards (section II.C), namely the indicator (section II.C.1),
averaging time and form (section II.C.2), and level (section II.C.3). A
summary of the final decisions on revisions to the primary Pb standards
is presented in section II.D.
1. Overview of Multimedia, Multipathway Considerations and Background
    This section briefly summarizes the information presented in
section II.A of the proposal and chapter 2 of the Staff Paper on
multimedia, multipathway and background considerations of the Pb NAAQS
review. As was true in the setting of the current standard, multimedia
distribution of and multipathway exposure to Pb that has been emitted
into the ambient air play a key role in the Agency's consideration of
the Pb NAAQS. Some key multimedia and multipathway considerations in
the review include:
    (1) Lead is emitted into the air from many sources encompassing a
wide variety of stationary and mobile source types. Lead emitted to the
air is predominantly in particulate form, with the particles occurring
in various sizes. Once emitted, the 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. As summarized in sections II.A.1 and
II.E.1 of the proposal, airborne concentrations of Pb at sites near
sources are much higher, and the representation of larger particles is
greater, than at sites not known to be directly influenced by sources.
    (2) Once deposited out of the air, Pb can subsequently be
resuspended into the ambient air and, because of the persistence of Pb,
Pb emissions contribute to media concentrations for some years into the
future.
    (3) Exposure to Pb emitted into the ambient air (air-related Pb)
can occur directly by inhalation, or indirectly by ingestion of Pb-
contaminated food, water or other materials including dust and
soil.\10\ 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. These exposure pathways are described more
fully in the proposal.
---------------------------------------------------------------------------

    \10\ In general, air-related pathways include those pathways
where Pb passes through ambient air on its path from a source to
human exposure.
---------------------------------------------------------------------------

    (4) Air-related exposure pathways are affected by changes to air
quality, including changes in concentrations of Pb in air and 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. Thus, because of the
roles of both air concentration and air deposition in human exposure
pathways, and because 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.
    Additionally, as when the standard was set, human exposures to Pb
include nonair or background contributions in addition to air-related
pathways. Some key aspects of the consideration of air and nonair
pathways in the review (described in more detail in the proposal) are
summarized here:
    (1) 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.
    (2) The pathways of human exposure to Pb that are not air-related
include ingestion of indoor Pb paint,\11\ Pb in diet as a result of
inadvertent additions during food processing, and Pb in drinking water
attributable to Pb in distribution systems, as well as other generally
less prevalent pathways, as described in the proposal (73 FR 29192) and
Criteria Document (CD, pp. 3-50 to 3-51).
---------------------------------------------------------------------------

    \11\ Weathering of outdoor Pb paint may also contribute to soil
Pb levels adjacent to the house.
---------------------------------------------------------------------------

    (3) 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 and may also derive from 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, policy-relevant background in air
is likely insignificant in comparison to the contributions from
exposures to nonair media.
    (4) The relative contribution of Pb from 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, while for young
children, ingestion of indoor dust can be a significant Pb exposure
pathway (e.g., via hand-to-mouth activity of very young children).
    (5) Estimating separate contributions to human Pb exposure from air
and nonair sources is complicated by the existence of multiple and
varied air-related pathways, 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
indoor dust or outdoor dust/soil,

do not usually distinguish between air-related and other sources of Pb
or between air-related Pb associated with historical emissions and that
from recent emissions.\12\
---------------------------------------------------------------------------

    \12\ The exposure assessment for children performed for this
review employed available data and methods to develop estimates
intended to inform a characterization of these pathways (as
described in the proposal and the final Risk Assessment Report).
---------------------------------------------------------------------------

