Document ID: EPA-HQ-OAR-2006-0735-4805
Agency: epa
Document Type: Proposed Rule
Title: National Ambient Air Quality Standards for Lead
Posted Date: 2007-12-17T05:00Z

[Federal Register: December 17, 2007 (Volume 72, Number 241)]
[Proposed Rules]               
[Page 71487-71544]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr17de07-32]                         

[[Page 71487]]

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Part II

Environmental Protection Agency

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40 CFR Part 50

National Ambient Air Quality Standards for Lead; Proposed Rule

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 50

[EPA-HQ-OAR-2006-0735; FRL-8503-8 ]
RIN 2060-AN83

 
National Ambient Air Quality Standards for Lead

AGENCY: Environmental Protection Agency (EPA).

ACTION: Advance notice of proposed rulemaking (ANPR).

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SUMMARY: EPA is issuing this ANPR to invite comment from all interested 
parties on policy options and other issues related to the Agency's 
ongoing review of the national ambient air quality standards (NAAQS) 
for lead (Pb). Consistent with recent modifications the Agency has made 
to its process for reviewing NAAQS, we are seeking broad public comment 
at this time to help inform the Agency's future proposed decisions on 
the adequacy of the current Pb NAAQS and on any revisions of the Pb 
NAAQS that may be appropriate. EPA is also soliciting comment on 
retaining Pb on the list of criteria pollutants and on maintaining 
NAAQS for Pb.
    As part of this review, the Agency has released several key 
documents that will inform the Agency's rulemaking. These documents 
include the Air Quality Criteria for Lead, released in 2006, which 
critically assesses and integrates relevant scientific information; 
risk assessment reports including the most recent report, Lead: Human 
Exposure and Health Risk Assessment for Selected Case Studies, which 
documents quantitative exposure analyses and risk assessments conducted 
for this review; and a recently released Staff Paper, Review of the 
National Ambient Air Quality Standards for Lead: Policy Assessment of 
Scientific and Technical Information, which presents an evaluation by 
staff in EPA's Office of Air Quality Planning and Standards (OAQPS) of 
the policy implications of the scientific information and quantitative 
assessments and OAQPS staff conclusions and recommendations on a range 
of policy options for the Agency's consideration.
    Under the terms of a court order, the Administrator will sign by 
September 1, 2008 a Notice of Final Rulemaking for publication in the 
Federal Register. To meet this schedule, we anticipate the 
Administrator will sign a Notice of Proposed Rulemaking in March 2008 
for publication in the Federal Register, at which time further 
opportunity for public comment will be provided.

DATES: Comments must be received by January 16, 2008.

ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-
OAR-2006-0735 by one of the following methods:
     http://www.regulations.gov: Follow the on-line 

instructions for submitting comments.
     E-mail: a-and-r-Docket@epa.gov.
     Fax: 202-566-9744.
     Mail: Docket No. EPA-HQ-OAR-2006-0735, Environmental 
Protection Agency, Mail code 6102T, 1200 Pennsylvania Ave., NW., 
Washington, DC 20460. Please include a total of two copies.
     Hand Delivery: Docket No. EPA-HQ-OAR-2006-0735, 
Environmental Protection Agency, EPA West, Room 3334, 1301 Constitution 
Ave., NW., Washington, DC. Such deliveries are only accepted during the 
Docket's normal hours of operation, and special arrangements should be 
made for deliveries of boxed information.
    Instructions: Direct your comments to Docket ID No. EPA-HQ-OAR-
2006-0735. The EPA's policy is that all comments received will be 
included in the public docket without change and may be made available 
online at http://www.regulations.gov, including any personal 

information provided, unless the comment includes information claimed 
to be Confidential Business Information (CBI) or other information 
whose disclosure is restricted by statute. Do not submit information 
that you consider to be CBI or otherwise protected through http://www.regulations.gov or e-mail. The http://www.regulations.gov Web site 

is an ``anonymous access'' system, which means EPA will not know your 
identity or contact information unless you provide it in the body of 
your comment. If you send an e-mail comment directly to EPA without 
going through http://www.regulations.gov, your e-mail address will be 

automatically captured and included as part of the comment that is 
placed in the public docket and made available on the Internet. If you 
submit an electronic comment, EPA recommends that you include your name 
and other contact information in the body of your comment and with any 
disk or CD-ROM you submit. If EPA cannot read your comment due to 
technical difficulties and cannot contact you for clarification, EPA 
may not be able to consider your comment. Electronic files should avoid 
the use of special characters, any form of encryption, and be free of 
any defects or viruses. For additional information about EPA's public 
docket, visit the EPA Docket Center homepage at http://www.epa.gov/epahome/dockets.htm
.

    Docket: All documents in the docket are listed in the http://www.regulations.gov
 index. Although listed in the index, some 

information is not publicly available, e.g., CBI or other information 
whose disclosure is restricted by statute. Certain other material, such 
as copyrighted material, will be publicly available only in hard copy. 
Publicly available docket materials are available either electronically 
in http://www.regulations.gov or in hard copy at the Air and Radiation 

Docket and Information Center, EPA/DC, EPA West, Room 3334, 1301 
Constitution Ave., NW., Washington, DC. The Public Reading Room is open 
from 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding legal 
holidays. The telephone number for the Public Reading Room is (202) 
566-1744 and the telephone number for the Air and Radiation Docket and 
Information Center is (202) 566-1742.

FOR FURTHER INFORMATION 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: 919-
541-0237; e-mail: Murphy.deirdre@epa.gov.

SUPPLEMENTARY INFORMATION: 

General Information

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

    1. Submitting CBI. Do not submit this information to EPA through 
http://www.regulations.gov or e-mail. Clearly mark the part or all of 

the information that you claim to be CBI. For CBI information in a disk 
or CD ROM that you mail to EPA, mark the outside of the disk or CD ROM 
as CBI and then identify electronically within the disk or CD ROM the 
specific information that is claimed as CBI. In addition to one 
complete version of the comment that includes information claimed as 
CBI, a copy of the comment that does not contain the information 
claimed as CBI must be submitted for inclusion in the public docket. 
Information so marked will not be disclosed except in accordance with 
procedures set forth in 40 CFR part 2.
    2. Tips for Preparing Your Comments. When submitting comments, 
remember to:
     Identify the rulemaking by docket number and other 
identifying

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information (subject heading, Federal Register date and page number).
     Follow directions--the agency may ask you to respond to 
specific questions or organize comments by referencing a Code of 
Federal Regulations (CFR) part or section number.
     Explain why you agree or disagree, suggest alternatives, 
and substitute language for your requested changes.
     Describe any assumptions and provide any technical 
information and/or data that you used.
     If you estimate potential costs or burdens, explain how 
you arrived at your estimate in sufficient detail to allow for it to be 
reproduced.
     Provide specific examples to illustrate your concerns, and 
suggest alternatives.
     Explain your views as clearly as possible, avoiding the 
use of profanity or personal threats.
     Make sure to submit your comments by the comment period 
deadline identified.

Availability of Related Information

    A number of documents relevant to this rulemaking, including the 
Air Quality Criteria for Lead (Criteria Document) (USEPA, 2006a), the 
Staff Paper, related risk assessment reports, and other related 
technical documents are available on EPA's Office of Air Quality 
Planning and Standards (OAQPS) Technology Transfer Network (TTN) Web 
site at http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html. 

These and other related documents are also available for inspection and 
copying in the EPA docket identified above.

Table of Contents

    The following topics are discussed in this preamble:

I. Introduction
II. Background
    A. Legislative Requirements
    B. History of Lead NAAQS Reviews
    C. Current Related Lead Control Programs
    D. Current Lead NAAQS Review
    E. Implementation Considerations
III. The Primary Standard
    A. Health Effects Information
    1. Internal Disposition--Blood Lead as Dose Metric
    2. Nature of Effects
    3. Lead-Related Impacts on Public Health
    a. At-Risk Subpopulations
    b. Potential Public Health Impacts
    4. Key Observations
    B. Human Exposure and Health Risk Assessments
    1. Overview of Risk Assessment From Last Review
    2. Design Aspects of Exposure and Risk Assessments
    a. CASAC Advice
    b. Health Endpoint, Risk Metric and Concentration-Response 
Functions
    c. Case Study Approach
    d. Air Quality Scenarios
    e. Categorization of Policy-Relevant Exposure Pathways
    f. Analytical Steps
    g. Generating Multiple Sets of Risk Results
    h. Key Limitations and Uncertainties
    3. Summary of Results
    a. Blood Pb Estimates
    b. IQ Loss Estimates
    C. Considerations in Review of the Standard
    1. Background on the Current Standard
    a. Basis for Setting the Current Standard
    b. Policy Options Considered in the Last Review
    2. Approach for Current Review
    3. Adequacy of the Current Standard
    a. Evidence-Based Considerations
    b. Exposure- and Risk-Based Considerations
    c. CASAC Advice and Recommendations
    d. Policy Options
    4. Elements of the Standard
    a. Indicator
    b. Averaging Time and Form
    c. Level
IV. The Secondary Standard
    A. Welfare Effects Information
    B. Screening Level Ecological Risk Assessment
    1. Design Aspects of the Assessment and Associated Uncertanties
    2. Summary of Results
    C. Considerations in Review of the Standard
    1. Background on the Current Standard
    2. Approach for Current Review
    3. Adequacy of the Current Standard
    a. Evidence-Based Considerations
    b. Risk-Based Considerations
    c. CASAC Advice and Recommendations
    d. Policy Options
    4. Elements of the Standard
V. Considerations for Ambient Monitoring
    A. Sampling and Analysis Methods
    B. Network Design
    C. Sampling Schedule
    D. Data Handling
    E. Monitoring for the Secondary NAAQS
VI. Solicitation of Comment
VII. Statutory and Executive Order Reviews
     References

I. Introduction

    In the past year EPA has instituted a number of changes to the 
process that the Agency uses in reviewing the NAAQS to help to improve 
the efficiency of the process 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 
(described at http://www.epa.gov/ttn/naaqs/). These changes apply to 

the four major components of the NAAQS review process: planning, 
science assessment, risk/exposure assessment, and policy assessment/
rulemaking. The process improvements will help the Agency meet the goal 
of reviewing each NAAQS on a 5-year cycle as required by the Clean Air 
Act (CAA) without compromising the scientific integrity of the process. 
These changes are being incorporated into the various ongoing NAAQS 
reviews being conducted by the Agency, including the current review of 
the Pb NAAQS.
    The issuance of this ANPR is one of the key features of the new 
NAAQS review process. Historically, a policy assessment that evaluates 
the policy implications of the available scientific information and 
risk/exposure assessments has been presented in the form of a Staff 
Paper, prepared by staff in EPA's OAQPS, which included OAQPS staff 
conclusions and recommendations on a range of policy options for the 
Agency's consideration. The new process will enable broader 
participation of the scientific community and the public early in the 
NAAQS review by providing scientific information, risk/exposure 
assessments, and policy options in an ANPR rather than a Staff Paper. 
The purpose of the ANPR is to identify conceptual evidence- and risk-
based approaches for reaching policy judgments, discuss what the 
science and risk/exposure assessments say about the adequacy of the 
current standards, and describe a range of options for standard 
setting, in terms of indicators, averaging times, forms, and ranges of 
levels for any alternative standards. Discussion of alternative 
standards is to include a description of the underlying interpretations 
of the scientific evidence and risk/exposure information that might 
support such alternative standards and that could be considered by the 
Administrator in making NAAQS decisions. The issuance of an ANPR 
provides the opportunity for the Clean Air Scientific Advisory 
Committee (CASAC) \1\ and the public to evaluate and provide comment on 
a broad range of policy options being considered by the Administrator.
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    \1\ As discussed below in section II, CASAC is the independent 
scientific review committee that provides advice and recommendations 
to the EPA Administrator related to periodic reviews of NAAQS, as 
mandated by the Clean Air Act.
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    In the case of this Pb NAAQS review, which was initiated well 
before changes were instituted to the NAAQS review process, both an 
OAQPS Staff Paper and an ANPR are being issued. As discussed below in 
section II, the issuance of both documents reflects the terms of a 
court order that governs this review and requires that a final OAQPS 
Staff Paper be issued. As a consequence, in addition to soliciting 
comment, this ANPR summarizes information from the OAQPS Staff Paper 
(referred to as Staff Paper throughout this notice) and from

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the Agency's risk assessment and Criteria Document. This ANPR is 
structured such that policy options on adequacy of the current 
standards and aspects of potential alternative standards are discussed 
in Sections III.C and IV.C. Preceding those policy discussions are 
sections focused on health and welfare effects in Sections III.A and 
IV.A, respectively, and on human exposure and risk and ecological risk 
in Sections III.B and IV.B, respectively.

II. Background

A. Legislative Requirements

    Two sections of the Clean Air Act (Act) govern the establishment 
and revision of the NAAQS. Section 108 (42 U.S.C. 7408) directs the 
Administrator to identify and list each air pollutant that ``in his 
judgment, cause or contribute to air pollution which may reasonably be 
anticipated to endanger public health and welfare'' and whose 
``presence * * * in the ambient air results from numerous or diverse 
mobile or stationary sources'' and to issue air quality criteria for 
those that are listed. Air quality criteria are to ``accurately reflect 
the latest scientific knowledge useful in indicating the kind and 
extent of all identifiable effects on public health or welfare which 
may be expected from the presence of [a] pollutant in ambient air * * 
*''. Section 108 also states that the Administrator ``shall, from time 
to time * * * revise a list'' that includes these pollutants, which 
provides the authority for a pollutant to be removed from or added to 
the list of criteria pollutants.
    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.'' \2\ 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.'' \3\
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    \2\ 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)
    \3\ 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 (DC 
Cir 1980), cert. denied, 449 U.S. 1042 (1980); American Petroleum 
Institute v. Costle, 665 F.2d 1176, 1186 (D.C. Cir. 1981), cert. 
denied, 455 U.S. 1034 (1982). Both kinds of uncertainties are 
components of the risk associated with pollution at levels below those 
at which human health effects can be said to occur with reasonable 
scientific certainty. Thus, in selecting primary standards that include 
an adequate margin of safety, the Administrator is seeking not only to 
prevent pollution levels that have been demonstrated to be harmful but 
also to prevent lower pollutant levels that may pose an unacceptable 
risk of harm, even if the risk is not precisely identified as to nature 
or degree.
    In selecting a margin of safety, EPA considers such factors as the 
nature and severity of the health effects involved, the size of the 
sensitive population(s) at risk, and the kind and degree of the 
uncertainties that must be addressed. The selection of any particular 
approach to providing an adequate margin of safety is a policy choice 
left specifically to the Administrator's judgment. Lead Industries 
Association v. EPA, supra, 647 F.2d at 1161-62.
    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. In so doing, EPA may not consider the 
costs of implementing the standards. See generally Whitman v. American 
Trucking Associations, 531 U.S. 457, 471, 475-76 (2001).
    Section 109(d)(1) of the Act requires that ``Not later than 
December 31, 1980, and at 5-year intervals thereafter, the 
Administrator shall complete a thorough review of the criteria 
published under section 108 and the national ambient air quality 
standards 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. The Administrator may review and revise criteria or 
promulgate new standards earlier or more frequently than required under 
this paragraph.'' 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, 
``Not 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.'' \4\ Since the early 1980's, this 
independent review function has been performed by the Clean Air 
Scientific Advisory Committee (CASAC) of EPA's Science Advisory Board.
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    \4\ In addition to the provisions of Section 109(d)(2)(B), 
concerning the role of CASAC in providing advice and recommendations 
to the Administrator on the criteria and standards, Section 
109(d)(2)(C) provides that CASAC shall also, ``(i) advise the 
Administrator of areas in which additional knowledge is required to 
appraise the adequacy and basis of existing, new, or revised 
national ambient air quality standards, (ii) describe the research 
efforts necessary to provide the required information, (iii) advise 
the Administrator on the relative contribution to air pollution 
concentrations of natural as well as anthropogenic activity, and 
(iv) advise the Administrator of any adverse public health, welfare, 
social economic, or energy effects which may result from various 
strategies for attainment and maintenance of such national ambient 
air quality standards.''
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B. History of Lead NAAQS Reviews

    On October 5, 1978 EPA promulgated primary and secondary NAAQS for 
Pb under section 109 of the Act (43 FR 46246). Both primary and 
secondary standards were set at a level of 1.5 micrograms per cubic 
meter ([mu]g/m\3\), measured as Pb in total suspended particulate 
matter (Pb-TSP), not to be exceeded by the maximum arithmetic mean 
concentration averaged over a calendar quarter. This standard was based 
on the 1977 Air Quality Criteria for Lead (USEPA, 1977).

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    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, as 
noted above, 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.

C. Current Related Lead Control Programs

    States are primarily responsible for ensuring attainment and 
maintenance of 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 (SIP's) 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 identified above that focus on air pollution control 
provide for nationwide reductions in environmental releases and human 
exposures. 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).\5\ 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). And, 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).\6\ By 
Executive Orders issued in October 2001 and April 2003, President Bush 
extended the work for the Task Force for an additional three and a half 
years beyond its original charter (66 FR 52013 and 68 FR 19931). The 
Task Force set a Federal goal of eliminating childhood Pb poisoning by 
the year 2010 and reducing Pb poisoning in children was the Task 
Force's top priority.
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    \5\ As described in Section III below the CDC stated in 2005 
that no ``safe'' threshold for blood Pb levels in young children has 
been identified (CDC, 2005a).
    \6\ Co-chaired by the Secretary of the HHS and the Administrator 
of the EPA, the Task Force consisted of representatives from 16 
Federal departments and agencies.
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    Federal abatement programs provide for the reduction in human 
exposures and environmental releases from in-place materials containing 
Pb (e.g., Pb-based paint, urban soil and dust and contaminated waste 
sites). Federal regulations on disposal of Pb-based paint waste help 
facilitate the removal of Pb-based paint from residences (See 
``Criteria for Classification of Solid Waste Disposal Facilities and 
Practices and Criteria for Municipal Solid Waste Landfills: Disposal of 
Residential Lead-Based Paint Waste; Final Rule'' EPA-HQ-RCRA-2001-
0017). Further, in 1991, EPA lowered the maximum levels of Pb permitted 
in public water systems from 50 parts per billion (ppb) to 15 ppb (56 
FR 26460).
    Federal programs to reduce exposure to Pb in paint, dust and soil 
are specified under the comprehensive federal strategy developed under 
the Residential Lead-Based Paint Hazard Reduction Act (Title X). Under 
Title X and Title IV of the Toxic Substances Control Act, EPA has 
established regulations in the following four categories: (1) Training 
and certification requirements for persons engaged in lead-based paint 
activities; accreditation of training providers; 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 lead in paint, dust and soil; and (4) 
Providing information on lead hazards to the public, including steps 
that people can take to protect themselves and their families from 
lead-based paint hazards.
    Under Title X of TSCA, EPA established dust lead standards for 
residential housing and soil dust in 2001. This regulation supports the 
implementation of other regulations which deal with worker training and 
certification, lead hazard disclosure in real estate transactions, lead 
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 
lead hazard control. In addition, this regulation also establishes, 
among other things, under authority of TSCA section 402, residential 
lead dust cleanup levels and amendments to dust and soil sampling 
requirements (66 FR 1206). The Title X term ``lead-based paint hazard'' 
implemented through this regulation identifies lead-based paint and all 
residential lead-containing dusts and soils regardless of the source of 
lead, 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

[[Page 71492]]

were to set unreasonable standards (e.g., standards that would 
recommend removal of all lead from paint, dust and soil), States and 
Tribes may choose to opt out of the Title X lead 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.
    On January 10, 2006, EPA issued a Notice of Proposed Rulemaking 
covering renovations performed for compensation in target housing. The 
2006 Proposal contains requirements designed to address lead hazards 
created by renovation, repair, and painting activities that disturb 
lead-based paint. The 2006 Proposal includes requirements for training 
renovators, other renovation workers, and dust sampling technicians; 
for certifying renovators, dust sampling technicians, and renovation 
firms; for accrediting providers of renovation and dust sampling 
technician training; for renovation work practices; and for 
recordkeeping. The 2006 Proposal proposes to make the rule effective in 
two stages. Initially, the rule proposes to apply to all renovations 
for compensation performed in target housing where a child with an 
increased blood lead level resided and rental target housing built 
before 1960. The proposed rule also proposes application to owner-
occupied target housing built before 1960, unless the person performing 
the renovation obtained a statement signed by the owner-occupant that 
the renovation would occur in the owner's residence and that no child 
under age 6 resided there. As proposed, the rule would take effect one 
year later in all rental target housing built between 1960 and 1978 and 
owner-occupied target housing built between 1960 and 1978. EPA also 
proposes to allow interested States, Territories, and Indian Tribes the 
opportunity to apply for and receive authorization to administer and 
enforce all of the elements of the new renovation provisions.
    A significant number of commenters observed that the proposal did 
not cover buildings where children under age 6 spend a great deal of 
time, such as day care centers and schools. Commenters noted that the 
risk posed to children from lead-based paint hazards in schools and 
day-care centers is likely to be equal to, if not greater than, the 
risk posed from these hazards at home. These commenters suggested that 
EPA expand its proposal to include such places, and several suggested 
that EPA use the existing definition of ``child-occupied facility'' in 
40 CFR Sec.  745.223 to define the expanded scope of coverage. EPA felt 
that these comments had merit, and, because adding child-occupied 
facilities was beyond the scope of the 2006 Proposal, an expansion of 
the 2006 Proposal was necessary to give this issue full and fair 
consideration. Accordingly, on June 5, 2007, EPA issued a Supplemental 
Notice of Proposed Rulemaking to add child-occupied facilities to the 
universe of buildings covered by the 2006 Proposal. EPA is working 
expeditiously to finalize this rulemaking and expects to do so in the 
first calendar quarter of 2008.
    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 (e.g., ``Hazardous 
Waste Management System; Identification and Listing of Hazardous Waste: 
Inorganic Chemical Manufacturing Wastes; Land Disposal Restrictions for 
Newly Identified Wastes and CERCLA Hazardous Substance Designation and 
Reportable Quantities; Final Rule'', http://www.epa.gov/epaoswer/hazwaste/state/revision/frs/fr195.pdf and http://www.epa.gov/epaoswer/

http://www.epa.gov/epaoswer/

batteries in municipal solid waste facilitate the collection and 
recycling or proper disposal of batteries containing Pb (e.g., See 
``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
). 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/
).

    A variety of federal nonregulatory programs also provide for 
reduced environmental release of Pb containing materials through more 
general encouragement of pollution prevention, promote reuse and 
recycling, reduce priority and toxic chemicals in products and waste, 
and conserve energy and materials. These include the Resource 
Conservation Challenge (http://www.epa.gov/epaoswer/osw/conserve/index.htm), the National Waste Minimization Program (http://

http://www.epa.gov/epaoswer/hazwaste/minimize/leadtire.htm), ``Plug in to 

eCycling'' (a partnership between EPA and consumer electronics 
manufacturers and retailers; http://www.epa.gov/epaoswer/hazwaste/recycle/electron/crt.htm#crts
), and activities to reduce the practice 

of backyard trash burning (http://www.epa.gov/msw/backyard/pubs.htm).

    Efforts such as those programs described above have been successful 
in that blood Pb levels in all segments of the population have dropped 
significantly from levels 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 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 \7\ are at the low end of the 
historic range of blood Pb levels for general population of children 
aged 1-5 years and are below a level of 5 [mu]g/dL--a level that has 
been associated with adverse effects with a higher degree of certainty 
in the published literature (than levels such as 2 [mu]g/dL) and is a 
level where cognitive deficits were identified with statistical 
significance (Lanphear et al., 2000). The decline in blood Pb levels in 
the United States has resulted from coordinated, intensive efforts at 
the national, state and local levels. The Agency has continued to 
grapple with soil and dust Pb levels from the historical use of Pb in 
paint and gasoline and other sources. In doing so, the agency has faced 
the difficulty of determining the level at which to set standards for 
residential dust levels given the uncertainties at what environmental 
levels and in which specific medium may actually cause particular blood 
Pb levels that are

[[Page 71493]]

associated with adverse effects (66 FR 1206).\8\
---------------------------------------------------------------------------

    \7\ It is noted that although the 95th percentile value for the 
2003-2004 NHANES is not currently available, that value for 2001-
2002 was 5.8 [mu]g/dL. Also, as discussed in Section III.A.1 
(including footnote 15), levels have been found to vary among 
children of different socioeconomic status and other demographic 
characteristics (CD, p. 4-21).
    \8\ See 2001 regulation to establish standards for lead-based 
paint hazards in most pre-1978 housing and child-occupied facilities 
(66 FR 1206).
---------------------------------------------------------------------------

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

D. Current Lead NAAQS Review

    EPA initiated the current review of the air quality criteria for Pb 
on November 9, 2004 with a general call for information (69 FR 64926). 
A project work plan (USEPA, 2005a) for the preparation of the Criteria 
Document was released in January 2005 for CASAC and public review. EPA 
held a series of workshops in August 2005, with invited recognized 
scientific experts to discuss initial draft materials that dealt with 
various lead-related issues being addressed in the Pb air quality 
criteria document. The first draft of the Criteria Document (USEPA, 
2005b) was released for CASAC and public review in December 2005 and 
discussed at a CASAC meeting held on February 28-March 1, 2006.
    A second draft Criteria Document (USEPA, 2006b) was released for 
CASAC and public review in May 2006, and discussed at the CASAC meeting 
on June 28, 2006. A subsequent draft of Chapter 7--Integrative 
Synthesis (Chapter 8 in the final Criteria Document), released on July 
31, 2006, was discussed at an August 15, 2006 CASAC teleconference. The 
final Criteria Document was released on September 30, 2006 (USEPA, 
2006a; cited throughout this preamble as CD). While the Criteria 
Document focuses on new scientific information available since the last 
review, it integrates that information with scientific criteria from 
previous reviews.
    In February 2006, EPA released the Plan for Review of the National 
Ambient Air Quality Standards for Lead (USEPA 2006c) that described 
Agency plans and a timeline for reviewing the air quality criteria, 
developing human exposure and risk assessments and an ecological risk 
assessment, preparing a policy assessment, and developing the proposed 
and final rulemakings.
    In May 2006, EPA released for CASAC and public review a draft 
Analysis Plan for Human Health and Ecological Risk Assessment for the 
Review of the Lead National Ambient Air Quality Standards (USEPA, 
2006d), which was discussed at a June 29, 2006 CASAC meeting 
(Henderson, 2006). The May 2006 assessment plan discussed two 
assessment phases: a pilot phase and a full-scale phase. The pilot 
phase of both the human health and ecological risk assessments was 
presented in the draft Lead Human Exposure and Health Risk Assessments 
and Ecological Risk Assessment for Selected Areas (ICF, 2006; 
henceforth referred to as the first draft Risk Assessment Report) which 
was released for CASAC and public review in December 2006. The first 
draft Staff Paper, also released in December 2006, discussed the pilot 
assessments and the most policy-relevant science from the Criteria 
Document. These documents were reviewed by CASAC and the public at a 
public meeting on February 6-7, 2007 (Henderson, 2007a).
    Subsequent to that meeting, EPA conducted full-scale human exposure 
and health risk assessments, although no further work was done on the 
ecological assessment due to resource limitations. A second draft Risk 
Assessment Report (USEPA, 2007a), containing 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 
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 review the primary and secondary Pb NAAQS. 
Such an evaluation 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 policy 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 air quality standards: Indicator,\9\ 
averaging time, form,\10\ and level. These elements, which together 
serve to define each standard, must be considered collectively in 
evaluating the 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.
---------------------------------------------------------------------------

    \9\ The ``indicator'' of a standard defines the chemical species 
or mixture that is to be measured in determining whether an area 
attains the standard.
    \10\ 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.
---------------------------------------------------------------------------

    The schedule for completion of this review is governed by a 
judicial order resolving a lawsuit filed in May 2004, alleging that EPA 
had failed to complete the current review within the period provided by 
statute. Missouri Coalition for the Environment, v. EPA (No. 
4:04CV00660 ERW, Sept. 14, 2005). The order that now governs this 
review, entered by the court on September 14, 2005, provides that EPA 
finalize the Staff Paper no later than November 1, 2007, which we have 
done. The order also specifies that EPA sign, for publication, notices 
of proposed and final rulemaking concerning its review of the Pb NAAQS 
no later than May 1, 2008 and September 1, 2008, respectively. To 
ensure that the ordered final rulemaking deadline will be met, EPA has 
set an interim target date for a proposed rulemaking of March 2008.

[[Page 71494]]

    The EPA invites general, specific, and/or technical comments on all 
issues discussed in this ANPR, including issues related to the Agency's 
review of the primary and secondary Pb NAAQS (sections III and IV 
below) and associated monitoring considerations (section V below). EPA 
also invites comments on all information, findings, and recommendations 
presented in this notice (section VI below).
    A public meeting of the CASAC will be held on December 12-13, 2007 
for the purpose of providing advice and recommendations to the 
Administrator based on its review of this ANPR and the recently 
released final Staff Paper and Risk Assessment Report. Information 
about this meeting was published in the Federal Register on November 
20, 2007 (72 FR 65335-65336).

E. Implementation Considerations

    Currently only two areas in the United States are designated as 
non-attainment of the Pb NAAQS. If the Pb NAAQS is significantly 
lowered as a result of this review, it is likely (based on a review of 
the current air quality monitoring data) that many more areas would be 
classified as non-attainment (see section 2.3.2.5 of the Staff Paper 
for more details). States with Pb non-attainment areas would be 
required to develop ``State Implementation Plans'' that identify and 
implement specific air pollution control measures that would reduce the 
ambient Pb concentrations to below the Pb NAAQS. If the Pb NAAQS is 
revised to a lower level, States may be able to attain the revised 
NAAQS by implementing air pollution controls on lead emitting 
industrial sources. These controls include such measures as fabric 
filter particulate controls and fugitive dust controls. However, at 
some of the lower Pb concentration levels that have been identified for 
consideration in this review, it may become necessary in some areas to 
implement controls on nonindustrial sources such as dust from roadways, 
dust from construction, and/or demolition sites.
    As described in further detail in the Staff Paper (see Section 
2.2), Pb is emitted from a wide variety of source types. The top five 
categories of sources of Pb emissions included in the EPA's 2002 
National Emissions Inventory (NEI) include: Mobile sources; \11\ 
industrial, commercial, institutional and process boilers; utility 
boilers; iron and steel foundries; and primary Pb smelting (see Staff 
Paper Section 2.2).
---------------------------------------------------------------------------

    \11\ The emissions estimates identified as mobile sources in the 
current NEI are currently limited to combustion of general aviation 
gas in piston-engine aircraft. Lead emissions estimates for other 
mobile source emissions of Pb (e.g., brake wear, tire wear, and 
others) are not included in the current NEI.
---------------------------------------------------------------------------

III. The Primary Standard

    This section presents information relevant to the review of the 
primary Pb NAAQS, including information on the health effects 
associated with Pb exposures, results of the human exposure and health 
risk assessment, and considerations related to evaluating the adequacy 
of the current standard and alternative standards that might be 
appropriate for the Administrator to consider.

A. Health Effects Information

    The following summary focuses on health endpoints associated with 
the range of exposures considered to be most relevant to current 
exposure levels and makes note of several key aspects of the health 
evidence for Pb. First, because exposure to atmospheric Pb particles 
occurs not only via direct inhalation of airborne particles, but also 
via ingestion of deposited particles (e.g., associated with soil and 
dust), the exposure being assessed is multimedia and multi-pathway in 
nature, occurring via both the inhalation and ingestion routes. In 
fact, ingestion of indoor dust can be recognized as a significant Pb 
exposure pathway, particularly for young children, for which dust 
ingested via hand-to-mouth activity can be a more important source of 
Pb exposure than inhalation, although dust can be resuspended through 
household activities and pose an inhalation risk as well (CD, p. 3-27 
to 3-28).\12\ Some studies have found that dietary intake of Pb may be 
a predominant source of Pb exposure among adults, greater than 
consumption of water and beverages or inhalation (CD, p. 3-43).\13\ 
Second, the exposure index or dose metric most commonly used and 
associated with health effects information is an internal biomarker 
(i.e., blood Pb). Additionally, the exposure duration of interest 
(i.e., that influencing internal dose pertinent to health effects of 
interest) may span months to potentially years, as does the time scale 
of the environmental processes influencing Pb deposition and fate. 
Lastly, the nature of the evidence for the health effects of greatest 
interest for this review, neurological effects in young children, are 
epidemiological data substantiated by toxicological data that provide 
biological plausibility and insights on mechanisms of action (CD, 
sections 5.3, 6.2 and 8.4.2).
---------------------------------------------------------------------------

    \12\ For example, the Criteria Document states the following: 
``Given the large amount of time people spend indoors, exposure to 
Pb in dusts and indoor air can be significant. For children, dust 
ingested via hand-to-mouth activity is often a more important source 
of Pb exposure than inhalation. Dust can be resuspended through 
household activities, thereby posing an inhalation risk as well. 
House dust Pb can derive both from Pb-based paint and from other 
sources outside the home. The latter include Pb-contaminated 
airborne particles from currently operating industrial facilities or 
resuspended soil particles contaminated by deposition of airborne Pb 
from past emissions.'' (CD, p. E-6)
    \13\ Some recent exposure studies have evaluated the relative 
importance of diet to other routes of Pb exposure. In reports from 
the NHEXAS, Pb concentrations measured in households throughout the 
Midwest were significantly higher in solid food compared to 
beverages and tap water (Clayton et al., 1999; Thomas et al., 1999). 
However, beverages appeared to be the dominant dietary pathway for 
Pb according to the statistical analysis (Clayton et al., 1999), 
possibly indicating greater bodily absorption of Pb from liquid 
sources (Thomas et al., 1999). Dietary intakes of Pb were greater 
than those calculated for intake from home tap water or inhalation 
on a [mu]g/day basis (Thomas et al., 1999). The NHEXAS study in 
Arizona showed that, for adults, ingestion was a more important Pb 
exposure route than inhalation (O'Rourke et al., 1999). (CD, p. 3-
43)
---------------------------------------------------------------------------

    In recognition of the multi-pathway aspects of Pb, and the use of 
an internal exposure metric in health risk assessment, the next section 
describes the internal disposition or distribution of Pb, and the use 
of blood Pb as an internal exposure or dose metric. This is followed by 
a discussion of the nature of Pb-induced health effects that emphasizes 
those with the strongest evidence. Potential impacts of Pb exposures on 
public health, including recognition of potentially susceptible or 
vulnerable subpopulations, are then discussed. Finally, key 
observations about Pb-related health effects are summarized.
1. Internal Disposition--Blood Lead as Dose Metric
    The health effects of Pb are remote from the portals of entry to 
the body (i.e., the respiratory system and gastrointestinal tract). 
Consequently, the internal disposition and distribution of Pb is an 
integral aspect of the relationship between exposure and effect. This 
section briefly summarizes the current state of knowledge of Pb 
disposition pertaining to both inhalation and ingestion routes of 
exposure as described in the Criteria Document.
    Inhaled Pb particles deposit in the different regions of the 
respiratory tract as a function of particle size (CD, pp. 4-3 to 4-4). 
Lead associated with smaller particles, which are predominantly 
deposited in the pulmonary region, may, depending on solubility, be 
absorbed into the general circulation or transported to the 
gastrointestinal tract (CD, pp. 4-3). Lead associated with larger 
particles, which are predominantly deposited in the head and conducting 
airways (e.g., nasal

[[Page 71495]]

pharyngeal and tracheobronchial regions of respiratory tract), may be 
transported into the esophagus and swallowed, thus making its way to 
the gastrointestinal tract (CD, pp. 4-3 to 4-4), where it may be 
absorbed into the blood stream. Thus, Pb can reach the gastrointestinal 
tract either directly through the ingestion route or indirectly 
following inhalation.
    Once in the blood stream, where approximately 99% of the Pb 
associates with red blood cells, the Pb is quickly distributed 
throughout the body (e.g., within days) with the bone serving as a 
large, long-term storage compartment, and soft tissues (e.g., kidney, 
liver, brain, etc) serving as smaller compartments, in which Pb may be 
more mobile (CD, sections 4.3.1.4 and 8.3.1.). Additionally, the 
epidemiologic evidence indicates that Pb freely crosses the placenta 
resulting in continued fetal exposure throughout pregnancy, and that 
exposure increases during the later half of pregnancy (CD, section 
6.6.2).
    During childhood development, bone represents approximately 70% of 
a child's body burden of Pb, and this accumulation continues through 
adulthood, when more than 90% of the total Pb body burden is stored in 
the bone (CD, section 4.2.2). Accordingly, levels of Pb in bone are 
indicative of a person's long-term, cumulative exposure to Pb. In 
contrast, blood Pb levels are usually indicative of recent exposures. 
Depending on exposure dynamics, however, blood Pb may--through its 
interaction with bone--be indicative of past exposure or of cumulative 
body burden (CD, section 4.3.1.5).
    Throughout life, Pb in the body is exchanged between blood and 
bone, and between blood and soft tissues (CD, section 4.3.2), with 
variation in these exchanges reflecting ``duration and intensity of the 
exposure, age and various physiological variables'' (CD, p. 4-1). Past 
exposures that contribute Pb to the bone, consequently, may influence 
current levels of Pb in blood. Where past exposures were elevated in 
comparison to recent exposures, this influence may complicate 
interpretations with regard to recent exposure (CD, sections 4.3.1.4 to 
4.3.1.6). That is, higher blood Pb concentrations may be indicative of 
higher cumulative exposures or of a recent elevation in exposure (CD, 
pp. 4-34 and 4-133).
    In several recent studies investigating the relationship between Pb 
exposure and blood Pb in children (e.g., Lanphear and Roghmann 1997; 
Lanphear et al., 1998), blood Pb levels have been shown to reflect Pb 
exposures, with particular influence associated with exposures to Pb in 
surface dust. Further, as stated in the Criteria Document ``these and 
other studies of populations near active sources of air emissions 
(e.g., smelters, etc.), substantiate the effect of airborne Pb and 
resuspended soil Pb on interior dust and blood Pb'' (CD, p. 8-22).
    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 4.3.1.3 and 8.3.2) and toxicological 
studies of Pb health effects and dose-response relationships (CD, 
Chapter 5). The prevalence of the use of blood Pb as an exposure index 
or biomarker is related to both the ease of blood sample collection 
(CD, p. 4-19; Section 4.3.1) and by findings of association with a 
variety of health effects (CD, Section 8.3.2). For example, the U.S. 
Centers for Disease Control and Prevention (CDC), and its predecessor 
agencies, have for many years used blood Pb level as a metric for 
identifying children at risk of adverse health effects and for 
specifying particular public health recommendations (CDC, 1991; CDC, 
2005a). In 1978, when the current Pb NAAQS was established, the CDC 
recognized a blood Pb level of 30 [mu]g/dL as a level warranting 
individual intervention (CDC, 1991). In 1985, the CDC recognized a 
level of 25 [mu]g/dL for individual child intervention, and in 1991, 
they recognized a level of 15 [mu]g/dL for individual intervention and 
a level of 10 [mu]g/dL for implementing community-wide prevention 
activities (CDC, 1991; CDC, 2005). In 2005, with consideration of a 
review of the evidence by their advisory committee, CDC revised their 
statement on Preventing Lead Poisoning in Young Children, specifically 
recognizing the evidence of adverse health effects in children with 
blood Pb levels below 10 [mu]g/dL 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).\14\
---------------------------------------------------------------------------

    \14\ With the 2005 statement, CDC identified a variety of 
reasons, reflecting both scientific and practical considerations, 
for not lowering the 1991 level of concern, including a lack of 
effective clinical or public health interventions to reliably and 
consistently reduce blood Pb levels that are already below 10 [mu]g/
dL, the lack of a demonstrated threshold for adverse effects, and 
concerns for deflecting resources from children with higher blood Pb 
levels (CDC, 2005a). CDC's Advisory Committee on Childhood Lead 
Poisoning Prevention recently provided recommendations regarding 
interpreting and managing blood Pb levels below 10 [mu]g/dL in 
children and reducing childhood exposures to Pb (ACCLPP, 2007).
---------------------------------------------------------------------------

    Since 1976, the CDC has been monitoring blood Pb levels nationally 
through the National Health and Nutrition Examination Survey (NHANES). 
This survey 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 4.3.1.3 and 8.3.3; Schwemberger et 
al., 2005). The Criteria Document summarizes related information as 
follows (CD, p. E-6).

