[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]
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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
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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
).
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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\
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\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.
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\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).
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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 describ