    (6) Relative contributions to a child's total Pb exposure from air-
related exposure pathways 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) and access to other
sources of Pb exposure such as Pb paint, tap water affected by plumbing
containing Pb, and lead-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.
In other cases, such as children living in older housing with peeling
paint or where renovations have occurred, the dominant source of Pb
exposure may be lead paint used in the house in the past. Depending on
Pb levels in a home's tap water, drinking water can sometimes be a
significant source. In still other cases, there may be more of a
mixture of contributions from multiple sources, with no one source
dominating.
2. Overview of Health Effects Information
    This section summarizes information presented in section II.B of
the proposal pertaining to health endpoints associated with the range
of exposures considered to be most relevant to current exposure levels.
In recognition of the role of multiple exposure pathways and routes and
the use of an internal exposure or dose metric in evaluating health
risk for Pb, the following section summarizes key aspects of the
internal disposition or distribution of Pb, the use of blood Pb as an
internal exposure or dose metric, and the evidence with regard to the
quantitative relationship between air Pb and blood Pb levels (section
II.A.2.a). This is followed first by a summary of the broad array of
Pb-induced health effects and recognition of at-risk subpopulations
(section II.A.2.b) and then by a summary of neurological effects in
children and quantitative concentration-response relationships for
blood Pb and IQ (section II.A.2.c).
a. Blood Lead
(i) Internal Disposition of Lead
    Lead enters the body via the respiratory system and
gastrointestinal tract, from which it is quickly absorbed into the
blood stream and distributed throughout the body.\13\ Lead
bioaccumulates in the body, with the bone serving as a large, long-term
storage compartment; soft tissues (e.g., kidney, liver, brain, etc.)
serve as smaller compartments, in which Pb may be more mobile (CD,
sections <IP_ADDRESS> and 8.3.1). 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).
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).
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    \13\ Additionally, Pb freely crosses the placenta resulting in
continued fetal exposure throughout pregnancy, with that exposure
increasing during the latter half of pregnancy (CD, section 6.6.2).
---------------------------------------------------------------------------

    The bone pool of Pb in children 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>).
(ii) Use of Blood Pb 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 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). Most recently, 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 \14\ 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).\15\
---------------------------------------------------------------------------

    \14\ 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).
    \15\ 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 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, pp. 2-3). The preface for the CDC
statement included the following: ``Although there is evidence of
adverse health effects in children with blood lead levels below 10
[mu]g/dL, CDC has not changed its level of concern, which remains at
levels >10 [mu]g/dL. We believe it critical to focus available
resources where the potential adverse effects remain the greatest.
If no threshold level exists for adverse health effects, setting a
new BLL of concern somewhere below 10 [mu]g/dL would be based on an
arbitrary decision. In addition, the feasibility and effectiveness
of individual interventions to further reduce BLLs below 10 [mu]g/dL
has not been demonstrated.'' [CDC, 2005a, p. ix] CDC further stated
``Nonetheless, the sources of lead exposure and the population-based
interventions that can be expected to reduce lead exposure are
similar in children with BLLs <10 [mu]g/ dL and >10 [mu]g/dL, so
preventive lead hazard control measures need not be deferred pending
further research findings or consensus.'' [CDC, 2005a, p. 2] 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 in multiple
age groups nationally through the National Health and Nutrition
Examination Survey (NHANES).\16\ 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).
---------------------------------------------------------------------------

    \16\ This information documents a variation in mean blood Pb
levels across the various age groups monitored. For example, mean
blood Pb levels 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
[mu]g/dL, respectively (CD, p. 4-22).

    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 blood Pb 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), and racial/ethnic and income disparities
in blood Pb levels in children persist. For example, as described in
the proposal, blood Pb levels for lower income and African American
children are higher than those for the general population. The recently
released RRP rule (discussed above in section I.C) is expected to
contribute to further reductions in blood Pb levels for children living
in houses with Pb paint.
(iii) Air-to-Blood Relationships
    As described in section II.A.1 above and discussed in section II.A
of the proposal, 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 (discussed in section II.B.1.c of the proposal), which is often
termed a slope or ratio, describes the increase in blood Pb (in [mu]g/
dL) estimated to be associated with each unit increase of air Pb (in
[mu]g/m\3\).\17\
---------------------------------------------------------------------------

    \17\ 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,\18\ 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.
---------------------------------------------------------------------------

    \18\ We note that the 2006 Criteria Document did not include a
discussion of more recent studies relating to air-to-blood ratios;
more recent studies were discussed in the Staff Paper, including
discussion by CASAC in their review of those documents.
---------------------------------------------------------------------------

    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
inhalation and ingestion exposure pathways affects the magnitude of the
resultant air-to-blood estimates, such that fewer pathways included as
``air-related'' yields 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 \19\ 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).
---------------------------------------------------------------------------

    \19\ 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). The proposal noted 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 higher historical ambient air Pb levels to
have influenced blood Pb levels (see Section V.B.1 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, the
proposal observed 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 age six in 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).\20\ 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).
---------------------------------------------------------------------------

    \20\ 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).