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

While levels in the U.S. general population, including geometric mean 
levels in children aged 1-5, have declined significantly, mean levels 
have been found to vary among children of different socioeconomic 
status (SES) and other demographic characteristics (CD, p. 4-21).\15\
---------------------------------------------------------------------------

    \15\ For example, while the 2001-2004 median blood level for 
children aged 1-5 of all races and ethnic groups is 1.6 [mu]g/dL, 
the median for the subset living below the poverty level is 2.3 
[mu]g/dL and 90th percentile values for these two groups are 4.0 
[mu]g/dL and 5.4 [mu]g/dL, respectively. Similarly, the 2001-2004 
median blood level for black, non-hispanic children aged 1-5 is 2.5 
[mu]g/dL, while the median level for the subset of that group living 
below the poverty level is 2.9 [mu]g/dL and the median level for the 
subset living in a household with income more than 200% of the 
poverty level is 1.9 [mu]g/dL. Associated 90th percentile values for 
2001-2004 are 6.4 [mu]g/dL (for black, non-hispanic children aged 1-
5), 7.7 [mu]g/dL (for the subset of that group living below the 
poverty level) and 4.1 [mu]g/dL (for the subset living in a 
household with income more than 200% of the poverty level). (http://www.epa.gov/envirohealth/children/body_burdens/b1-table.htm_then
 

click on ``Download a universal spreadsheet file of the Body Burdens 
data tables'').
---------------------------------------------------------------------------

    Bone measurements, as a result of the generally slower Pb turnover 
in bone, are recognized as providing a better measure of cumulative Pb 
exposure (CD, Section 8.3.2). The bone pool of Pb in children, however, 
is thought to be much more labile than that in adults due to the more 
rapid turnover of bone mineral as a result of growth (CD, p. 4-27). As 
a result, changes in blood Pb concentration in children more closely 
parallel changes in total body burden (CD, pp. 4-20 and 4-27). This is 
in contrast to adults, whose bone has accumulated decades of Pb 
exposures (with past exposures often greater than current ones), and 
for whom the bone may be a significant source long after exposure has 
ended (CD, Section 4.3.2.5).

[[Page 71496]]

    Accordingly, blood Pb level in children is the index of exposure or 
exposure metric in the risk assessment discussed below in section 
III.B. The use of concentration-response functions that rely on blood 
Pb (e.g., rather than ambient Pb concentration) as the exposure metric 
reduces uncertainty in the causality aspects of Pb risk estimates. The 
relationship between specific sources and pathways of exposure and 
blood Pb level is needed, however, in order to identify the specific 
risk contributions associated with those sources and pathways of 
greatest interest to this assessment (i.e., those related to Pb emitted 
into the air). For example, the blood Pb-response relationships 
developed in epidemiological studies of Pb exposed populations do not 
distinguish among different sources or pathways of Pb exposure (e.g., 
inhalation, ingestion of indoor dust, ingestion of dust containing 
leaded paint). In the exposure assessment for this review, models that 
estimate blood Pb levels associated with Pb exposure (e.g., CD, Section 
4.4) are used to inform estimates of contributions to blood Pb arising 
from ambient air related Pb as compared to contributions from other 
sources.
2. Nature of Effects
    Lead has been demonstrated to exert ``a broad array of deleterious 
effects on multiple organ systems via widely diverse mechanisms of 
action'' (CD, p. 8-24 and Section 8.4.1). This array of health effects 
includes 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).\16\
---------------------------------------------------------------------------

    \16\ Lead has been classified as a probable human carcinogen by 
the International Agency for Research on Cancer, based mainly on 
sufficient animal evidence, and as reasonably anticipated to be a 
human carcinogen by the U.S. National Toxicology Program (CD, 
Section 6.7.2). U.S. EPA considers Pb a probable carcinogen (http://www.epa.gov/iris/subst/0277.htm
; CD, p. 6-195).

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

    This review is focused on those effects most pertinent to ambient 
exposures, which given the reductions in ambient Pb levels over the 
past 30 years, are generally those associated with blood Pb levels in 
children and adults in the range of 10 [mu]g/dL and lower. Tables 8-5 
and 8-6 in the Criteria Document highlight the key such effects 
observed in children and adults, respectively (CD, pp. 8-60 to 8-62). 
The effects include neurological, hematological and immune effects for 
children, and hematological, cardiovascular and renal effects for 
adults. As evident from the discussions in Chapters 5, 6 and 8 of the 
Criteria Document, ``neurotoxic effects in children and cardiovascular 
effects in adults are among those best substantiated as occurring at 
blood Pb concentrations as low as 5 to 10 [mu]g/dL (or possibly lower); 
and these categories are currently clearly of greatest public health 
concern'' (CD, p. 8-60). 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 blood Pb levels extend below 5 
[mu]g/dL, and some studies have observed these effects at the lowest 
blood levels considered. Threshold levels for these effects cannot be 
discerned from the currently available studies. For example, the 
Criteria Document also states the following (CD, p. 6-269).

    Recent studies of Pb neurotoxicity in children consistently 
indicate that blood Pb levels < 10 [mu]g/dL are associated with 
neurocognitive deficits. The data are also suggestive that these 
effects may be seen at blood Pb levels ranging down to 5 [mu]g/dL, 
or perhaps somewhat lower, but the evidence is less definitive.\17\

    \17\ The Criteria Document further 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)

    Since effects on children's developing nervous system are 
considered to be the sentinel effects in this review, and are the focus 
of the quantitative risk assessment conducted for this review 
(discussed below in section III.B), these effects are discussed briefly 
below. Other neurological effects associated with Pb exposures indexed 
by blood Pb levels near or below 10 [mu]g/dL include behavioral 
effects, such as delinquent behavior (CD, Sections 6.2.6 and 8.4.2.2), 
sensory effects, such as those related to hearing and vision (CD, 
Sections 6.2.7, 7.4.2.3 and 8.4.2.3), and deficits in neuromotor 
function (CD, p. 8-36). The differing evidence and associated strength 
of the evidence for these different effects is described in detail in 
the Criteria Document.
    The nervous system has long been recognized as a target of Pb 
toxicity, with the developing nervous system affected at lower 
exposures than the mature system (CD, Sections 5.3, 6.2.1, 6.2.2, and 
8.4). While blood Pb levels in U.S. children ages one to five years 
have decreased notably since the late 1970s, newer studies have 
investigated and reported associations of effects on the 
neurodevelopment of children with these more recent blood Pb levels 
(CD, Chapter 6). Functional manifestations of Pb neurotoxicity during 
childhood include sensory, motor, cognitive and behavioral impacts. 
Numerous epidemiological studies have reported neurocognitive, 
neurobehavioral, sensory, and motor function effects in children at 
blood Pb levels below 10 [mu]g/dL (CD, Section 6.2). 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).
    Cognitive effects associated with Pb exposures that have been 
observed in epidemiological studies have included decrements in 
intelligence test results, such as the widely used IQ score, and in 
academic achievement as assessed by various standardized tests as well 
as by class ranking and graduation rates (CD, Section 6.2.16 and pp. 8-
29 to 8-30). As noted in the Criteria Document with regard to the 
latter, ``Associations between Pb exposure and academic achievement 
observed in the above-noted studies were significant even after 
adjusting for IQ, suggesting that Pb-sensitive neuropsychological 
processing and learning factors not reflected by global intelligence 
indices might contribute to reduced performance on academic tasks'' 
(CD, pp. 8-29 to 8-30).
    Other cognitive effects observed in studies of children have 
included effects on attention, executive functions, language, memory, 
learning and visuospatial processing (CD, Sections 5.3.5, 6.2.5 and 
8.4.2.1), 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 8.4.2.1; p. 8-31), which provide strong biological 
plausibility of Pb effects on learning ability, memory and attention

[[Page 71497]]

(CD, Section 5.3.5), as well as associated mechanistic findings. With 
regard to persistence of effects the Criteria Document states the 
following (CD, p. 8-67):

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

The evidence with regard to persistence of Pb-induced deficits observed 
in animal and epidemiological studies is described in discussion of 
those studies in the Criteria Document (CD, Sections 5.3.5, 6.2.11, and 
8.5.2). It is additionally important to note that there may be long-
term consequences of such deficits over a lifetime. Poor academic 
skills and achievement can have ``enduring and important effects on 
objective parameters of success in real life,'' as well as increased 
risk of antisocial and delinquent behavior (CD, Section 6.2.16).
    As discussed in the Criteria Document, while there is no direct 
animal test parallel to human IQ tests, ``in animals a wide variety of 
tests that assess attention, learning, and memory suggest that Pb 
exposure {of animals{time}  results in a global deficit in functioning, 
just as it is indicated by decrements in IQ scores in children'' (CD, 
p. 8-27). The animal and epidemiological evidence for this endpoint are 
consistent and complementary (CD, p. 8-44). As stated in the Criteria 
Document (p. 8-44):

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

    Epidemiologic studies of Pb and child development have demonstrated 
inverse associations between blood Pb concentrations and children's IQ 
and other outcomes at successively lower Pb exposure levels over the 
past 30 years (CD, p. 6-64). This is supported by multiple studies 
performed over the past 15 years (see CD, Section 6.2.13); ``the most 
compelling evidence for effects at blood Pb levels < 10 [mu]g/dL comes 
from an international pooled analysis of seven prospective cohort 
studies (n = 1,333) by Lanphear et al. (2005)'' (CD, p. 6-67 and 
sections 6.2.13 and 6.2.3.1.11). This pooled analysis estimated a 
decline of 6.2 points in full scale IQ (with a 95% confidence interval 
bounded by 3.8 and 8.6) occurring between approximately 1 and 10 [mu]g/
dL blood Pb level, measured concurrent with the IQ test (CD, p. 6-76). 
As discussed below in section III.B, this analysis (Lanphear et al., 
2005) was relied upon in the quantitative risk assessment.
3. Lead-Related Impacts on Public Health
    In addition to the advances in our knowledge and understanding of 
Pb health effects at lower exposures (e.g., using blood Pb as the 
index), there has been some change with regard to the U.S. population 
Pb burden since the time of the last Pb NAAQS review. For example, the 
geometric mean blood Pb level for U.S. children aged 1-5, as estimated 
by the U.S. Centers for Disease Control, declined from 2.7 [mu]g/dL 
(95% CI: 2.5-3.0) in the 1991-1994 survey period to 1.7 [mu]g/dL (95% 
CI: 1.55-1.87) in the 2001-2002 survey period (CD, Section 
4.3.1.3).\18\ Blood Pb levels have also declined in the U.S. adult 
population over this time period (CD, Section 4.3.1.3).\19\ As noted in 
the Criteria Document, ``blood-Pb levels have been declining at 
differential rates for various general subpopulations, as a function of 
income, race, and certain other demographic indicators such as age of 
housing'' (CD, p. 8-21).
---------------------------------------------------------------------------

    \18\ These levels are in contrast to the geometric mean blood Pb 
level of 14.9 [mu]g/dL reported for U.S. children (aged 6 months to 
5 years) in 1976-1980 (CD, Section 4.3.1.3). Median and 90th 
percentile values have also declined from 15 [mu]g/dL and 25 [mu]g/
dL, respectively, in 1976-1980, to 1.6 [mu]g/dL and 3.9 [mu]g/dL, 
respectively in 2003-04 (http://www.epa.gov/envirohealth/children/body_burdens/b1-table.htm
).

    \19\ For example, NHANES data for older adults (60 years of age 
and older) indicate a decline in overall population geometric mean 
blood Pb level from 3.4 [mu]g/dL in 1991-1994 to 2.2 [mu]g/dL in 
1999-2002; the trend for adults between 20 and 60 years of age is 
similar to that for children 1 to 5 years of age (http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5420a5.htm
).

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

a. At-Risk Subpopulations
    Potentially at-risk subpopulations include those with increased 
susceptibility (i.e., physiological factors contributing to a greater 
response for the same exposure) and those with increased exposure 
(including that resulting from behavior leading to increased contact 
with contaminated media) (USEPA 1986a, p. 1-154). A behavioral factor 
of great impact on Pb exposure is the incidence of hand-to-mouth 
activity that is prevalent in very young children (CD, Section 4.4.3). 
Physiological factors include both conditions contributing to a 
subgroup's increased risk of effects at a given blood Pb level, and 
those that contribute to blood Pb levels higher than those otherwise 
associated with a given Pb exposure (CD, Section 8.5.3). We also 
considered evidence pertaining to vulnerability to pollution-related 
effects which additionally encompasses situations of elevated exposure, 
such as residing in old housing with Pb-containing paint or 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) that can contribute to increased risk of adverse health 
effects from Pb.
    Three particular physiological factors contributing to increased 
risk of Pb effects at a given blood Pb level are recognized in the 
Criteria Document (e.g., CD, Section 8.5.3): Age, health status, and 
genetic composition. With regard to age, the susceptibility of young 
children to the neurodevelopmental effects of Pb is well recognized 
(e.g., CD, Sections 5.3, 6.2, 8.4, 8.5, 8.6.2), although the specific 
ages of vulnerability have not been established (CD, pp. 6-60 to 6-64). 
Early childhood may also be a time of increased susceptibility for Pb 
immunotoxicity (CD, Sections 5.9.10, 6.8.3 and 8.4.6). Further early 
life exposures have been associated with increased risk of 
cardiovascular effects in humans later in life (CD, p. 8-74). Early 
life exposures have also been associated with increased risk, in 
animals, of neurodegenerative effects later in life (CD, p. 8-74).\20\ 
Health status is another

[[Page 71498]]

physiological factor in that subpopulations with pre-existing health 
conditions may be more susceptible (as compared to the general 
population) for particular Pb-associated effects, with this being most 
clear for renal and cardiovascular outcomes. For example, African 
Americans as a group, have a higher frequency of hypertension than the 
general population or other ethnic groups (NCHS, 2005), and as a result 
may face a greater risk of adverse health impact from Pb-associated 
cardiovascular effects. A third physiological factor relates to genetic 
polymorphisms. That is, subpopulations defined by particular genetic 
polymorphisms (e.g., presence of the [delta]-aminolevulinic acid 
dehydratase-2 [ALAD-2] allele) have also been recognized as sensitive 
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, 6.4.7.3 and 6.3.6).
---------------------------------------------------------------------------

    \20\ Specifically, among young adults who lived as children in 
an area heavily polluted by a smelter and whose current Pb exposure 
was low, higher bone Pb levels were associated with higher systolic 
and diastolic blood pressure (CD, p. 8-74). In adult rats, greater 
early exposures to Pb are associated with increased levels of 
amyloid protein precursor, a marker of risk for neurodegenerative 
disease (CD, p. 8-74).
---------------------------------------------------------------------------

    While early childhood is recognized as a time of increased 
susceptibility, a difficulty in identifying a discrete period of 
susceptibility from epidemiological studies has been that the period of 
peak exposure, reflected in peak blood Pb levels, is around 18-27 
months when hand-to-mouth activity is at its maximal (CD, p. 6-60). The 
earlier Pb literature described the first 3 years of life as a critical 
window of vulnerability to the neurodevelopmental impacts of Pb (CD, p. 
6-60). Recent epidemiologic studies, however, have indicated a 
potential for susceptibility of children to concurrent Pb exposure 
extending to school age (CD, pp. 6-60 to 6-64). The evidence indicates 
both the sensitivity of the first 3 years of life, and a sustained 
sensitivity throughout the lifespan as the human central nervous system 
continues to mature and be vulnerable to neurotoxicants (CD, Section 
8.4.2.7). The animal evidence helps inform an understanding of specific 
periods of development with increased vulnerability to specific types 
of effect (CD, Section 5.3), and indicates the potential importance of 
exposures of duration on the order of months. Evidence of a differing 
sensitivity of the immune system to Pb across and within different 
periods of life stages indicates the potential importance of exposures 
of duration as short as weeks to months. For example, the animal 
studies suggest that the gestation period is the most sensitive life 
stage followed by early neonatal stage, and that within these life 
stages, critical windows of vulnerability are likely to exist (CD, 
Section 5.9 and p. 5-245).
    In summary, there are a variety of ways in which Pb exposed 
populations might be characterized and stratified for consideration of 
public health impacts. Age or lifestage was used to distinguish 
potential groups on which to focus the quantitative risk assessment 
because of its influence on exposure and susceptibility. Young children 
were selected as the priority population for the risk assessment in 
consideration of the health effects evidence regarding endpoints of 
greatest public health concern. The Criteria Document recognizes, 
however, other population subgroups as described above may also be at 
risk of Pb-related health effects of public health concern.
b. Potential Public Health Impacts
    As discussed in the Criteria Document, there are potential public 
health implications of low-level Pb exposure, indexed by blood Pb 
levels, associated with several health endpoints identified in the 
Criteria Document (CD, Section 8.6).\21\ These include potential 
impacts on population IQ, which is the focus of the quantitative risk 
assessment conducted for this review, as well as heart disease and 
chronic kidney disease, which are not included in the quantitative risk 
assessment (CD, Sections 8.6, 8.6.2, 8.6.3 and 8.6.4). It is noted that 
there is greater uncertainty associated with effects at the lower 
levels of blood Pb, and that there are differing weights of evidence 
across the effects observed.\22\ With regard to potential implications 
of Pb effects on IQ, the Criteria Document recognizes the ``critical'' 
distinction between population and individual risk, noting 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).\23\ 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).\24\ 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 handicap (CD, p. 8-77).
---------------------------------------------------------------------------

    \21\ The differing evidence and associated strength of the 
evidence for these different effects is described in detail in the 
Criteria Document.
    \22\ As is described in Section III.B.2.a, CASAC, in their 
comments on the analysis plan for the risk assessment described in 
this notice, placed higher priority on modeling the child IQ metric 
than the adult endpoints (e.g., cardiovascular effects).
    \23\ Similarly, ``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).
    \24\ 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).
---------------------------------------------------------------------------

    The magnitude of a public health impact is dependent upon the size 
of population affected and type or severity of the effect. As 
summarized above, there are several population groups that may be 
susceptible or vulnerable to effects associated with exposure to Pb, 
including young children, particularly those in families of low SES 
(CD, p. E-15), as well as individuals with hypertension, diabetes, and 
chronic renal insufficiency (CD, p. 8-72). Although comprehensive 
estimates of the size of these groups residing in proximity to policy-
relevant sources of ambient Pb have not been developed, total estimates 
of these population subpopulations within the U.S. are substantial (as 
noted in Table 3-3 of the Staff Paper).\25\
---------------------------------------------------------------------------

    \25\ For example, approximately 4.8 million children live in 
poverty, while the estimates of numbers of adults with hypertension, 
diabetes or chronic kidney disease are on the order of 20 to 50 
million (see Table 3-3 of Staff Paper).
---------------------------------------------------------------------------

    With regard to estimates of the size of potentially vulnerable 
subpopulations living in areas of increased exposure related to ambient 
Pb, the information is still more limited. The limited information 
available on air and surface soil concentrations of Pb indicates 
elevated concentrations near stationary sources as compared with areas 
remote from such sources (CD, Sections 3.2.2 and 3.8). Air quality 
analyses (presented in Chapter 2 of the Staff Paper) indicate 
dramatically higher Pb concentrations at monitors near sources as 
compared with those more remote. As described in Section 2.3.2.1 of the 
Staff Paper, however, since the 1980s the number of Pb monitors has 
been significantly reduced by states (with EPA guidance that 
monitorings well below the current NAAQS could be shut down) and a lack 
of monitors near some large sources may lead to underestimates of the 
extent of occurrences of relatively higher Pb concentrations. The 
significant limitations of our monitoring and emissions information 
constrain our efforts to characterize the size of at-risk populations 
in areas influenced by

[[Page 71499]]

policy-relevant sources of ambient Pb. For example, the limited size 
and spatial coverage of the current Pb monitoring network constrains 
our ability to characterize current levels of airborne Pb in the U.S. 
Further, the available information on emissions and locations of 
sources indicates that the network is inconsistent in its coverage of 
the largest sources identified in the 2002 National Emissions Inventory 
(NEI), with monitors within a mile of only 2 of 26 facilities in the 
2002 NEI with emissions greater than 5 tons per year (tpy). 
Additionally, there are various uncertainties and limitations 
associated with source information in the NEI.
    In recognition of the significant limitations associated with the 
currently available information on Pb emissions and airborne 
concentrations in the U.S. and the associated exposure of potentially 
at-risk populations, Chapter 2 of the Staff Paper summarizes the 
information in several different ways. For example, analyses of the 
current monitoring network indicated the numbers of monitoring sites 
that would exceed alternate standard levels, taking into consideration 
different statistical forms. These analyses are also summarized with 
regard to population size in counties home to those monitoring sites 
(see Appendix 5.A of the Staff Paper). Information for the monitors and 
from the NEI indicates a range of source sizes in proximity to monitors 
at which various levels of Pb are reported. Together this information 
suggests that there is variety in the magnitude of Pb emissions from 
sources that could influence air Pb concentrations. Identifying 
specific emissions levels of sources expected to result in air Pb 
concentrations of interest, however, would be informed by a 
comprehensive analysis using detailed source characterization 
information that was not feasible within the time and data constraints 
of this review. Instead, we have developed a summary of the emissions 
and demographic information for Pb sources that includes estimates of 
the numbers of people residing in counties in which the aggregate Pb 
emissions from NEI sources is greater than or equal to 0.1 tpy or in 
counties in which the aggregate Pb emissions is greater than or equal 
to 0.1 tpy per 1000 square miles (see Tables 3-4 and 3-5, respectively, 
in the Staff Paper).
    Additionally, the potential for historically deposited Pb near 
roadways to contribute to increased risks of Pb exposure and associated 
risk to populations residing nearby is suggested in the Criteria 
Document. Although estimates of the number of individuals, including 
children, living within close proximity to roadways specifically 
recognized for this potential have not been developed, these numbers 
may be substantial. \26\
---------------------------------------------------------------------------

    \26\ For example, the 2005 American Housing Survey, conducted by 
the U.S. Census Bureau indicates that some 14 million (or 
approximately 13% of) housing units are ``within 300 feet of a 4-or-
more-lane roadway, railroad or airport'' (U.S. Census Bureau, 2006). 
Additionally, estimates developed for Colorado, Georgia and New York 
indicate that approximately 15-30% of the populations in those 
states reside within 75 meters of a major roadway (i.e., a ``Limited 
Access Highway'', ``Highway'', ``Major Road'' or ``Ramp'', as 
defined by the U.S. Census Feature Class Codes) (ICF, 2005).
---------------------------------------------------------------------------

4. Key Observations
    The following key observations are based on the available health 
effects evidence and the evaluation and interpretation of that evidence 
in the Criteria Document.
     Lead exposures occur both by inhalation and by ingestion 
(CD, Chapter 3). As stated in the Criteria Document, ``given the large 
amount of time people spend indoors, exposure to Pb in dusts and indoor 
air can be significant'' (CD, p. 3-27).
     Children, in general and especially low SES children, are 
at increased risk for Pb exposure and Pb-induced adverse health 
effects. This is due to several factors, including enhanced exposure to 
Pb via ingestion of soil Pb and/or dust Pb due to normal childhood 
hand-to-mouth activity (CD, p. E-15, Chapter 3 and Section 6.2.1).
     Once inhaled or ingested, Pb is distributed by the blood, 
with long-term storage accumulation in the bone. Bone Pb levels provide 
a strong measure of cumulative exposure which has been associated with 
many of the effects summarized below, although difficulty of sample 
collection has precluded widespread use in epidemiological studies to 
date (CD, Chapter 4).
     Blood levels of Pb are well accepted as an index of 
exposure (or exposure metric) for which associations with the key 
effects (see below) have been observed. In general, associations with 
blood Pb are most robust for those effects for which past exposure 
history poses less of a complicating factor, i.e., for effects during 
childhood (CD, Section 4.3).
     Both epidemiological and toxicologic studies have shown 
that environmentally relevant levels of Pb affect many different organ 
systems (CD, p. E-8). Many associations of health effects with Pb 
exposure have been found at levels of blood Pb that are currently 
relevant for the U.S. population, with children having blood Pb levels 
of 5-10 [mu]g/dL, or, perhaps somewhat lower, being at notable risk for 
neurological effects (see subsequent bullet). Supportive evidence from 
toxicological studies provides biological plausibility for the observed 
effects. (CD, Chapters 5, 6 and 8)
     Pb exposure is associated with a variety of neurological 
effects in children, notably intellectual attainment and school 
performance. Both qualitative and quantitative evidence, with further 
support from animal research, indicates a robust and consistent effect 
of Pb exposure on neurocognitive ability at mean concurrent blood Pb 
levels in the range of 5 to 10 [mu]g/dL. A recent analysis of a 
nationally representative U.S. sample suggested Pb effects on 
intellectual attainment of young children at population mean concurrent 
blood Pb levels ranging down to as low as 2 [mu]g/dL. (CD, Sections 
5.3, 6.2, 8.4.2 and 6.10)
     Deficits in cognitive skills may have long-term 
consequences 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, Sections 6.1 and 8.4.2)
     For the quantitative risk assessment for neurocognitive 
ability in young children (described in Chapter 4 of the Staff Paper), 
the Staff Paper chose to use nonlinear concentration-response models 
that reflect the epidemiological evidence of a higher slope of the 
blood Pb concentration-response relationship at lower blood Pb levels, 
particularly below 10 [mu]g/dL (CD, Sections 6.2.13 and 8.6).
     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).
     In adults, with regard to cardiovascular outcomes, the 
Criteria Document included the following summary (CD, p. E-10).

    Epidemiological studies have consistently demonstrated 
associations between Pb exposure and enhanced risk of deleterious 
cardiovascular outcomes, including increased blood pressure and 
incidence of hypertension. \27\ A meta-analysis of

[[Page 71500]]

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. Studies have also found that cumulative past Pb exposure 
(e.g., bone Pb) may be as important, if not more, than present Pb 
exposure in assessing cardiovascular effects. The evidence for an 
association of Pb with cardiovascular morbidity and mortality is 
limited but supportive.
---------------------------------------------------------------------------

    \27\ The Criteria Document states that ``While several studies 
have demonstrated a positive correlation between blood pressure and 
blood Pb concentration, others have failed to show such association 
when controlling for confounding factors such as tobacco smoking, 
exercise, body weight, alcohol consumption, and socioeconomic 
status. Thus, the studies that have employed blood Pb level as an 
index of exposure have shown a relatively weak association with 
blood pressure. In contrast, the majority of the more recent studies 
employing bone Pb level have found a strong association between 
long-term Pb exposure and arterial pressure (Chapter 6). Since the 
residence time of Pb in the blood is relatively short but very long 
in the bone, the latter observations have provided rather compelling 
evidence for a positive relationship between Pb exposure and a 
subsequent rise in arterial pressure'' (CD, pp. 5-102 to 5-103). 
Further, in consideration of the meta-analysis also described here, 
the Criteria Document stated that ``The meta-analysis provides 
strong evidence for an association between increased blood Pb and 
increased blood pressure over a wide range of populations'' (CD, p. 
6-130) and ``the meta-analyses results suggest that studies not 
detecting an effect may be due to small sample sizes or other 
factors affecting precision of estimation of the exposure effect 
relationship'' (CD, p. 6-133).

Studies of nationally representative U.S. samples observed associations 
between blood Pb levels and increased systolic blood pressure at 
population mean blood lead levels less than 5 [mu]g/dL, particularly 
among African Americans (CD, Section 6.5.2). With regard to gender 
differences, the Criteria Document states the following (CD, p. 6-154).
    Although females often show lower Pb coefficients than males, and 
Blacks higher Pb coefficients than Whites, where these differences have 
been formally tested, they are usually not statistically significant. 
The tendencies may well arise in the differential Pb exposure in these 
strata, lower in women than in men, higher in Blacks than in Whites. 
The same sex and race differential is found with blood pressure.

Animal evidence provides confirmation of Pb effects on cardiovascular 
functions. (CD, Sections 5.5, 6.5, 8.4.3 and 8.6.3)
     Renal effects, evidenced by reduced renal filtration, have 
also been associated with Pb exposures indexed by bone Pb levels and 
also with mean blood Pb levels in the range of 5 to 10 [mu]g/dL in the 
general adult population, with the potential adverse impact of such 
effects being enhanced for susceptible subpopulations including those 
with diabetes, hypertension, and chronic renal insufficiency (CD, 
Sections 6.4, 8.4.5, and 8.6.4). The full significance of this effect 
is unclear, given that other evidence of more marked signs of renal 
dysfunction have not been detected at blood Pb levels below 30-40 
[mu]g/dL in large studies of occupationally-exposed Pb workers (CD, pp. 
6-270 and 8-50). \28\
---------------------------------------------------------------------------

    \28\ In the general population, both cumulative and circulating 
Pb has been found to be associated with longitudinal decline in 
renal functions. In the large NHANES III study, alterations in 
urinary creatinine excretion rate (one indicator of possible renal 
dysfunction) was observed in hypertensives at a mean blood Pb of 
only 4.2 [mu]g/dL. These results provide suggestive evidence that 
the kidney may well be a target organ for effects from Pb in adults 
at current U.S. environmental exposure levels. The magnitude of the 
effect of Pb on renal function ranged from 0.2 to -1.8 mL/min change 
in creatinine clearance per 1.0 [mu]g/dL increase in blood Pb in 
general population studies. However, the full significance of this 
effect is unclear, given that other evidence of more marked signs of 
renal dysfunction have not been detected at blood Pb levels below 
30-40 [mu]g/dL among thousands of occupationally-exposed Pb workers 
that have been studied. (CD, p. 6-270)
---------------------------------------------------------------------------

     Other Pb associated effects in adults occurring at or just 
above 10 [mu]g/dL include hematological (e.g., impact on heme synthesis 
pathway) and neurological effects, with animal evidence providing 
support of Pb effects on these systems and evidence regarding mechanism 
of action. (CD, Sections 5.2, 5.3, 6.3 and 6.9.2)

B. Human Exposure and Health Risk Assessments

    This section presents a brief summary of the human exposure and 
health risk assessments conducted by EPA for this review. The complete 
full-scale assessment, which includes specific analyses conducted to 
address CASAC comments and advice on an earlier draft assessment, is 
presented in the final Risk Assessment Report (USEPA, 2007b).
    The focus of this Pb NAAQS risk assessment is on Pb derived from 
those sources emitting Pb to ambient air. The design and implementation 
of this assessment needed to address significant limitations and 
complexity that go far beyond the situation for similar assessments 
typically performed for other criteria pollutants. Not only was the 
risk assessment constrained by the timeframe allowed for this review in 
the context of breadth of information to address, it was also 
constrained by significant limitations in data and modeling tools for 
the assessment. Furthermore, the multimedia and persistent nature of 
Pb, and the role of multiple exposure pathways, add significant 
complexity to the assessment as compared to other assessments that 
focus only on the inhalation pathway.
    Due to the limited data, models, and time available, the risk 
assessment could not fully incorporate all of the important 
complexities associated with Pb. Consequently, in characterizing risk 
associated with the ambient air-related \29\ (policy-relevant) sources 
and exposures, simplifying assumptions were made in several areas. For 
example, people are also exposed to Pb that originates from nonair 
sources, including leaded paint or drinking water distribution systems. 
For this assessment, the Pb from these nonair sources is collectively 
referred to as ``policy-relevant background.'' 30 31 
Although deposition of airborne Pb is a major source of Pb in food (CD, 
p. 3-54) and may also contribute to Pb in drinking water, the 
contribution from air pathways to these nonair exposure pathways could 
not be explicitly modeled, and these contributions are treated as 
though they were part of the policy-relevant background. \32\ This 
means that some benefits associated with emissions reductions are 
excluded to the extent that reduced air emissions will eventually mean 
less Pb in water and food.
---------------------------------------------------------------------------

    \29\ Ambient air related sources are those emitting Pb into the 
ambient air (including resuspension of previously emitted Pb, that 
may include Pb paint from older buildings which has weathered and 
impacted outdoor soil with subsequent resuspension), and ambient air 
related exposures include inhalation of ambient air Pb as well as 
ingestion of Pb deposited out of the air (e.g., onto outdoor soil/
dust or indoor dust).
    \30\ This categorization of policy-relevant sources and 
background exposures is not intended to convey any particular policy 
decision at this stage regarding the Pb standard. Rather, it is 
simply intended to define the focus of this analysis.
    \31\ In the context of NAAQS for other criteria pollutants which 
are not multimedia in nature, such as ozone, the term policy-
relevant background is used to distinguish anthropogenic air 
emissions from naturally occurring non-anthropogenic emissions to 
separate pollution levels that can be controlled by U.S. regulations 
from levels that are generally uncontrollable by the United States 
(USEPA, 2007d). In the case of Pb, however, due to the multimedia, 
multipathway nature of human exposures to Pb, policy-relevant 
background is defined more broadly to include not only the ``quite 
low'' levels of naturally occurring Pb emissions into the air from 
non-anthropogenic sources such as volcanoes, sea salt, and windborne 
soil particles from areas free of anthropogenic activity, but also 
Pb from nonair sources, generally including leaded paint or drinking 
water distribution systems, which are collectively referred to in 
the risk assessment described here as ``policy-relevant background'' 
(USEPA, 2007b, p. 2-28, p. 1-3).
    \32\ Furthermore, although Pb from indoor paint is considered a 
component of policy-relevant background, for this analysis, it may 
be reflected somewhat in estimates developed for policy-relevant 
sources due to modeling constraints (see USEPA, 2007b).
---------------------------------------------------------------------------

    An overview of the human health risk assessment completed in the 
last review of the Pb NAAQS in 1990 (USEPA, 1990a) is presented first 
below, followed

[[Page 71501]]

by a summary of key aspects of the approach used in this assessment, 
including key limitations and uncertainties. The key assessment results 
are then summarized.
1. Overview of Risk Assessment From Last Review
    The risk assessment conducted in support of the last review used a 
case study approach to compare air quality scenarios in terms of their 
impact on the percentage of modeled populations that exceeded specific 
blood Pb levels chosen with consideration of the health effects 
evidence at that time (USEPA, 1990b; USEPA, 1989). The case studies in 
that analysis, however, focused exclusively on Pb smelters including 
two secondary and one primary smelter and did not consider exposures in 
a more general urban context. Additionally, the analysis focused on 
children (birth through 7 years of age) and middle-aged men. The 
assessment evaluated impacts of alternate NAAQS on numbers of children 
and men with blood Pb levels above levels of concern based on health 
effects evidence at that time. The primary difference between the risk 
assessment approach used in the current analysis and the assessment 
completed in 1990 involves the risk metric employed. Rather than 
estimating the percentage of study populations with exposures above 
blood Pb levels of interest as was done in the last review (i.e., 10, 
12 and 15 [mu]g/dL), the current analysis estimates changes in health 
risk, specifically IQ loss, associated with Pb exposure for child 
populations at each of the case study locations with that IQ loss 
further differentiated between background Pb exposure and policy-
relevant exposures.
2. Design Aspects of Exposure and Risk Assessments
    This section provides an overview of key elements of the assessment 
design, inputs, and methods, and includes identification of key 
uncertainties and limitations.
a. CASAC Advice
    The CASAC conducted a consultation on the draft analysis plan for 
the risk assessment (USEPA, 2006c) in June, 2006 (Henderson, 2006). 
Some key comments provided by CASAC members on the plan included: (1) 
Placing a higher priority on modeling the child IQ metric than the 
adult endpoints (e.g., cardiovascular effects), (2) recognizing the 
importance of indoor dust loading by Pb contained in outdoor air as a 
factor in Pb-related exposure and risk for sources considered in this 
analysis, and (3) concurring with use of the IEUBK biokinetic blood Pb 
model. Taking these comments into account, a pilot phase assessment was 
conducted to test the risk assessment methodology being developed for 
the subsequent full-scale assessment. The pilot phase assessment is 
described in the first draft Staff Paper and accompanying technical 
report (ICF 2006), which was discussed by the CASAC Pb panel on 
February 6-7 (Henderson, 2007a).
    Results from the pilot assessment, together with comments received 
from CASAC and the public, informed the design of the full-scale 
analysis. The full-scale analysis included a substitution of a more 
generalized urban case study for the location-specific near-roadway 
case study evaluated in the pilot. In addition, a number of changes 
were made in the exposure and risk assessment approaches, including the 
development of a new indoor dust Pb model focused specifically on urban 
residential locations and specification of additional IQ loss 
concentration-response (C-R) functions to provide greater coverage for 
potential impacts at lower exposure levels.
    The draft full-scale assessment was presented in the July 2007 
draft risk assessment report (USEPA, 2007a) that was released for 
public comment and provided to CASAC for review. In their review of the 
July draft risk assessment report, the CASAC Pb Panel made several 
recommendations for additional exposure and health risk analyses 
(Henderson, 2007b). These included a recommendation that the general 
urban case study be augmented by the inclusion of risk analyses in 
specific urban areas of the U.S. In this regard, they specifically 
stated the following (Henderson, 2007b, p. 3).

