[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 described in this notice, a case study
approach was employed as described in Sections 2.2 (and subsections)
and 5.1.3 of the Risk Assessment Report (USEPA, 2007b). The four types
of case studies included in the assessment are the following:
Location-specific urban case studies: Three urban case
studies focus on specific urban areas (Cleveland, Chicago and Los
Angeles) to provide perspectives on the magnitude of ambient air Pb-
related risk in specific urban locations. Ambient air Pb concentrations
are characterized using source-oriented and other Pb-TSP monitors in
these cities. As stated above, these case studies were developed in
response to CASAC recommendations and there has not been review of the
completed analyses for these case studies by CASAC
General urban case study: The general urban case study is
a nonlocation-specific analysis that uses several simplifying
assumptions regarding ambient air Pb levels and demographics to produce
a simplified representation of urban areas.
Primary Pb smelter case study: \33\ This case study
estimates risk for children living in an area currently not in
attainment with the current NAAQS, that is impacted by Pb emissions
from a primary Pb smelter. As such, this case study characterizes risk
for a specific highly exposed population and also provides insights on
risk to child populations living in areas near large sources of Pb
emissions.
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\33\ See Section III.B.2.a for a summary of CASAC's comment with
regard to the primary and secondary Pb smelter case studies.
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Secondary Pb smelter case study: \34\ This case study was
included in the initial analyses for the full-scale assessment as an
example of areas influenced by smaller point sources of Pb emissions.
As discussed in Section III.B.2.g below, however, a variety of
significant limitations in the approaches employed for this case and
associated large uncertainties in these results are recognized that
preclude considering this case study to be illustrative of the larger
set of areas influenced by similarly sized Pb sources. Risk estimates
for this case study (presented in detail in the Risk Assessment Report
(USEPA, 2007b)) are lower than those for the other case studies.
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\34\ See Section III.B.2.a for a summary of CASAC's comment with
regard to the primary and secondary Pb smelter case studies.
---------------------------------------------------------------------------
d. Air Quality Scenarios
Air quality scenarios assessed include (a) a current conditions
scenario for the location-specific urban case studies, the general
urban case study and the secondary Pb smelter case study, (b) a current
NAAQS scenario for the location-specific urban case studies, the
general urban case study and the primary Pb smelter case study, and (c)
a range of alternative NAAQS scenarios for all case studies. The
alternative NAAQS scenarios include levels of 0.5, 0.2, 0.05, and 0.02
[mu]g/m\3\, with a monthly averaging time, as well as a level of 0.2
[mu]g/m\3\ scenario using a quarterly averaging time.\35\ The current
NAAQS scenario for the urban case studies assumes ambient air Pb
concentrations higher than actual current conditions. While it is
extremely unlikely that Pb concentrations in urban areas would rise to
meet the current NAAQS and there are limitations and uncertainties
associated with the approach used (as described in Section III.B.2.g
below), this scenario was included to provide some perspective on risks
associated with just meeting the current NAAQS relative to current
conditions. When evaluating these results it is important to keep the
limitations and uncertainties in mind.
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\35\ For further discussion of the air quality scenarios and
averaging times included in the risk assessment, see section 2.3.1
of the Risk Assessment Report (USEPA, 2007b)
---------------------------------------------------------------------------
Current conditions for the three location-specific urban case
studies in terms of maximum quarterly average air Pb concentrations are
0.09, 0.14 and 0.36 [mu]g/m\3\ for the study areas in Los Angeles,
Chicago and Cleveland, respectively. In terms of maximum monthly
average the values are 0.17 [mu]g/m\3\, 0.31 [mu]g/m\3\ and 0.56 [mu]g/
m\3\ for the study areas in Los Angeles, Chicago and Cleveland,
respectively. Two current conditions scenarios were considered for the
general urban case study: One based on the mean value for ambient air
Pb levels in large urban areas (0.14 [mu]g/m\3\ as a maximum quarterly
average) and a high-end ambient air Pb level in large urban areas (0.87
[mu]g/m\3\ as a maximum quarterly average).