---------------------------------------------------------------------------

    The proposal identified sources of uncertainty related to air-to-
blood ratios obtained from Hilts (2003). 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. \21\
---------------------------------------------------------------------------

    \21\ 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.\22\ 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 et al. (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.\23\
---------------------------------------------------------------------------

    \22\ EPA is not basing its 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 considered
by CASAC and the public.
    \23\ 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.
---------------------------------------------------------------------------

    In their advice to the Agency prior to the proposal, 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).\24\
---------------------------------------------------------------------------

    \24\ 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).
---------------------------------------------------------------------------

    In the proposal, beyond considering the evidence presented in the
published literature and that reviewed in Pb Criteria Documents, we
also considered air-to-blood ratios derived from the exposure
assessment for this review (summarized below in section II.A.3 and
described in detail in USEPA, 2007b). 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 U.S. Department of Housing
and Urban Development (HUD) survey 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 (as described in the Risk Assessment Report, Volume II, Appendix
G, Attachment G-1). Given this application of the HUD dataset, there is
the potential that the nonlinear 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\.\25\ 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.
---------------------------------------------------------------------------

    \25\ Air-to-blood ratios for the full study area of the primary
Pb smelter range from 1:3 to 1:7 across the range of alternative
standard levels from 1.5 down to 0.02 [mu]g/m\3\ (USEPA, 2007b).
---------------------------------------------------------------------------

    In summary, EPA's view in the proposal was that 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. EPA invited comment on this range as well as the appropriate
weight to place on specific ratios within this range. Advice from CASAC
and comments from the public on this issue are discussed below in
section II.C.3.
b. Array of Health Effects and At-Risk Subpopulations
    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).\26\
---------------------------------------------------------------------------

    \26\ Lead has been classified as a probable human carcinogen by
the International Agency for Research on Cancer (inorganic lead
compounds), based mainly on sufficient animal evidence, and as
reasonably anticipated to be a human carcinogen by the U.S. National
Toxicology Program (lead and lead compounds) (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.
These key effects include neurological, hematological and immune \27\
effects for children, and hematological, cardiovascular and renal
effects for adults (CD, Tables 8-5 and 8-6, pp. 8-60 to 8-62). 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).28 29 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. 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).
---------------------------------------------------------------------------

    \27\ At mean blood Pb levels, in children, on the order of 10
[mu]g/dL, and somewhat lower, associations have been found with
effects to the immune system, including altered macrophage
activation, increased IgE levels and associated increased risk for
autoimmunity and asthma (CD, Sections 5.9, 6.8, and 8.4.6).
    \28\ 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)
    \29\ Epidemiological studies have consistently demonstrated
associations between Pb exposure and enhanced risk of deleterious
cardiovascular outcomes, including increased blood pressure and
incidence of hypertension. A meta-analysis of numerous studies
estimates that a doubling of blood-Pb level (e.g., from 5 to 10
[mu]g/dL) is associated with ~1.0 mm Hg increase in systolic blood
pressure and ~0.6 mm Hg increase in diastolic pressure (CD, p. E-
10).
---------------------------------------------------------------------------

    We note that many studies over the past decade, in investigating
effects at lower blood Pb levels, have utilized the CDC advisory level
or level of concern for individual children (10 [mu]g/dL) \30\ 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.
---------------------------------------------------------------------------

    \30\ This level has variously been called an advisory level or
level of concern (http://www.atsdr.cdc.gov/csem/lead/pb_
standards2.html). In addressing children's blood Pb levels, CDC has
stated ``Specific strategies that target screening to high-risk
children are essential to identify children with BLLs >= 10 [mu]g/
dL.'' (CDC, 2005, p.1)
---------------------------------------------------------------------------

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

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

    As described in the proposal, physiological, behavioral and
demographic factors contribute to increased risk of Pb-related health
effects. Potentially at-risk subpopulations, also referred to as
sensitive sub-populations, include those with increased susceptibility
(i.e., physiological factors contributing to a greater response for the
same exposure), as well as those with greater vulnerability (i.e.,
those with increased exposure such as through exposure to higher media
concentrations or resulting from behavior leading to increased contact
with contaminated media), or those affected by socioeconomic factors,
such as reduced access to health care or low socioeconomic status.
    While adults are susceptible to Pb effects at lower blood Pb levels
than previously understood (e.g., CD, p. 8-25), the greater influence
of past exposures on their current blood Pb levels (as summarized above
in section II.A.2.a) leads us to give greater prominence to children as
the sensitive subpopulation in this review. Children are at increased
risk of Pb-related health effects due to various factors that enhance
their exposures (e.g., via the hand-to-mouth activity that is prevalent
in very young children, CD, section 4.4.3) and susceptibility. While
children are considered to be at a period of