    * * * the CASAC strongly believes that it is important that EPA 
staff make estimates of exposure that will have national 
implications for, and relevance to, urban areas; and that, 
significantly, the case studies of both primary lead (Pb) smelter 
sites as well as secondary smelter sites, while relevant to a few 
atypical locations, do not meet the needs of supporting a Lead 
NAAQS. The Agency should also undertake case studies of several 
urban areas with varying lead exposure concentrations, based on the 
prototypic urban risk assessment that OAQPS produced in the 2nd 
Draft Lead Human Exposure and Health Risk Assessments. In order to 
estimate the magnitude of risk, the Agency should estimate exposures 
and convert these exposures to estimates of blood levels and IQ loss 
for children living in specific urban areas.

Hence, EPA included additional case studies in the risk assessment. 
Further, CASAC recommended using a concentration-response function with 
a change in slope near 7.5 [mu]g/dL. Accordingly, EPA included such an 
additional concentration-response function in the risk assessment. 
Results from the initial full-scale analyses, along with comments from 
CASAC, such as those described here, and the public resulted in a final 
version of the full-scale assessments which is summarized in this 
notice and presented in greater detail in the Risk Assessment Report 
and associated appendices (USEPA, 2007b). While these additional 
analyses were developed in response to CASAC recommendations, there has 
not been review of the completed analyses by CASAC.
b. Health Endpoint, Risk Metric and Concentration-Response Functions
    The health endpoint on which the quantitative health risk 
assessment focuses is developmental neurotoxicity in children, with IQ 
decrement as the risk metric. Among the wide variety of health 
endpoints associated with Pb exposures, there is general consensus that 
the developing nervous system in young children is the most sensitive 
and that neurobehavioral effects (specifically neurocognitive 
deficits), including IQ decrements, appear to occur at lower blood 
levels than previously believed (i.e., at levels < 10 [mu]g/dL). For 
example, the overall weight of the available evidence, described in the 
Criteria Document, provides clear substantiation of neurocognitive 
decrements being associated in young children with blood Pb levels in 
the range of 5 to 10 [mu]g/dL, and some analyses indicate Pb effects on 
intellectual attainment of young children ranging from 2 to 8 [mu]g/dL 
(CD, Sections 6.2, 8.4.2, and 8.4.2.6). That is, while blood Pb levels 
in U.S. children ages one to five years have decreased notably since 
the late 1970s, newer studies have investigated and reported 
associations of effects on the neurodevelopment of children with these 
more recent blood Pb levels (CD, Chapter 6).
    The evidence for neurotoxic effects in children is a robust 
combination of epidemiological and toxicological evidence (CD, Sections 
5.3, 6.2, and 8.5). The epidemiological evidence is supported by animal 
studies that substantiate the biological plausibility of the 
associations, and provides an understanding of mechanisms of action for 
the effects (CD, Section 8.4.2). The selection of children's IQ for the 
quantitative risk assessment reflects consideration of the evidence 
presented in the Criteria Document as well as advice received from 
CASAC (Henderson, 2006, 2007a).
    The epidemiological studies that have investigated blood Pb effects 
on IQ (see

[[Page 71502]]

CD, Section 6.2.3) have considered a variety of specific blood Pb 
metrics, including: (1) Blood concentration ``concurrent'' with the 
response assessment (e.g., at the time of IQ testing), (2) average 
blood concentration over the ``lifetime'' of the child at the time of 
response assessment (e.g., average of measurements taken over child's 
first 6 or 7 years), (3) peak blood concentration during a particular 
age range, and (4) early childhood blood concentration (e.g., the mean 
of measurements between 6 and 24 months age). All four specific blood 
Pb metrics have been correlated with IQ (see CD, p. 6-62; Lanphear et 
al., 2005). In the international pooled analysis by Lanphear and others 
(2005), however, the concurrent and lifetime averaged measurements were 
considered ``stronger predictors of lead-associated intellectual 
deficits than was maximal measured (peak) or early childhood blood lead 
concentrations,'' with the concurrent blood Pb level exhibiting the 
strongest relationship (CD, p. 6-29). It is not clear in this case, or 
for similar findings in other studies, whether the cognitive deficits 
observed were due to Pb exposure that occurred during early childhood 
or were a function of concurrent exposure. Nevertheless, concurrent 
blood Pb levels likely reflected both ongoing exposure and preexisting 
body burden (CD, p. 6-32).
    Given the evidence described in detail in the Criteria Document 
(Chapters 6 and 8), and in consideration of CASAC recommendations 
(Henderson, 2006, 2007a, 2007b), the risk assessment for this review 
relies on the functions presented by Lanphear and others (2005) that 
relate absolute IQ as a function of concurrent blood Pb or of the log 
of concurrent blood Pb, and lifetime average blood Pb, respectively. As 
discussed in the Criteria Document (CD, p. 8-63 to 8-64), the slope of 
the concentration-response relationship described by these functions is 
greater at the lower blood Pb levels (e.g., less than 10 [mu]g/dL). As 
discussed in the Criteria Document, threshold blood Pb levels for these 
effects cannot be discerned from the currently available 
epidemiological studies, and the evidence in the animal Pb 
neurotoxicity literature does not define a threshold for any of the 
toxic mechanisms of Pb (CD, Sections 5.3.7 and 6.2).
    In applying relationships observed with the pooled analysis 
(Lanphear et al., 2005) to the risk assessment, which includes blood Pb 
levels below the range represented by the pooled analysis, several 
alternative blood Pb concentration-response models were considered in 
recognition of a reduced confidence in our ability to characterize the 
quantitative blood Pb concentration-response relationship at the lowest 
blood Pb levels represented in the recent epidemiological studies. The 
functions considered and employed in the initial risk analyses for this 
review include the following.
     Log-linear function with low-exposure linearization, for 
both concurrent and lifetime average blood metrics, applies the 
nonlinear relationship down to the blood Pb concentration representing 
the lower bound of blood Pb levels for that blood metric in the pooled 
analysis and applies the slope of the tangent at that point to blood Pb 
concentrations estimated in the risk assessment to fall below that 
level.
     Log-linear function with cutpoint, for both concurrent and 
lifetime average blood metrics, also applies the nonlinear relationship 
at blood Pb concentrations above the lower bound of blood Pb 
concentrations in the pooled analysis dataset for that blood metric, 
but then applies zero risk to all lower blood Pb concentrations 
estimated in the risk assessment.
    In the additional risk analyses performed subsequent to the August 
2007 CASAC public meeting, the two functions listed above and the 
following two functions were employed (see Section 5.3.1 of the Risk 
Assessment Report for details on the forms of these functions as 
applied in this risk assessment).
     Population stratified dual linear function for concurrent 
blood Pb, derived from the pooled dataset stratified at peak blood Pb 
of 10 [mu]g/dL and
     Population stratified dual linear function for concurrent 
blood Pb, derived from the pooled dataset stratified at 7.5 [mu]g/dL 
peak blood Pb.
    In interpreting risk estimates derived using the various functions, 
consideration should be given to the uncertainties with regard to the 
precision of the coefficients used for each analysis. The coefficients 
for the log-linear model from Lanphear et al. (2005) had undergone a 
careful development process, including sensitivity analyses, using all 
available data from 1,333 children. The shape of the exposure-response 
relationship was first assessed through tests of linearity, then by 
evaluating the restricted cubic spline model. After determining that 
the log-linear model provided a good fit to the data, covariates to 
adjust for potential confounding were included in the log-linear model 
with careful consideration of the stability of the parameter estimates. 
After the multiple regression models were developed, regression 
diagnostics were employed to ascertain whether the Pb coefficients were 
affected by collinearity or influential observations. To further 
investigate the stability of the model, a random-effects model (with 
sites random) was applied to evaluate the results and also the effect 
of omitting one of the seven cohorts on the Pb coefficient. In the 
various sensitivity analyses performed, the coefficient from the log-
linear model was found to be robust and stable. The log-linear model, 
however, is not biologically plausible at very low blood Pb 
concentrations as they approach zero; therefore, in the first two 
functions the log-linear model is applied down to a cutpoint (of 1 
[mu]g/dL for the concurrent blood Pb metric), selected based on the low 
end of the blood Pb levels in the pooled dataset, followed by a 
linearization or an assumption of zero risk at levels below that point.
    In contrast, the coefficients from the two analyses using the 
population stratified dual linear function with stratification at 7.5 
[mu]g/dL and 10 [mu]g/dL, peak blood Pb, have not undergone such 
careful development. These analyses were primarily done to compare the 
lead-associated decrement at lower blood Pb concentrations and higher 
blood Pb concentrations. For these analyses, the study population was 
stratified at the specified peak blood Pb level and separate linear 
models were fitted to the concurrent blood Pb data for the children in 
the two study population subgroups. The fit of the model or sensitivity 
analyses were not conducted (or reported) on these coefficients. While 
these analyses are quite suitable for the purpose of investigating 
whether the slope at lower concentration levels are greater compared to 
higher concentration levels, use of such coefficients in a risk 
analysis to assess public health impact may be inappropriate. Further, 
only 103 children had maximal blood Pb levels less than 7.5 [mu]g/dL 
and 244 children had maximal blood Pb levels less than 10 [mu]g/dL. 
While these children may better represent current blood Pb levels, not 
fitting a single model using all available data may lead to bias. Slob 
et al. (2005) noted that the usual argument for not considering data 
from the high dose range is that different biological mechanisms may 
play a role at higher doses compared to lower doses. However, this does 
not mean a single curve across the entire exposure range cannot 
describe the relationship. The fitted curve merely assumes that the 
underlying dose-response follows a

[[Page 71503]]

smooth curve over the whole dose range. If biological mechanisms change 
when going from lower to higher doses, this change will result in a 
gradually changing slope of the dose-response. The major strength of 
the Lanphear et al. (2005) study was the large sample size and the 
pooled analysis of data from seven different cohorts. In the case of 
the study population subgroup with peak blood Pb below 7.5 [mu]g/dL, 
less than 10% of the available data is used in the analysis, with more 
than half of the data coming from one cohort (Rochester) and the six 
other cohorts contributing zero to 13 children to the analysis. Such an 
analysis dissipates the strength of the Lanphear et al. study.
    In consideration of the preceding discussion, greater confidence is 
placed in the log-linear model form compared to the dual-linear 
stratified models for purposes of the risk assessment described in this 
notice. Further, in considering risk estimates derived from the four 
core functions (log-linear function with low-exposure linearization, 
log-linear function with cutpoint, dual linear function, stratified at 
7.5 [mu]g/dL peak blood Pb, and dual linear function, stratified at 10 
[mu]g/dL peak blood Pb), greatest confidence is assigned to risk 
estimates derived using the log-linear function with low-exposure 
linearization since this function (a) is a nonlinear function that 
describes greater response per unit blood Pb at lower blood Pb levels 
consistent with multiple studies identified in the discussion above, 
(b) is based on fitting a function to the entire pooled dataset (and 
hence uses all of the data in describing response across the range of 
exposures), (c) is supported by sensitivity analyses showing the model 
coefficients to be robust, and (d) provides an approach for predicting 
IQ loss at the lowest exposures simulated in the assessment (consistent 
with the lack of evidence for a threshold). Note, however, that risk 
estimates generated using the other three concentration-response 
functions are also presented to provide perspective on the impact of 
uncertainty in this key modeling step.
c. Case Study Approach
    For the risk assessment described in this notice, a case study 
approach was employed as described in Sections 2.2 (and subsections) 
and 5.1.3 of the Risk Assessment Report (USEPA, 2007b). The four types 
of case studies included in the assessment are the following:
     Location-specific urban case studies: Three urban case 
studies focus on specific urban areas (Cleveland, Chicago and Los 
Angeles) to provide perspectives on the magnitude of ambient air Pb-
related risk in specific urban locations. Ambient air Pb concentrations 
are characterized using source-oriented and other Pb-TSP monitors in 
these cities. As stated above, these case studies were developed in 
response to CASAC recommendations and there has not been review of the 
completed analyses for these case studies by CASAC
     General urban case study: The general urban case study is 
a nonlocation-specific analysis that uses several simplifying 
assumptions regarding ambient air Pb levels and demographics to produce 
a simplified representation of urban areas.
     Primary Pb smelter case study: \33\ This case study 
estimates risk for children living in an area currently not in 
attainment with the current NAAQS, that is impacted by Pb emissions 
from a primary Pb smelter. As such, this case study characterizes risk 
for a specific highly exposed population and also provides insights on 
risk to child populations living in areas near large sources of Pb 
emissions.
---------------------------------------------------------------------------

    \33\ See Section III.B.2.a for a summary of CASAC's comment with 
regard to the primary and secondary Pb smelter case studies.
---------------------------------------------------------------------------

     Secondary Pb smelter case study: \34\ This case study was 
included in the initial analyses for the full-scale assessment as an 
example of areas influenced by smaller point sources of Pb emissions. 
As discussed in Section III.B.2.g below, however, a variety of 
significant limitations in the approaches employed for this case and 
associated large uncertainties in these results are recognized that 
preclude considering this case study to be illustrative of the larger 
set of areas influenced by similarly sized Pb sources. Risk estimates 
for this case study (presented in detail in the Risk Assessment Report 
(USEPA, 2007b)) are lower than those for the other case studies.
---------------------------------------------------------------------------

    \34\ See Section III.B.2.a for a summary of CASAC's comment with 
regard to the primary and secondary Pb smelter case studies.
---------------------------------------------------------------------------

d. Air Quality Scenarios
    Air quality scenarios assessed include (a) a current conditions 
scenario for the location-specific urban case studies, the general 
urban case study and the secondary Pb smelter case study, (b) a current 
NAAQS scenario for the location-specific urban case studies, the 
general urban case study and the primary Pb smelter case study, and (c) 
a range of alternative NAAQS scenarios for all case studies. The 
alternative NAAQS scenarios include levels of 0.5, 0.2, 0.05, and 0.02 
[mu]g/m\3\, with a monthly averaging time, as well as a level of 0.2 
[mu]g/m\3\ scenario using a quarterly averaging time.\35\ The current 
NAAQS scenario for the urban case studies assumes ambient air Pb 
concentrations higher than actual current conditions. While it is 
extremely unlikely that Pb concentrations in urban areas would rise to 
meet the current NAAQS and there are limitations and uncertainties 
associated with the approach used (as described in Section III.B.2.g 
below), this scenario was included to provide some perspective on risks 
associated with just meeting the current NAAQS relative to current 
conditions. When evaluating these results it is important to keep the 
limitations and uncertainties in mind.
---------------------------------------------------------------------------

    \35\ For further discussion of the air quality scenarios and 
averaging times included in the risk assessment, see section 2.3.1 
of the Risk Assessment Report (USEPA, 2007b)
---------------------------------------------------------------------------

    Current conditions for the three location-specific urban case 
studies in terms of maximum quarterly average air Pb concentrations are 
0.09, 0.14 and 0.36 [mu]g/m\3\ for the study areas in Los Angeles, 
Chicago and Cleveland, respectively. In terms of maximum monthly 
average the values are 0.17 [mu]g/m\3\, 0.31 [mu]g/m\3\ and 0.56 [mu]g/
m\3\ for the study areas in Los Angeles, Chicago and Cleveland, 
respectively. Two current conditions scenarios were considered for the 
general urban case study: One based on the mean value for ambient air 
Pb levels in large urban areas (0.14 [mu]g/m\3\ as a maximum quarterly 
average) and a high-end ambient air Pb level in large urban areas (0.87 
[mu]g/m\3\ as a maximum quarterly average).
    Details of the assessment scenarios, including a description of the 
derivation of Pb concentrations for air and other media are presented 
in Sections 2.3 (and subsections) and Section 5.1.1 of the Risk 
Assessment Report (USEPA, 2007b).
e. Categorization of Policy-Relevant Exposure Pathways
    To inform policy aspects of the Pb NAAQS review, the assessment 
estimates for blood Pb and IQ loss were divided into two components: 
The fraction associated with policy-relevant pathways, which include 
inhalation, outdoor soil/dust ingestion and indoor dust ingestion, and 
the fraction associated with background (e.g., diet and drinking 
water). The policy-relevant pathways are further divided into two 
categories, ``recent air'' and ``past air''. Conceptually, the recent 
air category includes those pathways involving Pb that is or has 
recently been in the outdoor ambient air, including inhalation and 
ingestion of indoor dust Pb derived from recent ambient air (i.e.,

[[Page 71504]]

air Pb that has penetrated into the residence recently and loaded 
indoor dust). Past air includes exposure contributions from ingestion 
of outdoor soil/dust that is contacted on surfaces outdoors, and 
ingestion of indoor dust Pb that is derived from past air sources 
(i.e., impacts from Pb that was in the ambient air in the past and has 
not been recently resuspended into ambient air). In this assessment, as 
discussed further below, that portion of indoor dust Pb not associated 
with recent air, is classified as ``other'' and, due to technical 
limitations includes not only past air impacts, but also contributions 
from indoor Pb paint. In the risk assessment, estimates of contribution 
to blood Pb and IQ loss were developed for the following pathways or 
pathway combinations:
     Inhalation of ambient air Pb (i.e., ``recent air'' Pb): 
This is derived using the blood Pb estimate resulting from Pb exposure 
limited to the inhalation pathway (and will include exposures to Pb in 
ambient air from all sources contributing to the ambient air 
concentration estimate).
     Ingestion of ``recent air'' indoor dust Pb: This is 
derived using the blood Pb estimate resulting from Pb exposure limited 
to ingestion of the Pb in indoor dust that is predicted to be 
associated with ambient air concentrations (i.e., via the air 
concentration coefficient in the regression-based dust models or via 
the mechanistic component of the hybrid blood Pb model (see Section 
3.1.4 of the Risk Assessment Report). For the primary Pb smelter case 
study, estimates for this pathway are not separated from estimates for 
the pathway described in the subsequent bullet due to uncertainty 
regarding this categorization with the model used for this case study 
(Section 3.1.4.2 of the Risk Assessment Report).
     Ingestion of ``other'' indoor dust Pb: This is derived 
using the blood Pb estimate resulting from Pb exposure limited to 
ingestion of the Pb in indoor dust that is not predicted to be 
associated with ambient air concentrations (i.e., that predicted by the 
intercept in the dust models plus that predicted by the outdoor soil 
concentration coefficient, for models that include an intercept 
(Section 3.1.4 of the Risk Assessment Report)). This is interpreted to 
represent indoor paint, outdoor soil/dust, and additional sources of Pb 
to indoor dust including historical air (see Risk Assessment Report, 
Section 2.4.3). As the intercept in regression dust models will be 
inclusive of error associated with the model coefficients, this 
category also includes some representation of dust Pb associated with 
current ambient air concentrations (described in previous bullet). For 
the primary Pb smelter case study, estimates for this pathway are not 
separated from estimates for the pathway described above due to 
uncertainty regarding this categorization with the model used for this 
case study (Risk Assessment Report, Section 3.1.4.2). This pathway is 
included in the ``past air'' category.
     Ingestion of outdoor soil/dust Pb: This is derived using 
the blood Pb estimate resulting from Pb exposure limited to ingestion 
of outdoor soil/dust Pb. This pathway is included in the ``past air'' 
category (and could include contamination from historic Pb emissions 
from automobiles and Pb paint).
     Ingestion of drinking water Pb: This is derived using the 
blood Pb estimate resulting from Pb exposure limited to ingestion of 
drinking water Pb. This pathway is included in the policy-relevant 
background category.
     Ingestion of dietary Pb: This is derived using the blood 
Pb estimate resulting from Pb exposure limited to ingestion of dietary 
Pb. This pathway is included in the policy-relevant background 
category.
    In simulating reductions in exposure associated with reducing 
ambient air Pb levels through alternative NAAQS (and increases in 
exposure if the current NAAQS was reached in certain case studies), 
modeling for the assessment has only affected the exposure pathways 
categorized as recent air (inhalation and ingestion of that portion of 
indoor dust associated with outdoor ambient air). The assessment has 
not simulated decreases in past air-related exposure pathways (e.g., 
reductions in outdoor soil Pb levels following reduction in ambient air 
Pb levels and a subsequent decrease in exposure through incidental soil 
ingestion and the contribution of outdoor soil to indoor dust). This 
aspect of the analysis will tend to underestimate the reductions in 
risk associated with alternative NAAQS. However, this does not mean 
that overall risk has been underestimated. The net effect of all 
sources of uncertainty or bias in the analysis, which may also tend to 
under- or overestimate risk, could not be quantified.
    Additionally, there is uncertainty related to parsing out exposure 
and risk between background and policy-relevant exposure pathways (and 
subsequent parsing of recent air and past air) resulting from a number 
of technical limitations. Key among these is that, while conceptually, 
indoor Pb paint contributions to indoor dust Pb would be considered 
background and included in modeling background exposures, due to 
technical limitations related to indoor dust Pb modeling, ultimately, 
Pb paint was included as part of ``other'' indoor dust Pb (i.e., as 
part of past air exposure). The inclusion of indoor lead Pb as a 
component of ``other'' indoor air (and consequently as a component of 
``past air'' exposure) represents a source of potential high bias in 
our prediction of total exposure and risk associated with past air 
because conceptually, exposure to indoor paint Pb is considered part of 
background exposure.
    In summary, because of limitations in the assessment design, data 
and modeling tools, the risk attributable to policy-relevant exposure 
pathways is bounded on the low end by the risk estimated for the 
``recent air'' category and on the upper end by the risk estimated for 
the ``recent air'' plus ``past air'' categories.
f. Analytical Steps
    The risk assessment includes four analytical steps, briefly 
described below and presented in detail in Sections 2.4.4, 3.1, 3.2, 
4.1, and 5.1 of the Risk Assessment Report (USEPA, 2007b).
     Characterization of Pb in ambient air: The 
characterization of outdoor ambient air Pb levels uses different 
approaches depending on the case study (as explained in more detail 
below): (a) Source-oriented and non-source oriented monitors are 
assumed to represent different exposure zones in the city-specific case 
studies, (b) a single exposure level is assumed, based on monitoring 
data for various cities, for the general urban case study, and (c) 
ambient levels are estimated using air dispersion modeling based on Pb 
emissions from a particular facility in the point source case studies.
     Characterization of outdoor soil/dust and indoor dust Pb 
concentrations: Outdoor soil Pb levels are estimated using empirical 
data and/or fate and transport modeling. Indoor dust Pb levels are 
predicted using a combination of (a) regression-based models that 
relate indoor dust to ambient air Pb and/or outdoor soil Pb, and (b) 
mechanistic models.\36\
---------------------------------------------------------------------------

    \36\ Additional detail on the methods used in characterizing Pb 
concentrations in outdoor soil and indoor dust are presented in 
Sections 3.1.3 and 3.1.4 of the Risk Assessment, respectively. Data, 
methods and assumptions here used in characterizing Pb 
concentrations in these exposure media may differ from those in 
other analyses that serve different purposes.
---------------------------------------------------------------------------

     Characterization of blood Pb levels: Blood Pb levels for 
each exposure zone are derived from central-tendency blood Pb 
concentrations estimated using the

[[Page 71505]]

Integrated Exposure and Uptake Biokinetic (IEUBK) model, and concurrent 
or lifetime average blood Pb is estimated from these outputs as 
described in Section 3.2.1.1 of the Risk Assessment Report (USEPA, 
2007b). For the point source and location-specific urban case studies, 
a probabilistic exposure model is used to generate population 
distributions of blood Pb concentrations based on: (a) The central 
tendency blood Pb levels for each exposure zone, (b) demographic data 
for the distribution of children (less than 7 years of age) across 
exposure zones in a study area, and (c) a geometric standard deviation 
(GSD) intended to characterize interindividual variability in blood Pb 
(e.g., reflecting differences in behavior and biokinetics related to 
Pb). For the general urban case study, as demographic data for a 
specific location are not considered, the GSD is applied directly to 
the central tendency blood Pb level to estimate a population 
distribution of blood Pb levels. Additional detail on the methods used 
to model population blood Pb levels is presented in Sections 3.2.2 and 
5.2.2.3 of the Risk Assessment Report (USEPA, 2007b).
     Risk characterization (estimating IQ loss): Concurrent or 
lifetime average blood Pb estimates for each simulated child in each 
case study population are converted into total Pb-related IQ loss 
estimates using the concentration-response functions described above.
    Key limitations and uncertainties associated with the application 
of these specific analytical steps are summarized in Section III.B.2.g 
below.
g. Generating Multiple Sets of Risk Results
    In the initial analyses for the full-scale assessment (USEPA, 
2007a), EPA implemented multiple modeling approaches for each case 
study scenario in an effort to characterize the potential impact on 
exposure and risk estimates of uncertainty associated with the 
limitations in the tools, data and methods available for this risk 
assessment and with key analytical steps in the modeling approach. 
These multiple modeling approaches are described in Section 2.4.6.2 of 
the final Risk Assessment Report (USEPA, 2007b). In consideration of 
comments provided by CASAC (Henderson, 2007b) on these analyses 
regarding which modeling approach they felt had greater scientific 
support, a pared down set of modeling combinations was identified as 
the core approach for the subsequent analyses. This core modeling 
approach includes the following key elements:
     Ambient air Pb estimates (based on monitors or modeling 
and proportional rollbacks, as described below),
     Background exposure from food and water (as described 
above),
     The hybrid indoor dust model specifically developed for 
urban residential applications (which predicts Pb in indoor dust as a 
function of ambient air Pb and nonair contribution),
     The IEUBK blood Pb model (which predicts blood Pb in young 
children exposed to Pb from multiple exposure pathways),
     The concurrent blood Pb metric,
     A GSD for concurrent blood Pb of 2.1 to characterize 
interindividual variability in blood Pb levels for a given ambient 
level, and
     four different functions relating concurrent blood Pb to 
IQ loss, including two log-linear models (one with a cutpoint and one 
with low-exposure linearization) and two dual-linear models with 
stratification, one stratified at 7.5 [mu]g/dL peak blood Pb and the 
other at 10 [mu]g/dL peak blood Pb.
    For each case study, the core modeling approach employs a single 
set of modeling elements to estimate exposure and the four different 
concentration-response functions referenced above to derive four sets 
of risk results from the single set of exposure estimates. The spread 
of estimates resulting from application of all four functions captures 
much of the uncertainty associated model choice in this analytical 
step. Among these four functions, greater confidence is associated with 
estimates derived using the log-linear with low-exposure linearization 
concentration-response function as discussed above.
    In addition to employing multiple concentration-response functions, 
the assessment includes various sensitivity analyses to characterize 
the potential impact of uncertainty in other key analysis steps on 
exposure and risk estimates. The sensitivity analyses and uncertainty 
characterization completed for the risk analysis are described in 
Sections 3.5, 4.3, 5.2.5 and 5.3.3 of the Risk Assessment Report 
(USEPA, 2007b).
h. Key Limitations and Uncertainties
    As recognized above, EPA has made simplifying assumptions in 
several areas of this assessment due to the limited data, models, and 
time available. These assumptions and related limitations and 
uncertainties are described in the Risk Assessment Report (USEPA, 
2007b). Key assumptions, limitations and uncertainties are briefly 
identified below. EPA considers these aspects of the assessment to be 
important to the interpretation of the exposure and risk estimates. In 
the presentation below, limitations (and associated uncertainty) are 
listed, beginning with those regarding design of the assessment or case 
studies, followed by those regarding estimation of Pb concentrations in 
ambient air indoor dust, outdoor soil/dust, and blood, and lastly 
regarding estimation of Pb-related IQ Loss.
     Temporal aspects: Exposure for the simulated child 
population begins at birth (including a prenatal maternal contribution) 
and continues for 7 years, with Pb concentrations in all exposure media 
remaining constant throughout the period, and children residing in the 
same exposure zone throughout the period. In characterizing exposure 
media concentrations, annual averages are derived and held constant 
through the seven year period. Exposure factors and physiological 
parameters vary with age of the cohort through the seven year exposure 
period, several exposure factors and physiological parameters are 
varied on an annual basis within the blood Pb modeling step. These 
aspects are a simplification of population exposures that contributes 
some uncertainty to our exposure and risk estimates.
     General urban case study: This case study differs from the 
others in several ways. It is by definition a general case study and 
not based on a specific location. There is a single exposure zone for 
the case study within which all media concentrations of Pb are assumed 
to be spatially uniform; that is, no spatial variation within the area 
is simulated. Additionally, the case study does not rely on any 
specific demographic values. Within the single exposure zone a 
theoretical population of unspecified size is assumed to be uniformly 
distributed. Thus this case study is a simplified representation of 
urban areas intended to inform our assessment of the impact of changes 
in ambient Pb concentrations on risk, but which carries with it 
attendant uncertainties in our interpretation of the associated 
exposure and risk estimates. For example, the risk estimates for this 
case study, while generally representative of an urban residential 
population exposed to the specified ambient air Pb levels, cannot be 
readily related to a specific urban population. Specific urban 
populations are spatially distributed in a nonuniform pattern and 
experience ambient air Pb levels that vary through time and space. 
Consequently, interpretations of the associated blood Pb and risk 
estimates with regard to their relevance to specific urban residential 
exposures carry

[[Page 71506]]

substantial uncertainty and presumably an upward bias in risk, 
particularly for large areas, across which air concentrations may vary 
substantially.
     Point source case studies: Dispersion modeling was used to 
characterize ambient air Pb levels in the point source case studies. 
This approach simulates spatial gradients related to dispersion and 
deposition of Pb from emitting sources. The details of this modeling is 
presented in the Risk Assessment Report (USEPA, 2007b). In the case of 
the point sources modeled, sources were limited to those associated 
with the smelter operations, and did not include other sources such as 
resuspension of roadside Pb not related to facility operations, and 
other stationary sources of Pb within or near the study area. This 
means that, with distance from the facility, there is likely 
underestimation of ambient air-related Pb exposure because with 
increased distance from the facility there would be increasing 
influence of other sources relative to that of the facility. This 
limitation is likely to have more significant impact on risk estimates 
associated with the full study than on those for the subareas (which 
are the portions of the study area with 1.5 km from the smelter 
facilities), and to perhaps have a more significant impact on risk 
estimates associated with the smaller secondary Pb smelter (see below). 
As noted above, in their review of the July draft risk assessment 
report, the CASAC Pb Panel made several recommendations for additional 
exposure and health risk analyses (Henderson, 2007b), including a 
recommendation that the general urban case study be augmented by the 
inclusion of risk analyses in specific urban areas of the U.S. In this 
regard, they specifically stated the following (Henderson, 2007b, p. 
3):

The CASAC strongly believes that it is important that EPA staff make 
estimates of exposure that will have national implications for, and 
relevance to, urban areas; and that, significantly, the case studies 
of both primary lead (Pb) smelter sites as well as secondary smelter 
sites, while relevant to a few atypical locations, do not meet the 
needs of supporting a Lead NAAQS. The Agency should also undertake 
case studies of several urban areas with varying lead exposure 
concentrations, based on the prototypic urban risk assessment that 
OAQPS produced in the 2nd Draft Lead Human Exposure and Health Risk 
Assessments.