Details of the assessment scenarios, including a description of the
derivation of Pb concentrations for air and other media are presented
in Sections 2.3 (and subsections) and Section 5.1.1 of the Risk
Assessment Report (USEPA, 2007b).
e. Categorization of Policy-Relevant Exposure Pathways
To inform policy aspects of the Pb NAAQS review, the assessment
estimates for blood Pb and IQ loss were divided into two components:
The fraction associated with policy-relevant pathways, which include
inhalation, outdoor soil/dust ingestion and indoor dust ingestion, and
the fraction associated with background (e.g., diet and drinking
water). The policy-relevant pathways are further divided into two
categories, ``recent air'' and ``past air''. Conceptually, the recent
air category includes those pathways involving Pb that is or has
recently been in the outdoor ambient air, including inhalation and
ingestion of indoor dust Pb derived from recent ambient air (i.e.,
[[Page 71504]]
air Pb that has penetrated into the residence recently and loaded
indoor dust). Past air includes exposure contributions from ingestion
of outdoor soil/dust that is contacted on surfaces outdoors, and
ingestion of indoor dust Pb that is derived from past air sources
(i.e., impacts from Pb that was in the ambient air in the past and has
not been recently resuspended into ambient air). In this assessment, as
discussed further below, that portion of indoor dust Pb not associated
with recent air, is classified as ``other'' and, due to technical
limitations includes not only past air impacts, but also contributions
from indoor Pb paint. In the risk assessment, estimates of contribution
to blood Pb and IQ loss were developed for the following pathways or
pathway combinations:
Inhalation of ambient air Pb (i.e., ``recent air'' Pb):
This is derived using the blood Pb estimate resulting from Pb exposure
limited to the inhalation pathway (and will include exposures to Pb in
ambient air from all sources contributing to the ambient air
concentration estimate).
Ingestion of ``recent air'' indoor dust Pb: This is
derived using the blood Pb estimate resulting from Pb exposure limited
to ingestion of the Pb in indoor dust that is predicted to be
associated with ambient air concentrations (i.e., via the air
concentration coefficient in the regression-based dust models or via
the mechanistic component of the hybrid blood Pb model (see Section
3.1.4 of the Risk Assessment Report). For the primary Pb smelter case
study, estimates for this pathway are not separated from estimates for
the pathway described in the subsequent bullet due to uncertainty
regarding this categorization with the model used for this case study
(Section 3.1.4.2 of the Risk Assessment Report).
Ingestion of ``other'' indoor dust Pb: This is derived
using the blood Pb estimate resulting from Pb exposure limited to
ingestion of the Pb in indoor dust that is not predicted to be
associated with ambient air concentrations (i.e., that predicted by the
intercept in the dust models plus that predicted by the outdoor soil
concentration coefficient, for models that include an intercept
(Section 3.1.4 of the Risk Assessment Report)). This is interpreted to
represent indoor paint, outdoor soil/dust, and additional sources of Pb
to indoor dust including historical air (see Risk Assessment Report,
Section 2.4.3). As the intercept in regression dust models will be
inclusive of error associated with the model coefficients, this
category also includes some representation of dust Pb associated with
current ambient air concentrations (described in previous bullet). For
the primary Pb smelter case study, estimates for this pathway are not
separated from estimates for the pathway described above due to
uncertainty regarding this categorization with the model used for this
case study (Risk Assessment Report, Section 3.1.4.2). This pathway is
included in the ``past air'' category.
Ingestion of outdoor soil/dust Pb: This is derived using
the blood Pb estimate resulting from Pb exposure limited to ingestion
of outdoor soil/dust Pb. This pathway is included in the ``past air''
category (and could include contamination from historic Pb emissions
from automobiles and Pb paint).
Ingestion of drinking water Pb: This is derived using the
blood Pb estimate resulting from Pb exposure limited to ingestion of
drinking water Pb. This pathway is included in the policy-relevant
background category.