maximum exposure around 18-27 months, the current evidence has found
even stronger associations between blood Pb at school age and IQ at
school age. The evidence ``supports the idea that Pb exposure continues
to be toxic to children as they reach school age, and [does] not lend
support to the interpretation that all the damage is done by the time
the child reaches 2 to 3 years of age'' (CD, section 6.2.12). The
following physiological and demographic factors can further affect risk
of Pb-related effects in some children.
     Children with particular genetic polymorphisms (e.g.,
presence of the [delta]-aminolevulinic acid dehydratase-2 [ALAD-2]
allele) have increased sensitivity to Pb toxicity, which may be due to
increased susceptibility to the same internal dose and/or to increased
internal dose associated with same exposure (CD, p. 8-71, sections
6.3.5, <IP_ADDRESS> and 6.3.6).
     Some children may have blood Pb levels higher than those
otherwise associated with a given Pb exposure (CD, section 8.5.3) as a
result of nutritional status (e.g., iron deficiency, calcium intake),
as well as genetic and other factors (CD, chapter 4 and sections 3.4,
5.3.7 and 8.5.3).
     Situations of elevated exposure, such as residing near
sources of ambient Pb, as well as socioeconomic factors, such as
reduced access to health care or low socioeconomic status (SES) (USEPA,
2003, 2005c) can also contribute to increased blood Pb levels and
increased risk of associated health effects from air-related Pb.
     As described in the proposal (sections II.B.1.b and
II.B.3), children in poverty and black, non-Hispanic children have
notably higher blood Pb levels than do economically well-off children
and white children, in general.
c. 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 children is among the, if not the, most sensitive. 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 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).\32\ 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).
---------------------------------------------------------------------------

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

    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).
    With regard to potential implications of Pb effects on IQ, the
Criteria Document recognizes the ``critical'' distinction between
population and individual risk, identifying issues regarding declines
in IQ for an individual and for the population. The Criteria Document
further states that a ``point estimate indicating a modest mean change
on a health index at the individual level can have substantial
implications at the population level'' (CD, p. 8-77).\33\ A downward
shift in the mean IQ value is associated with both substantial
decreases in percentages achieving very high scores and substantial
increases in the percentage of individuals achieving very low scores
(CD, p. 8-81).\34\ For an individual functioning in the low IQ range
due to the influence of developmental risk factors other than Pb, a Pb-
associated IQ decline of several points might be sufficient to drop
that individual into the range associated with increased risk of
educational, vocational, and social failure (CD, p. 8-77).
---------------------------------------------------------------------------

    \33\ As an example, the Criteria Document states ``although an
increase of a few mmHg in blood pressure might not be of concern for
an individual's well-being, the same increase in the population mean
might be associated with substantial increases in the percentages of
individuals with values that are sufficiently extreme that they
exceed the criteria used to diagnose hypertension'' (CD, p. 8-77).
    \34\ For example, for a population mean IQ of 100 (and standard
deviation of 15), 2.3% of the population would score above 130, but
a shift of the population to a mean of 95 results in only 0.99% of
the population scoring above 130 (CD, pp. 8-81 to 8-82).
---------------------------------------------------------------------------

    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.
    The persistence of such Pb-induced effects is described in the
proposal and the Criteria Document (e.g., CD, sections 5.3.5, 6.2.11,
and 8.5.2). The persistence or irreversibility of such effects can be
the result of damage occurring without adequate repair offsets or of
the persistence of Pb in the body (CD, section 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).
    Multiple 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 (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>).
Thus, 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, lower blood Pb levels (CD,