     Secondary Pb smelter case study: Air Pb concentration 
estimates derived from the air dispersion modeling completed for the 
secondary Pb smelter case study are subject to appreciably greater 
uncertainty than that for those for the primary Pb smelter case study 
due to a number of factors, including: (a) A more limited and less 
detailed accounting of emissions and emissions sources associated with 
the facility (particularly fugitive emissions), (b) a lack of prior air 
quality modeling analyses and performance analyses, and (c) a 
substantially smaller number of Pb-TSP monitors in the area that could 
be used to evaluate and provide confidence in model performance.\37\ 
Further, as mentioned in the previous bullet, no air sources of Pb 
other than those associated with the facility were accounted for in the 
modeling. Given the relatively smaller magnitude of emissions from the 
secondary Pb smelter, the underestimating potential of this limitation 
with regard to air concentrations with distance from the facility has a 
greater relative impact on risk estimates for this case study than for 
the primary Pb smelter case study. The aggregate uncertainty of all of 
these factors results in low confidence in estimates for this case 
study. It is observed that exposure and risk estimates are lower than 
those for the other case studies. Although this case study was 
initially intended to be used as an example of areas near stationary 
sources of intermediate size (smaller than the primary Pb smelter), 
experience with this analysis indicates that substantially more data 
and multiple case studies differing in several aspects would be needed 
to broadly characterize risks for such a category of Pb exposure 
scenarios.
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    \37\ The information supporting the air dispersion modeling for 
the primary Pb smelter case study provides substantially greater 
confidence in estimates for that case study.
---------------------------------------------------------------------------

     Location-specific urban case studies: The Pb-TSP 
monitoring network is currently quite limited. The number of monitors 
available to represent air concentrations in these case studies ranged 
from six for Cleveland to 11 for Chicago. Accordingly, our estimates of 
the magnitude of and spatial variation of air Pb concentrations are 
subject to uncertainty associated with the limited data. In applying 
the available data to each of these case studies, exposure zones, one 
corresponding to each monitor, were created and U.S. Census block 
groups (and the children within those demographic units) were 
distributed among the exposure zones. The details of the approach used 
are described in Section 5.1.3 of the Risk Assessment Report (USEPA, 
2007b). Although this approach provides a spatial gradient across the 
study area due to differences in monitor values for each exposure zone, 
this approach assumes a constant concentration within each exposure 
zone (i.e., no spatial gradient within a zone). Additionally, the 
nearest neighbor approach to assign block groups to exposure zones 
assumes that a monitor adequately represents all locations that are 
closer to that monitor than to any of the others in the study area. In 
reality, across block groups there are more variable spatial gradients 
in a study area than those reflected in the approach used here. This 
introduces significant uncertainty into the characterization of risk 
for the urban case studies. As recognized in Section, III.B.2.a, the 
analyses for these case studies were developed in response to CASAC 
recommendations on the July 2007 draft Risk Assessment (Henderson, 
2007b) and there has not been review of the completed analyses by 
CASAC.
     Current NAAQS air quality scenarios: For the location-
specific urban case studies, proportional roll-up procedures were used 
to adjust ambient air Pb concentrations up to just meet the current 
NAAQS (see Sections 2.3.1 and 5.2.2.1 of the Risk Assessment Report, 
USEPA, 2007b, for detailed discussion). EPA recognizes that it is 
extremely unlikely that Pb concentrations in urban areas would rise to 
meet the current NAAQS and that there is substantial uncertainty with 
our simulation of such conditions. In these case studies a proportional 
roll-up was simulated, such that it is assumed that the current spatial 
distribution of air concentrations (as characterized by the current 
data) is maintained and increased Pb emissions contribute to increased 
Pb concentrations, the highest of which just meets the current 
standard. There are many other types of changes within a study area 
that could result in a similar outcome such as increases in emissions 
from just one specific industrial operation that could lead to air 
concentrations in a part of the study area that just meet the current 
NAAQS, while the remainder of the study area remained largely unchanged 
(at current conditions). For the primary Pb smelter case study, where 
current conditions exceed the current NAAQS, attainment of the current 
NAAQS was simulated using air quality modeling, emissions and source 
parameters used in developing the 2007 proposed revision to the State 
Implementation Plan for the area (see Section 3.1.1.2 of the Risk 
Assessment Report (USEPA, 2007b)).
     Alternative NAAQS air quality scenarios: In all case 
studies, proportional roll-down procedures were used to adjust ambient 
air Pb concentrations downward to attain

[[Page 71507]]

alternative NAAQS (see Sections 2.3.1 and 5.2.2.1 of the Risk 
Assessment Report, USEPA, 2007b). There is significant uncertainty in 
simulating conditions associated with the implementation of emissions 
reduction actions to meet a lower standard. There are a variety of 
changes other than that represented by a proportional roll-down that 
could result in air concentrations that just meet lower alternative 
standards. For example, control measures might be targeted only at the 
specific area exceeding the standard, resulting in a reduction of air 
Pb concentrations to the alternate standard while concentrations in the 
rest of the study area remain unchanged (at current conditions). 
Consequently, there is significant uncertainty associated with 
estimates for the alternate NAAQS scenarios.
     Estimates of outdoor soil/dust Pb concentrations: Outdoor 
soil Pb concentration for both the urban case studies and the primary 
Pb smelter case study are based on empirical data (see Section 3.1.3 of 
the Risk Assessment). To the extent that the underlying sampling data 
included areas containing older structures, the impact of Pb paint 
weathered from older structures on soil Pb levels will be reflected in 
these empirical estimates. In the case of the urban case studies, a 
mean value from a sample of houses built between 1940 and 1998 was used 
to represent soil Pb levels (see Section 3.1.3.1 of the Risk 
Assessment). Outdoor soil/dust Pb concentrations in all air quality 
scenarios have been set equal to the values for the current conditions 
scenarios. An impact of changes in air Pb concentrations on soil 
concentrations, and the associated impact on dust concentrations, blood 
Pb and risk estimates were not simulated. In areas where air 
concentrations have been greater in the past, however, implementation 
of a reduced NAAQS might be expected to yield reduced soil Pb levels 
over the long term. As described in Section 2.3.3 of the Risk 
Assessment Report (USEPA, 2007b), however, there is potentially 
significant uncertainty associated with this specification, 
particularly with regard to implications for areas in which a Pb source 
may locate where one of comparable size had not been previously. 
Additionally, it is possible that control measures implemented to meet 
alternative NAAQS may result in changes to soil Pb concentrations; 
these are not reflected in the assessment.
     Estimates of indoor dust Pb concentrations for the urban 
case studies (application of the hybrid model): The hybrid mechanistic-
empirical model for estimating indoor dust Pb for the urban case 
studies (see Section 3.1.4.1 of the Risk Assessment Report, USEPA, 
2007b) has several sources of uncertainty that could significantly 
impact its estimates. These include: (a) Failure to consider house-to-
house variability in factors related to infiltration of outdoor ambient 
air Pb indoors and subsequent buildup on indoor surfaces, (b) 
limitations in data available on the rates and efficiency of indoor 
dust cleaning and removal, (c) limitations in the method for converting 
model estimates of dust Pb loading to dust Pb concentration needed for 
blood Pb modeling, and (d) the approach employed to partition estimates 
of dust Pb concentration into ``recent air'' and ``other'' components 
(see Section 5.3.3.4 of the Risk Assessment Report, USEPA, 2007b). 
These last two sources of uncertainty reduce our confidence in 
estimates of apportionment of dust Pb between ``recent air'' and 
``other''. In recognition of this limitation, in evaluating exposure 
and risk reduction trends related to reducing ambient air Pb levels, 
focus has been placed on changes in total blood Pb rather than on 
estimates of ``recent air'' blood Pb.
     Estimates of indoor dust Pb concentrations for the primary 
Pb smelter case study (application of the site-specific regression 
model): There is uncertainty associated with the site-specific 
regression model applied in the remediation zone (see Section 3.1.4.2 
of the Risk Assessment Report), and relatively greater uncertainty 
associated with its application to air quality scenarios that simulate 
notably lower air Pb levels. Limitations in the dataset from which the 
model was derived limited its form to that of a simple regression that 
predicts dust Pb concentration as a function of air Pb concentration 
plus a constant (intercept). However there may be variables in addition 
to air that influence dust Pb concentrations and their absence in the 
regression contributes uncertainty to the resulting estimates. To the 
extent that these unaccounted-for variables are spatially related to 
the smelter facility Pb sources, our estimates could be biased, not 
with regard to the absolute dust Pb concentration, but with regard to 
differences in dust Pb concentration estimate between different air 
quality scenarios. Those differences may be overestimated because of 
potential overestimation of the air coefficient and underestimation of 
the intercept in the regression model. Examples of such unaccounted-for 
variables are roadside dust Pb and historical contributions to current 
levels of indoor dust Pb (e.g., Pb that entered a house in the past and 
continues to contribute to current dust Pb levels).
     Characterizing interindividual variability using a GSD: 
There is uncertainty associated with the GSD specified for each case 
study (see Sections 3.2.3 and 5.2.2.3 of the Risk Assessment Report). 
Two factors are described here as contributors to that uncertainty. 
Interindividual variability in blood Pb levels for any study population 
(as described by the GSD) will reflect, to a certain extent, spatial 
variation in media concentrations, including outdoor ambient air Pb 
levels and indoor dust Pb levels. For each case study, there is 
significant uncertainty in the specification of spatial variability in 
ambient air Pb levels and associated indoor dust Pb levels, as noted 
above. In addition, there are a limited number of datasets for 
different types of residential child populations from which a GSD can 
be derived (e.g., NHANES datasets \38\ for more heterogeneous 
populations and individual study datasets for likely more homogeneous 
populations near specific industrial Pb sources). This uncertainty 
associated with the GSDs introduces significant uncertainty in exposure 
and risk estimates for the 95th population percentile.
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    \38\ For example, the GSD for the urban case studies, in the 
risk assessment described in this notice, was derived using NHANES 
data for the years 1999-2000.
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     Exposure pathway apportionment for higher percentile blood 
Pb level and IQ loss estimates: Apportionment of blood Pb levels for 
higher population percentiles is assumed to be the same as that 
estimated using the central tendency estimate of blood Pb in an 
exposure zone. This introduces significant uncertainty into projections 
of pathway apportionment for higher population percentiles of blood Pb 
and IQ loss. In reality, pathway apportionment may differ in higher 
exposure percentiles. For example, paint and/or drinking water 
exposures may increase in importance, with air-related contributions 
decreasing as an overall percentage of blood Pb levels and associated 
risk. Because of this uncertainty related to pathway apportionment, as 
mentioned earlier, greater confidence is placed in estimates of total 
Pb exposure and risk in evaluating the impact of the current NAAQS and 
alternative NAAQS relative to current conditions.
     Relating blood Pb levels to IQ loss: Specification of the 
quantitative relationship between blood Pb level and

[[Page 71508]]

IQ loss is subject to significant uncertainty at lower blood Pb levels 
(e.g., below 5 [mu]g/dL concurrent blood Pb). As discussed earlier, 
there are limitations in the datasets and concentration-response 
analyses available for characterizing the concentration-response 
relationship at these lower blood Pb levels. For example, the pooled 
international dataset analyzed by Lanphear and others (2005) includes 
relatively few children with blood Pb levels below 5 [mu]g/dL and no 
children with levels below 1 [mu]g/dL. In recognition of the 
uncertainty in specifying a quantitative concentration-response 
relationship at such levels, our core modeling approach involves the 
application of four different functions to generate a range of risk 
estimates (see Section 4.2.6 and Section 5.3.1 of the Risk Assessment 
Report, USEPA, 2007b). The difference in absolute IQ loss estimates for 
the four concentration-response functions for a given case study/air 
quality scenario combination is typically close to a factor of 3. 
Estimates of differences in IQ loss between air quality scenarios (in 
terms of percent), however, are more similar across the four functions, 
although the function producing higher overall risk estimates (the dual 
linear function, stratified at 7.5 [mu]g/dL, peak blood Pb) also 
produces larger absolute reductions in IQ loss compared with the other 
three functions.
3. Summary of Results
    This section presents blood Pb and IQ loss estimates generated in 
the exposure and risk assessments. Blood Pb estimates are presented 
first, followed by IQ loss estimates.
a. Blood Pb Estimates
    This section presents blood Pb estimates for the median (Table 1) 
and 95th (Table 2) population percentiles.\39\ Each table presents 
estimates of blood Pb levels resulting from total Pb exposure across 
all pathways (policy relevant and background), as well as estimates of 
the percent contribution from ``recent air'' and ``recent plus past 
air'' exposure categories. As noted in Sections 4.2.4 of the Staff 
Paper and Section 3.4 of the Risk Assessment Report, given the various 
limitations of our modeling tools, the contribution to blood Pb levels 
from air-related exposure pathways and current levels of Pb emitted to 
the air (including via resuspension) are likely to fall between 
contributions attributed to ``recent air'' and those attributed to 
``recent plus past air''. Key uncertainties regarding partitioning dust 
Pb into ``recent air'' and ``other'' categories are summarized above 
(and in Section 4.2.7 of the Staff Paper). The ``recent air'' component 
of indoor dust Pb is the projected level associated with outdoor 
ambient air Pb levels, with outdoor ambient air potentially including 
resuspended, previously deposited Pb which may reflect the resuspension 
of historic levels of Pb from gasoline and from exterior house and 
building Pb paint. In presenting the 95th population percentile 
estimates, it is recognized that 5 percent of the child study 
population at each case study are estimated to have blood Pb levels 
above these estimates. Due to technical limitations, however, we 
believe that it is not possible at this point to reasonably predict the 
distribution of blood Pb levels for that top 5 percent. Observations 
regarding the blood Pb results presented in Tables 1 and 2 are 
presented in Section 4.3 of the Staff Paper.
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    \39\ Blood Pb level estimates for current conditions for these 
cases studies differ from the national values associated with 
NHANES. For example, median blood Pb levels presented in Table 1 for 
the current conditions scenario for the urban case studies are 
somewhat larger than the national median from the NHANES data for 
2003-2004. Specifically, values for the three location-specific 
urban case studies range from 1.7 to 1.8 [mu]g/dL with the general 
urban case study having a value of 1.9 [mu]g/dL (current-conditions 
mean) (see Table 1), while the median value from NHANES (2003-2004) 
is 1.6 [mu]g/dL (http://www.epa.gov/envirohealth/children/body_burdens/b1-table.htm
). NHANES values for the 95th percentile were 

not available for 2003-2004, precluding a comparison of modeled 
estimates presented in Table 2 against NHANES data. We note, 
however, that the 95th percentile value in 2001-2002 was 5.8 [mu]g/
dL (see footnote 7). However, NHANES values for the 90th percentile 
(for 2003-2004) were identified and these values can be compared 
against 90th percentile estimates generated for the urban case 
studies (see Risk Assessment Report, Appendix O, Section O.3.2 for 
the location-specific urban case study and Appendix N, Section 
N.2.1.2 for the general urban case study). The 90th percentile blood 
Pb levels for the current conditions scenario, for the three 
location-specific urban case studies range from 4.5 to 4.6 [mu]g/dL, 
while the estimate for the general urban case study is 5.0 [mu]g/dL. 
These 90th percentile values for the case study populations are 
larger than the 90th percentile value of 3.9 [mu]g/dL reported by 
NHANES for all children in 2003-2004. It is noted that ambient air 
levels reflected in the urban case studies are likely to differ from 
those underlying the NHANES data.

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[[Page 71509]]

     
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    \40\ As noted in footnote 39, median blood Pb levels generated 
for the three location-specific urban case studies and the general 
urban case study for the current conditions scenario are somewhat 
larger than the median value from NHANES for 2003-2004.
    \41\ As recognized in section III.B.2.d above, to simulate air 
concentrations associated with the current NAAQS, a proportional 
roll-up of concentrations from those for current conditions was 
performed for the location-specific urban case studies. This was not 
necessary for the primary Pb smelter case study in which air 
concentrations currently exceed the current standard.
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    \42\ As noted in footnote 39, 90th percentile blood Pb levels 
generated for the three location specific urban case studies and the 
general urban case study for the current conditions scenario are 
larger than the 90th percentile value from NHANES for 2003-2004. 
Note, 95th percentile values were not available for the NHANES 2003-
2004 dataset, preventing a direct comparison to modeled estimates 
presented in Table 2. However, in 2001-2002, the 95th percentile 
value was 5.8 [mu]g/dL (see footnote 7).
    \43\ As recognized in section III.B.2.d above, to simulate air 
concentrations associated with the current NAAQS, a proportional 
roll-up of concentrations from those for current conditions was 
performed for the location-specific urban case studies. This was not 
necessary for the primary Pb smelter case study in which air 
concentrations currently exceed the current standard.

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[[Page 71511]]

b. IQ Loss Estimates
    This section presents IQ loss estimates in Tables 3 through 6. 
These IQ loss estimates need to be understood in the context of the 
broader and more comprehensive and detailed presentation provided Risk 
Assessment Report (USEPA, 2007b). The tables presented here include 
three types of risk estimates:
     Estimates of IQ loss for all air quality scenarios (based 
on total Pb exposure): Tables 3 and 4 present IQ loss estimates for 
total Pb exposure for each of the air quality scenarios simulated for 
each case study. Table 3 presents estimates for the population median 
and Table 4 presents results for the 95th population percentile. These 
results included both median and 95th population percentile estimates. 
To reflect the variation in estimates derived from the four different 
concentration-response functions included in the analysis, three 
categories of estimates are considered including (a) IQ loss estimates 
generated using the low concentration-response function (the model that 
generated the lowest IQ loss estimates), (b) estimates generated using 
the log-linear with low-exposure linearization (LLL) model, and (c) IQ 
loss estimates generated using the high concentration-response function 
(the model that generated the highest IQ loss estimates). For reasons 
described above, estimates generated using the LLL model have been 
given emphasis in the summary below.
     Estimates of IQ loss under the current NAAQS air quality 
scenario (with pathway apportionment): Tables 5 and 6 present IQ loss 
estimates for total Pb exposure based on simulation of just meeting the 
current NAAQS for the case studies to which the core modeling approach 
was applied. Specifically, Table 5 presents estimates of the total Pb-
related IQ loss for the population median and Table 6 presents 
estimates for the 95th population percentile. Both of these tables 
present total IQ loss estimates for (a) total Pb exposure (including 
both policy-relevant pathways and background sources) and (b) policy-
relevant exposures alone (bounded by estimates for ``recent air'' and 
for ``recent plus past air'').
     IQ loss incidence estimates for the three location-
specific urban case studies: Estimates of the number of children for 
each location-specific urban case study projected to have total Pb-
related IQ loss greater than one point are summarized in Table 7, and 
similar estimates for IQ loss greater than 7 points are summarized in 
Table 8. Also presented are the changes in incidence of the current 
NAAQS and alternative NAAQS scenarios compared to current conditions, 
with emphasis placed on estimates generated using the LLL 
concentration-response function. Estimates are presented for each of 
the four concentration-response functions used in the core analysis. 
The complete set of incidence results is presented in Risk Assessment 
Report Appendix O, Section O.3.4.
    The IQ loss results presented in Tables 3 through 8 need to be 
understood in the context of the broader and more comprehensive and 
detailed presentation provided in the Risk Assessment Report. 
Observations regarding the IQ loss results presented in Tables 3 
through 8 are presented in Section 4.4 of the Staff Paper.
    It is important to point out that the range of absolute IQ loss 
estimates generated using the four models for a given case study and 
air quality scenario is typically around a factor of three. However, 
the relative (proportional) change in IQ loss across air quality 
scenarios (i.e., the pattern of IQ loss reduction across air quality 
scenarios for the same case study) is fairly consistent across all four 
models. This suggests uncertainty in estimates of absolute IQ loss for 
a median or 95th percentile child with exposures related to a given 
ambient air Pb level. Accordingly, we have greater confidence in 
predicting incremental changes in IQ loss across air quality scenarios 
and this is reflected in the observations presented in Section 4.4 of 
the Staff Paper. As with the blood Pb estimates, 5 percent of the child 
study population at each case study location is estimated to have IQ 
loss above the 95th percentile estimates presented here, however, due 
to technical limitations of our modeling tools, it is not feasible at 
this point to reasonably predict the distribution of IQ loss levels for 
that top 5 percent.
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    \44\ As recognized in section III.B.2.d above, to simulate air 
concentrations associated with the current NAAQS, a proportional 
roll-up of concentrations from those for current conditions was 
performed for the location-specific urban case studies. This was not 
necessary for the primary Pb smelter case study in which air 
concentrations currently exceed the current standard.

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[[Page 71513]]

     
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    \45\ As recognized in section III.B.2.d above, to simulate air 
concentrations associated with the current NAAQS, a proportional 
roll-up of concentrations from those for current conditions was 
performed for the location-specific urban case studies. This was not 
necessary for the primary Pb smelter case study in which air 
concentrations currently exceed the current standard.
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    \46\ As recognized in section III.B.2.d above, to simulate air 
concentrations associated with the current NAAQS, a proportional 
roll-up of concentrations from those for current conditions was 
performed for the location-specific urban case studies. This was not 
necessary for the primary Pb smelter case study in which air 
concentrations currently exceed the current standard.
    \47\ As recognized in section III.B.2.d above, to simulate air 
concentrations associated with the current NAAQS, a proportional 
roll-up of concentrations from those for current conditions was 
performed for the location-specific urban case studies. This was not 
necessary for the primary Pb smelter case study in which air 
concentrations currently exceed the current standard.
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    \48\ As recognized in section III.B.2.d above, to simulate air 
concentrations associated with the current NAAQS, a proportional 
roll-up of concentrations from those for current conditions was 
performed for the location-specific urban case studies. This was not 
necessary for the primary Pb smelter case study in which air 
concentrations currently exceed the current standard.
[GRAPHIC] [TIFF OMITTED] TP17DE07.005

[[Page 71516]]

     
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    \49\ As recognized in section III.B.2.d above, to simulate air 
concentrations associated with the current NAAQS, a proportional 
roll-up of concentrations from those for current conditions was 
performed for the location-specific urban case studies. This was not 
necessary for the primary Pb smelter case study in which air 
concentrations currently exceed the current standard.
[GRAPHIC] [TIFF OMITTED] TP17DE07.006

BILLING CODE 6560-50-C

[[Page 71517]]

C. Considerations in Review of the Standard

    This section presents an integrative synthesis of information in 
the Criteria Document together with EPA analyses and evaluations. EPA 
notes that the final decision on retaining or revising the current 
primary Pb standard is a public health policy judgment to be made by 
the Administrator. The Administrator's final decision will draw upon 
scientific information and analyses about health effects, population 
exposure and risks, as well as judgments about the appropriate response 
to the range of uncertainties that are inherent in the scientific 
evidence and analyses. These judgments will be informed by a 
recognition that the available health effects evidence generally 
reflects a continuum consisting of ambient levels at which scientists 
generally agree that health effects are likely to occur, through lower 
levels at which the likelihood and magnitude of the response become 
increasingly uncertain.
    This approach is consistent with the requirements of the NAAQS 
provisions of the Act and with how EPA and the courts have historically 
interpreted the Act. These provisions require the Administrator to 
establish primary standards that, in the Administrator's judgment, are 
requisite to protect public health with an adequate margin of safety. 
In so doing, the Administrator seeks to establish standards that are 
neither more nor less stringent than necessary for this purpose. The 
Act does not require that primary standards be set at a zero-risk level 
but rather at a level that avoids unacceptable risks to public health, 
including the health of sensitive groups.
    The following discussion starts with background information on the 
current standard (section III.C.1), including both the basis for 
derivation of the current standard and considerations and conclusions 
from the 1990 Staff Paper (USEPA, 1990b). This is followed by a summary 
of the general approach for this current review (section III.C.2). 
Considerations with regard to the adequacy of the current standard are 
discussed in section III.C.3, with evidence and exposure-risk-based 
considerations in subsections III.C.3.a and b, respectively, followed 
by a summary of CASAC advice and recommendations (section III.C.3.c) 
and, lastly, solicitation of comment on the broad range of policy 
options (section III.C.3.d). Considerations with regard to elements of 
alternative standards--indicator, averaging time and form, and level--
are discussed in sections III.C.4.a., III.C.4.b, and III.C.4.c, 
respectively. The discussion with regard to level includes subsections 
on evidence and exposure-risk-based considerations (sections III.C.4.a 
and b), followed by a summary of CASAC advice and recommendations 
(section III.C.4.c) and, lastly, solicitation of comment on the broad 
range of policy options (section III.C.4.d).
1. Background on the Current Standard
a. Basis for Setting the Current Standard
    The current primary standard is set at a level of 1.5 [mu]g/
m3, measured as Pb-TSP, not to be exceeded by the maximum 
arithmetic mean concentration averaged over a calendar quarter. The 
standard was set in 1978 to provide protection to the public, 
especially children as the particularly sensitive population subgroup, 
against Pb-induced adverse health effects (43 FR 46246). The basis for 
selecting each of the elements of the standard is described below.
i. Level
    EPA's objective in selecting the level of the current standard was 
``to estimate the concentration of Pb in the air to which all groups 
within the general population can be exposed for protracted periods 
without an unacceptable risk to health'' (43 FR 46252). Consistent with 
section 109 of the Clean Air Act, the Agency selected a level for the 
current standard that was below the concentration that was at that time 
identified as a threshold for adverse health effects (i.e., 40 [mu]g/dl 
blood Pb), so as to provide an adequate margin of safety. As stated in 
the notice of final rulemaking, ``This estimate was based on EPA's 
judgment in four key areas:
    (1) Determining the ``sensitive population'' as that group within 
the general population which has the lowest threshold for adverse 
effects or greatest potential for exposure. EPA concludes that young 
children, aged 1 to 5, are the sensitive population.
    (2) Determining the safe level of total lead exposure for the 
sensitive population, indicated by the concentration of lead in the 
blood. EPA concludes that the maximum safe level of blood lead for an 
individual child is 30 [mu]g Pb/dl and that population blood lead, 
measured as the geometric mean, must be 15 [mu]g Pb/dl in order to 
place 99.5 percent of children in the United States below 30 [mu]g Pb/
dl.
    (3) Attributing the contribution to blood lead from nonair 
pollution sources. EPA concludes that 12 [mu]g Pb/dl of population 
blood lead for children should be attributed to nonair exposure.
    (4) Determining the air lead level which is consistent with 
maintaining the mean population blood lead level at 15 [mu]g Pb/dl [the 
maximum safe level]. Taking into account exposure from other sources 
(12 [mu]g Pb/dl), EPA has designed the standard to limit air 
contribution after achieving the standard to 3 [mu]g Pb/dl. On the 
basis of an estimated relationship of air lead to blood lead of 1 to 2, 
EPA concludes that the ambient air standard should be 1.5 [mu]g Pb/
m3.'' (43 FR 46252)
    EPA's judgments in these key areas, as well as margin of safety 
considerations, are discussed below.
    The assessment of the science that was presented in the 1977 
Criteria Document (USEPA, 1977), indicated young children, aged 1 to 5, 
as the population group at particular risk from Pb exposure. Children 
were recognized to have a greater physiological sensitivity than adults 
to the effects of Pb and a greater exposure. In identifying young 
children as the sensitive population, EPA also recognized the 
occurrence of subgroups with enhanced risk due to genetic factors, 
dietary deficiencies or residence in urban areas. Yet information was 
not available to estimate a threshold for adverse effects for these 
subgroups separate from that of all young children. Additionally, EPA 
recognized both a concern regarding potential risk to pregnant women 
and fetuses, and a lack of information to establish that these 
subgroups are more at risk than young children. Accordingly, young 
children, aged 1 to 5, were identified as the group which has the 
lowest threshold for adverse effects of greatest potential for exposure 
(i.e., the sensitive population) (43 FR 46252).
    In identifying the maximum safe exposure, EPA relied upon the 
measurement of Pb in blood (43 FR 46252-46253). The physiological 
effect of Pb that had been identified as occurring at the lowest blood 
Pb level was inhibition of an enzyme integral to the pathway by which 
heme (the oxygen carrying protein of human blood) is synthesized, i.e., 
delta-aminolevulinic acid dehydratase ([delta]-ALAD). The 1977 Criteria 
Document reported a threshold for inhibition of this enzyme in children 
at 10 [mu]g Pb/dL. The 1977 Criteria Document also reported a threshold 
of 15-20 [mu]g/dL for elevation of protoporphyrin (EP), which is an 
indication of some disruption of the heme synthesis pathway. EPA 
concluded that this effect on the heme synthesis pathway (indicated by 
EP) was potentially adverse. EPA further described a range of blood 
levels associated with a progression in

[[Page 71518]]

detrimental impact on the heme synthesis pathway. At the low end of the 
range (15-20 [mu]g/dL), the initial detection of EP associated with 
blood Pb was not concluded to be associated with a significant risk to 
health. The upper end of the range (40 [mu]g/dL), the threshold 
associated with clear evidence of heme synthesis impairment and other 
effects contributing to clinical symptoms of anemia, was regarded as 
clearly adverse to health. EPA also recognized the existence of 
thresholds for additional adverse effects (e.g., nervous system 
deficits) occurring for some children at just slightly higher blood Pb 
levels (e.g., 50 [mu]g/dL). Additionally, EPA stated that the maximum 
safe blood level should not be higher than the blood Pb level 
recognized by the CDC as ``elevated'' (and indicative of the need for 
intervention). In 1978, that level was 30 [mu]g/dL. \50\
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    \50\ The CDC subsequently revised their advisory level for 
children's blood Pb to 25 [mu]g/dL in 1985, and to 10 [mu]g/dL 1991. 
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 and the data demonstrating that no ``safe'' threshold for 
blood Pb in children had been identified, and emphasizing the 
importance of preventative measures (CDC, 2005a). Recently, CDC's 
Advisory Committee on Childhood Lead Poisoning Prevention noted the 
2005 CDC statements and reported on a review of the clinical 
interpretation and management of blood Pb levels below 10 [mu]g/dL 
(ACCLPP, 2007). More details on this level are provided in Section 
III.A.1.
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    Having identified the maximum safe blood level in individual 
children, EPA next made a public health policy judgment regarding the 
target mean blood level for the U.S. population of young children (43 
FR 46252-46253). With this judgment, EPA identified a target of 99.5 
percent of this population to be brought below the maximum safe blood 
Pb level. This judgment was based on consideration of the size of the 
sensitive subpopulation, and the recognition that there are special 
high-risk groups of children within the general population. The 
population statistics available at the time (the 1970 U.S. Census) 
indicated a total of 20 million children younger than 5 years of age, 
with 15 million residing in urban areas and 5 million in center cities 
where Pb exposure was thought likely to be ``high''. Concern about 
these high-risk groups influenced EPA's determination of 99.5 percent, 
deterring EPA from selecting a population percentage lower than 99.5 
(43 FR 46253). EPA then used standard statistical techniques to 
calculate the population mean blood Pb level that would place 99.5 
percent of the population below the maximum safe level. Based on the 
then available data, EPA concluded that blood Pb levels in the 
population of U.S. children were normally distributed with a GSD of 
1.3. Based on standard statistical techniques, EPA determined that a 
thus described population in which 99.5 percent of the population has 
blood Pb levels below 30 [mu]g/dL would have a geometric mean blood 
level of 15 [mu]g/dL. EPA described 15 [mu]g/dL as ``the maximum safe 
blood lead level (geometric mean) for a population of young children'' 
(43 FR 46247).
    When setting the current NAAQS, EPA recognized that the air 
standard needed to take into account the contribution to blood Pb 
levels from Pb sources unrelated to air pollution. Consequently, the 
calculation of the current NAAQS included the subtraction of Pb 
contributed to blood Pb from nonair sources from the estimate of a safe 
mean population blood Pb level. Without this subtraction, EPA 
recognized that the combined exposure to Pb from air and nonair sources 
would result in a blood Pb concentration exceeding the safe level (43 
FR 46253). In developing an estimate of this nonair contribution, EPA 
recognized the lack of detailed or widespread information about the 
relative contribution of various sources to children's blood Pb levels, 
such that an estimate could only be made by inference from other 
empirical or theoretical studies, often involving adults. Additionally, 
EPA recognized the expectation that the contribution to blood Pb levels 
from nonair sources would vary widely, was probably not in constant 
proportion to air Pb contribution, and in some cases may alone exceed 
the target mean population blood Pb level (43 FR 46253-46254). The 
amount of blood Pb attributed to nonair sources was selected based 
primarily on findings in studies of blood Pb levels in areas where air 
Pb levels were low relative to other locations in U.S. The air Pb 
levels in these areas ranged from 0.1 to 0.7 [mu]g/m\3\. The average of 
the reported blood Pb levels for children of various ages in these 
areas was on the order of 12 [mu]g/dL. Thus, 12 [mu]g/dL was identified 
as the nonair contribution, and subtracted from the population mean 
target level of 15 [mu]g/dL to yield a value of 3 [mu]g/dL as the limit 
on the air contribution to blood Pb.
    In determining the air Pb level consistent with an air contribution 
of 3 [mu]g Pb/dL, EPA reviewed studies assessed in the 1977 Criteria 
Document that reported changes in blood Pb with different air Pb 
levels. These studies included a study of children exposed to Pb from a 
primary Pb smelter, controlled exposures of adult men to Pb in fine 
particulate matter, and a personal exposure study involving several 
male cohorts exposed to Pb in a large urban area in the early 1970s (43 
FR 46254). Using all three studies, EPA calculated an average slope or 
ratio over the entire range of data. That value was 1.95 (rounded to 2 
[mu]g/dL blood Pb concentration to 1 [mu]g/m\3\ air Pb concentration), 
and is recognized to fall within the range of values reported in the 
1977 Criteria Document. On the basis of this 2-to-1 relationship, EPA 
concluded that the ambient air standard should be 1.5 [mu]g Pb/m\3\ (43 
FR 46254).
    In consideration of the appropriate margin of safety during the 
development of the current NAAQS, EPA identified the following factors: 
(1) The 1977 Criteria Document reported multiple biological effects of 
Pb in practically all cell types, tissues and organ systems, of which 
the significance for health had not yet been fully studied; (2) no 
beneficial effects of Pb at then current environmental levels were 
recognized; (3) data were incomplete as to the extent to which children 
are indirectly exposed to air Pb that has moved to other environmental 
media, such as water, soil and dirt, and food; (4) Pb is chemically 
persistent and with continued uncontrolled emissions would continue to 
accumulate in human tissue and the environment; and (5) the possibility 
that exposure associated with blood Pb levels previously considered 
safe might influence neurological development and learning abilities of 
the young child (43 FR 46255). Recognizing that estimating an 
appropriate margin of safety for the air Pb standard was complicated by 
the multiple sources and media involved in Pb exposure, EPA chose to 
use margin of safety considerations principally in establishing a 
maximum safe blood Pb level for individual children (30 [mu]g Pb/dL) 
and in determining the percentage of children to be placed below this 
maximum level (about 99.5 percent). Additionally, in establishing other 
factors used in calculating the standard, EPA used margin of safety 
considerations in the sense of making careful judgment based on 
available data, but these judgments were not considered to be at the 
precautionary extreme of the range of data available at the time (43 FR 
46251).
    EPA further recognized that, because of the variability between 
individuals in a population experiencing a given level of Pb exposure, 
it was considered impossible to provide the same margin

[[Page 71519]]

of safety for all members in the sensitive population or to define the 
margin of safety in the standard as a simple percentage. EPA believed 
that the factors it used in designing the standards provided an 
adequate margin of safety for a large proportion of the sensitive 
population. The Agency did not believe that the margin was excessively 
large or on the other hand that the air standard could protect everyone 
from elevated blood Pb levels (43 FR 46251).
ii. Averaging Time, Form, and Indicator
    The averaging time for the current standard is a calendar quarter. 
In the decision for this aspect of the standard, the Agency also 
considered a monthly averaging period, but concluded that ``a 
requirement for the averaging of air quality data over calendar quarter 
will improve the validity of air quality data gathered without a 
significant reduction in the protectiveness of the standards.'' As 
described in the notice for this decision (43 FR 46250), this 
conclusion was based on several points, including the following:
     An analysis of ambient measurements available at the time 
indicated that the distribution of air Pb levels was such that there 
was little possibility that there could be sustained periods greatly 
above the average value in situations where the quarterly standard was 
achieved.
     A recognition that the monitoring network may not actually 
represent the exposure situation for young children, such that it 
seemed likely that elevated air Pb levels when occurring would be close 
to Pb air pollution sources where young children would typically not 
encounter them for the full 24-hour period reported by the monitor.
     Medical evidence available at the time indicated that 
blood Pb levels re-equilibrate slowly to changes in air exposure, a 
finding that would serve to dampen the impact of short-term period of 
exposure to elevated air Pb.
     Direct exposure to air is only one of several routes of 
total exposure, thus lessening the impact of a change in air Pb on 
blood Pb levels.
    The statistical form of the current standard is as a not-to-be-
exceeded or maximum value. EPA set the standard as a ceiling value with 
the conclusion that this air level would be safe for indefinite 
exposure for young children (43 FR 46250).
    The indicator is total airborne Pb collected by a high volume 
sampler (43 FR 46258). EPA's selection of Pb-TSP as the indicator for 
the standard was based on explicit recognition both of the significance 
of ingestion as an exposure pathway for Pb that had deposited from the 
air and of the potential for Pb deposited from the air to become re-
suspended in respirable size particles in the air and available for 
human inhalation exposure. As stated in the final rule, ``a significant 
component of exposure can be ingestion of materials contaminated by 
deposition of lead from the air,'' and that, ``in addition to the 
indirect route of ingestion and absorption from the gastrointestinal 
tract, non-respirable Pb in the environment may, at some point become 
respirable through weathering or mechanical action'' (43 FR 46251).
b. Policy Options Considered in the Last Review
    During the 1980s, EPA initiated a review of the air quality 
criteria and NAAQS for Pb. CASAC and the public were fully involved in 
this review, which led to the publication of a criteria document with 
associated addendum and a supplement (USEPA, 1986a, 1986b, 1990a), an 
exposure analysis methods document (USEPA, 1989) and a staff paper 
(USEPA, 1990b).
    Total emissions to air were estimated to have dropped by 94 percent 
between 1978 and 1987, with the vast majority of it attributed to the 
reduction of Pb in gasoline. Accordingly, the focus of the last review 
was on areas near stationary sources of Pb emissions. Although such 
sources were not considered to have made a significant contribution (as 
compared to Pb in gasoline) to the overall Pb pollution across large, 
urban or regional areas, Pb emissions from such sources were considered 
to have the potential for a significant impact on a local scale. Air Pb 
concentrations, and especially soil and dust Pb concentrations had been 
associated with elevated levels of Pb absorption in children and adults 
in numerous Pb point source community studies. Exceedances of the 
current NAAQS were found at that time only in the vicinity of 
nonferrous smelters or other point sources of Pb.
    In summarizing and interpreting the health evidence presented in 
the 1986 Criteria Document and associated documents, the 1990 Staff 
Paper described the collective impact on children of the effects at 
blood Pb levels above 15 [mu]g/dL as representing a clear pattern of 
adverse effects worthy of avoiding. This is in contrast to EPA's 
identification of 30 [mu]g/dL as a safe blood Pb level for individual 
children when the NAAQS was set in 1978. The Staff Paper further stated 
that at blood Pb levels of 10-15 [mu]g/dL, there was a convergence of 
evidence of Pb-induced interference with a diverse set of physiological 
functions and processes, particularly evident in several independent 
studies showing impaired neurobehavioral function and development. 
Further, the available data did not indicate a clear threshold in this 
blood Pb range. Rather, it suggested a continuum of health risks down 
to the lowest levels measured.\51\
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    \51\ In 1991, the CDC reduced their advisory level for 
children's blood Pb from 25 [mu]g/dL to 10 [mu]g/dL.
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    For the purposes of comparing the relative protectiveness of 
alternative Pb NAAQS, the staff conducted analyses to estimate the 
percentages of children with blood Pb levels above 10 [mu]g/dL and 
above 15 [mu]g/dL for several air quality scenarios developed for a 
small set of stationary source exposure case studies. The results of 
the analyses of child populations living near two Pb smelters indicated 
that substantial reductions in Pb exposure could be achieved through 
just meeting the current Pb NAAQS. According to the best estimate 
analyses, over 99.5% of children living in areas significantly affected 
by the smelters would have blood Pb levels below 15 [mu]g/dL if the 
current standard was achieved. Progressive changes in this number were 
estimated for the alternative monthly Pb NAAQS levels evaluated in 
those analyses, which ranged from 1.5 [mu]g/m\3\ to 0.5 [mu]g/m\3\.
    In light of the health effects evidence available at the time, the 
1990 Staff Paper presented air quality, exposure, and risk analyses, 
and other policy considerations, as well as the following staff 
conclusions with regard to the primary Pb NAAQS (USEPA, 1990b, pp. xii 
to xiv):
    (1) ``The range of standards * * * should be from 0.5 to 1.5 [mu]g/
m\3\.''
    (2) ``A monthly averaging period would better capture short-term 
increases in lead exposure and would more fully protect children's 
health than the current quarterly average.''
    (3) ``The most appropriate form of the standard appears to be the 
second highest monthly averages {sic{time}  in a 3-year span. This form 
would be nearly as stringent as a form that does not permit any 
exceedances and allows for discounting of one ``bad'' month in 3 years 
which may be caused, for example, by unusual meteorology.''
    (4) ``With a revision to a monthly averaging time more frequent 
sampling is needed, except in areas, like roadways remote from lead 
point sources, where the standard is not expected to be violated. In 
those situations, the current 1-in-6 day sampling schedule would 
sufficiently reflect air quality and trends.''