Ingestion of dietary Pb: This is derived using the blood
Pb estimate resulting from Pb exposure limited to ingestion of dietary
Pb. This pathway is included in the policy-relevant background
category.
In simulating reductions in exposure associated with reducing
ambient air Pb levels through alternative NAAQS (and increases in
exposure if the current NAAQS was reached in certain case studies),
modeling for the assessment has only affected the exposure pathways
categorized as recent air (inhalation and ingestion of that portion of
indoor dust associated with outdoor ambient air). The assessment has
not simulated decreases in past air-related exposure pathways (e.g.,
reductions in outdoor soil Pb levels following reduction in ambient air
Pb levels and a subsequent decrease in exposure through incidental soil
ingestion and the contribution of outdoor soil to indoor dust). This
aspect of the analysis will tend to underestimate the reductions in
risk associated with alternative NAAQS. However, this does not mean
that overall risk has been underestimated. The net effect of all
sources of uncertainty or bias in the analysis, which may also tend to
under- or overestimate risk, could not be quantified.
Additionally, there is uncertainty related to parsing out exposure
and risk between background and policy-relevant exposure pathways (and
subsequent parsing of recent air and past air) resulting from a number
of technical limitations. Key among these is that, while conceptually,
indoor Pb paint contributions to indoor dust Pb would be considered
background and included in modeling background exposures, due to
technical limitations related to indoor dust Pb modeling, ultimately,
Pb paint was included as part of ``other'' indoor dust Pb (i.e., as
part of past air exposure). The inclusion of indoor lead Pb as a
component of ``other'' indoor air (and consequently as a component of
``past air'' exposure) represents a source of potential high bias in
our prediction of total exposure and risk associated with past air
because conceptually, exposure to indoor paint Pb is considered part of
background exposure.
In summary, because of limitations in the assessment design, data
and modeling tools, the risk attributable to policy-relevant exposure
pathways is bounded on the low end by the risk estimated for the
``recent air'' category and on the upper end by the risk estimated for
the ``recent air'' plus ``past air'' categories.
f. Analytical Steps
The risk assessment includes four analytical steps, briefly
described below and presented in detail in Sections 2.4.4, 3.1, 3.2,
4.1, and 5.1 of the Risk Assessment Report (USEPA, 2007b).
Characterization of Pb in ambient air: The
characterization of outdoor ambient air Pb levels uses different
approaches depending on the case study (as explained in more detail
below): (a) Source-oriented and non-source oriented monitors are
assumed to represent different exposure zones in the city-specific case
studies, (b) a single exposure level is assumed, based on monitoring
data for various cities, for the general urban case study, and (c)
ambient levels are estimated using air dispersion modeling based on Pb
emissions from a particular facility in the point source case studies.
Characterization of outdoor soil/dust and indoor dust Pb
concentrations: Outdoor soil Pb levels are estimated using empirical
data and/or fate and transport modeling. Indoor dust Pb levels are
predicted using a combination of (a) regression-based models that
relate indoor dust to ambient air Pb and/or outdoor soil Pb, and (b)
mechanistic models.\36\
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\36\ Additional detail on the methods used in characterizing Pb
concentrations in outdoor soil and indoor dust are presented in
Sections 3.1.3 and 3.1.4 of the Risk Assessment, respectively. Data,
methods and assumptions here used in characterizing Pb
concentrations in these exposure media may differ from those in
other analyses that serve different purposes.