chapter 6; and as discussed in section II.B.2.b of the proposal).
    The current evidence reviewed in the Criteria Document with regard
to the quantitative relationship between neurocognitive decrement, such
as IQ, and blood Pb levels indicates that the slope for Pb effects on
IQ is nonlinear and is steeper at lower blood Pb levels, such that each
[mu]g/dL increase in blood Pb may have a greater effect on IQ at lower
blood Pb levels (e.g., below 10 [mu]g/dL) than at higher levels (CD,
section 6.2.13; pp. 8-63 to 8-64; Figure 8-7). As stated in the CD,
``the most compelling evidence for effects at blood Pb levels <10
[mu]g/dL, as well as a nonlinear relationship between blood Pb levels
and IQ, comes from the international pooled analysis of seven
prospective cohort studies (n=1,333) by Lanphear et al. (2005)'' (CD,
pp. 6-67 and 8-37 and section <IP_ADDRESS>.11). Using the full pooled
dataset with concurrent blood Pb level as the exposure metric and IQ as
the response from the pooled dataset of seven international studies,
Lanphear and others (2005) employed mathematical models of various
forms, including linear, cubic spline, log-linear, and piece-wise
linear, in their investigation of the blood Pb concentration-response
relationship (CD, p. 6-29; Lanphear et al., 2005). They observed for
this pooled dataset that the shape of the concentration-response
relationship is nonlinear and the log-linear model provides a better
fit over the full range of blood Pb measurements \35\ than a linear one
(CD, p. 6-29 and pp. 6-67 to 6-70; Lanphear et al., 2005). In addition,
they found that no individual study among the seven was responsible for
the estimated nonlinear relationship between Pb and deficits in IQ (CD
p. 6-30). Others have also analyzed the same dataset and similarly
concluded that, across the range of the dataset's blood Pb levels, a
log-linear relationship was a significantly better fit than the linear
relationship (p=0.009) with little evidence of residual confounding
from included model variables (CD, section 6.2.13; Rothenberg and
Rothenberg, 2005).
---------------------------------------------------------------------------

    \35\ The median of the concurrent blood Pb levels modeled was
9.7 [mu]g/dL; the 5th and 95th percentile values were 2.5 and 33.2
[mu]g/dL, respectively (Lanphear et al., 2005).
---------------------------------------------------------------------------

    As noted in the Criteria Document, a number of examples of non- or
supralinear dose-response relationships exist in toxicology (CD, pp. 6-
76 and 8-38 to 8-39). With regard to the effects of Pb on
neurodevelopmental outcome such as IQ, the Criteria Document suggests
that initial neurodevelopmental effects at lower Pb levels may be
disrupting very different biological mechanisms (e.g., early
developmental processes in the central nervous system) than more severe
effects of high exposures that result in symptomatic Pb poisoning and
frank mental retardation (CD, p. 6-76). The Criteria Document describes
this issue in detail with regard to Pb (summarized in CD at p. 8-39).
Various findings within the toxicological evidence, presented in the
Criteria Document (described in the proposal), provide biologic
plausibility for a steeper IQ loss at low blood levels, with a
potential explanation being that the predominant mechanism at very low
blood-Pb levels is rapidly saturated and that a different, less-
rapidly-saturated process, becomes predominant at blood-Pb levels
greater than 10 [mu]g/dL.
    The current evidence includes multiple studies that have examined
the quantitative relationship between IQ and blood Pb level in analyses
of children with individual blood Pb concentrations below 10 [mu]g/dL.
In comparing across the individual epidemiological studies and the
international pooled analysis, the Criteria Document observed that at
higher blood Pb levels (e.g., above 10 [mu]g/dL), the slopes (for
change in IQ with blood Pb) derived for log-linear and linear models
are almost identical, and for studies with lower blood Pb levels, the
slopes appear to be steeper than those observed in studies involving
higher blood Pb levels (CD, p. 8-78, Figure 8-7). In making these
observations, the Criteria Document focused on the curves from the
models from the 10th percentile to the 90th percentile saying that the
``curves are restricted to that range because log-linear curves become
very steep at the lower end of the blood Pb levels, and this may be an
artifact of the model chosen''.
    The quantitative relationship between IQ and blood Pb level has
been examined in the Criteria Document using studies where all or the
majority of study subjects had blood Pb levels below 10 [mu]g/dL and
also where an analysis was performed on a subset of children whose
blood Pb levels have never exceeded 10 [mu]g/dL (CD, Table 6-1).\36\
The datasets for three of these studies included concurrent blood Pb
levels above 10 [mu]g/dL; the concentration-response (C-R) relationship
reported for one of the three was linear while it was log-linear for
the other two. For the one study among these three that reported a
linear C-R relationship, the highest blood Pb level was just below 12
[mu]g/dL and the population mean was 7.9 [mu]g/dL (Kordas et al.,
2006). Of the two studies with log-linear functions, one reported 69%
of the children with blood Pb levels below 10 [mu]g/dL and a population
mean blood Pb level of 7.44 [mu]g/dL (Al-Saleh et al., 2001), and the
second reported a population median blood Pb level of 9.7 [mu]g/dL and
a 95th percentile of 33.2 [mu]g/dL (Lanphear et al., 2005). In order to
compare slopes across all of these studies (linear and log-linear) in
the Criteria Document, EPA estimated, for each, the average slope of
change in IQ with change in blood Pb between the 10th percentile \37\
blood Pb level and 10 [mu]g/dL (CD, Table 6-1). The resultant group of
reported and estimated average linear slopes for IQ change with blood
Pb levels up to 10 [mu]g/dL range from -0.4 to -1.8 IQ points per
[mu]g/dL blood Pb (CD, Tables 6-1 and 8-7), with a median of -0.9 IQ
points per [mu]g/dL blood Pb (CD, p. 8-80).\38\ These slopes from