[[Page 71520]]

    (5) ``Because exposure to atmospheric lead particles occurs not 
only via direct inhalation, but via ingestion of deposited particles as 
well, especially among young children, the hi-volume sampler provides a 
reasonable indicator for determining compliance with a monthly standard 
and should be retained as the instrument to monitor compliance with the 
lead NAAQS until more refined instruments can be developed.''
    Based on its review of a draft Staff Paper, which contained the 
above recommendations, the CASAC strongly recommended to the 
Administrator that EPA should actively pursue a public health goal of 
minimizing the Pb content of blood to the extent possible, and that the 
Pb NAAQS is an important component of a multimedia strategy for 
achieving that goal (CASAC, 1990, p. 4). In noting the range of levels 
recommended by staff, CASAC recommended consideration of a revised 
standard that incorporates a ``wide margin of safety, because of the 
risk posed by Pb exposures, particularly to the very young whose 
developing nervous system may be compromised by even low level 
exposures'' (id., p. 3). More specifically, CASAC judged that a 
standard within the range of 1.0 to 1.5 [mu]g/m\3\ would have 
``relatively little, if any, margin of safety;'' that greater 
consideration should be given to a standard set below 1.0 [mu]g/m\3\; 
and, to provide perspective in setting the standard, it would be 
appropriate to consider the distribution of blood Pb levels associated 
with meeting a monthly standard of 0.25 [mu]g/m\3\, a level below the 
range considered by staff (id.).
    After consideration of the documents developed during the review, 
EPA chose not to propose revision of the NAAQS for Pb. During the same 
time period, the Agency published and embarked on the implementation of 
a broad, multi-program, multi-media, integrated national strategy to 
reduce Pb exposures (USEPA, 1991). As part of implementing this 
integrated Pb strategy, the Agency focused efforts primarily on 
regulatory and remedial clean-up actions aimed at reducing Pb exposures 
from a variety of non-air sources judged to pose more extensive public 
health risks to U.S. populations, as well as on actions to reduce Pb 
emissions to air, particularly near stationary sources. This focus 
reflected in part the dramatic reduction of Pb in gasoline that 
occurred since the standard was set in 1978, which resulted in orders-
of-magnitude reductions in airborne emissions of Pb, and a significant 
shift in the types of sources with the greatest Pb emissions. EPA 
established standards for Pb-based paint hazards and Pb dust cleanup 
levels in most pre-1978 housing and child-occupied facilities. 
Additionally, EPA has developed standards for the management of Pb in 
solid and hazardous waste, oversees the cleanup of Pb contamination at 
Superfund sites, and has issued regulations to reduce Pb in drinking 
water (http://www.epa.gov/lead/regulation.htm). Beyond these specific 

regulatory actions, the Agency's Lead Awareness Program has continued 
to work to protect human health and the environment against the dangers 
of Pb by conducting research and designing educational outreach 
activities and materials (http://www.epa.gov/lead/). Actions to reduce 

Pb emissions to air during the 1990s included enforcement of the NAAQS, 
as well as the promulgation of regulations under Section 112 of the 
Clean Air Act, including national emissions standards for hazardous air 
pollutants at primary and secondary Pb smelters, as well as other Pb 
sources.
2. Approach for Current Review
    To evaluate whether it is appropriate to consider retaining the 
current primary Pb standard, or whether consideration of revisions is 
appropriate, EPA is considering an approach in this review like that 
used in the Staff Paper. As discussed below, this approach builds upon 
the general approach used in the initial setting of the standard, as 
well as that used in the last review, and reflects the broader body of 
evidence and information now available.
    This approach is based on an integration of information on health 
effects associated with exposure to ambient Pb; expert judgment on the 
adversity of such effects on individuals; and policy judgments as to 
when the standard is requisite to protect public health with an 
adequate margin of safety, which are informed by air quality and 
related analyses, quantitative exposure and risk assessments when 
possible, and qualitative assessment of impacts that could not be 
quantified.
    In conducting this assessment, EPA is aware of the dramatic 
reductions in air Pb emissions in the U.S. in recent decades.\52\ In 
addition to the dramatic reduction of Pb in gasoline, an additional 
circumstance that has changed since the standard was set is the 
enactment of the Clean Air Act Amendments of 1990, which amended Clean 
Air Act Section 112 to list Pb compounds as hazardous air pollutants 
(HAP) and to require technology-based and risk-based standards, as 
appropriate, for major stationary sources of HAP.\53\ EPA is also aware 
that these significantly changed circumstances have raised the question 
in this review of whether it is still appropriate to maintain a NAAQS 
for Pb or to retain Pb on the list of criteria pollutants. As a result, 
this evaluation will consider the status of Pb as a criteria pollutant 
and assesses whether revocation of the standard is an appropriate 
option for the Administrator to consider.
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    \52\ Detailed information on air Pb emissions, and temporal 
trends in emissions since 1980 is provided in Section 2.2 of the 
Staff Paper.
    \53\ The use of Pb paint in new houses has declined 
substantially over the 20\th\ century. For example ``an estimated 
68% of U.S. homes built before 1940 have Pb hazards, as do 43% of 
those built during 1940-1959 and 8% of those built during 1960-
1977'' (ACCLPP, 2007). We are uncertain of the implications of these 
reductions for ambient air.
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    As discussed below, in conducting this evaluation, EPA will take 
into account both evidence-based and quantitative exposure- and risk-
based considerations. To the extent that the available information 
suggests that revision of the current standard may be appropriate to 
consider, EPA will also evaluate the currently available information to 
determine the extent to which it supports consideration of a revised 
standard. In this evaluation, EPA will consider the specific elements 
of the standard to identify options (in terms of an indicator, 
averaging time, level, and form) for consideration in making public 
health policy judgments, based on the currently available information, 
as to the degree of protection that is requisite to protect public 
health with an adequate margin of safety.
    To help inform the Agency's consideration of the quantitative 
exposure and risk assessments, summarized above in section III.B, EPA 
solicits comment on the appropriate weight to be placed on the results 
from these assessments in evaluating the adequacy of the current 
primary standard and in considering alternative standards. 
Specifically, we solicit comment on a number of aspects of the design 
of the assessments and interpretation of the assessment results, 
including in particular: (1) The appropriateness of rolling up ambient 
Pb concentrations to simulate just meeting the current standard for 
areas in which current concentrations are well below the level of the 
current standard; \54\ (2) the use of a proportional

[[Page 71521]]

method to roll-up and roll-down Pb concentrations to simulate just 
meeting the current and alternative standards; \55\ (3) the 
categorization and apportionment of policy-relevant exposure pathways 
and policy-relevant background, particularly with regard to exposures 
related to historically deposited Pb from leaded gasoline and from Pb 
paint; and (4) the weight to be given to risk estimates derived using 
various concentration-response functions. More broadly, we also solicit 
comment on the approach of considering exposures and risks resulting 
from the ingestion of historically emitted Pb that may now be present 
in indoor dust and outdoor soil (e.g., that associated with past use of 
Pb in gasoline or Pb paint) impacted by ambient air Pb as being policy-
relevant for the purpose of setting a NAAQS.
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    \54\ We have not in the past used such an approach in developing 
risk assessments for other NAAQS reviews since other risk 
assessments (i.e., for ozone and PM) included a number of areas that 
did not meet the current NAAQS such that rolling up ambient 
pollutant concentrations was not needed to characterize risks 
associated with just meeting the current standard.
    \55\ There are other methods that might be used.
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3. Adequacy of the Current Standard
    In considering the adequacy of the current standard, EPA will first 
consider whether it is appropriate to maintain a NAAQS for Pb or to 
retain Pb on the list of criteria pollutants. As noted above, this 
question has arisen in this review as a result of the dramatic 
alteration in the basic patterns of air Pb emissions in the U.S. since 
the standard was set, that primarily reflects the dramatic reduction of 
Pb in gasoline, which resulted in orders-of-magnitude reductions in 
airborne emissions of Pb and a significant shift in the types of 
sources with the greatest Pb emissions. In addition, Section 112 of the 
Clean Air Act was amended in 1990 to include Pb compounds on the list 
of HAP and to require EPA to establish technology-based emission 
standards for those listed major source categories emitting Pb 
compounds, and to establish risk-based standards, as appropriate, for 
those categories of sources.
    EPA notes that CASAC specifically examined several scientific 
issues and related public health (and public welfare) policy issues 
that the CASAC Lead Review Panel \56\ judged to be essential in 
determining whether delisting Pb or revoking the Pb NAAQS would be 
appropriate options for the Administrator to consider. In its letter to 
the Administrator of March 27, 2007, based on its review of the first 
draft Staff Paper (Henderson, 2007a; Attachment A of the Staff Paper), 
CASAC's examination of these issues was framed by the following series 
of questions:
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    \56\ This Lead Panel includes the statutorily defined seven-
member CASAC and additional subject-matter experts needed to provide 
an appropriate breadth of expertise for this review of the Pb NAAQS.
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    (1) Does new scientific information accumulated since EPA's 
promulgation of the current primary Lead NAAQS of 1.5 [mu]g/m\3\ in 
1978 suggest that science previously overstated the toxicity of lead?
    (2) Have past regulatory and other controls on lead decreased PbB 
[blood lead] concentrations in human populations so far below levels of 
concern as to suggest there is now an adequate margin of safety 
inherent in those PbB levels?
    (3) Have the activities that produced emissions and atmospheric 
redistribution of lead in the past changed to such an extent that 
society can have confidence that emissions will remain low even in the 
absence of NAAQS controls?
    (4) Are airborne concentrations and amounts of lead sufficiently 
low throughout the United States that future regulation of lead 
exposures can be effectively accomplished by regulation of lead-based 
products and allowable amounts of lead in soil and/or water?
    (5) If lead were de-listed as a criteria air pollutant, would it be 
appropriately regulated under the Agency's Hazardous Air Pollutants 
(HAP) program?
    For the reasons presented in its March 2007 letter, the CASAC Lead 
Review Panel judged that the answer to each of these questions was 
``no,'' leading the Panel to conclude that ``the existing state of 
science is consistent with continuing to list ambient lead as a 
criteria pollutant for which fully-protection NAAQS are required'' (id, 
p. 5). Further, in a subsequent letter to the Administrator of 
September 27, 2007, based on its review of the second draft Risk 
Assessment Report (Henderson, 2007b; Attachment B of the Staff Paper), 
CASAC strongly reiterated its opposition to any considered delisting of 
Pb, and expressed its unanimous support for maintaining fully-
protective NAAQS (id., p. 2). The EPA seeks comment and supporting 
information on the issue of whether it would be appropriate for EPA to 
determine that emissions of Pb no longer contribute to air pollution 
that may reasonably be anticipated to endanger public heath. EPA also 
solicits comment and supporting information on the extent to which 
reductions in the ambient air Pb standard would benefit public health.
    In considering the adequacy of the current standard, EPA will 
consider the available evidence and quantitative exposure- and risk-
based information, summarized below.
a. Evidence-Based Considerations
    In considering the broad array of health effects evidence assessed 
in the Criteria Document with respect to the adequacy of the current 
standard, EPA will focus on those health endpoints associated with the 
Pb exposure and blood levels most pertinent to ambient exposures. 
Additionally, we will give particular weight to evidence available 
today that differs from that available at the time the standard was set 
with regard to its support of the current standard.
    First, with regard to the sensitive population, the susceptibility 
of young children to the effects of Pb is well recognized, in addition 
to more recent recognition of effects of chronic exposure to low level 
Pb with advancing age (CD, Sections 5.3.7 and pp. 8-73 to 8-75). The 
prenatal period and early childhood are periods of increased 
susceptibility to Pb exposures, with evidence of adverse effects on the 
developing nervous system that generally appear to persist into later 
childhood and adolescence (CD, Section 6.2).\57\ Thus, while the 
sensitivity of the elderly and other particular subgroups is 
recognized, as at the time the standard was set, young children 
continue to be recognized as the key sensitive population for Pb 
exposures.
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    \57\ For example, the following statement is made in the 
Criteria Document ``Negative Pb impacts on neurocognitive ability 
and other neurobehavioral outcomes are robust in most recent studies 
even after adjustment for numerous potentially confounding factors 
(including quality of care giving, parental intelligence, and 
socioeconomic status). These effects generally appear to persist 
into adolescence and young adulthood.'' (CD, p.E-9)
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    With regard to the exposure levels at which adverse health effects 
occur, the current evidence demonstrates the occurrence of adverse 
health effects at appreciably lower blood Pb levels than those 
demonstrated by the evidence at the time the standard was set. This 
change in the evidence since the time the standard was set is reflected 
in changes made by the CDC in their advisory level for Pb in children's 
blood, and changes they have made in their characterization of that 
level. Although CDC recognized a level of 30 [mu]g/dL blood Pb as 
warranting individual intervention in 1978 when the Pb NAAQS was set, 
in 2005 they recognized the evidence of adverse health effects in 
children with blood Pb levels below 10 [mu]g/dL and the data 
demonstrating that no ``safe'' threshold for blood Pb had been 
identified (CDC, 1991; CDC, 2005).
    The Criteria Document describes current evidence regarding the 
occurrence of a variety of adverse health

[[Page 71522]]

effects, including those on the developing nervous system, associated 
with blood Pb levels extending well below 10 [mu]g/dL to 5 [mu]g/dL and 
possibly lower (CD, Sections 8.4 and 8.5).\58\ With regard to the 
evidence of effects on the developing nervous system at these low 
levels, EPA notes, in particular, the international pooled analysis by 
Lanphear and others (2005), studies of individual cohorts such as the 
Rochester, Boston, and Mexico City cohorts (Canfield et al., 2003a; 
Canfield et al., 2003b; Bellinger and Needleman, 2003; Tellez-Rojo et 
al., 2006), the study of African-American inner-city children from 
Detroit (Chiodo et al., 2004), and the cross-sectional analysis of a 
nationally representative sample from the NHANES III (conducted from 
1988-1994), in which the mean blood Pb level was 1.9 [mu]g/dL (Lanphear 
et al., 2000). Further, current evidence does not indicate a threshold 
for the more sensitive health endpoints such as adverse effects on the 
developing nervous system (CD, pp. 5-71 to 5-74 and Section 6.2.13).
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    \58\ For context, it is noted that the 2001-2004 median blood 
level for children aged 1-5 of all races and ethnic groups is 1.6 
[mu]g/dL, the median for the subset living below the poverty level 
is 2.3 [mu]g/dL and 90th percentile values for these two groups are 
4.0 [mu]g/dL and 5.4 [mu]g/dL, respectively. Similarly, the 2001-
2004 median blood level for black, non-hispanic children aged 1-5 is 
2.5 [mu]g/dL, while the median level for the subset of that group 
living below the poverty level is 2.9 [mu]g/dL and the median level 
for the subset living in a household with income more than 200% of 
the poverty level is 1.9 [mu]g/dL. Associated 90th percentile values 
for 2001-2004 are 6.4 [mu]g/dL (for black, non-hispanic children 
aged 1-5), 7.7 [mu]g/dL (for the subset of that group living below 
the poverty level) and 4.1 [mu]g/dL (for the subset living in a 
household with income more than 200% of the poverty level). (http://www.epa.gov/envirohealth/children/body_burdens/b1-table.htm_then
 

click on ``Download a universal spreadsheet file of the Body Burdens 
data tables'').
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    As when the standard was set in 1978, EPA recognizes that there 
remain today contributions to blood Pb levels from nonair sources. 
Estimating contributions from nonair sources are complicated by 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 do not usually 
distinguish between outdoor soil/dust Pb resulting from historical 
emissions and outdoor soil/dust Pb resulting from recent emissions. 
Further, while indoor dust Pb has been identified as being a 
predominant contributor to children's blood Pb, available studies do 
not distinguish the different pathways (air-related and other) 
contributing to indoor dust Pb. As recognized in Section III.A. above 
(including footnote 13), some studies have found that dietary intake of 
Pb may be a predominant source of Pb exposure among adults, greater 
than consumption of water and beverages or inhalation (CD, p. 3-43). 
The exposure assessment for children performed for this review has 
employed available data and methods to develop estimates intended to 
inform a characterization of these pathways.
    Consistent with reductions in air Pb concentrations \59\ which 
contribute to blood Pb, nonair contributions have also been reduced. 
For example, the use of Pb paint in new houses has declined 
substantially over the 20th century, such that ``an estimated 68% of 
U.S. homes built before 1940 have Pb hazards, as do 43% of those built 
during 1940-1959 and 8% of those built during 1960-1977'' (ACCLPP, 
2007). Additionally, Pb contributions to diet have been reported to 
have declined significantly since 1978, perhaps as much as 70% or more 
between then and 1990 (WHO, 1995) and the 2006 Criteria Document 
identifies a drop in dietary Pb intake by 2 to 5 year olds of 96% 
between the early 1980s and mid 1990s. The 1977 Criteria Document 
included a dietary Pb intake estimate for the general population of 100 
to 350 [mu]g Pb/day (USEPA 1977, p. 1-2) and the 2006 Criteria Document 
cites recent studies indicating a dietary intake ranging from 2 to 10 
[mu]g Pb/day (CD, Section 3.4 and p. 8-14). Reductions in elevated 
blood Pb levels in urban areas indicate that other nonair contributions 
to blood Pb (e.g., drinking water distribution systems, and Pb-based 
paint) have also been reduced since the late 1970s. In their March 2007 
letter to the Administrator, the CASAC Pb Panel recommended that 1.0-
1.4 [mu]g/dL or lower be considered as an estimate of the nonair 
component of blood Pb.
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    \59\ Air Pb concentrations nationally are estimated to have 
declined more than 90% since the early 1980s.
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    As in 1978, the evidence demonstrates that Pb in ambient air 
contributes to Pb in blood, with the pertinent exposure routes 
including both inhalation and ingestion (CD, Sections 3.1.3.2, 4.2 and 
4.4; Hilts et al., 2003). In 1978, the evidence indicated a 
quantitative relationship between ambient air Pb and blood Pb--i.e., 
the ratio describing the increase in blood Pb per unit of air Pb--that 
ranged from 1:1 to 1:2 (USEPA, 1977). In setting the standard, the 
Agency relied on a ratio of 1:2, i.e., 2 [mu]g/dL blood Pb per 1 [mu]g/
m\3\ air Pb (43 FR 46252). The evidence now and in the past on this 
relationship is limited by the circumstances in which the data are 
collected. Specific measurements of Pb in blood that derived from Pb 
that had been in the air are not available. Rather, estimates are 
available for the relationship between Pb concentrations in air and Pb 
levels in blood, developed from populations in differing Pb exposure 
circumstances, which inform this issue. Many of the currently available 
reviews of estimates for air-to-blood ratios, which include air 
contributions from both inhalation and ingestion exposure pathways, 
indicate that such ratios generally fall between 1:3 to 1:5, with some 
higher \60\ (USEPA 1986a, pp. 11-99 to 11-100 and 11-106; Brunekreef, 
1984). Findings of a recent study of changes in children's blood Pb 
levels associated with reduced Pb emissions and associated air 
concentrations near a Pb smelter in Canada indicates a ratio on the 
order of 1:7 (CD, pp. 3-23 to 3-24; Hilts et al., 2003). In their 
advice to the Agency, CASAC identified values 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).\61\ While there is uncertainty in the absolute 
value of the air-to-blood relationship, the current evidence indicates 
a notably greater ratio, with regard to increase in blood Pb, than the 
1978 1:2 relationship e.g., on the order of 1:3 to 1:5 with some higher 
estimates (see footnote 60) and some lower estimates (down to 1:1). 
EPA's consideration of this issue in 1986 indicated that ratios which 
consider both inhalation and ingestion pathways are ``necessarily 
higher than those estimates for inhaled air lead alone'' (USEPA, 1986a, 
p. 11-106). We solicit comment on data or studies that may help inform 
our understanding of this important parameter.
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    \60\ For example, adjusted ratios from Brunekreef (1984, Table 
1) ranged up to 1:8.5 and unadjusted ratios extended above 1:10.
    \61\ The CASAC Panel stated ``The Schwartz and Picher analysis 
showed that in 1978, the midpoint of the National Health and 
Nutrition Examination Survey (NHANES) II, gasoline lead was 
responsible for 9.1 [mu]g/dL of blood lead 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 lead from gasoline was 
completed, air lead 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 lead, taking all pathways into 
account.'' (Henderson, 2007a, page D-2 to D-3).
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    Based on this information, the Staff Paper concluded that young 
children remain the sensitive population of primary focus in this 
review, there is now no recognized safe level of Pb in

[[Page 71523]]

children's blood, and studies appear to show adverse effects at mean 
concurrent blood Pb levels as low as 2 ug/dL (CD, pp. 6-31 to 6-32; 
Lanphear et al., 2000). Further, while the nonair contribution to blood 
Pb has declined, perhaps to a range of 1.0-1.4 [mu]g/dL, the air-to-
blood ratio appears to be higher at today's lower blood Pb levels than 
the estimates at the time the standard was set, with current estimates 
on the order of 1:3 to 1:5 and perhaps up to 1:10. Using the framework 
employed in setting the standard in 1978, the more recently available 
evidence and more recently available estimates may suggest a level for 
the standard that is lower by an order of magnitude or more.
b. Exposure- and Risk-Based Considerations
    In addition to the evidence-based considerations, EPA will also 
consider exposures and health risks estimated to occur upon meeting the 
current Pb standard to help inform judgments about the extent to which 
exposure and risk estimates may be judged to be important from a public 
health perspective, taking into account key uncertainties associated 
with the estimated exposures and risks.
    As discussed above, young children are the sensitive population of 
primary focus in this review. The exposure and risk assessment 
estimates Pb exposure for children (less than 7 years of age), and 
associated risk of neurocognitive effects in terms of IQ decrements. In 
addition to the risks (IQ decrement) that were quantitatively 
estimated, EPA recognizes that there may be long-term adverse 
consequences of such deficits over a lifetime, that there is evidence 
of other health effects occurring at similar or higher exposures for 
young children, and that other health evidence demonstrates 
associations between Pb exposure and adverse health effects in adults. 
As noted in section III.B above, the risk assessment results focus 
predominantly on risk estimates derived using the log-linear with low-
exposure linearization (LLL) concentration-response function, with the 
range associated with the other three functions also being noted.
    As noted in the Criteria Document, a modest change in the mean for 
a health index at the individual level can have substantial 
implications at the population level (CD, p. 8-77, Sections 8.6.1 and 
8.6.2; Bellinger, 2004; Needleman et al., 1982; Weiss, 1988; Weiss, 
1990)). For example, for an individual functioning in the low range of 
IQ due to the influence of risk factors other than Pb, a Pb-associated 
IQ decline of a few points might be sufficient to drop that individual 
into the range associated with increased risk of educational, 
vocational, and social handicap (CD, p. 8-77). Further, given a 
somewhat uniform manifestation of Pb-related decrements across the 
range of IQ scores in a population, a downward shift in the mean IQ 
value is not associated only with a substantial increase in the 
percentage of individuals achieving very low scores, but also with 
substantial decreases in percentages achieving very high scores (CD, p. 
8-81). The CASAC Pb Panel has advised on this point that ``a population 
loss of 1-2 IQ points is highly significant from a public health 
perspective'' (Henderson, 2007a, p. 6).
    In this section, risk estimates for the median and for an upper 
percentile, the 95th are discussed. In setting the standard in 1978, 
EPA accorded risk management significance to the 99.5th percentile by 
selecting a mean blood Pb level intended to bring 99.5 percent of the 
population to or below the then described maximum safe blood Pb level. 
Similarly, in their advice to EPA in this review, CASAC stated that 
``the primary lead standard should be set so as to protect 99.5% of the 
population'' (Henderson, 2007a, p. 6). In considering estimates from 
the quantitative assessment that will inform conclusions consistent 
with this objective, however, EPA and CASAC also recognize 
uncertainties in the risk estimates at the edges of the distribution 
and consequently the 95th percentile is reported as the estimate of the 
high end of the risk distribution (Henderson, 2007b, p. 3). In so 
doing, however, EPA notes that there are individuals in the population 
expected to have higher risk, the consideration of which is important 
given the risk management objectives for the current standard when set 
in 1978 with regard to the 99.5th percentile.
    In addition to estimating IQ loss associated with the combined 
exposure to Pb from all exposure pathways, EPA estimated IQ loss for 
two policy-relevant categories of exposure pathways. These are ``recent 
air'', which conceptually is intended to include contributions to blood 
Pb associated with Pb that has recently been in the air, and ``past 
air'', intended to include contributions to blood Pb associated with Pb 
that was in the air in the past but not in the air recently. In the 
exposure modeling conducted for the risk assessment, the exposure 
pathways assigned to the recent air category were inhalation of ambient 
air Pb and ingestion of the component of indoor dust Pb that is 
predicted to be associated with ambient air concentrations. The 
exposure pathways assigned to the past air category were ingestion of 
outdoor soil/dust Pb and ingestion of the component of indoor dust Pb 
not assigned to recent air. There are various limitations associated 
with our modeling tools that affected the estimates for these two 
categories. As a result, blood Pb levels and associated risks of 
greatest interest in this review--those associated with exposure 
pathways involving ambient air Pb and current levels of Pb emitted to 
the air (including via resuspension)--are likely to fall between 
estimates for recent air and those for the sum of recent plus past 
air.\62\ Accordingly, this notice presents these two sets of estimates 
as providing a range of interest, with regard to policy-relevant Pb, 
for this review.
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    \62\ Comparisons of blood Pb levels estimated for individual 
case study populations (from all exposure sources in current 
conditions scenarios) to national population values from NHANES are 
noted in footnote 39 in Section III.B.3.a.
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    In considering the adequacy of the current standard, it is 
important to note that the standard is currently met throughout the 
country with very few exceptions. The national composite average 
maximum quarterly mean based on 198 active monitoring sites during 
2003-2005 is 0.17 [mu]g/m\3\, an order of magnitude below the current 
standard, indicating that most of the monitored areas of the country 
are well below the standard. Review of the current monitoring network 
in light of current information on Pb sources and emissions, however, 
indicated that monitors are not located near many of the larger 
sources. Therefore, the assessment may be underestimating Pb 
concentrations.
    Using the current monitoring data, EPA estimated exposure and risk 
associated with current conditions in a general urban case study and in 
three location-specific urban case studies in areas where air 
concentrations fall significantly below the current standard.\63\ Two 
current conditions scenarios were assessed for the general urban case 
study, one based on the 95th percentile of levels in large urban areas 
(0.87 [mu]g/m\3\, maximum quarterly mean) and one based on mean levels 
in such

[[Page 71524]]

areas (0.14 [mu]g/m\3\, maximum quarterly. Levels in the three 
location-specific case studies ranged from 0.09 to 0.35 [mu]g/m\3\, in 
terms of maximum quarterly average. For the general urban case study, 
which is a simplified representation of urban areas, median estimates 
of total Pb-related IQ loss range from 1.5 to 6.3 points (across all 
four concentration-response functions), with estimates based on the LLL 
function of 4.5 and 4.7 points, for the mean and high-end current 
conditions scenarios, respectively. Associated estimates for exposure 
pathway contributions to total IQ loss (LLL estimate) at the population 
median in these two scenarios indicate that IQ loss associated with 
policy-relevant Pb falls somewhere between 1.3 and 3.6 points. At the 
95th percentile for total IQ loss (LLL estimate), IQ loss associated 
with policy-relevant Pb is estimated to fall somewhere between 2.2 and 
6.0 points (Risk Assessment Report, Table 5-9).
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    \63\ Comparisons of median and 90th percentile blood Pb levels 
estimated for individual case study populations (from all exposure 
sources in current conditions scenarios) to national population 
values from NHANES are noted in footnote 39 in Section III.B.3.a. 
That comparison suggests that modeled estimates generated for the 
location-specific urban case studies for both population percentiles 
are somewhat larger than values cited in NHANES (for 2003-2004). 
However, as mentioned earlier, factors related to Pb exposure, 
including ambient air levels, are likely to differ for the urban 
case study populations compared with the national population 
underlying NHANES.
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    For the three location-specific areas, median estimates of total 
Pb-related IQ loss for current conditions range from 1.4 to 5.2 points 
(across all four concentration-response functions), with estimates 
based on the LLL function all being 4.2 points.\64\ Median IQ loss 
associated with policy-relevant Pb (LLL function) is estimated to fall 
between 0.6 to 2.9 points IQ loss. The 95th percentile estimates for 
total Pb-related IQ loss across the three location-specific urban case 
studies range from 4.1 to 11.4 points (across all four concentration-
response functions), with estimates based on the LLL function ranging 
from 7.5 to 7.6 points. At the 95th percentile for the three location-
specific urban case studies, IQ loss associated with policy-relevant Pb 
(LLL function) is estimated to fall between 1.2 to 5.2 points IQ loss 
(Risk Assessment Report, Tables 5-9 and 5-10).
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    \64\ Although the maximum quarterly average concentration for 
the highest monitor in each study area differs among the three areas 
by a factor of 4 (0.09 to 0.36 [mu]g/m\3\), the population weighted 
air Pb concentrations for these three study areas are more similar 
and differ by approximately a factor of 2, with the study area with 
highest maximum quarterly average concentration having a lower 
population-weighted air concentration that is more similar to the 
other two areas. This similarity in population weighted 
concentrations explains the finding of similar total IQ loss across 
the three study areas.
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    In order to consider exposure and risk associated with the current 
standard, EPA developed estimates for a case study based on air quality 
projected to just meet the standard in a location of the country where 
air concentrations do not meet the current standard (the primary Pb 
smelter case study). In so doing, we consider it extremely unlikely 
that air concentrations in urban areas across the U.S. that are 
currently well below the current standard would increase to just meet 
the standard. However, we recognize the potential for air Pb 
concentrations in some areas currently well below the standard to 
increase to just meet the standard by way of, for example, expansion of 
existing sources (e.g., facilities operating as secondary smelters may 
exercise previously used capabilities as primary smelters) or by the 
congregation of multiple Pb sources in adjacent locations. We have 
simulated this scenario (increased Pb concentrations to just meet the 
current standard) in a general urban case study and three location-
specific urban case studies. In this scenario, we note substantial 
uncertainty in simulating how the profile of Pb concentrations might 
change in the hypothetical case where concentrations increase to just 
meet the current standard.
    Turning first to the estimates of total blood Pb for the current 
NAAQS scenario simulated for the location-specific urban case studies, 
we note the extent to which exposures associated with increased air Pb 
concentrations that simulate just meeting the current standard are 
estimated to increase blood Pb levels in young children. The magnitude 
of this for the median total blood Pb ranges from 0.3 [mu]g/dL (an 
increase of 20 percent) in the case of the Cleveland study area for 
which current conditions are estimated to be approximately one fourth 
of the current NAAQS, up to approximately 1 [mu]g/dL (an increase of 50 
to 70%) for the Chicago and Los Angeles study areas for which current 
conditions are estimated to be at or below one tenth of the current 
NAAQS.
    Estimates of IQ loss (for child with median total IQ loss estimate) 
associated with recent air plus past air Pb at exposures allowed by 
just meeting the current NAAQS in the primary Pb smelter case study 
differ when considering the full study area (10 km radius) or the 1.5 
km radius subarea. Estimates for median IQ loss associated with the 
recent air plus past air categories of exposure pathways for the full 
study area range from 0.6 point to 2.3 points (for the range of 
concentration-response functions), while these estimates for the 
subarea range from 3.2 points to 9.4 points IQ loss. The estimates 
(recent plus past) for the median based on the LLL concentration-
response function are 1.9 points IQ loss for the full study area and 
6.0 points for the subarea. The 95th percentile estimates of total IQ 
loss in the subarea range from 5.0 to 12.4 points, with an associated 
range for the recent air plus past air of 4.2 to 10.4 points.
    For the current NAAQS scenario in the three location-specific case 
studies, estimates of IQ loss associated with policy-relevant Pb for 
the median total IQ loss range from 0.6 points loss (recent air 
estimate using low-end concentration-response function) to 7.4 points 
loss (recent plus past air estimate using the high-end concentration-
response function). The corresponding estimates based on the LLL 
concentration-response function range from 2.7 points (lowest location-
specific recent air estimate) to 4.7 points IQ loss (highest location-
specific recent plus past air estimate). The comparable estimates of IQ 
loss for children at the 95th percentile range from 2.6 to 7.6 points 
for the LLL concentration-response function.
    Further, in comparing current NAAQS scenario estimates to current 
conditions estimates for the three location-specific urban case 
studies, the estimated difference in total Pb-related IQ loss for the 
median is about 0.5 to 1.4 points using the LLL concentration-response 
function and a similar magnitude of difference is estimated for the 
95th percentile. The corresponding estimate for the general urban case 
study is 1.1 to 1.3 points higher total Pb-related IQ loss for the 
current NAAQS scenario compared to the two current conditions 
scenarios.
    Estimates of median and 95th percentile IQ loss associated with 
policy-relevant Pb exposure for air quality scenarios under current 
conditions (which meet the current NAAQS) and, particularly those 
reflecting conditions simulated to just meet the current standard,\65\ 
indicate levels of IQ loss that some may reasonably consider to be 
significant from a public health perspective. Further, for the three 
location-specific urban case studies, the estimated differences in 
incidences of children with IQ loss greater than one point and with IQ 
loss greater than seven points in comparing current conditions to those 
associated with the current NAAQS indicate the potential for 
significant numbers of children to be negatively affected if air Pb 
concentrations increased to levels just meeting the