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Characterization of blood Pb levels: Blood Pb levels for
each exposure zone are derived from central-tendency blood Pb
concentrations estimated using the
[[Page 71505]]
Integrated Exposure and Uptake Biokinetic (IEUBK) model, and concurrent
or lifetime average blood Pb is estimated from these outputs as
described in Section 3.2.1.1 of the Risk Assessment Report (USEPA,
2007b). For the point source and location-specific urban case studies,
a probabilistic exposure model is used to generate population
distributions of blood Pb concentrations based on: (a) The central
tendency blood Pb levels for each exposure zone, (b) demographic data
for the distribution of children (less than 7 years of age) across
exposure zones in a study area, and (c) a geometric standard deviation
(GSD) intended to characterize interindividual variability in blood Pb
(e.g., reflecting differences in behavior and biokinetics related to
Pb). For the general urban case study, as demographic data for a
specific location are not considered, the GSD is applied directly to
the central tendency blood Pb level to estimate a population
distribution of blood Pb levels. Additional detail on the methods used
to model population blood Pb levels is presented in Sections 3.2.2 and
5.2.2.3 of the Risk Assessment Report (USEPA, 2007b).
Risk characterization (estimating IQ loss): Concurrent or
lifetime average blood Pb estimates for each simulated child in each
case study population are converted into total Pb-related IQ loss
estimates using the concentration-response functions described above.
Key limitations and uncertainties associated with the application
of these specific analytical steps are summarized in Section III.B.2.g
below.
g. Generating Multiple Sets of Risk Results
In the initial analyses for the full-scale assessment (USEPA,
2007a), EPA implemented multiple modeling approaches for each case
study scenario in an effort to characterize the potential impact on
exposure and risk estimates of uncertainty associated with the
limitations in the tools, data and methods available for this risk
assessment and with key analytical steps in the modeling approach.
These multiple modeling approaches are described in Section 2.4.6.2 of
the final Risk Assessment Report (USEPA, 2007b). In consideration of
comments provided by CASAC (Henderson, 2007b) on these analyses
regarding which modeling approach they felt had greater scientific
support, a pared down set of modeling combinations was identified as
the core approach for the subsequent analyses. This core modeling
approach includes the following key elements:
Ambient air Pb estimates (based on monitors or modeling
and proportional rollbacks, as described below),
Background exposure from food and water (as described
above),
The hybrid indoor dust model specifically developed for
urban residential applications (which predicts Pb in indoor dust as a
function of ambient air Pb and nonair contribution),
The IEUBK blood Pb model (which predicts blood Pb in young
children exposed to Pb from multiple exposure pathways),
The concurrent blood Pb metric,
A GSD for concurrent blood Pb of 2.1 to characterize
interindividual variability in blood Pb levels for a given ambient
level, and
four different functions relating concurrent blood Pb to
IQ loss, including two log-linear models (one with a cutpoint and one
with low-exposure linearization) and two dual-linear models with
stratification, one stratified at 7.5 [mu]g/dL peak blood Pb and the
other at 10 [mu]g/dL peak blood Pb.
For each case study, the core modeling approach employs a single
set of modeling elements to estimate exposure and the four different
concentration-response functions referenced above to derive four sets
of risk results from the single set of exposure estimates. The spread
of estimates resulting from application of all four functions captures
much of the uncertainty associated model choice in this analytical
step. Among these four functions, greater confidence is associated with
estimates derived using the log-linear with low-exposure linearization
concentration-response function as discussed above.
In addition to employing multiple concentration-response functions,
the assessment includes various sensitivity analyses to characterize
the potential impact of uncertainty in other key analysis steps on
exposure and risk estimates. The sensitivity analyses and uncertainty
characterization completed for the risk analysis are described in
Sections 3.5, 4.3, 5.2.5 and 5.3.3 of the Risk Assessment Report
(USEPA, 2007b).
h. Key Limitations and Uncertainties
As recognized above, EPA has made simplifying assumptions in
several areas of this assessment due to the limited data, models, and
time available. These assumptions and related limitations and
uncertainties are described in the Risk Assessment Report (USEPA,
2007b). Key assumptions, limitations and uncertainties are briefly
identified below. EPA considers these aspects of the assessment to be
important to the interpretation of the exposure and risk estimates. In
the presentation below, limitations (and associated uncertainty) are
listed, beginning with those regarding design of the assessment or case
studies, followed by those regarding estimation of Pb concentrations in
ambient air indoor dust, outdoor soil/dust, and blood, and lastly
regarding estimation of Pb-related IQ Loss.