Tables 6-1 and 8-7 of the Criteria Document are presented in the second
set of slopes in Table 1 below (adapted from Table 1 of the proposal).
In this second set are studies (included in the Criteria Document Table
6-1) that examined the quantitative relationships of IQ and blood Pb in
study populations for which most blood Pb levels were below 10 [mu]g/dL
and for which a linear slope restricted to blood Pb levels below about
10 [mu]g/dL could be estimated.
---------------------------------------------------------------------------

    \36\ The tests for cognitive function in these studies include
age-appropriate Wechsler intelligence tests (Lanphear et al., 2005;
Bellinger and Needleman, 2003), the Stanford-Binet intelligence test
(Canfield et al., 2003), the Test of Non-Verbal Intelligence (Al-
Saleh et al., 2001), an abbreviated form of the Wechsler tests
(Kordas et al., 2006) and the Bayley Scales of Infant Development
(Tellez-Rojo et al., 2006). The Wechsler and Stanford-Binet tests
are widely used to assess neurocognitive function in children and
adults, however, these tests are not appropriate for children under
age three. For such children, studies generally use the age-
appropriate Bayley Scales of Infant Development as a measure of
cognitive development.
    \37\ In the Criteria Document analysis, the 10th percentile was
chosen as a common point of comparison for the loglinear (and
linear) models at a point prior to the lowest end of the blood Pb
levels.
    \38\ One of these slopes (CD, Table 6-1) is for the IQ-blood Pb
(concurrent) relationship for children whose peak blood Pb levels
are below 10 [mu]g/dL in the international pooled dataset studied by
Lanphear and others (2005); these authors reported this slope along
with the companion slope, from the same (piece-wise) model, for the
remaining children whose peak blood Pb level equals or is above 10
[mu]g/dL (Lanphear et al., 2005). In the economic analysis for EPA's
recent Lead Renovation, Repair and Painting (RRP) Program rule
(described above in section I.C) for children living in houses with
lead-based paint, changes in IQ were estimated as a function of
changes in lifetime average blood Pb level using the corresponding
piece-wise model for lifetime average blood Pb derived from the
pooled dataset (USEPA, 2008; USEPA, 2007d). The piecewise models
that gave greater weight to impacts in this blood Pb range were
chosen because peak blood Pb levels are likely to be less than 10
[mu]g/dL for the vast majority of children exposed to Pb during
renovation activities. Further, while Lanphear et al. (2005) used
peak blood Pb concentrations to determine which segment of a model
to apply, for the hypothetical children to whom the approach is
discussed in the RRP Program rule, only lifetime averages were used
(in the RRP analysis). To counter the impact of assigning additional
hypothetical RRP children to the steeper of the two slopes than
would have been the case if they could be assigned based on peak
blood Pb levels (as a child's lifetime average blood Pb is lower
than peak blood Pb), the RRP analysis used the piece-wise model with
node at 10 [mu]g/dL, for which the steeper of the two slopes is less
steep than it is for the model with node at 7.5 [mu]g/dL. As stated
in the RRP economic analysis document, ``[s]electing a model with a
node, or changing one segment to the other, at a lifetime average
blood Pb concentration of 10 [mu]g/dL rather than at 7.5 [mu]g/dL,
is a small protection against applying an incorrectly rapid change
(steep slope with increasingly smaller effect as concentrations
lower) to the calculation'' (USEPA, 2008). We note here that the
slope for the less-than-10-[mu]g/dL portion of the model used in the
RRP analysis (-0.88) is similar to the median for the slopes
included in the Criteria Document analysis of quantitative
relationships for studies in which the majority of blood Pb levels
were below 10 [mu]g/dL.
---------------------------------------------------------------------------