[[Page 71525]]

current standard. Estimates of the additional number of children with 
IQ loss greater than one point (based on the LLL concentration-response 
function) in these three study areas with the current NAAQS scenario 
compared to current conditions range from 100 to 6,000 across the three 
locations. The corresponding estimates for the additional number of 
children with IQ loss greater than seven points, for the current NAAQS 
as compared to the current conditions scenario range from 600 to 
35,000. These latter values for the change in incidence of children 
with greater than seven points Pb-related IQ loss represent 5 to 17 
percent of the children (aged less than 7 years of age) in these study 
areas. This increase corresponds to approximately a doubling in the 
number of children with this magnitude of Pb-related IQ loss in the 
study area most affected.
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    \65\ As recognized in section III.B.2.d above, to simulate air 
concentrations associated with the current NAAQS, a proportional 
roll-up of concentrations from those for current conditions was 
performed for the location-specific urban case studies. This was not 
necessary for the primary Pb smelter case study in which air 
concentrations currently exceed the current standard.
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    While the risk assessment has quantified risks associated with IQ 
impacts in childhood, there are other, unquantified adverse 
neurocognitive effects that may occur at similarly low exposures which 
might additionally contribute to reduced academic performance, which 
may have adverse consequences over a lifetime (CD, pp. 8-29 to 8-30). 
Additional impacts at low levels of childhood exposure that were not 
quantified in the risk assessment include: other neurological effects 
(sensory, motor, cognitive and behavioral), immune system effects 
(including some related to allergic responses and asthma), and early 
effects related to anemia.
c. CASAC Advice and Recommendations
    Beyond the evidence- and risk/exposure-based information discussed 
above, in considering the adequacy of the current standard, EPA will 
also consider the advice and recommendations of CASAC, based on their 
review of the Criteria Document and the drafts of the Staff Paper and 
the related technical support document, as well as comments from the 
public on drafts of the Staff Paper and related technical support 
document.\66\ With regard to the public comments, those that addressed 
adequacy of the current standard concluded that the current standard is 
inadequate and should be revised, suggesting appreciable reductions in 
the level. No comments were received expressing the view that the 
current standard is adequate. One comment was received arguing not that 
the standard was inadequate but rather that conditions justified that 
it should be revoked. In both the 1990 review and this review of the 
standard set in 1978, CASAC, has recommended consideration of more 
health protective NAAQS. In CASAC's review of the 1990 Staff Paper, as 
discussed in Section 5.2.2, they generally recommended consideration of 
levels below 1.0 [mu]g/m\3\, specifically recommended analyses of a 
standard set at 0.25 [mu]g/m\3\, and also recommended a monthly 
averaging time (CASAC, 1990). In two letters to the Administrator 
during the current review, CASAC has consistently recommended that the 
primary NAAQS should be ``substantially lowered'' from the current 
level of 1.5 [mu]g/m\3\ to a level of ``0.2 [mu]g/m\3\ or less'' 
(Henderson, 2007a, b). CASAC drew support for this recommendation from 
the current evidence, described in the Criteria Document, of health 
effects occurring at dramatically lower blood Pb levels than those 
indicated by the evidence available when the standard was set.
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    \66\ All written comments submitted to the Agency will be 
available in the docket for this rulemaking, as will be transcripts 
of the public meeting held in conjunction with CASAC's review of the 
first draft of the Staff Paper and the first draft of the related 
technical support document, and of draft and final versions of the 
Criteria Document.
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    CASAC concluded that the current Pb NAAQS ``are totally inadequate 
for assuring the necessary decreases of lead exposures in sensitive 
U.S. populations below those current health hazard markers identified 
by a wealth of new epidemiological, experimental and mechanistic 
studies'', and stated that ``Consequently, it is the CASAC Lead Review 
Panel's considered judgment that the NAAQS for Lead must be decreased 
to fully-protect both the health of children and adult populations'' 
(Henderson, 2007a, p. 5).
d. Policy Options
    In considering the adequacy of the current standard, EPA first 
notes the dramatic changes in the basic patterns of air Pb emissions in 
the U.S. since the standard was set, reflecting the phase-out of Pb in 
gasoline, as well as changes to the CAA related to the inclusion of Pb 
compounds on the list of HAPs and associated requirements for 
technology- and risk-based standards for major stationary sources. We 
are aware that questions have been raised about the appropriateness of 
retaining Pb on the list of criteria pollutants and/or maintaining a 
NAAQS for Pb in light of these changed circumstances. We take note of 
the views of CASAC, summarized above, and the conclusions and 
recommendations in the OAQPS Staff Paper on these questions, which do 
not support delisting Pb or revoking the Pb NAAQS. We recognize, 
however, that there may be differing views on interpreting or weighing 
the available information. Thus, EPA solicits comment related to the 
questions of delisting and revocation. The EPA also solicits comment on 
whether the broad range of current multimedia Federal and State Pb 
control programs, summarized above in section II.C, are sufficient to 
provide appropriate public health protection in lieu of a Pb NAAQS.
    In further considering the adequacy of the current standard, EPA 
will focus on the body of available evidence (summarized above in 
section III.A and discussed in the Criteria Document) that is much 
expanded from that available when the current standard was set. The 
presentation of the evidence in the Criteria Document describes the 
occurrence of adverse health effects at appreciably lower blood Pb 
levels than those demonstrated by the evidence at the time the standard 
was set. We recognize that the current health effects evidence together 
with findings from the exposure and risk assessments (summarized above 
in section III.B), like the information available at the time the 
standard was set, supports the conclusion that air-related Pb exposure 
pathways (by inhalation and ingestion) contribute to blood Pb levels in 
young children. Furthermore, we take note of the information that 
suggests that the air-to-blood relationship (i.e., the air-to-blood 
ratio), is likely larger, with regard to increase in blood Pb per unit 
air concentration, when air inhalation and ingestion are considered 
than that estimated when the standard was set using only inhalation and 
may be several times larger. EPA recognizes there is uncertainty in 
estimates of this relationship and solicits comment on on ratios 
supported by the current evidence.
    In areas projected to just meet the current standard, the 
quantitative estimates of risk (for IQ decrement) associated with 
policy-relevant Pb indicate risk of a magnitude that some may consider 
to be significant from a public health perspective.\67\ Further, 
although the current monitoring data indicate few areas with airborne 
Pb near or just exceeding the current standard, we recognize 
significant limitations with the current monitoring network and thus 
the potential that the prevalence of such levels of Pb

[[Page 71526]]

concentrations may be underestimated by currently available data.
---------------------------------------------------------------------------

    \67\ As recognized in section III.B.2.d above, to simulate air 
concentrations associated with the current NAAQS, a proportional 
roll-up of concentrations from those for current conditions was 
performed for the location-specific urban case studies. This was not 
necessary for the primary Pb smelter case study in which air 
concentrations currently exceed the current standard.
---------------------------------------------------------------------------

    As summarized above, CASAC conclusions and recommendations and 
recommendations presented in the OAQPS Staff Paper reflect the view 
that the current standard is not adequate and support consideration of 
a revised standard to provide an adequate margin of safety for 
sensitive groups. Taking these views into account, we recognize that 
one approach is to consider a revised standard. We also recognize that 
there may be differing interpretations of the available information. 
Thus, EPA solicits comment on delisting, revocation, and the adequacy 
of the current standard and the rationale upon which such views are 
based.
4. Elements of the Standard
    The four elements of the standard--indicator, averaging time, form 
and level serve to define the standard and must be considered 
collectively in evaluating the health and welfare protection afforded 
by the standard. In considering revisions to the current primary Pb 
standard, as discussed in the following sections, EPA will consider 
each of the four elements of the standard as to how they might be 
revised to provide a primary standard for Pb that is requisite to 
protect public health with an adequate margin of safety.
a. Indicator
    The indicator for the current standard is Pb-TSP. When the standard 
was set, the Agency considered identifying Pb in particles less than or 
equal to 10 [mu]m in diameter (Pb-PM10) as the indicator in 
response to comments expressing concern that because only a fraction of 
airborne particulate matter is respirable, an air standard based on 
total air Pb is unnecessarily stringent. The Agency responded that 
while it agreed that some Pb particles are too small or too large to be 
deposited in the respiratory system, a significant component of 
exposures can be ingestion of materials contaminated by deposition of 
Pb from the air. In addition to the route of ingestion and absorption 
from the gastrointestinal tract, nonrespirable Pb in the environment 
may, at some point, become respirable through weathering or mechanical 
action. EPA concluded that total airborne Pb, both respirable and 
nonrespirable fractions should be addressed by the air standard.
    More recently, in the 1990 Staff Paper, this issue was reconsidered 
in light of information regarding limitations of the high-volume 
sampler used for the Pb-TSP measurements and the continued use of total 
suspended particulate matter (TSP) as the indicator was supported by 
OAQPS staff (USEPA, 1990).

    Given that exposure to lead occurs not only via direct 
inhalation, but via ingestion of deposited particles as well, 
especially among young children, the hi-vol provides a more complete 
measure of the total impact of ambient air lead. * * * Despite its 
shortcomings, the staff believes the high-volume sampler will 
provide a reasonable indicator for determination of compliance * * *
    In the current review, CASAC has recommended that EPA consider a 
change in the indicator to utilize low-volume PM10 sampling 
(Henderson, 2007a, b). In so doing, CASAC recognized that a scaling of 
the NAAQS level would be needed to accommodate the loss of very large 
coarse-mode Pb particles and concurrent Pb-PM10 and Pb-TSP 
sampling would be needed to inform development of scaling factors. The 
September 2007 CASAC letter states that the CASAC Lead Panel ``strongly 
encourages the Agency to consider revising the Pb reference method to 
allow sample collection by PM10, rather than TSP samplers, 
accompanied by analysis with low-cost multi-elemental techniques like 
X-Ray Fluorescence (XRF) or Inductively Coupled Plasma-Mass 
Spectroscopy (ICP-MS).'' While recognizing the importance of coarse 
dust contributions to total Pb exposure via the ingestion route and 
acknowledging that TSP sampling is likely to capture additional very 
coarse particles which are excluded by PM10 samplers, the 
Panel raised some concerns. The concerns were regarding the precision 
and variability of TSP samplers, and the inability to efficiently 
capture the non-homogeneity of very coarse particles in a national 
monitoring network, which the Panel indicated may need to be addressed 
in implementing additional monitoring sites and an increased frequency 
of sample collection that might be required with the substantial 
reduction in the level of the standard and shorter averaging time that 
they recommend (Henderson, 2007b).
    In considering the appropriate indicator, EPA takes note of and 
solicits comment on previous Agency conclusions that the health 
evidence indicates that Pb in all particle size fractions, not just 
respirable Pb, contributes to Pb in blood and to associated health 
effects. Additionally, the current information does not support the 
derivation of a single scaling factor, which might be used to relate a 
level for Pb-TSP to a monitoring result using Pb-PM10 on a 
national scale. The EPA recognizes, however, that an indicator that 
exhibits low spatial variability is desirable such that it facilitates 
implementation of an effective monitoring network, i.e., one that 
assures identification of areas with the potential to exceed the NAAQS.
    To the extent that Pb-PM10 exhibits less spatial 
variability and that a ``crosswalk'' can be developed between a level 
in terms of Pb-TSP, EPA recognizes that it is appropriate to consider 
moving to a Pb-PM10 indicator in the future. One of the 
issues to consider when moving to a Pb-PM10 indicator is 
whether regulating concentrations of Pb-PM10 will lead to 
appropriate controls on Pb emissions from sources with a large 
percentage of Pb in the greater than 10 micron size range (e.g., 
fugitive dust emissions from Pb smelters). It is reasonable to believe 
that Pb-PM10/Pb-TSP ratios are sensitive to distance from 
emissions sources (due to faster deposition of larger particles). As 
such, the use of a Pb-PM10 indicator may have a significant 
influence on the degree of Pb controls needed from emission sources.
    The EPA will consider several options that might improve the 
available database and facilitate such a move in the future, while 
retaining Pb-TSP as the indicator for the NAAQS at this time, 
consistent with the recommendations in the Staff Paper. For example, we 
might consider describing a FEM in terms of PM10 that might 
be acceptably applied on a site-by-site basis where an appropriate 
relationship between Pb-TSP and Pb-PM10 can be developed 
based on site-specific data. Alternatively, use of such an FEM might be 
approved, in combination with more limited Pb-TSP monitoring, in areas 
where the Pb-TSP data indicate ambient Pb levels are well below the 
NAAQS level.
    These examples were intended purely for purposes of illustrating 
the types of options the Agency might consider. Specific details of any 
options would need to be supported by appropriate data analyses. We 
solicit information and comments that would help inform such analyses 
and the Agency's views on the indicator for the primary Pb NAAQS.
b. Averaging Time and Form
    The basis for the averaging time of the current standard reflects 
consideration of the evidence available when the Pb NAAQS were 
promulgated in 1978. At that time, the Agency had concluded that the 
level of the standards, 1.5 [mu]g/m\3\, would be a ``safe ceiling for 
indefinite exposure of young children'' (43 FR 46250), and that the 
slightly greater possibility of elevated air Pb levels within the 
quarterly averaging

[[Page 71527]]

period as contrasted to the monthly averaging period proposed in 1977 
(43 FR 63076), was not significant for health. These conclusions were 
based in part on the Agency's interpretation of the health effects 
evidence as indicating that 30 [mu]g/dL was the maximum safe level of 
blood Pb for an individual child.
    As discussed above, the currently available health effects evidence 
\68\ indicates a variety of neurological effects, as well as immune 
system and hematological effects, associated with levels below 10 
[mu]g/dL as a central tendency metric of study cohorts of young 
children. Further, EPA recognizes that today ``there is no level of Pb 
exposure that can yet be identified, with condfidence, as clearly not 
being associated with some risk of deleterious health effects'' (CD, p. 
8-63). Accordingly, to the extent that air Pb contributes to variation 
in blood Pb, we currently cannot identify a safe ceiling for indefinite 
exposure of young children.
---------------------------------------------------------------------------

    \68\ The differing evidence and associated strength of the 
evidence for these different effects is described in detail in the 
Criteria Document.
---------------------------------------------------------------------------

    Additionally, several aspects of the current health effects 
evidence for Pb pertain to the consideration of averaging time:
     Children are exposed to ambient Pb via inhalation and 
ingestion, with Pb taken into the body absorbed through the lungs and 
through the gastrointestinal tract. Studies on Pb uptake, elimination 
and distribution show that Pb is absorbed into peripheral tissues in 
adults within a few days (USEPA 1986a; USEPA 1990b, p. IV-2). 
Absorption of Pb from the gastrointestinal tract appears to be greater 
and faster in children as compared to adults (CD, Section 4.2.1). Once 
absorbed, it is quickly distributed from plasma to red blood cells and 
throughout the body.
     Lead accumulates in the body and is only slowly removed, 
with bone Pb serving as a blood Pb source for years after exposure and 
as a source of fetal Pb exposure during pregnancy (CD, Sections 4.3.1.4 
and 4.3.1.5).
     Blood Pb levels, including levels of the toxicologically 
active fraction, respond quickly to increased Pb exposure, such that an 
abrupt increase in Pb uptake rapidly changes blood Pb levels, with the 
time to reach a new quasi-steady state with the total body burden after 
such an occurrence projected to be approximately 75 to 100 days (CD, p. 
4-27).
     The elimination half-life, which describes the time for 
blood Pb levels to stabilize after a reduction in exposure, for the 
dominant phase for blood Pb responses to changes in exposure is on the 
order of 20 to 30 days for adults (CD, p. 4-25). Blood elimination 
half-lives are influenced by contributions from bone. Given the tighter 
coupling in children of bone stores with blood levels, children's blood 
Pb is expected to respond more quickly than adults (CD, pp. 4-20 and 4-
27).
     Data from NHANES II and an analysis of the temporal 
relationship between gasoline consumption data and blood lead data 
generally support the inference of a prompt response of children's 
blood Pb levels to changes in exposure in that children's blood Pb 
levels and the number of children with elevated blood Pb levels appear 
to respond to monthly variations in Pb emissions from Pb in gasoline 
(EPA, 1986a, p. 11-39; Rabinowitz and Needleman, 1983; Schwartz and 
Pitcher, 1989).
     The evidence with regard to sensitive neurological effects 
is limited in what it indicates regarding the specific duration of 
exposure associated with effect, although it indicates both the 
sensitivity of the first 3 years of life and a sustained sensitivity 
throughout the lifespan as the human central nervous system continues 
to mature and be vulnerable to neurotoxicants (CD, Section 8.4.2.7). 
The animal evidence supports our understanding of periods of 
development with increased vulnerability to specific types of effect 
(CD, Section 5.3), and indicates a potential importance of exposures on 
the order of months.
     Evidence of a differing sensitivity of the immune system 
to Pb across and within different periods of life stages indicates a 
potential importance of exposures as short as weeks to months duration. 
For example, the animal evidence suggests that the gestation period is 
the most sensitive life stage followed by early neonatal stage, and 
within these life stages, critical windows of vulnerability are likely 
to exist (CD, Section 5.9 and p. 5-245).
    Further, evidence described in the Criteria Document and the risk 
assessment indicate that ingestion of dust can be a predominant 
exposure pathway for young children to policy-relevant Pb, and that 
there is a strong association between indoor dust Pb levels and 
children's blood Pb levels. As stated in the Criteria Document, ``given 
the large amount of time people spend indoors, exposure to Pb in dusts 
and indoor air can be significant'' (CD, p. 3-27). The Criteria 
Document further describes studies that evaluated the influence of dust 
Pb exposure on children's blood Pb: ``Using a structural equation 
model, Lanphear and Roghmann (1997) also found the exposure pathway 
most influential on blood Pb was interior dust Pb loading, directly or 
through its influence on hand Pb. Both soil and paint Pb influenced 
interior dust Pb; with the influence of paint Pb greater than that of 
soil Pb. Interior dust Pb loading also showed the strongest influence 
on blood Pb in a pooled multivariate regression analysis (Lanphear et 
al., 1998).'' (CD, p. 4-134).
    While some of these aspects of the health effects evidence would be 
consistent with a quarterly averaging time, taken as a whole, and in 
combination with information on potential response time for indoor dust 
Pb levels, EPA recognizes that there is also support for consideration 
of an averaging time shorter than a calendar quarter.
    When the standard was set in 1978, an analysis of ambient 
measurements available at the time indicated that the distribution of 
air Pb levels was such that there was little possibility that there 
could be sustained periods greatly above the average value in 
situations where the quarterly standard was achieved. This may have 
been related to the pattern of Pb emissions at the time the standard 
was set, which differed from the pattern today in that, due to 
emissions from cars and trucks at that time, emissions were more 
spatially distributed. In this review, based on data from 2003-2005, 
the air quality analysis in Chapter 2 of the Staff Paper indicates the 
presence of areas in the U.S. currently where temporal variability does 
create differences between average quarterly levels and levels 
sustained for shorter than quarterly periods. For example, four percent 
of the monitoring sites in the three-year analysis dataset that meet 
the current standard as an average over a calendar quarter exceed the 
level of the current standard when considering an average for any 
individual month. The same analysis indicates that this number is as 
high as ten percent for some alternate lower levels.
    In further considering the appropriate form of the standard that 
might accompany a shorter averaging time, EPA will take into account 
analyses using air quality data for 2003-2005 that characterize maximum 
quarterly average and various monthly statistics for each year across 
the three year Pb-TSP dataset and also across the three year period. 
The latter time period is consistent with the three calendar year 
attainment period that has been adopted for the ozone and particulate 
matter

[[Page 71528]]

NAAQS subsequent to the promulgation of the Pb NAAQS. For the three 
year period, the monthly statistics derived are maximum monthly mean, 
second maximum monthly mean, average of three overall highest monthly 
means, and average of three annual maximum monthly means; these 
statistical forms were also considered in the 1990 Staff paper. 
Additionally, the maximum and 2nd maximum monthly means for each year 
of the three year data set was derived, as well as the averages of 
these individual year statistics.
    With regard to comparison of monthly forms with the maximum 
quarterly mean, the average Pb-TSP maximum monthly mean among all 189 
sites in the analysis is notably higher (nearly a factor of two) than 
the average of the average maximum quarterly mean among these sites. 
Further, this difference is slightly greater for source-oriented sites 
than non source-oriented sites or urban sites (e.g., a factor of 
approximately 1.8 as compared to one of approximately 1.6), indicating 
perhaps an influence of variability in emissions. The alternate forms 
of a monthly averaging time that were analyzed yield an across-site 
average that is similar although slightly higher than the quarterly 
average (e.g., Figure 2-8 in Chapter 2 of the Staff Paper).
    The analyses described in Chapter 2 of the Staff Paper consider 
both a period of three calendar years and one of an individual calendar 
year (with the form of the current standard being the maximum quarterly 
mean in any one year). These analyses indicate that with regard to 
either single-year or 3-year statistics for the 2003-2005 dataset, a 
2nd maximum monthly mean yields very similar, although just slightly 
greater, numbers of sites exceeding various alternate levels as a 
maximum quarterly mean, with both yielding fewer exceedances than a 
maximum monthly mean.
    In their advice to the Agency, CASAC has recommended that 
consideration be given to changing from a calendar quarter to a monthly 
averaging time (Henderson, 2007a, b). In making that recommendation, 
CASAC emphasizes support from studies that suggest that blood Pb 
concentrations respond at shorter time scales than would be captured 
completely by quarterly values, as indicated by their description of 
their recommendation for adoption of a monthly averaging time as ``more 
protective of human health in light of the response of blood lead 
concentrations that occur at sub-quarterly time scales'' (Henderson, 
2007b).
    With regard to form of the standard, CASAC stated that one could 
``consider having the lead standards based on the second highest 
monthly average, a form that appears to correlated well with using the 
maximum quarterly value'', while also indicating that ``the most 
protective form would be the highest monthly average in a year.''
    The following observations support consideration of a monthly 
averaging time: (1) The health evidence indicates that very short 
exposures can lead to increases in blood Pb Pb levels, (2) the time 
period of response of indoor dust Pb to airborne Pb can be on the order 
of weeks and, (3) the health evidence indicates that adverse effects 
may occur with exposures during relatively short windows of 
susceptibility, such as prenatally and in developing infants. EPA also 
recognizes the limited available evidence specific to the consideration 
of the particular duration of sustained airborne Pb levels having the 
potential to contribute to the adverse health effects identified as 
most relevant to this review.
    Based on the information and air quality analyses discussed above, 
EPA is requesting comment on a range of options, including the 
recommendations in the Staff Paper that include changing the averaging 
time to monthly, with a form of maximum or second maximum, as well as 
retaining the quarterly averaging time. The EPA is also requesting 
comment on, the options of changing the form to apply to a three-year 
period as well as retaining a single-year period. We solicit comments 
on these ranges of averaging times and forms as well as views and 
related rationales that might support alternative options.
c. Level
    At this time, the Agency is interested in soliciting comment on a 
wide range of possible options for consideration when making a proposed 
decision on the level of the primary Pb NAAQS. These policy options 
range from lowering the standard, to the levels recommended by CASAC 
and the OAQPS Staff paper or lower, as well as on other alternative 
levels, up to and including the current level, and the rationale upon 
which such views are based.
i. Evidence-Based Considerations
    The EPA recognizes that there are several aspects to the body of 
epidemiological evidence available in this review that complicate 
efforts to translate the evidence into the basis for selecting an 
appropriate level for an ambient air quality standard. As an initial 
matter, as summarized above and discussed in greater depth in the 
Criteria Document (CD, Sections 4.3 and 6.1.3), the epidemiological 
evidence that associates Pb exposures with health effects uses blood Pb 
as the dose metric, not ambient air concentrations. Further, for the 
health effects receiving greatest emphasis in this review (neurological 
effects on the developing nervous system), no threshold levels can be 
discerned from the evidence. As was recognized at the time of the last 
review, estimating a threshold for toxic effects of Pb on the central 
nervous system entails a number of difficulties (CD, pp. 6-10 to 6-11). 
The task is made still more complex by support in the evidence for a 
nonlinear rather than linear relationship of blood Pb with 
neurocognitive decrement, with greater risk of decrement-associated 
changes in blood Pb at the lower levels of blood Pb in the exposed 
population (Section 3.3.7; CD, Section 6.2.13).
    In considering how this evidence can help inform the selection of 
the level of the standard, EPA will consider how the framework applied 
in the establishment of the standard may be applied to the much 
expanded body of evidence that is now available. This consideration 
builds upon the evidence-based considerations of the adequacy of the 
current standard, discussed above in Section III.C.3.a.
    As noted above, this review focuses on young children as the key 
sensitive population for Pb exposures, the same population identified 
in 1978. In this sensitive population, the current evidence 
demonstrates the occurrence of adverse health effects, including those 
on the developing nervous system, associated with blood Pb levels 
extending well below 10 [mu]g/dL to 5 [mu]g/dL and possibly lower. Some 
studies indicate Pb effects on intellectual attainment of young 
children at blood Pb levels ranging from 2 to 8 [mu]g/dL (CD, Sections 
6.2, 8.4.2 and 8.4.2.6), including findings of similar Pb-related 
effects in a study of a nationally representative sample of children in 
which the mean blood Pb level was 1.9 [mu]g/dL (CD, pp. 6-31 to 6-32; 
Lanphear et al., 2000).\69\ Further, the current evidence does not 
indicate a threshold for the more sensitive health endpoints such as 
adverse effects on the

[[Page 71529]]

developing nervous system (CD, pp. 5-71 to 5-74 and Section 6.2.13). 
This differs from the Agency's inference in the 1978 rulemaking of a 
threshold of 40 [mu]g/dL blood Pb for effects of Pb considered clearly 
adverse to health at that time, i.e., impairment of heme synthesis and 
other effects which result in anemia. Thus, the level of Pb in 
children's blood associated with adverse health effect has dropped 
substantially.
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    \69\ These findings include significant associations in the 
study sample subsets of children with blood Pb levels less than 10 
[mu]g/dL, less than 7.5 [mu]g/dL and less than 5 [mu]g/dL. A 
positive, but not statistically significant association, was 
observed in the less than 2.5 [mu]g/dL subset, although the effect 
estimate for this subset was largest among all the subsets. The lack 
of statistical significance for this subset may be due to the 
smaller sample size of this subset which would lead to lower 
statistical power.
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    As when the standard was set in 1978, EPA recognizes that there 
remain today contributions to blood Pb levels from nonair sources. As 
discussed above, these contributions have been reduced since 1978, with 
estimates of reduction in the dietary component of 70 to 95 percent 
(CD, Section 3.4). The evidence is limited with regard to the aggregate 
reduction since 1978 of all nonair sources to blood Pb. However, the 
available evidence and some preliminary analysis led CASAC to recommend 
consideration of 1.0 to 1.4 [mu]g/dL or lower as an estimate of the 
nonair component of blood Pb (Henderson, 2007a). The value of 1.4 
[mu]g/dL was the mean blood Pb level derived from a simulation of 
current nonair exposures using the IEUBK model (Henderson, 2007a, pp. 
F-60 to F-61). These current estimates are roughly an order of 
magnitude lower than the value of 12 [mu]g/dL that was used in setting 
the 1978 standard.
    Regarding the relationship between air and blood, while the 
evidence demonstrates that airborne Pb influences blood Pb 
concentrations through a combination of inhalation and ingestion 
exposure pathways, estimates of the precise quantitative relationship 
(i.e., air-to-blood ratio) available in the evidence vary (USEPA, 
1986a; Brunekreef, 1984) and there is uncertainty as to the values that 
pertain to current exposures. Studies summarized in the 1986 Criteria 
Document typically yield estimates in the range of 1:3 to 1:5, with 
some as high as 1:10 or higher (USEPA, 1986a; Brunekreef, 1984). 
Findings in a more recent study identified in the Criteria Document of 
blood Pb response to reduced air concentrations indicate a ratio on the 
order of 1:7 (CD, pp. 3-23 to 3-24; Hilts et al., 2003). A value of 1:5 
has been used by the World Health Organization (2000). These ratios are 
appreciably higher than the ratio of 1:2 that was used in setting the 
1978 standard.
    A standard setting approach being considered is to apply the 
framework relied upon in setting the standard in 1978 to the currently 
available information. In applying that framework, however, EPA 
recognizes that today ``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). However, there 
is increasing uncertainty with regard to the magnitude and type of 
effects at levels below 5 [mu]g/dL \70\. This is in contrast to the 
situation in 1978 when the Agency judged that the maximum safe blood Pb 
level (geometric mean) for a population of young children was 15 [mu]g/
dL based on its conclusion that the maximum safe blood Pb level of an 
individual child was 30 [mu]g/dL. \71\
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    \70\ As stated in the Criteria Document ``Some recent studies of 
Pb neurotoxicity in infants have observed effects at population 
average blood-Pb levels of only 1 or 2 [mu]g/dL; and some 
cardiovascular, renal, and immune outcomes have been reported at 
blood-Pb levels below 5 [mu]g/dL.'' (CD, p. E-16).
    \71\ More specifically, the 1978 target of 15 [mu]g/dL was 
described as the geometric mean level associated with a 99.5 
percentile of 30 [mu]g/dL which the Agency described as a ``safe 
level'' for an individual child (43 FR 46247-49).
---------------------------------------------------------------------------

    In illustrating the application of the 1978 framework, two blood Pb 
levels are used here for illustrative purposes. A level of 2 [mu]g/dL 
was used because it represents some of the lowest population levels 
associated with adverse effect in the current evidence (e.g., CD, p. E-
9; Lanphear et al., 2000). In addition, a level of 5 [mu]g/dL has been 
used. This level has been associated with adverse health effects with a 
higher degree of certainty in the published literature, and is a level 
where cognitive deficits were identified with statistical significance 
(Lanphear et al., 2000).
    Using a blood Pb target of 2 [mu]g/dL as a substitute for the 1978 
target of 15 [mu]g/dL for the child population geometric mean, then 
subtracting 1 to 1.4 [mu]g/dL for background, yields 0.6 to 1 [mu]g/dL 
as a target for the air contribution to blood Pb. Dividing the air 
target by 5, consistent with currently available information on the 
ratio of air Pb to blood Pb, yields a potential standard level of 0.1 
to 0.2 [mu]g/m\3\. Alternatively, using the same approach substituting 
5 [mu]g/dL for the child population geometric mean and subtracting 1 to 
1.4 [mu]g/dL for background, yields 3.6 to 4 [mu]g/dL as a target for 
the air contribution to blood Pb. Dividing the air target by 5, 
consistent with currently available information on the ratio of air Pb 
to blood Pb, yields a level of 0.7 to 0.8 [mu]g/m\3\. Similarly, 
substitution of other blood Pb targets would result in still other 
levels.
    In light of the current CDC blood Pb ``level of concern'' of 10 
[mu]g/dL, some might consider a blood Pb value of 10 [mu]g/dL as a 
target blood Pb value for this calculation to derive a level for the 
primary standard. EPA notes, however, that the CDC does not consider 
this level of concern as a safe blood Pb level or one without evidence 
of adverse effects (CDC, 2005a). Rather, it is used by CDC to identify 
children with elevated blood Pb levels for follow-up activities \72\ at 
the individual level and to trigger communitywide prevention activities 
(CDC, 2005a). The level of concern has been frequently misinterpreted 
as a definitive toxicologic threshold (CDC, 2005a). As summarized in 
Section III.A and above, and as described in detail in the Criteria 
Document, various adverse effects have been associated with children's 
blood Pb levels below 10 [mu]g/dL. For example, the Criteria Document 
states that the currently available toxicologic and epidemiologic 
information ``includes assessment of new evidence substantiating risks 
of deleterious effects on certain health endpoints beng 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). Accordingly, EPA has not used a mean or an 
individual target blood Pb value of 10 [mu]g/dL as the basis for an 
illustrative example of deriving a standard that is intended to protect 
public health with an adequate margin of safety. In recognition of 
differing views on this subject, however, we solicit comment on the 
appropriateness of using a mean or individual target blood Pb value of 
10 [mu]g/dL as the foundation for deriving a level for the primary Pb 
standard.
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    \72\ Activities such as taking an environmental history, 
educating parents about Pb and conducting follow-up blood Pb 
monitoring were among those suggested for children with blood Pb 
levels greater than or equal to 10 [mu]g/dL (CDC, 2005a). Recently, 
CDC's Advisory Committee on Childhood Lead Poisoning Prevention has 
also provided information and recommendations relevant to clinical 
management of children with blood Pb levels below 10 [mu]g/dL 
(ACCLPP, 2007).
---------------------------------------------------------------------------

    The above examples focus on the mean target blood Pb level for the 
sensitive population by way of illustrating application of the 1978 
framework. The EPA solicits comment on mean target blood Pb levels as 
well as other factors that would be important in applying the 1978 
framework. For example, the distribution of blood Pb levels within the 
sensitive population is an important aspect of the 1978 framework. When 
the standard was set in 1978, the Agency stated that the population 
mean, measured as the geometric mean, must be 15 [mu]g/dL in order to 
ensure that 99.5 percent of children in the United States would

[[Page 71530]]

have a blood Pb level below 30 [mu]g/dL, which was identified as the 
maximum safe blood Pb level for individual children based on the 
information available at that time (43 FR 46252). Target values for the 
mean of the population necessarily imply higher values for individuals 
associated with the upper percentiles of the blood Pb distribution. For 
example, the 2001-2002 NHANES information indicates that a geometric 
mean blood level of 1.7 [mu]g/dL for children nationally, aged 1-5 
years, is associated with a 95th percentile blood Pb level of 5.8 
[mu]g/dL (CDC, 2005b).
    Additionally, the nonair (background) contribution to total blood 
Pb is an important input to the framework and we solicit comment on the 
definition and appropriate values for this parameter.\73\ In the 
assessment presented in this notice, contributions attributed to 
``recent air'' and to ``recent plus past air'' may include some Pb from 
the historic use of Pb in paint and gasoline and other sources.
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    \73\ As noted above, in 2001 when establishing standards for 
lead-based paint hazards in most pre-1978 housing and child-occupied 
facilities (66 FR 1206), the Agency grappled with the uncertainties 
in what environmental levels of historic Pb in soil and dust (from 
the historical use of Pb in paint and gasoline) in which specific 
medium may cause blood Pb levels that are associated with adverse 
effects (see Section II.C).
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    Further, there are a range of estimates for the air-to-blood ratio 
that include estimates higher than that used in 1978 when the standard 
was set. We solicit comment and supporting information regarding the 
air-to-blood ratio and differences in the available estimates. All of 
these factors are important in applying a framework such as that used 
in 1978, and we solicit comment, along with supporting information, on 
all of these factors.
    Beyond the 1978 framework illustrated above, EPA recognizes a 
variety of approaches can be used in translating the current evidence 
to a level for the standard. With this notice, EPA solicits comment on 
the 1978 standard setting framework and on alternate approaches and the 
factors that are relevant to those approaches.
ii. Exposure- and Risk-Based Considerations
    To inform judgments about a range of levels for the standard that 
could provide an appropriate degree of public health protection, in 
addition to considering the health effects evidence, EPA will also 
consider the quantitative estimates of exposure and health risks 
attributable to policy-relevant Pb upon meeting specific alternative 
levels of alternative Pb standards and the uncertainties in the 
estimated exposures and risks, as discussed above in Section III.B. As 
discussed above, the risk assessment conducted by EPA is based on 
exposures that have been estimated for children of less than 7 years of 
age in six case studies. The assessment estimated the risk of adverse 
neurocognitive effects in terms of IQ decrements associated with total 
and policy-relevant Pb exposures, including incidence of different 
levels of IQ loss in three of the six case studies. In so doing, EPA is 
mindful of the important uncertainties and limitations that are 
associated with the exposure and risk assessments. For example, with 
regard to the risk assessment important uncertainties include those 
related to estimation of blood Pb concentration-response functions, 
particularly for blood Pb concentrations at and below the lower end of 
those represented in the epidemiological studies characterized in the 
Criteria Document.
    EPA also recognizes important limitations in the design of, and 
data and methods employed in, the exposure and risk analyses. For 
example, the available monitoring data for Pb, relied upon for 
estimating current conditions for the urban case studies is quite 
limited, in that monitors are not located near some of the larger known 
Pb sources, which provides the potential for underestimation of current 
conditions, and there is uncertainty about the proximity of existing 
monitors to other Pb sources potentially influencing exposures, such as 
old urban roadways and areas where housing with Pb paint has been 
demolished. All of these limitations raise uncertainty as to whether 
these data adequately capture the magnitude of ambient Pb 
concentrations to which the target population is currently exposed. 
Additionally, EPA recognizes that there is not sufficient information 
available to evaluate all relevant sensitive groups (e.g., adults with 
chronic kidney disease) or all Pb-related adverse health effects (e.g., 
neurological effects other than IQ decrement, immune system effects, 
adult cardiovascular or renal effects), and the scope of our analyses 
was generally limited to estimating exposures and risks in six case 
studies intended to illustrate a variety of Pb exposure situations 
across the U.S., with three of them focused on specific areas in three 
cities. As noted above, however, coordinated intensive efforts over the 
last 20 years have yielded a substantial decline in blood Pb levels in 
the United States. Recent NHANES data (2003-2004) yield blood lead 
level estimates for children age 1 to 5 years of 1.6 [mu]g/dL (median) 
and 3.9 [mu]g/dL (90th percentile). These median and 90th percentile 
national-level data are lower than modeled values generated for the 
three location-specific urban case studies current conditions scenarios 
(see footnote 39). It is noted, however, that the urban case studies 
and the NHANES study are likely to differ with regard to factors 
related to Pb exposure, including ambient air levels.
    EPA also recognizes limitations in our ability to characterize the 
contribution of policy-relevant Pb to total Pb exposure and Pb-related 
health risk. For example, given various limitations of our modeling 
tools, blood Pb levels associated with air-related exposure pathways 
and current levels of Pb emitted to the air (including via 
resuspension) may fall between the estimates for ``recent air'' and 
those for ``recent'' plus ``past air''. However, there are limitations 
associated with the indoor dust Pb models that affect our ability to 
discern differences in the recent air category among different 
alternate air quality scenarios and both categories may include Pb in 
soil and dust from the historical use of Pb in paint.
    With these limitations in mind, EPA will consider the estimates of 
IQ loss associated with policy-relevant Pb at air Pb concentrations 
near those currently occurring in urban areas as illustrated by 
conditions in the three cities chosen for the location-specific urban 
case studies, e.g., 0.09 to 0.36 [mu]g/m\3\ as a maximum quarterly 
average or 0.17 to 0.56 [mu]g/m\3\ as a maximum monthly average. 
Recognizing, as described above, that estimates of IQ loss associated 
with air-related exposure pathways and current levels of Pb emitted to 
the air (including via resuspension) may fall between the estimates for 
``recent air'' and those for ``recent'' plus ``past air'', EPA will 
consider ranges reflecting those two categories. Further, as noted 
above, we will focus on risk estimates derived using the LLL (log-
linear with low exposure linearization) concentration-response 
function.
    The ambient air Pb related IQ loss (based on LLL function) 
associated with the median IQ loss for current conditions in the three 
location-specific case studies (see Tables 5-9 and 5-10 of the Risk 
Assessment Report)--estimated to fall between the estimates for recent 
air (0.6-0.7 points) and those for recent plus past air (2.9 points)--
appears to be of a magnitude in the range that CASAC considered to be 
highly significant from a public health perspective (e.g., a