Temporal aspects: Exposure for the simulated child
population begins at birth (including a prenatal maternal contribution)
and continues for 7 years, with Pb concentrations in all exposure media
remaining constant throughout the period, and children residing in the
same exposure zone throughout the period. In characterizing exposure
media concentrations, annual averages are derived and held constant
through the seven year period. Exposure factors and physiological
parameters vary with age of the cohort through the seven year exposure
period, several exposure factors and physiological parameters are
varied on an annual basis within the blood Pb modeling step. These
aspects are a simplification of population exposures that contributes
some uncertainty to our exposure and risk estimates.
General urban case study: This case study differs from the
others in several ways. It is by definition a general case study and
not based on a specific location. There is a single exposure zone for
the case study within which all media concentrations of Pb are assumed
to be spatially uniform; that is, no spatial variation within the area
is simulated. Additionally, the case study does not rely on any
specific demographic values. Within the single exposure zone a
theoretical population of unspecified size is assumed to be uniformly
distributed. Thus this case study is a simplified representation of
urban areas intended to inform our assessment of the impact of changes
in ambient Pb concentrations on risk, but which carries with it
attendant uncertainties in our interpretation of the associated
exposure and risk estimates. For example, the risk estimates for this
case study, while generally representative of an urban residential
population exposed to the specified ambient air Pb levels, cannot be
readily related to a specific urban population. Specific urban
populations are spatially distributed in a nonuniform pattern and
experience ambient air Pb levels that vary through time and space.
Consequently, interpretations of the associated blood Pb and risk
estimates with regard to their relevance to specific urban residential
exposures carry
[[Page 71506]]
substantial uncertainty and presumably an upward bias in risk,
particularly for large areas, across which air concentrations may vary
substantially.
Point source case studies: Dispersion modeling was used to
characterize ambient air Pb levels in the point source case studies.
This approach simulates spatial gradients related to dispersion and
deposition of Pb from emitting sources. The details of this modeling is
presented in the Risk Assessment Report (USEPA, 2007b). In the case of
the point sources modeled, sources were limited to those associated
with the smelter operations, and did not include other sources such as
resuspension of roadside Pb not related to facility operations, and
other stationary sources of Pb within or near the study area. This
means that, with distance from the facility, there is likely
underestimation of ambient air-related Pb exposure because with
increased distance from the facility there would be increasing
influence of other sources relative to that of the facility. This
limitation is likely to have more significant impact on risk estimates
associated with the full study than on those for the subareas (which
are the portions of the study area with 1.5 km from the smelter
facilities), and to perhaps have a more significant impact on risk
estimates associated with the smaller secondary Pb smelter (see below).
As noted above, in their review of the July draft risk assessment
report, the CASAC Pb Panel made several recommendations for additional
exposure and health risk analyses (Henderson, 2007b), including a
recommendation that the general urban case study be augmented by the
inclusion of risk analyses in specific urban areas of the U.S. In this
regard, they specifically stated the following (Henderson, 2007b, p.
3):
The CASAC strongly believes that it is important that EPA staff make
estimates of exposure that will have national implications for, and
relevance to, urban areas; and that, significantly, the case studies
of both primary lead (Pb) smelter sites as well as secondary smelter
sites, while relevant to a few atypical locations, do not meet the
needs of supporting a Lead NAAQS. The Agency should also undertake
case studies of several urban areas with varying lead exposure
concentrations, based on the prototypic urban risk assessment that
OAQPS produced in the 2nd Draft Lead Human Exposure and Health Risk
Assessments.