    Among this group of quantitative IQ-blood Pb relationships examined
in the Criteria Document (CD, Tables 6-1 and 8-7), the steepest slopes
for change in IQ with change in blood Pb level are those derived for
the subsets of children in the Rochester and Boston cohorts for which
peak blood Pb levels were <10 [mu]g/dL; these slopes, in terms of IQ
points per [mu]g/dL blood Pb, are -1.8 (for concurrent blood Pb
influence on IQ) and -1.6 (for 24-month blood Pb influence on IQ),
respectively. The mean blood Pb levels for children in these subsets of
the Rochester and Boston cohorts are 3.32 (Canfield, 2008) and 3.8
[mu]g/dL (Bellinger, 2008), respectively, which are the lowest
population mean levels among the datasets included in the table. Other
studies with analyses involving similarly low blood Pb levels (e.g.,
mean levels below 4 [mu]g/dL) also had slopes steeper than -1.5 points
per [mu]g/dL blood Pb. These include the slope of -1.71 points per
[mu]g/dL blood Pb \39\ for the subset of 24-month old children in the
Mexico City cohort with blood Pb levels less than 5 [mu]g/dL (n=193),
for which the mean concurrent blood Pb level was 2.9 [mu]g/dL (Tellez-
Rojo et al. 2006, 2008),\40\ and the slope of -2.94 points per [mu]g/dL
blood Pb for the subset of 6-10 year old children whose peak blood Pb
levels never exceeded 7.5 [mu]g/dL (n=112), and for which the mean
concurrent blood Pb level was 3.24 [mu]g/dL (Lanphear et al. 2005;
Hornung 2008a). Thus, from these subset analyses, the slopes range from
-1.71 to -2.94 IQ points per [mu]g/dL of concurrent blood Pb, as shown
in the first set of slopes in Table 1. In this first set are studies
that included quantitative relationships for IQ and blood Pb that
focused on lower individual blood Pb levels (below 7.5 [mu]g/dL). We
also note that for blood Pb levels up to approximately 3.7 [mu]g/dL,
the slope of the nonlinear C-R function in which greatest confidence is
placed in estimating IQ loss in the quantitative risk assessment (the
LLL function) \41\ falls intermediate between these two values.
---------------------------------------------------------------------------

    \39\ This slope reflects effects on cognitive development in
this cohort of 24-month old children based on the age-appropriate
test described earlier, and is similar in magnitude to slopes for
the cohorts of older children described here. The strengths and
limitations of this age-appropriate test, the Mental Development
Index (MDI) of the Bayley Scales of Infant Development (BSID), were
discussed in a letter to the editor by Black and Baqui (2005). The
letter states that ``the MDI is a well-standardized,
psychometrically strong measure of infant mental development.'' The
MDI represents a complex integration of empirically-derived
cognitive skills, for example, sensory/perceptual acuities,
discriminations, and response; acquisition of object constancy;
memory learning and problem solving; vocalization and beginning of
verbal communication; and basis of abstract thinking. Black and
Baqui additionally state that although the MDI is one of the most
well-standardized, widely used assessment of infant mental
development, evidence indicates low predictive validity of the MDI
for infants younger than 24 months to subsequent measures of
intelligence. They explain that the lack of continuity may be
partially explained by ``the multidimensional and rapidly changing
aspects of infant mental development and by variations in
performance during infancy, variations in tasks used to measure
intellectual functioning throughout childhood, and variations in
environmental challenges and opportunities that may influence
development.'' Martin and Volkmar (2007) also noted that
correlations between BSID performance and subsequent IQ assessments
were variable, but they also reported high test-retest reliability
and validity, as indicated by the correlation coefficients of 0.83
to 0.91, as well as high interrater reliability, correlation
coefficient of 0.96, for the MDI. Therefore, the BSID has been found
to be a reliable indicator of current development and cognitive
functioning of the infant. Martin and Volkmar (2007) further note
that ``for the most part, performance on the BSID does not
consistently predict later cognitive measures, particularly when
socioeconomic status and level of functioning are controlled''.
    \40\ In this study, the slope for blood Pb levels between 5 and
10 [mu]g/dL (population mean blood Pb of 6.9 [mu]g/dL; n=101) was -
0.94 points per [mu]g/dL blood Pb but was not statistically
significant, with a p value of 0.12. The difference in the slope
between the <5 [mu]g/dL and the 5-10 [mu]g/dL groups was not
statistically significant (Tellez-Rojo et al., 2006; Tellez-Rojo,
2008).
    \41\ The LLL function is the loglinear function from Lampshear
et al. (2005), with linearization at low exposures (as described in
sections 2.1.5 and <IP_ADDRESS> ofthe Risk Assessment Report).