[[Page 71531]]

population IQ loss of 1-2 points). Comparable estimates for the current 
conditions scenarios in the general urban case study are still more 
significant with estimates for the general urban case study ranging 
from 1.3-1.8 for recent air and 3.2-3.6 for recent plus past air. For 
the primary Pb smelter case study, in which air quality exceeds the 
current NAAQS, IQ loss reductions in the recent plus past air category 
associated with the alternate NAAQS levels of 0.2 and 0.5 [mu]g/m\3\ 
ranging from 4.0 to 4.9 points IQ loss for the subarea.
    Focusing only on the recent air estimates, estimates of IQ loss 
(based on the LLL function) associated with policy-relevant Pb at the 
95th percentile of population total IQ loss are greater than 1 point 
for all current conditions scenarios in all three urban case studies 
for which the lowest air Pb concentrations are 0.09 [mu]g/m\3\ maximum 
quarterly average, and 0.17 [mu]g/m\3\ maximum monthly average.
    EPA will also consider the extent to which alternative standard 
levels below current conditions are estimated to reduce blood Pb levels 
and associated health risk in young children (Tables 4-1 through 4-4 in 
the Staff Paper), looking first to the estimates of total blood Pb. In 
the general urban case study, blood Pb levels for the median of the 
population associated with the lowest alternative NAAQS (0.02 [mu]g/
m\3\) are estimated to be reduced from levels in the two current 
conditions scenarios by 14% (0.3 [mu]g/dL) and 24% (0.5 [mu]g/dL), 
respectively. For the 95th percentile of the population, the estimated 
reductions are similar in terms of percentage, but are higher in 
absolute values (1.7 and 1.0 [mu]g/dL). For the three location-specific 
urban case studies, median blood Pb estimates associated with the 
lowest alternative standard are reduced from those associated with 
current conditions by approximately 10% in the Chicago and Cleveland 
study areas and 6% in the Los Angeles study area; similar percent 
reductions are estimated at the 95th percentile total blood Pb. For the 
localized subarea of the primary Pb smelter case study, a 65% reduction 
in both median and 95th percentile blood Pb (3 and 8.1 [mu]g/dL, 
respectively) is estimated for the lowest alternative NAAQS as compared 
to the current NAAQS.\74\
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    \74\ This can be compared to reductions in blood Pb, for the 
primary Pb smelter case study subarea estimated to be associated 
with a change in the level from the current standard to the 0.2 
[mu]g/m\3\ level (either averaging time) which are approximately 45-
50% for both the median and 95th percentile values.
---------------------------------------------------------------------------

    EPA will also consider the extent to which specific levels of 
alternative Pb standards reduce the estimated risks in terms of IQ loss 
attributable to policy-relevant exposures to Pb (Tables 4-3 and 4-4 in 
the Staff Paper). For the general urban case study, estimated 
reductions in median Pb-related IQ loss associated with reduced 
exposures at the lowest alternative NAAQS level (0.02 [mu]g/m\3\) were 
0.5 and 0.7 points (LLL function) for the two current conditions 
scenarios. Reductions at the 95th percentile were of a similar 
magnitude. Among the three location-specific case study areas, 
estimated reductions in median Pb-related IQ loss associated with 
reduced exposures at the lowest alternate NAAQS as compared to current 
conditions range from 0.4 to 0.6 points for the high-end concentration-
response function to 0.1 to 0.2 points for the low-end concentration-
response functions, with estimates for the LLL function ranging from 
0.2 to 0.3 points. The reduction at the 95th percentile, based on the 
LLL function, is 0.3-0.4 points. Reduced exposures associated with the 
lowest alternative NAAQS in the primary Pb smelter case study subarea 
as compared with the current NAAQS (which is not currently met by this 
area) were more substantial, ranging from 2.8 points at the median and 
3 points at the 95th percentile (based on LLL function).
    Based on estimated reductions in Pb-associated IQ loss discussed 
above, EPA observes that estimates for the 95th percentile of the 
population are quite similar to (for the LLL concentration-response 
function) or smaller (for the high- and low-end concentration-response 
functions) than those at the median for all case studies. This is 
because of the nonlinear relationship between IQ decrement and blood Pb 
level such that relatively smaller IQ decrement is associated with 
changes in blood Pb at higher blood Pb levels.
    Reductions in air Pb concentrations from current conditions to meet 
the lower alternative NAAQS (0.02 and 0.05 [mu]g/m\3\, maximum monthly 
mean) are estimated to reduce the number of children having Pb-related 
IQ loss greater than one point by one half to one percent in each of 
the three location-specific urban case studies. More specifically, 
within the three study areas this corresponds to a range of 
approximately 100 to 3,000 fewer children having total IQ loss greater 
than 1.0 for an alternative standard of 0.02 [mu]g/m\3\, maximum 
monthly mean. Further, just meeting the lowest alternative standard in 
these three study areas is estimated to reduce the number of children 
having an IQ loss greater than seven points by one to two percent. This 
corresponds to a range of approximately 350 (for the Cleveland study 
area) up to 8,000 (for the Chicago study area) fewer children with 
total Pb-related IQ loss greater than 7.0.
    As discussed above, CASAC considered a population IQ loss of 1-2 
points to be highly significant from a public health perspective. 
Estimates of IQ loss associated with policy-relevant Pb are of a 
magnitude that appears to fall near or within this range for air 
quality scenarios involving levels at or above 0.09 [mu]g/m\3\, maximum 
quarterly mean, or 0.17 [mu]g/m\3\, maximum monthly mean. Estimated 
reductions in risk associated with reducing air Pb concentrations from 
current conditions (in the urban case studies) to the two lower 
alternative levels evaluated (0.02 and 0.05 [mu]g/m\3\) appear to range 
from a few tenths to just below one IQ point (for the LLL 
concentration-response function) (and up to 1.5 IQ points for the 
highest concentration-response function). Based on estimated changes in 
risk across the population associated with the two lower alternative 
levels (as compared to current conditions), reductions in the number of 
children with total Pb-related IQ loss greater than 1 or greater than 7 
are estimated to be on the order of hundreds to thousands of children 
in the three location-specific urban case studies.
    In considering the exposure and risk information with regard to a 
level for the standard, EPA notes that at the time the standard was 
set, the Agency recognized a particular blood Pb level as ``safe''. 
Today, current evidence does not support the recognition of a ``safe'' 
level. This is generally reflected in the concentration-response 
functions used in the risk assessment and in CASAC recommendations on 
these functions with regard to a lack of a threshold. EPA will 
therefore consider a different approach in this review.
    In considering these risk estimates, EPA is mindful of CASAC's 
recommendation regarding the public health significance of a population 
loss of 1 to 2 IQ points, the significant implications of potential 
shifts in the distribution of IQ for the exposed population, and other 
unquantified Pb-related health effects. Based on these factors and the 
range of estimates summarized above for IQ loss associated with policy-
relevant Pb for the current conditions scenarios of the location-
specific case studies, we recognize that some may consider reducing the 
NAAQS as important from a public health perspective (from air-related 
ambient Pb) relative to that afforded by the current standard.

[[Page 71532]]

    In considering the public health significance of IQ loss beyond 
CASAC's recommendation on this issue, we note that some may consider 
that any IQ loss at the population level is of potential public health 
significance. That is, there is no amount of IQ loss at the population 
level that is clearly recognized as being of no importance from a 
public health perspective. On the other hand, we also recognize that 
some may hold different views. Thus, the magnitude of IQ loss that 
could be allowed by a standard that protects public health with an 
adequate margin of safety is clearly a public health policy judgment to 
be made by the Administrator.
    In considering the magnitudes of IQ loss estimated in our 
assessment for the lowest alternative levels considered, EPA will focus 
on total IQ loss and on the contribution to total IQ loss from policy-
relevant pathways. In so doing, we recognize that nonair contributions 
to total Pb-related IQ loss are estimated to reach and exceed an IQ 
loss of 1-2 points, and we also recognize that air Pb contributions are 
generally of a much smaller magnitude. Thus, we recognize that it may 
be appropriate to consider smaller estimates of IQ loss from air Pb 
contributions (e.g., less than 1 point IQ loss) in identifying the 
appropriate target for the policy-relevant component.
    Placing weight on incremental changes in policy-relevant Pb-related 
IQ loss of less than one point IQ would lead to consideration of the 
lower standard levels evaluated in the risk assessment as part of a 
judgment as to what standard would protect public health with an 
adequate margin of safety. EPA recognizes, however, the significant 
uncertainties in the quantitative risk estimates and that uncertainty 
in the estimates increases with increasing difference of the air 
quality scenarios from current conditions. Thus, to the extent that 
incremental exposure reductions achieved through lowering the NAAQS 
might contribute to incremental reductions in children's blood Pb and 
to associated reductions in health effects, consideration of NAAQS 
levels below 0.1 [mu]g/m\3\ (e.g., the lower levels included in the 
risk assessment of 0.02 and 0.05 [mu]g/m\3\) may be appropriate. On the 
other hand, to the extent that the uncertainties and limitations in the 
exposure and risk assessments are judged to be so great as to prevent 
meaningful conclusions from being drawn for these low alternative 
standard levels, consideration of such low levels may not be 
appropriate.
    If the policy goal for the Pb NAAQS was to be defined, for example, 
so as to provide protection that limited estimates of IQ loss from 
policy-relevant exposures to no more than 1-2 points IQ loss at the 
population-level, EPA notes that standard levels in the range of 0.1 to 
0.2 [mu]g/m\3\ may achieve that goal. We also note that even with lower 
levels of the standard evaluated, while the range of policy-relevant IQ 
loss estimates is lower, the upper end of the range still extends up to 
and in some cases above 1 point IQ loss. We note, however, appreciably 
greater uncertainty associated with these estimates that increases with 
increasing difference of the alternative standards from current 
conditions.
    Alternatively, if the policy goal was to be defined so as to 
provide somewhat greater public health protection by limiting the air-
related component of risk to somewhat less than 1 point IQ loss at the 
population level, this would suggest greater consideration for 
standards in the lower part of the range evaluated (0.02-0.05 [mu]g/
m\3\). Such a goal might reflect recognition that nonair sources, in 
and of themselves, are estimated to contribute 1-2 points or more of IQ 
loss, such that the incremental risk for policy-relevant Pb is adding 
to a level of total Pb exposure that is already in a range that can be 
reasonably judged to be highly significant from a public health 
perspective. We note, however that considering standards in this lower 
range places greater weight on the more highly uncertain risk estimates 
and thus would be more precautionary in nature.
iii. CASAC Advice and Recommendations
    Beyond the evidence- and risk/exposure-based information discussed 
above, EPA's consideration of the level for the NAAQS will also take 
into account the advice and recommendations of CASAC, based on their 
review of the Criteria Document and drafts of the Staff Paper and the 
related technical support document, as well as comments from the public 
on drafts of the Staff Paper and related technical support document. 
Public comments pertaining to the level of the standard recommended 
appreciable reductions in the level, e.g., setting it at 0.2 [mu]g/m\3\ 
or less.
    In their advice to the Agency during this review CASAC has 
recognized the importance of both the health effects evidence and the 
exposure and risk information in selecting the level for the standard 
(Henderson, 2007a,b). In two separate letters, CASAC has stated that it 
is the unanimous judgement of the CASAC Lead Panel that the primary 
NAAQS should be ``substantially lowered'' to ``a level of about 0.2 
[mu]g/m\3\ or less'', reflecting their view of the health effects 
evidence (Henderson, 2007a,b). In their March 2007 letter conveying 
comments on the pilot phase risk assessment, CASAC based their 
recommendation as to level on consideration of the health effects 
evidence they provided initial recommendations that the level should be 
substantially lower, reflecting their view of the evidence itself.
    The CASAC Pb Panel also provided advice regarding how the Agency 
should consider IQ loss estimates derived from the risk assessment in 
selecting a level for the standard. The Panel stated that they consider 
a population loss of 1-2 IQ points to be ``highly significant from a 
public health perspective.'' Further they recommended that ``the 
primary Pb standard should be set so as to protect 99.5% of the 
population from exceeding that IQ loss.'' The Agency anticipates 
further advice from CASAC with regard to level at the time of their 
review of this ANPR.
iv. Policy Options
    In considering alternative levels of the primary Pb standard, EPA 
will consider the health effects evidence and the exposure and risk 
assessment, as well as the important uncertainties and limitations in 
the evidence and the assessment results. To help inform public health 
policy judgments, we specifically solicit comment on levels of IQ loss 
considered to be significant from a public health perspective. 
Additionally, we solicit comment on the magnitude of IQ loss associated 
with exposures to ambient Pb by the pathways categorized as ``recent 
air'' in the risk assessment described in this notice that are 
considered to be significant from a public health perspective. We also 
solicit comment on the approach of adopting a public health policy goal 
of limiting policy-relevant air exposure such that the incremental 
blood Pb level (and the associated resulting IQ loss) are below a 
specified level (e.g., to a magnitude of 0.5 or 1 [mu]g/dL, or other 
alternative values).
    The EPA takes note of the views of CASAC on these matters, 
summarized above, the conclusions and recommendations in the OAQPS 
Staff Paper,\75\ and the views of public commenters. We also note other 
views,

[[Page 71533]]

including retaining the current standard level or a range of 
alternative levels that includes the upper end of the alternative 
standards considered in the risk assessment (i.e., 0.5 [mu]g/m\3\ as a 
maximum monthly average). The EPA recognizes that there may be 
differing interpretations of the available evidence, the public health 
significance of various changes in population IQ loss, and various 
aspects of the evidence and exposure and risk assessments, including 
important uncertainties and limitations associated with the evidence 
and assessments. Thus, EPA solicits comment on the range of alternative 
standard levels identified above, as well as on other alternative 
levels, up to and including the current level, and the rationale upon 
which such views are based.
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    \75\ The OAQPS Staff Paper recommends consideration of a range 
of alternative standard levels from as high as 0.1 to 0.2 [mu]g/m\3\ 
down to the lower levels evaluated in the risk assessment of 0.02 to 
0.05 [mu]g/m\3\.
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IV. The Secondary Standard

    This section presents information relevant to the review of the 
secondary Pb NAAQS, including information on the welfare effects 
associated with Pb exposures, results of the screening-level ecological 
risk assessment, and considerations related to evaluating the adequacy 
of the current standard and alternative standards that might be 
appropriate for the Administrator to consider.

A. Welfare Effects Information

    Welfare effects addressed by the secondary NAAQS include, but are 
not limited to, effects on soils, water, crops, vegetation, manmade 
materials, animals, wildlife, weather, visibility and climate, damage 
to and deterioration of property, and hazards to transportation, as 
well as effects on economic values and on personal comfort and well-
being. A qualitative assessment of welfare effects evidence related to 
ambient Pb is summarized in this section, drawing from Chapter 6 of the 
Staff Paper. The presentation here first recognizes several key aspects 
of the welfare evidence for Pb. Lead is persistent in the environment 
and accumulates in soils, aquatic systems (including sediments), and 
some biological tissues of plants, animals and other organisms, thereby 
providing long-term, multipathway exposures to organisms and 
ecosystems. Additionally, EPA recognizes that there have been a number 
of uses of Pb, especially as an ingredient in automobile fuel but also 
in other products such as paint, lead-acid batteries, and some 
pesticides, which have significantly contributed to widespread 
increases in Pb concentrations in the environment, a portion of which 
remains today (e.g., CD, Chapters 2 and 3).
    Ecosystems near smelters, mines and other industrial sources of Pb 
have demonstrated a wide variety of adverse effects including decreases 
in species diversity, loss of vegetation, changes to community 
composition, decreased growth of vegetation, and increased number of 
invasive species. Apportioning these effects between Pb and other 
stressors is complicated because these point sources also emit a wide 
variety of other heavy metals and sulfur dioxide which may cause toxic 
effects. There are no field studies which have investigated effects of 
Pb additions alone but some studies near large point sources of Pb have 
found significantly reduced species composition and altered community 
structures. While these effects are significant, they are spatially 
limited: The majority of contamination occurs within 20 to 50 km of the 
emission source (CD, AX7.1.4.2).
    By far, the majority of Pb found in terrestrial ecosystems was 
deposited in the past during the use of Pb additives in gasoline. This 
gasoline-derived Pb was emitted predominantly in small size particles 
which were widely dispersed and transported across large distances. 
Many sites receiving Pb predominantly through such long-range transport 
have accumulated large amounts of Pb in soils (CD, p.l AX7-98). There 
is little evidence that terrestrial sites exposed as a result of this 
long range transport of Pb have experienced significant effects on 
ecosystem structure or function (CD, AX7.1.4.2, p. AX7-98). Strong 
complexation of Pb by soil organic matter may explain why few 
ecological effects have been observed (CD, p. AX7-98). Studies have 
shown decreasing levels of Pb in vegetation which seems to correlate 
with decreases in atmospheric deposition of Pb resulting from the 
removal of Pb additives to gasoline (CD, AX7.1.4.2).
    Terrestrial ecosystems remain primarily sinks for Pb but amounts 
retained in various soil layers vary based on forest type, climate, and 
litter cycling (CD, Section 7.1). Once in the soil, the migration and 
distribution of Pb is controlled by a multitude of factors including 
pH, precipitation, litter composition, and other factors which govern 
the rate at which Pb is bound to organic materials in the soil (CD, 
Section 2.3.5).
    Like most metals the solubility of Pb is increased at lower pH. 
However, the reduction of pH may in turn decrease the solubility of 
dissolved organic material (DOM). Given the close association between 
Pb mobility and complexation with DOM, a reduced pH does not 
necessarily lead to increased movement of Pb through terrestrial 
systems and into surface waters. In areas with moderately acidic soil 
(i.e., pH of 4.5 to 5.5) and abundant DOM, there is no appreciable 
increase in the movement of Pb into surface waters compared to those 
areas with neutral soils (i.e., pH of approximately 7.0). This appears 
to support the theory that the movement of Pb in soils is limited by 
the solubilization and transport of DOM. In sandy soils without 
abundant DOM, moderate acidification appears likely to increase outputs 
of Pb to surface waters (CD, AX7.1.4.1).
    Lead exists in the environment in various forms which vary widely 
in their ability to cause adverse effects on ecosystems and organisms. 
Current levels of Pb in soil also vary widely depending on the source 
of Pb but in all ecosystems Pb concentrations exceed natural background 
levels. The deposition of gasoline-derived Pb into forest soils has 
produced a legacy of slow moving Pb that remains bound to organic 
materials despite the removal of Pb from most fuels and the resulting 
dramatic reductions in overall deposition rates. For areas influenced 
by point sources of air Pb, concentrations of Pb in soil may exceed by 
many orders of magnitude the concentrations which are considered 
harmful to laboratory organisms. Adverse effects associated with Pb 
include neurological, physiological and behavioral effects which may 
influence ecosystem structure and functioning. Ecological soil 
screening levels (Eco-SSLs) have been developed for Superfund site 
characterizations to indicate concentrations of Pb in soils below which 
no adverse effects are expected to plants, soil invertebrates, birds 
and mammals. Values like these may be used to identify areas in which 
there is the potential for adverse effects to any or all of these 
receptors based on current concentrations of Pb in soils.
    Atmospheric Pb enters aquatic ecosystems primarily through the 
erosion and runoff of soils containing Pb and deposition (wet and dry). 
While overall deposition rates of atmospheric Pb have decreased 
dramatically since the removal of Pb additives from gasoline, Pb 
continues to accumulate and may be re-exposed in sediments and water 
bodies throughout the United States (CD, Section 2.3.6).
    Several physical and chemical factors govern the fate and 
bioavailability of Pb in aquatic systems. A significant portion of Pb 
remains bound to suspended particulate matter in the water column and 
eventually settles into the substrate. Species, pH, salinity, 
temperature,

[[Page 71534]]

turbulence and other factors govern the bioavailability of Pb in 
surface waters (CD, Section 7.2.2).
    Lead exists in the aquatic environment in various forms and under 
various chemical and physical parameters which determine the ability of 
Pb to cause adverse effects either from dissolved Pb in the water 
column or Pb in sediment. Current levels of Pb in water and sediment 
also vary widely depending on the source of Pb. Conditions exist in 
which adverse effects to organisms and thereby ecosystems may be 
anticipated given experimental results. It is unlikely that dissolved 
Pb in surface water constitutes a threat to ecosystems that are not 
directly influenced by point sources. For Pb in sediment, the evidence 
is less clear. It is likely that some areas with long-term historical 
deposition of Pb to sediment from a variety of sources as well as areas 
influenced by point sources have the potential for adverse effects to 
aquatic communities. The long residence time of Pb in sediment and its 
ability to be resuspended by turbulence make Pb likely to be a factor 
for the foreseeable future. Criteria have been developed to indicate 
concentrations of Pb in water and sediment below which no adverse 
effects are expected to aquatic organisms. These values may be used to 
identify areas in which there is the potential for adverse effects to 
receptors based on current concentrations of Pb in water and sediment.

B. Screening Level Ecological Risk Assessment

    This section presents a brief summary of the screening-level 
ecological risk assessment conducted by EPA for this review. The 
assessment is described in detail in Lead Human Exposure and Health 
Risk Assessments and Ecological Risk Assessment for Selected Areas, 
Pilot Phase (ICF, 2006). Funding constraints have precluded performance 
of a full-scale ecological risk assessment. The discussion here is 
focused on the screening level assessment performed in the pilot phase 
(ICF, 2006) and takes into consideration CASAC recommendations with 
regard to interpretation of this assessment (Henderson, 2007a, b). The 
following summary focuses on key features of the approach used in the 
assessment and presents only a brief summary of the results of the 
assessment. A complete presentation of results is provided in the pilot 
phase Risk Assessment Report (ICF, 2006) and summarized in Chapter 6 of 
the Staff Paper.
1. Design Aspects of Assessment and Associated Uncertainties
    The screening level risk assessment involved several location-
specific case studies and a national-scale surface water and sediment 
screen. The case studies included areas surrounding a primary Pb 
smelter and a secondary Pb smelter, as well as a location near a 
nonurban roadway. An additional case study for an ecologically 
vulnerable location was identified and described (ICF, 2006), but 
resource constraints have precluded risk analysis for this location.
    The case study analyses were designed to estimate the potential for 
ecological risks associated with exposures to Pb emitted into ambient 
air. Soil, surface water, and/or sediment concentrations were estimated 
from available monitoring data or modeling analysis, and then compared 
to ecological screening benchmarks to assess the potential for 
ecological impacts from Pb that was emitted into the air. Results of 
these comparisons are not definitive estimates of risk, but rather 
serve to identify those locations at which there is the greatest 
likelihood for adverse effect. Similarly, the national-scale screening 
assessment evaluated surface water and sediment monitoring locations 
across the United States for the potential for ecological impacts 
associated with atmospheric deposition of Pb. The reader is referred to 
the pilot phase Risk Assessment Report (ICF, 2006) for details on the 
use of this information and models in the screening assessment.
    The measures of exposure for these analyses are total Pb 
concentrations in soil, dissolved Pb concentrations in fresh surface 
waters (water column), and total Pb concentrations in freshwater 
sediments. The hazard quotient (HQ) approach was then used to compare 
Pb media concentrations with ecological screening values. The exposure 
concentrations were estimated for the three case studies and the 
national-scale screening analyses as described below:
     For the primary Pb smelter case study, measured 
concentrations of total Pb in soil, dissolved Pb in surface waters, and 
total Pb in sediment were used to develop point estimates for sampling 
clusters thought to be associated with atmospheric Pb deposition, 
rather than Pb associated with nonair sources, such as runoff from 
waste storage piles.
     For the secondary Pb smelter case study, concentrations of 
Pb in soil were estimated using fate and transport modeling based on 
EPA's MPE methodology (USEPA, 1998) and data available from similar 
locations.
     For the near roadway nonurban case study, measured soil 
concentration data collected from two interstate sampling locations, 
one with fairly high-density development (Corpus Christi, Texas) and 
another with medium-density development (Atlee, Virginia), were used to 
develop estimates of Pb in soils for each location.
     For the national-scale surface water and sediment 
screening analyses, measurements of dissolved Pb concentrations in 
surface water and total Pb in sediment for locations across the United 
States were compiled from available databases (USGS, 2004). Air 
emissions, surface water discharge, and land use data for the areas 
surrounding these locations were assessed to identify locations where 
atmospheric Pb deposition may be expected to contribute to potential 
ecological impacts. The exposure assessment focused on these locations.
    The ecological screening values used in this assessment were 
developed from the Eco-SSLs methodology, EPA's recommended ambient 
water quality criteria, and sediment screening values developed by 
MacDonald and others (2000, 2003). Soil screening values were derived 
for this assessment using the Eco-SSL methodology with the toxicity 
reference values for Pb (USEPA, 2005d, 2005e) and consideration of the 
inputs on diet composition, food intake rates, incidental soil 
ingestion, and contaminant uptake by prey (details are presented in 
Section 7.1.3.1 and Appendix L, of ICF, 2006). Hardness-specific 
surface water screening values were calculated for each site based on 
EPA's recommended ambient water quality criteria for Pb (USEPA, 1984). 
For sediment screening values, the assessment relied on sediment 
``threshold effect concentrations'' and ``probable effect 
concentrations'' developed by MacDonald et al. (2000). The methodology 
for these sediment criteria is described more fully in section 7.1.3.3 
and Appendix M of the pilot phase Risk Assessment Report (ICF, 2006).
    The HQ is calculated as the ratio of the media concentration to the 
ecotoxicity screening value, and represented by the following equation:

HQ = (estimated Pb media concentration) / (ecotoxicity screening value)

    For each case study, HQ values were calculated for each location 
where either modeled or measured media concentrations were available. 
Separate soil HQ values were calculated for each

[[Page 71535]]

ecological receptor group for which an ecotoxicity screening value has 
been developed (i.e., birds, mammals, soil invertebrates, and plants). 
HQ values less than 1.0 suggest that Pb concentrations in a specific 
medium are unlikely to pose significant risks to ecological receptors. 
HQ values greater than 1.0 indicate that the expected exposure exceeds 
the ecotoxicity screening value and that there is a potential for 
adverse effects.
    There are several uncertainties that apply across case studies 
noted below:
     The ecological risk screen is limited to specific case 
study locations and other locations for which dissolved Pb data were 
available and evaluated in the national-scale surface water and 
sediment screens. In identifying sites for inclusion in the assessment, 
efforts were made to ensure that the Pb exposures assessed were 
attributable to airborne Pb and not dominated by nonair sources. 
However, there is uncertainty as to whether other sources might have 
actually contributed to the Pb exposure estimates.
     A limitation to using the selected ecotoxicity screening 
values is that they might not be sufficient to identify risks to some 
threatened or endangered species or unusually sensitive aquatic 
ecosystems (e.g., CD, p. AX7-110).
     The methods and database from which the surface water 
screening values (i.e., the AWQC for Pb) were derived is somewhat 
dated. New data and approaches (e.g., use of pH as indicator of 
bioavailability) may now be available to estimated the aquatic toxicity 
of Pb (CD, Sections AX7.2.1.2 and AX7.2.1.3).
     No adjustments were made for sediment-specific 
characteristics that might affect the bioavailability of Pb in 
sediments in the derivation of the sediment quality criteria used for 
this ecological risk screen (CD, Sections 7.2.1 and AX7.2.1.4; Appendix 
M, ICF, 2006). Similarly, characteristics of soils for the case study 
locations were not evaluated for measures of bioavailability.
     Although the screening value for birds used in this 
analysis is based on reasonable estimates for diet composition and 
assimilation efficiency parameters, it was based on a conservative 
estimate of the relative bioavailability of Pb in soil and natural 
diets compared with water soluble Pb added to an experimental pellet 
diet (Appendix L, ICF, 2006).
2. Summary of Results
    The following is a brief summary of key observations related to the 
results of the screening-level ecological risk assessment. A more 
complete discussion of the results is provided in Chapter 6 of the 
Staff Paper and the complete presentation of the assessment and results 
is presented in the pilot phase Risk Assessment Report (ICF, 2006).
     The national-scale screen of surface water data initial 
identified some 42 sample locations of which 15 were then identified as 
unrelated to mining sites and having water column levels of dissolved 
Pb that were greater than hardness adjusted chronic criteria for the 
protection of aquatic life (with one location having a HQ of 15), 
indicating a potential for adverse effect if concentrations were 
persistent over chronic periods. Acute criteria were not exceeded at 
any of these locations. The extent to which air emissions of Pb have 
contributed to these surface water Pb concentrations is unclear.
     In the national-scale screen of sediment data associated 
with the 15 surface water sites described above, threshold effect 
concentration-based HQs at nine of these sites exceeded 1.0. 
Additionally, HQs based on probable effect concentrations exceeded 1.0 
at five of the sites, indicating probable adverse effects to sediment 
dwelling organisms. Thus, sediment Pb concentrations at some sites are 
high enough that there is a likelihood that they would cause adverse 
effects to sediment dwelling organisms. However, the contribution of 
air emissions to these concentrations is unknown.
     In the primary Pb smelter case study, all three of the 
soil sampling clusters (including the ``reference areas'') had HQs that 
exceeded 1.0 for birds. Samples from one cluster also had HQs greater 
than 1.0 for plants and mammals. The surface water sampling clusters 
all had measurements below the detection limit of 3.0 [mu]g/L. However, 
three sediment sample clusters had HQs greater than 1.0. In summary, 
the concentrations of Pb in soil and sediments exceed screening values 
for these media indicating potential for adverse effects to terrestrial 
organisms (plants, birds and mammals) and to sediment dwelling 
organisms. While the contribution to these Pb concentrations from air 
as compared to nonair sources is not quantified, air emissions from 
this facility are substantial (see Appendix D, USEPA 2007b; ICF 2006).
     In the secondary Pb smelter case study, the soil 
concentrations, developed from soil data for similar locations, 
resulted in avian HQs greater than 1.0 for all distance intervals 
evaluated. The scaled soil concentrations within 1 km of the facility 
also showed HQs greater than 1.0 for plants, birds, and mammals. These 
estimates indicate a potential for adverse effect to those receptor 
groups.
     In the nonurban, near roadway case study, HQs for birds 
and mammals were greater than 1.0 at all but one of the distances from 
the road. Plant HQs were greater than 1.0 at the closest distance. In 
summary, HQs above one were estimated for plants, birds and mammals, 
indicating potential for adverse effect to these receptor groups.

C. Considerations in Review of the Standard

    This section presents an integrative synthesis of information in 
the Criteria Document together with EPA analyses and evaluations. EPA 
notes that the final decision on retaining or revising the current 
secondary Pb standard is a public policy judgment to be made by the 
Administrator. The Administrator's final decision will draw upon 
scientific information and analyses about welfare effects, exposure and 
risks, as well as judgments about the appropriate response to the range 
of uncertainties that are inherent in the scientific evidence and 
analyses.
    The NAAQS provisions of the Act require the Administrator to 
establish secondary standards that, in the judgment of the 
Administrator, are requisite to protect the public welfare from any 
known or anticipated adverse effects associated with the presence of 
the pollutant in the ambient air. In so doing, the Administrator seeks 
to establish standards that are neither more nor less stringent than 
necessary for this purpose. The Act does not require that secondary 
standards be set to eliminate all risk of adverse welfare effects, but 
rather at a level requisite to protect public welfare from those 
effects that are judged by the Administrator to be adverse.
    The following discussion starts with background information on the 
current standard (Section IV.C.1). The general approach for this 
current review is summarized in Section IV.C.2. Considerations with 
regard to the adequacy of the current standard are discussed in section 
IV.C.3, with evidence and exposure-risk-based considerations in 
subsections IV.C.3.a and b, respectively, followed by a summary of 
CASAC advice and recommendations (section IV.C.3.c) and, lastly, 
solicitation of comment on the broad range of policy options (section 
IV.C.3.d). Considerations with regard to elements of alternative 
standards are discussed in Section IV.C.4.

[[Page 71536]]

1. Background on the Current Standard
    The current standard was set in 1978 to be identical to the primary 
standard (1.5 [mu]g Pb/m\3\, as a maximum arithmetic mean averaged over 
a calendar quarter), the basis for which is summarized in Section 
III.C.1. At the time the standard was set, the Agency concluded that 
the primary air quality standard would adequately protect against known 
and anticipated adverse effects on public welfare, as the Agency stated 
that it did not have evidence that a more restrictive secondary 
standard was justified. In the rationale for this conclusion, the 
Agency stated that the available evidence cited in the 1977 Criteria 
Document indicated that ``animals do not appear to be more susceptible 
to adverse effects from lead than man, nor do adverse effects in 
animals occur at lower levels of exposure than comparable effects in 
humans'' (43 FR 46256). The Agency recognized that Pb may be deposited 
on the leaves of plants and present a hazard to grazing animals. With 
regard to plants, the Agency stated that Pb is absorbed but not 
accumulated to any great extent by plants from soil, and that although 
some plants may be susceptible to Pb, it is generally in a form that is 
largely nonavailable to them. Further the Agency stated that there was 
no evidence indicating that ambient levels of Pb result in significant 
damage to manmade materials and Pb effects on visibility and climate 
are minimal.
    The secondary standard was subsequently considered during the 1980s 
in development of the 1986 Criteria Document (USEPA, 1986a) and the 
1990 Staff Paper (USEPA, 1990). In summarizing OAQPS staff conclusions 
and recommendations at that time, the 1990 Staff Paper stated that a 
qualitative assessment of available field studies and animal 
toxicological data suggested that ``domestic animals and wildlife are 
as susceptible to the effects of lead as laboratory animals used to 
investigate human lead toxicity risks.'' Further, the 1990 Staff Paper 
highlighted concerns over potential ecosystem effects of Pb due to its 
persistence, but concluded that pending development of a stronger 
database that more accurately quantifies ecological effects of 
different Pb concentrations, consideration should be given to retaining 
a secondary standard at or below the level of the then-current 
secondary standard of 1.5 [mu]g/m\3\.
2. Approach for Current Review
    To evaluate whether it is appropriate to consider retaining the 
current secondary Pb standard, or whether consideration of revisions is 
appropriate, EPA is considering an approach in this review like that 
used in the Staff Paper that considers the evidence and risk analyses. 
This approach recognizes that the available welfare effects evidence 
generally reflects laboratory-based evidence of toxicological effects 
on specific organisms exposed to concentrations of Pb at which 
scientists generally agree that adverse effects are likely to occur. It 
is widely recognized, however, that environmental exposures are likely 
to be at lower concentrations and/or accompanied by significant 
confounding factors (e.g., other metals, acidification), which 
increases our uncertainty about the likelihood and magnitude of the 
organism and ecosystem response.
3. Adequacy of the Current Standard
a. Evidence-Based Considerations
    In considering the welfare effects evidence with respect to the 
adequacy of the current standard, EPA will consider not only the array 
of evidence newly assessed in the Criteria Document but also that 
assessed in the 1986 Criteria Document and summarized in the 1990 Staff 
Paper. As discussed extensively in the latter two documents, there was 
a significantly improved characterization of environmental effects of 
Pb in the ten years after the Pb NAAQS was set. And, in the subsequent 
nearly 20 years, many additional studies on Pb effects in the 
environment are now available (2006 Criteria Document). Some of the 
more relevant aspects of the evidence available since the standard was 
set include the following:
     A more quantitative determination of the mobility, 
distribution, uptake, speciation, and fluxes of atmospherically 
delivered Pb in terrestrial ecosystems shows that the binding of Pb to 
organic materials in the soil slows its mobility through soil and may 
prevent uptake by plants (CD, Sections 7.1.2, 7.1.5, AX7.1.4.1, 
AX7.1.4.2, AX7.1.4.3 and AX7.1.2 ). Therefore, while atmospheric 
deposition of Pb has decreased, Pb may be more persistent in some 
ecosystems than others and may remain in the active zone of the soil, 
where exposure may occur, for decades (CD, Sections 7.1.2, AX7.1.2 and 
AX7.1.4.3).
     Plant toxicity may occur at lower levels than previously 
identified as determined by data considered in development of Eco-SSLs 
(CD, pp. 7-11 to 7-12, AX7-16 and Section AX7.1.3.2), although the 
range of reported soil Pb effect levels is large (tens to thousands of 
mg/kg soil).
     Avian and mammalian toxicity may occur at lower levels 
than those previously identified, although the range of Pb effect 
levels is large (<1 to >1,000 mg Pb/kg bw-day) (CD, p. 7-12, Section 
AX7.1.3.3).
     There is an expanded understanding of the fate and effects 
of Pb in aquatic ecosystems and of the distribution and concentrations 
of Pb in surface waters throughout the United States (CD, Section 
AX7.2.2).
     New methods for assessing the toxicity of metals to water 
column and sediment-dwelling organisms and data collection efforts (CD, 
Sections 7.2.1, 7.2.2, AX7.2.2, and AX7.2.2.2) have improved our 
understanding of Pb aquatic toxicity and findings include an indication 
that in some estuarine systems Pb deposited during historic usage of 
leaded gasoline may remain in surface sediments for decades. (CD, p. 7-
23).
     A larger dataset of aquatic species assessed with regard 
to Pb toxicity, and findings of lower effect levels for previously 
untested species (CD, p. AX7-176 and Section AX7.2.4.3).
     Currently available studies have also shown effects on 
community structure, function and primary productivity, although some 
confounders (such as co-occurring pollutants) have not been well 
addressed (CD, Section AX7.1.4.2).
     Evidence in ecological research generally indicates the 
value of a critical loads approach; however, current information on Pb 
critical loads is lacking for many processes and interactions involving 
Pb in the environment and work is ongoing (CD, Section 7.3).
    Given the full body of current evidence, despite wide variations in 
Pb concentrations in soils throughout the country, Pb concentrations 
are likely in excess of concentrations expected from geologic or other 
non-anthropogenic forces. In particular, the deposition of gasoline-
derived Pb into forest soils has produced a legacy of slow moving Pb 
that remains bound to organic materials despite the removal of Pb from 
most fuels and the resulting dramatic reductions in overall deposition 
rates (CD, Section AX7.1.4.3). For areas influenced by point sources of 
air Pb that meet the current standard, concentrations of Pb in soil may 
exceed by many orders of magnitude the concentrations which are 
considered harmful to laboratory organisms (CD, Section 3.2 and 
AX7.1.2.3).
    There are several difficulties in quantifying the role of current 
ambient Pb in the environment: Some Pb deposited before the standard 
was

[[Page 71537]]

enacted is still present in soils and sediments; historic Pb from 
gasoline continues to move slowly through systems as does current Pb 
derived from both air and nonair sources. Additionally, the evidence of 
adversity in natural systems is very sparse due in no small part to the 
difficulty in determining the effects of confounding factors such as 
multiple metals or factors influencing bioavailability in field 
studies. However, the evidence summarized above and in Section 4.2 of 
the Staff Paper and described in detail in the Criteria Document 
informs our understanding of Pb in the environment today and evidence 
of environmental Pb exposures of potential concern.
    Conditions exist in which Pb-associated adverse effects to aquatic 
organisms and thereby ecosystems may be anticipated given experimental 
results. While the evidence does not indicate that dissolved Pb in 
surface water constitutes a threat to those ecosystems that are not 
directly influenced by point sources, the evidence regarding Pb in 
sediment is less clear (CD, Sections AX7.2.2.2.2 and AX7.2.4). It is 
likely that some areas with long term historical deposition of Pb to 
sediment from a variety of sources as well as areas influenced by point 
sources have the potential for adverse effects to aquatic communities. 
The long residence time of Pb in sediment and its ability to be 
resuspended by turbulence make Pb contamination likely to be a factor 
for the foreseeable future. Based on this information, the Staff Paper 
concluded that the evidence suggests that the environmental levels of 
Pb occurring under the current standard, set nearly thirty years ago, 
may pose risk of adverse environmental effect.
b. Risk-based Considerations
    In addition to the evidence-based considerations described in the 
previous section, the screening level ecological risk assessment is 
informative, taking into account key limitations and uncertainties 
associated with the analyses.
    The screening level risk assessment involved a comparison of 
estimates of environmental media concentrations of Pb to ecological 
screening levels to assess the potential for ecological impacts from Pb 
that was emitted into the air. Results of these comparisons are not 
considered to be definite predictors of risk, but rather serve to 
identify those locations at which there is greatest likelihood for 
adverse effect. Similarly, the national-scale screening assessment 
evaluated the potential for ecological impacts associated with the 
atmospheric deposition of Pb released into ambient air at surface water 
and sediment monitoring locations across the United States.
    The ecological screening levels employed in the screening level 
risk assessment for different media are drawn from different sources. 
Consequently there are somewhat different limitations and uncertainties 
associated with each. In general, their use here recognizes their 
strength in identifying media concentrations with the potential for 
adverse effect and their relative nonspecificity regarding the 
magnitude of risk of adverse effect.
    As discussed in the previous section, as a result of its 
persistence, Pb emitted in the past remains today in aquatic and 
terrestrial ecosystems of the United States. Consideration of the 
environmental risks associated with the current standard is complicated 
by the environmental burden associated with air Pb concentrations that 
exceeded the current standard, predominantly in the past.
    Concentrations of Pb in soil and sediments associated with the 
primary Pb smelter case study exceeded screening values for those media 
indicating potential for adverse effect in terrestrial organisms 
(plants, birds and mammals) and in sediment dwelling organisms. While 
the contribution to these Pb concentrations from air as compared to 
nonair sources has not been quantified, air emissions from this 
facility are substantial (see Appendix D, USEPA 2007b; ICF 2006). 
Additionally, estimates of Pb concentration in soils associated with 
the nonurban near roadway case study and the secondary Pb smelter case 
study were also associated with HQs above 1 for plants, birds and 
mammals, indicating potential for adverse effect to those receptor 
groups. The industrial facility in the secondary Pb smelter case study 
is much younger than the primary Pb smelter and apparently became 
active less than ten years prior to the establishment of the current 
standard.
    The national-scale screens, which are not focused on particular 
point source locations, indicate the ubiquitous nature of Pb in aquatic 
systems of the United States today. Further the magnitude of Pb 
concentrations in several aquatic systems exceeded screening values. In 
the case of the national-scale screen of surface water data, 15 
locations were identified with water column levels of dissolved Pb that 
were greater than hardness adjusted chronic criteria for the protection 
of aquatic life (with one location having a HQ as high as 15), 
indicating a potential for adverse effect if concentrations were 
persistent over chronic periods. Further, sediment Pb concentrations at 
some sites in the national-scale screen were high enough that the 
likelihood that they would cause adverse effects to sediment dwelling 
organisms may be considered ``probable''.
    A complicating factor in interpreting the findings for the 
national-scale screening assessments is the lack of clear apportionment 
of Pb contributions from air as compared to nonair sources, such as 
industrial and municipal discharges. While the contribution of air 
emissions to the elevated concentrations has not been quantified, 
documentation of historical trends in the sediments of many water 
bodies has illustrated the sizeable contribution that airborne Pb can 
have on aquatic systems (e.g., Section 2.8.1). This documentation also 
indicates the greatly reduced contribution in many systems as compared 
to decades ago (presumably reflecting the banning of Pb-additives from 
gasoline used by cars and trucks). However, the timeframe for removal 
of Pb from surface sediments into deeper sediment varies across 
systems, such that Pb remains available to biological organisms in some 
systems for much longer than in others (Section 2.8, CD, pages AX7-141 
to AX7-145).
    The case study locations included in the screening assessment, with 
the exception of the primary Pb smelter site, are currently meeting the 
current Pb standard, yet Pb occurs in some locations at concentrations, 
particularly in soil, and aquatic sediment above the screening levels, 
indicative of a potential for harm to some terrestrial and sediment 
dwelling organisms. While the role of airborne Pb in determining these 
Pb concentrations is unclear, the historical evidence indicates that 
airborne Pb can create such concentrations in sediments and soil. 
Further, environmental concentrations may be related to emissions prior 
to establishment of the current standard and such concentrations appear 
to indicate a potential for harm to ecological receptors today.
c. CASAC Advice and Recommendations
    In the CASAC letter transmitting advice and recommendations 
pertaining to the review of the first draft Staff Paper and draft Pb 
Exposure and Risk Assessments, the CASAC Pb panel provided 
recommendations regarding the need for a Pb NAAQS, and the adequacy of 
the current Pb NAAQS, as well as comments on the draft documents. With 
regard to the need for a Pb NAAQS and adequacy of the current NAAQS, 
the CASAC letter said:

[[Page 71538]]

    The unanimous judgment of the Lead Panel is that lead should not 
be delisted as a criteria pollutant, as defined by the Clean Air 
Act, for which primary (public health based) and secondary (public 
welfare based) NAAQS are established, and that both the primary and 
secondary NAAQS should be substantially lowered.

    Specifically with regard to the secondary NAAQS, the CASAC Pb Panel 
stated that the December 2006 draft documents presented ``compelling 
scientific evidence that current atmospheric Pb concentrations and 
deposition--combined with a large reservoir of historically deposited 
Pb in soils, sediments and surface waters--continue to cause adverse 
environmental effects in aquatic and/or terrestrial ecosystems, 
especially in the vicinity of large emissions sources.'' The Panel went 
on to state that ``These effects persist in some cases at locations 
where current airborne lead concentrations are below the level of the 
current primary and secondary lead standards'' and ``Thus, from an 
environmental perspective, there are convincing reasons to both retain 
lead as a regulated criteria air pollutant and to lower the level of 
the current secondary standard.''
    In making this recommendation, the CASAC Pb Panel also cites the 
persistence of Pb in the environment, the possibility of some of the 
large amount of historically deposited Pb becoming resuspended by 
natural events, and the expectation that humans are not uniquely 
sensitive among the many animal and plant species in the environment. 
In summary, with regard to the recommended level of a revised secondary 
standard, the CASAC panel stated that:

    Therefore, at a minimum, the level of the secondary Lead NAAQS 
should be at least as low as the lowest-recommended primary lead 
standard.

    CASAC provided further advice and recommendations on the Agency's 
consideration of the secondary standard in this review in their letter 
of September 2007 (Henderson, 2007b). In that letter they recognized 
the role of the secondary standard in influencing the long-term 
environmental burden of Pb and a need for environmental monitoring to 
assess the success of the standard in this role.
d. Policy Options
    In considering the adequacy of the current secondary standard, EPA 
will consider, for reasons discussed above in III.C.3.d on the primary 
standard, whether it is appropriate to maintain a NAAQS for Pb or to 
retain Pb on the list of criteria pollutants. We take note of the views 
of CASAC, summarized above, the conclusions and recommendations in the 
OAQPS Staff Paper, and the views of public commenters on these 
questions. We recognize that there may be differing views on 
interpreting or weighing the available information. Thus, EPA solicits 
comment related to the questions of delisting and revocation.
    In further considering the adequacy of the current standard in 
providing requisite protection from Pb-related adverse effects on 
public welfare, EPA will focus on the body of available evidence 
(briefly summarized above in Section IV.A). Depending on the 
interpretation, the available data and evidence, primarily qualitative, 
may suggest the potential for adverse environmental impacts under the 
current standard. Given the limited data on Pb effects in ecosystems, 
it is necessary to look at evidence of Pb effects on organisms and 
extrapolate to ecosystem effects. Therefore, taking into account the 
available evidence and current media concentrations in a wide range of 
areas, EPA seeks comment on whether the evidence suggests that adverse 
effects are occurring, particularly near point sources, under the 
current standard. While the role of current airborne emissions is 
difficult to apportion, it is conclusive that deposition of Pb from air 
sources is occurring and that this ambient Pb is likely to be 
persistent in the environment. Historically deposited Pb has persisted, 
although location-specific dynamics of Pb in soil result in differences 
in the timeframe during which Pb is retained in surface soils or 
sediments where it may be available to ecological receptors (USEPA, 
2007b, section 2.3.3). EPA seeks comment on the role of deposition of 
Pb from current sources and the availability of this Pb to ecological 
receptors.
    There is only very limited information available pertinent to 
assessing whether groups of organisms which influence ecosystem 
function are subject to similar effects as those in humans. The 
screening-level risk information, while limited and accompanied by 
various uncertainties, also suggests occurrences of environmental Pb 
concentrations existing under the current standard that could have 
adverse environmental effects. Environmental Pb levels today are 
associated with atmospheric Pb concentrations and deposition that have 
combined with a large reservoir of historically deposited Pb in 
environmental media.
    The EPA takes note of the views of CASAC, summarized above, the 
conclusions and recommendations in the OAQPS Staff Paper, and views of 
public commenters on the adequacy of the current standard. EPA solicits 
comment on the adequacy of the current standard and the rationale upon 
which such views are based.
4. Elements of the Standard
    The secondary standard is defined in terms of four basic elements: 
indicator, averaging time, level and form, which serve to define the 
standard and must be considered collectively in evaluating the welfare 
protection afforded by the standards. In considering a revision to the 
current standard, EPA will consider the four elements of the standard, 
the information available and advice and recommendations from CASAC 
regarding how the elements might be revised to provide a secondary 
standard for Pb that protects against adverse environmental effect.
    With regard to the pollutant indicator for use in a secondary NAAQS 
that provides protection for public welfare from exposure to Pb, EPA 
notes that Pb is a persistent pollutant to which ecological receptors 
are exposed via multiple pathways. While the evidence indicates that 
the environmental mobility and ecological toxicity of Pb are affected 
by various characteristics of its chemical form, and the media in which 
it occurs, information are insufficient to identify an indicator other 
than total Pb that would provide protection against adverse 
environmental effect in all ecosystems nationally.
    Lead is a cumulative pollutant with environmental effects that can 
last many decades. In considering the appropriate averaging time for 
such a pollutant the concept of critical loads may be useful (CD, 
Section 7.3). However, information is currently insufficient for such 
use in this review.
    There is a general lack of data that would indicate the appropriate 
level of Pb in environmental media that may be associated with adverse 
effects. The EPA notes the influence of airborne Pb on Pb in aquatic 
systems and of changes in airborne Pb on aquatic systems, as 
demonstrated by historical patterns in sediment cores from lakes and Pb 
measurements (Section 2.8.1; CD, Section AX7.2.2; Yohn et al., 2004; 
Boyle et al., 2005), as well as the comments of the CASAC Pb panel that 
a significant change to current air concentrations (e.g., via a 
significant change to the standard) is likely to have significant 
beneficial effects on the magnitude of Pb exposures in the environment 
and Pb toxicity impacts on natural and managed terrestrial and aquatic 
ecosystems in various regions of

[[Page 71539]]

the U.S., the Great Lakes and also U.S. territorial waters of the 
Atlantic Ocean (Henderson, 2007a, Appendix E). We concur with CASAC's 
conclusion that the Agency lacks the relevant data to provide a clear, 
quantitative basis for setting a secondary Pb NAAQS that differs from 
the primary in indicator, averaging time, level or form. Thus, EPA 
solicits comment on the option of a reduction in the secondary standard 
consistent with any reduction of the primary standard that would 
provide increased protection against adverse environmental effect.
    Beyond the views noted above, EPA recognizes that there may be 
differing interpretations of the available evidence and various aspects 
of the evidence and exposure and risk information, including on the 
important uncertainties and limitations associated with the evidence 
and assessment. Thus, EPA solicits additional information pertaining to 
and comment on the considerations described above, as well as on other 
views with regard to the elements of a secondary standard for Pb, and 
the rationale upon which such views are based.

V. Considerations for Ambient Monitoring

    A determination of compliance with the Pb NAAQS for any given area 
is made based on ambient air monitoring data collected by State and 
local monitoring agencies. This section discusses aspects of the Pb 
surveillance monitoring requirements with regards to the adequacy under 
the current primary Pb NAAQS as well as under options being considered 
for a revised primary Pb NAAQS. These aspects include the sampling and 
analysis methods, network design, sampling schedule, and data handling 
methods. In addition, this section discusses the need for monitoring in 
support of the secondary Pb NAAQS.

A. Sampling and Analysis Methods

    To be used in determination of compliance with the Pb NAAQS, the Pb 
data must be collected and analyzed using a Federal Reference Method 
(FRM), or a Federal Equivalent Method (FEM). The current FRM for Pb 
sampling and analyses is based on the use of a high-volume TSP sampler 
to collect the sample and the use of atomic absorption for the analysis 
of Pb in the sample (40 CFR 50 Appendix G). There are 21 FEMs currently 
approved for Pb-TSP (http://www.epa.gov/ttn/amtic/criteria.html). All 

21 FEMs are based on the use of high-volume TSP samplers, but with a 
variety of different analysis methods (e.g., XRF and ICP/MS).
    Concerns have been raised over the use of high-volume TSP samplers. 
CASAC has commented that TSP samplers have poor precision, that the 
upper particle cut size varies widely as a function of wind speed and 
direction, and that the spatial non-homogeneity of very coarse 
particles cannot be efficiently captured by a national monitoring 
network (Henderson, 2007b). For these reasons, CASAC recommended 
considering a revision to the Pb reference method to allow sample 
collection using PM10 samplers. CASAC suggested that it may 
be possible to develop a single quantitative adjustment factor from a 
short period of collocated sampling at multiple sites, or a Pb-
PM10/Pb-TSP equivalency ratio could be determined on a 
regional or site-specific basis.
    The EPA evaluated the precision and bias of the high-volume Pb-TSP 
sampler based on data reported to AQS for collocated samplers and 
results of in-field sampler flow audits and laboratory audits for Pb 
(Camalier and Rice, 2007). In this evaluation, we found that the 
average precision of the high-volume Pb-TSP sampler was approximately 
12%, with a standard deviation of 19%, and average sampling bias (based 
on flow audits) was -0.7%, with a standard deviation of 4.2%. We also 
estimated the average bias for the lab analyses at -1.1% (with a 
standard deviation of 5.5%) based on spiked filter audits. Total bias, 
which includes bias from both sampling and laboratory analysis, was 
estimated at -1.7%, with a standard deviation of 3.4%. This level of 
precision and bias is comparable to the goal of the FRM and FEM for 
other criteria pollutants (e.g., within 10% for PM2.5, 40 
CFR 58 Appendix A). We attempted to look at the precision of low-volume 
Pb-PM10 samplers based on data reported to AQS, however, we 
did not have enough data (18 paired data points for one site) to make 
any conclusions on the precision of this sampler.
    Evaluations of the high-volume TSP sampler have demonstrated that 
the sampler's cutpoint can vary between 25 and 50 [mu]m depending on 
wind speed and direction (Wedding et al., 1977, McFarland and Rodes, 
1979). A study was conducted during the last Pb NAAQS review to 
evaluate the effect of wind speed and direction on sampler efficiency 
(Purdue, 1988). This demonstration showed that the Pb collection 
efficiency of the high-volume TSP sampler ranged from 80% to 90% over a 
wide range of wind speeds and directions. In comparison, a study 
conducted near a primary Pb smelter indicated that the ratio of Pb-
PM10 to Pb-TSP ranged from 17% to 186% for 22 collocated 
samples (Brion, 1988). We believe that the variability of the 
collection efficiency of the high-volume TSP sampler does not warrant 
the discontinuation of its use. However, with this notice, we are 
soliciting comments on this issue.
    We analyzed data from a number of monitoring sites where collocated 
Pb-TSP and Pb-PM10 data have been collected in order to 
evaluate the appropriateness of using Pb-PM10 data as a 
surrogate for Pb-TSP (Cavender, 2007). From this analysis it is clear 
that a single relationship can not be made that would allow one to 
accurately estimate Pb-TSP concentrations from Pb-PM10 
measurements at all sites. However, at many locations it does appear a 
strong linear relationship can be shown between Pb-TSP and Pb-PM10 
concentrations. As such, it may be feasible for a monitoring agency to 
develop a site-specific relationship, using conservative assumptions, 
to estimate Pb-TSP based on Pb-PM10 measurements. We invite 
comments on the appropriateness of using Pb-PM10 data as a 
surrogate for Pb-TSP.
    While all current FRM and FEM are based on the high-volume TSP 
sampler, several vendors market low-volume TSP samplers. These samplers 
are identical to low-volume PM10 samplers with the exception 
of the sampling head and corresponding cut size. These samplers have a 
number of advantages over the high-volume TSP sampler including the 
capability of sequential sampling (i.e., the ability to collect more 
than one sample between operator visits). Sequential sampling would be 
highly desirable if the sampling frequency is increased as part of a 
change to a monthly averaging period. Currently, the FEM demonstration 
requirements [40 CFR 53.33(i)] dictate that the FEM testing must be 
performed with an ambient Pb-TSP concentration between 0.5 [mu]g/m\3\ 
to 4.0 [mu]g/m\3\. Due to the dramatic decrease in ambient Pb 
concentrations, there are few (if any) areas in the country where a 
vendor could be assured that the average ambient Pb-TSP concentrations 
would meet the FEM demonstration requirements during the field testing 
period. If the Pb NAAQS is lowered, we believe it is appropriate to 
lower the FEM requirement to a level more consistent with current 
ambient Pb concentrations and the lowered NAAQS to allow for continued 
development and approval of Pb-TSP FEM. We invite comment on the 
appropriate range of concentrations for an FEM demonstration.

[[Page 71540]]

    We also reviewed the method detection capabilities of the current 
lab methods for the FRM and FEM to ensure that these methods had the 
necessary sensitivity to accurately measure Pb-TSP at the low 
concentrations considered in the Risk Assessment Report and Staff 
Paper. Based on data submitted to AQS, the method detection limits for 
these methods are all 0.01 [mu]g/m\3\ or less (Rice, 2007). From these 
findings, we request comment on whether the current lab analysis 
methods are adequate for continued use even at the lowest alternative 
NAAQS levels considered in the Risk Assessment Report and Staff Paper.

B. Network Design

    The existing Pb-TSP network has decreased substantially over the 
last few decades. In 1980 there were over 900 Pb-TSP sites, this number 
has been reduced to approximately 200 sites. These reductions were made 
because of substantially reduced ambient Pb concentrations and shifting 
priorities to other criteria pollutants. Now several states have no Pb-
TSP monitors resulting in large portions of the country with no data on 
current ambient Pb-TSP concentrations. In addition, many of the largest 
Pb emitting sources in the country do not have nearby monitors, and 
there is substantial uncertainty about ambient air Pb levels resulting 
from historic Pb deposits near roadways. For these reasons, we request 
comment on whether the existing Pb-TSP network may not be adequate, and 
that additional monitoring sites may be needed to determine compliance 
with either the current or revised Pb NAAQS.
    The minimum network design requirements are given in 40 CFR 58 
Appendix D. The current network design requirements are for 2 FRM or 
FEM sites in any area where Pb concentrations exceed or have exceeded 
the NAAQS in the most recent 2 years. These requirements may make it 
difficult to persuade state and local monitoring agencies to add 
monitors in areas without existing monitors. As such, we believe that 
these requirements are not adequate and should be modified (as part of 
this rulemaking) to ensure monitoring is conducted in areas where NAAQS 
violations may occur.
    We request comment on options for improving the coverage of the Pb 
network. One option would be to adopt network requirements similar to 
those recently promulgated for PM2.5 and ozone which tie the 
number of required monitors to the population of the urban area and 
ambient Pb concentrations (40 CFR 58 Appendix D). Under this approach, 
more monitoring sites would be required in areas with larger 
populations and higher Pb concentrations. This approach would result in 
improved network coverage in urban areas. However, large Pb emitting 
sources that are not in urban areas may still not be monitored.
    A second option would be to require one or more monitors near large 
Pb emitting sources. For example, a monitor could be required at the 
point near the maximum predicted concentrations for sources with a 
potential Pb emission rate of 1 ton per year or more (as provided by 
the most recent National Emissions Inventory, or permit data). Clearly, 
some effort would be necessary to identify an appropriate emissions 
threshold to ensure that all emission sources with the potential to 
exceed the NAAQS are monitored without creating undue burden where 
there is no potential to exceed the NAAQS. This option would ensure 
coverage of the highest Pb emitting sources, but may not provide 
adequate coverage in many populated areas where a combination of 
smaller emissions sources and re-entrained dust may result in Pb 
concentrations in excess of the NAAQS.
    A third option could be created by the combination of the first two 
options discussed above: Establish a minimum number of required 
monitors in urban areas based on population and ambient Pb 
concentrations and require monitors near large Pb emission sources. 
This option would provide good monitoring coverage in urban areas and 
near Pb emissions sources. Again, care would need to be taken in 
establishing an emissions threshold.
    A fourth option would be to utilize the current PM10 
network if an acceptable regional or site-specific correlation of Pb-
TSP and Pb-PM10 can be made. This option would provide a 
substantial increase in monitoring coverage without requiring a large 
investment in new monitoring stations. The current PM10 
network has been carefully established to include both rural and urban 
ambient levels, though it was not designed to monitor near large Pb 
emitting sources. We invite comments on these options as well as 
suggestions for additional options to consider for improving the Pb 
network.

C. Sampling Schedule

    The current sampling frequency requirement is for one 24-hour 
sample every six days [40 CFR 58.12(b)]. For the current NAAQS, which 
is based on a quarterly average, the 1-in-6 sampling schedule yields 15 
samples per quarter on average with 100% completeness, or 12 samples 
with 75% completeness. A change to a monthly averaging period would 
result in between 4 and 6 samples per month at the current sampling 
frequency. If we change the averaging time to a monthly average, we 
would likely need to increase the sampling frequency as 4 samples would 
not result in a statistically valid estimate of the actual air quality 
for the period.
    Incomplete sampling results in increased uncertainty in the 
estimate of actual ambient air quality. While some degree of 
uncertainty is unavoidable due to the precision and bias inherent to 
the sampling technique, it is important to understand the level of 
uncertainty for each sampling option being considered and to select a 
sampling frequency which achieves an acceptable level of uncertainty. 
We plan to go through the Data Quality Objectives (DQO) process in 
order to help us select an appropriate sampling option. The DQO process 
is a series of logical steps that guides decision makers to a plan for 
the resource-effective acquisition of environmental data. The DQO 
process is used to establish performance and acceptance criteria, which 
serve as the basis for designing a plan for collecting data of 
sufficient quality and quantity to support the goals of the study (EPA, 
2006e, EPA/240/B-06/001).
    We are considering several options for sampling frequency. These 
options include maintaining the current 1-in-6 day sampling schedule, 
increasing the sampling frequency to 1-in-3 day, or increasing the 
sampling frequency to 1-in-1 day sampling (i.e., complete sampling). In 
addition, we will be considering an option that relates sampling 
frequency to recent ambient Pb-TSP concentrations, such that an 
increased sampling frequency is required as the recent ambient Pb-TSP 
concentrations approach the NAAQS level. Other options that we will be 
considering include--
     Increasing sampling time duration (e.g., changing from a 
24 hour sampling time duration to a 48 or 72 hour sampling time 
duration).
     Allowing for compositing of samples (i.e., analyzing 
sequential samples together).
     Allowing for multiple samplers at one site.
    We invite comments on the appropriateness of these sampling options 
and suggestions for additional options for consideration.

D. Data Handling

    A number of data handling conventions and computations are 
necessary when using ambient monitoring data to determine attainment

[[Page 71541]]

or non-attainment of the NAAQS. Recently, we have been codifying these 
data handling conventions and computations into a separate appendix for 
each NAAQS. As such, we intend to create an appendix for the 
interpretation of the Pb NAAQS as part of this rule making. Specific 
conventions we are considering and invite comments on at this time 
include the following--
     Design values will be developed based on the most recent 3 
calendar year period.
     Design values will be rounded to two significant figures 
using conventional rounding methodology.
     75% of the expected number of samples is needed for a 
quarter to be considered complete, or 50% for a month.
     Only one period (i.e., one month or one quarter depending 
on the final form of the standard) is needed to demonstrate non-
attainment. Two periods would be needed if the NAAQS is based on the 
2nd maximum.
     Three full consecutive years of complete data are needed 
to re-designate an area attainment from non-attainment.
     Incomplete periods can be used to demonstrate non-
attainment, but not attainment.

E. Monitoring for the Secondary NAAQS

    Currently, the secondary NAAQS is set equal to the primary NAAQS 
(1.5 [mu]g/m\3\, maximum quarterly average). We do not expect there to 
be ambient air concentrations in excess of the secondary NAAQS in rural 
areas that are not associated with a Pb emission source. If the 
secondary standard remains equal to the primary standard at the 
completion of the current review, we request comment on the option of 
developing Pb surveillance monitoring requirements for the primary 
NAAQS that will be sufficient to determine compliance with the 
secondary NAAQS.
    While additional monitoring may not be necessary to demonstrate 
compliance with the secondary NAAQS, CASAC has recommended additional 
monitoring to gather information to better inform consideration of the 
secondary NAAQS in the next and future reviews. Specifically, CASAC 
stated that ``the EPA needs to initiate new measurement activities in 
rural areas--which quantify and track changes in lead concentrations in 
the ambient air, soils, deposition, surface waters, sediments and 
biota, along with other information as may be needed to calculate and 
apply a critical loads approach for assessing environmental lead 
exposures and risks in the next review cycle'' (Henderson, 2007b).
    We currently monitor ambient Pb in PM2.5 as part of the 
IMPROVE network. There are 110 formally designated IMPROVE sites 
located in or near national parks and other Class I visibility areas, 
virtually all of these being rural. Approximately 80 additional sites 
at various urban and rural locations, requested and funded by various 
parties, are also informally treated as part of the network. While we 
believe it may not be appropriate to rely on either Pb-PM10 
or Pb-PM2.5 monitoring to demonstrate compliance with a Pb-
TSP NAAQS, we believe the Pb-PM2.5 measurements provided by 
the IMPROVE network can be used as a useful indicator to track changes 
in ambient Pb concentrations and resulting Pb deposition in rural areas 
that are not directly impacted by a Pb emission source. It may also be 
desirable to augment the IMPROVE network with a small ``sentinel'' 
network of collocated Pb-TSP monitors for a period of time in order to 
develop a better understanding of how Pb-PM2.5 and Pb-TSP 
relate in these rural areas. Alternatively, since it is likely that at 
rural locations nearly all Pb is in the less than 10 [mu]m size range, 
we could analyze the PM10 mass samples (which are already 
being collected) for Pb for a period of time to develop a better 
understanding of how Pb-PM2.5 and Pb-PM10 relate 
in these rural areas. We welcome comments on the value and 
appropriateness of use of the IMPROVE Pb-PM2.5 data for 
assessing trends in ambient air concentrations of Pb, and the need to 
collocate a small network of Pb-TSP or Pb-PM10 monitors at 
IMPROVE sites.
    The National Water-Quality Assessment (NAWQA), conducted by the 
United States Geological Survey, contains data on Pb concentrations in 
surface water, bed sediment, and animal tissue for more than 50 river 
basins and aquifers throughout the country (CD, AX7.2.2.2). NAWQA data 
are collected during long-term, cyclical investigations wherein study 
units undergo intensive sampling for 3 to 4 years, followed by low-
intensity monitoring and assessment of trends every 10 years. 
Similarly, the USGS is collaborating with Canadian and Mexican 
government agencies on a multi-national project called ``Geochemical 
Landscapes'' that has as its long-term goal a soil geochemical survey 
of North America (http://minerals.cr.usgs.gov/projects/geochemical_landscapes/index.html
). The Geochemical Landscapes project has the 

potential to fill the need for periodic Pb soil sampling. We note the 
value of the NAWQA and Geochemical Landscapes data in the assessment of 
trends in Pb concentrations in both soil and aquatic systems, and 
support the continued collection of this data by the USGS.

VI. Solicitation of Comment

    With the issuance of this ANPR, the Agency is soliciting broad 
public input to inform the Agency's proposed rulemaking related to the 
review of the Pb NAAQS. As noted in Section I above, this ANPR, as a 
consequence of the timing of the Pb NAAQS review relative to the 
Agency's initiation of the new NAAQS process, summarizes information 
from the OAQPS Staff Paper, and from the Agency's risk assessment and 
Criteria Document. In so doing, this notice presents OAQPS staff views 
on the adequacy of the current standard and on a range of policy 
options for the Administrator's consideration, together with the views 
of CASAC and the public as reflected in their comments on the related 
documents that have been previously made available for review. The 
Agency is soliciting comment on the range of views discussed above as 
well as any broader range of options that members of the public feel 
appropriate for the Administrator to consider. Comments are solicited 
together with the rationales for the views expressed in those comments. 
The Agency is also soliciting further advice from CASAC on the issues 
discussed in this notice at an upcoming public meeting (announced in a 
separate Federal Register notice).
    In soliciting public comment in advance of reaching proposed 
decisions on whether to retain or revise the NAAQS under review, the 
Agency is interested in general, specific, and technical comments on 
all aspects of the rulemaking discussed in this notice and the related 
documents. These aspects generally include characterization of Pb in 
the ambient environment, characterization of the health effects 
evidence and the assessment of human exposure and health risk, 
characterization of the environmental effects evidence and 
consideration of environmental exposure and risk, as well as an 
assessment of the adequacy of the current primary and secondary 
standards and of alternative standards for the Administrator's 
consideration in reaching proposed decisions in this review of the Pb 
NAAQS. We solicit broad comment on these aspects of this rulemaking, 
informed by the discussion presented in this notice as well as the more 
comprehensive discussion in the Criteria Document, the Staff Paper, and 
related risk assessment reports.
    Several types of information pertinent to the characterization of 
Pb in the

[[Page 71542]]

ambient environment are considered for this review. These include 
characterization of sources of Pb, including source distribution within 
the U.S. and associated estimates of the magnitude of air emissions. 
The currently available information on the magnitude, geographic 
distribution and variability of Pb levels in the ambient air is also 
considered. Further, given that Pb is a multimedia pollutant, 
characterization of Pb includes consideration of atmospheric deposition 
and Pb in ambient soil, surface waters and sediment. Comments, 
including information and views, are solicited in all of these areas as 
well as any other areas related to the characterization of Pb in the 
ambient environment that are relevant to this review.
    The current health effects evidence for Pb, evaluated in the 
Agency's Criteria Document, encompasses a broad range of information 
regarding human exposure to ambient Pb, toxicokinetics of Pb, 
biological markers and models of Pb burden in humans, toxicological 
effects of Pb in laboratory animals and in vitro test systems, and 
epidemiologic studies of human health effects associated with Pb 
exposure. In addition, based on the information in the Criteria 
Documents, quantitative assessments of human exposures to Pb and 
associated health risks as well as environmental exposures and related 
risks have been conducted and are presented in related risk assessment 
reports. We are soliciting comments, including information and views, 
informed by the Criteria Document, Staff Paper, and risk assessment 
reports, on characterization of the health effects evidence and 
consideration of human exposure and health risk associated with Pb 
exposures. Similarly, the Agency is soliciting comment on the 
characterization of the environmental effects evidence and 
environmental risks of Pb relevant to this review.
    With regard to the primary and secondary standards, a wide range of 
views have been expressed, reflecting differing conclusions about the 
scientific evidence and quantitative risk assessments and differing 
public health and welfare policy judgments about appropriate standards. 
These views range from asserting the need for significant strengthening 
of the standards to a recommendation in public comments that the Pb 
NAAQS should be revoked and/or Pb should be delisted as a criteria 
pollutant. We solicit comment on these views as well as on any other 
views that are thought to be appropriate for the Agency to consider, 
together with rationales for the views expressed. More specifically, we 
solicit comment, including views and associated rationale, informed by 
the Criteria Document, Staff Paper and related risk assessment reports, 
on the adequacy of the current primary and secondary standards. We also 
solicit comment on the range of alternative primary and secondary 
standards the Agency should consider, with a focus on the four basic 
elements of the standards, including indicator, averaging time, level, 
and form. Further, we are soliciting comment on the view that it is 
appropriate to revoke the NAAQS for Pb or to remove Pb from the list of 
criteria pollutants.
    Issues related to Pb surveillance monitoring requirements relevant 
to this review are also discussed in this notice. These issues fall 
into several areas, including sampling and analysis methods related to 
Pb-TSP and Pb-PM10 measurements, monitoring network design, 
sampling schedule, and data handling. Specific aspects of monitoring in 
support of the secondary standard are also discussed. We are soliciting 
comments on the issues related to Pb surveillance monitoring 
requirements identified in this notice as well as on other issues 
relevant to these requirements in this review.
    The Agency will consider comments received in response to this 
notice in reaching proposed decisions in this rulemaking. As noted 
above, the public will have an additional opportunity for comment on 
the proposed rulemaking, which will further inform the Administrator's 
final decisions on the Pb NAAQS.

VII. Statutory and Executive Order Reviews

Executive Order 12866: Regulatory Planning and Review

    Under Executive Order (EO) 12866 (58 FR 51735, October 4, 1993), 
this action is a ``significant regulatory action.'' Accordingly, EPA 
submitted this action to the Office of Management and Budget (OMB) for 
review under EO 12866 and any changes made in response to OMB 
recommendations have been documented in the docket for this action.

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List of Subjects in 40 CFR Part 50

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

    Dated: December 5, 2007.
Stephen L. Johnson,
Administrator.
[FR Doc. E7-23884 Filed 12-14-07; 8:45 am]

BILLING CODE 6560-50-P