                        Table 1--Summary of Quantitative Relationships of IQ and Blood Pb for Two Sets of Studies Discussed Above
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                Form of model    Average linear
                                                                                Range BLL \A\    Geometric mean BLL      from which        slope \B\
        Study/analysis             Study cohort     Analysis dataset     N         ([mu]g/dL)        \A\ ([mu]g/dL)      average slope      (points per
                                                                                derived          [mu]g/dL)
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                           Set of studies from which steeper slopes are drawn in the proposal
--------------------------------------------------------------------------------------------------------------------------------------------------------
Tellez-Rojo <5 subgroup.......  Mexico City, age   Children--BLL<5        193  0.8-4.9...........  2.9...............  Linear...........           -1.71
                                 24 mo.             [mu]g/dL.
--------------------------------------------------------------------------------------------------------------------------------------------------------
based on Lanphear et al 2005      Dataset from which the log-linear function is derived is the pooled International
 \C\, Log-linear with low-         dataset of 1333 children, age 6-10 yr, having median blood Pb of 9.7 [mu]g/dL and
 exposure linearization (LLL).                         5th-95th percentile of 2.5-33.2 [mu]g/dL.
                                    LLL \D\: -2.29 at 2 [mu]g/dL
                                         -1.89 at 3 [mu]g/dL
--------------------------------------------------------------------------------------------------------------------------------------------------------
Lanphear et al. 2005 \C\, <7.5  Pooled             Children--peak         103  0.9-7.4...........  3.24..............  Linear...........           -2.94
 peak subgroup.                  International,     BLL <7.5 [mu]g/
                                 age 6-10 yr.       dL.
--------------------------------------------------------------------------------------------------------------------------------------------------------

                            Set of studies with shallower slopes (Criteria Document Table 6-1) presented in the proposal \E\
--------------------------------------------------------------------------------------------------------------------------------------------------------
Canfield et al 2003 \C\, <10    Rochester, age 5   Children--peak          71  0.5-8.4...........  3.32..............  Linear...........           -1.79
 peak subgroup.                  yr.                BLL <10 [mu]g/dL.
Bellinger and Needleman 2003    Boston \B\ \F\...  Children--peak          48  1-9.3 \F\.........  \F\ 3.8...........  Linear...........           -1.56
 \C\.                                               BLL <10 [mu]g/dL.
Tellez-Rojo et al. 2006.......  Mexico City, age   Full dataset.....      294  0.8-9.8...........  4.28..............  Linear...........           -1.04
                                 24 mo.
Tellez-Rojo et al. 2006 full--  Mexico City, age   Full dataset.....      294  0.8-9.8...........  4.28..............  Log-linear.......       \G\ -0.94
 loglinear.                      24 mo.
Lanphear et al. 2005 \C\, <10   Pooled             Children--peak         244  0.1-9.8...........  4.30..............  Linear...........           -0.80
 peak \C\ subgroup.              International,     BLL <10 [mu]g/dL.
                                 age 6-10 yr.
Al-Saleh et al 2001 full--      Saudi Arabia, age  Full dataset.....      533  2.3-27.36 \H\.....  7.44..............  Log-linear.......       \G\ -0.76
 loglinear.                      6-12 yr.
Kordas et al 2006, <12          Torreon, Mexico,   Children--BLL <12      377  2.3-<12...........  7.9...............  Linear...........           -0.40
 subgroup.                       age 7 yr.          [mu]g/dL.
Lanphear et al 2005 \C\ full--  Pooled             Full dataset.....     1333  0.1-71.7..........  9.7 (median)......  Log-linear.......       \G\ -0.41
 loglinear.                      International,
                                 age 6-10 yr.
--------------------------------------------------------------------------------------------------------------------------------------------------------
    Median value........................................................................................................................       \D\ -0.9
--------------------------------------------------------------------------------------------------------------------------------------------------------
\A\ Blood Pb level (BLL) information provided here is drawn from publications listed in table, in some cases augmented by study authors (Bellinger,
  2008; Canfield, 2008a,b; Hornung, 2008a,b; Kordas, 2008; Tellez-Rojo, 2008).
\B\ Average linear slope estimates here are for relationship between IQ and concurrent blood Pb levels (BLL), except for Bellinger & Needleman which
  used 24 month BLLs with 10 year old IQ.
\C\ The Lanphear et al. 2005 pooled International study includes blood Pb data from the Rochester and Boston cohorts, although for different ages (6 and
  5 years, respectively) than the ages analyzed in Canfield et al 2003 and Bellinger and Needleman 2003.
\D\ The LLL function (described in section II.C.2.b) was developed from Lanphear et al 2005 loglinear model with a linearization of the slope at BLL