Secondary Pb smelter case study: Air Pb concentration
estimates derived from the air dispersion modeling completed for the
secondary Pb smelter case study are subject to appreciably greater
uncertainty than that for those for the primary Pb smelter case study
due to a number of factors, including: (a) A more limited and less
detailed accounting of emissions and emissions sources associated with
the facility (particularly fugitive emissions), (b) a lack of prior air
quality modeling analyses and performance analyses, and (c) a
substantially smaller number of Pb-TSP monitors in the area that could
be used to evaluate and provide confidence in model performance.\37\
Further, as mentioned in the previous bullet, no air sources of Pb
other than those associated with the facility were accounted for in the
modeling. Given the relatively smaller magnitude of emissions from the
secondary Pb smelter, the underestimating potential of this limitation
with regard to air concentrations with distance from the facility has a
greater relative impact on risk estimates for this case study than for
the primary Pb smelter case study. The aggregate uncertainty of all of
these factors results in low confidence in estimates for this case
study. It is observed that exposure and risk estimates are lower than
those for the other case studies. Although this case study was
initially intended to be used as an example of areas near stationary
sources of intermediate size (smaller than the primary Pb smelter),
experience with this analysis indicates that substantially more data
and multiple case studies differing in several aspects would be needed
to broadly characterize risks for such a category of Pb exposure
scenarios.
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\37\ The information supporting the air dispersion modeling for
the primary Pb smelter case study provides substantially greater
confidence in estimates for that case study.
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Location-specific urban case studies: The Pb-TSP
monitoring network is currently quite limited. The number of monitors
available to represent air concentrations in these case studies ranged
from six for Cleveland to 11 for Chicago. Accordingly, our estimates of
the magnitude of and spatial variation of air Pb concentrations are
subject to uncertainty associated with the limited data. In applying
the available data to each of these case studies, exposure zones, one
corresponding to each monitor, were created and U.S. Census block
groups (and the children within those demographic units) were
distributed among the exposure zones. The details of the approach used
are described in Section 5.1.3 of the Risk Assessment Report (USEPA,
2007b). Although this approach provides a spatial gradient across the
study area due to differences in monitor values for each exposure zone,
this approach assumes a constant concentration within each exposure
zone (i.e., no spatial gradient within a zone). Additionally, the
nearest neighbor approach to assign block groups to exposure zones
assumes that a monitor adequately represents all locations that are
closer to that monitor than to any of the others in the study area. In
reality, across block groups there are more variable spatial gradients
in a study area than those reflected in the approach used here. This
introduces significant uncertainty into the characterization of risk
for the urban case studies. As recognized in Section, III.B.2.a, the
analyses for these case studies were developed in response to CASAC
recommendations on the July 2007 draft Risk Assessment (Henderson,
2007b) and there has not been review of the completed analyses by
CASAC.
Current NAAQS air quality scenarios: For the location-
specific urban case studies, proportional roll-up procedures were used
to adjust ambient air Pb concentrations up to just meet the current
NAAQS (see Sections 2.3.1 and 5.2.2.1 of the Risk Assessment Report,
USEPA, 2007b, for detailed discussion). EPA recognizes that it is
extremely unlikely that Pb concentrations in urban areas would rise to
meet the current NAAQS and that there is substantial uncertainty with
our simulation of such conditions. In these case studies a proportional
roll-up was simulated, such that it is assumed that the current spatial
distribution of air concentrations (as characterized by the current
data) is maintained and increased Pb emissions contribute to increased
Pb concentrations, the highest of which just meets the current
standard. There are many other types of changes within a study area
that could result in a similar outcome such as increases in emissions
from just one specific industrial operation that could lead to air
concentrations in a part of the study area that just meet the current
NAAQS, while the remainder of the study area remained largely unchanged
(at current conditions). For the primary Pb smelter case study, where
current conditions exceed the current NAAQS, attainment of the current
NAAQS was simulated using air quality modeling, emissions and source
parameters used in developing the 2007 proposed revision to the State
Implementation Plan for the area (see Section 3.1.1.2 of the Risk
Assessment Report (USEPA, 2007b)).
Alternative NAAQS air quality scenarios: In all case
studies, proportional roll-down procedures were used to adjust ambient
air Pb concentrations downward to attain
[[Page 71507]]
alternative NAAQS (see Sections 2.3.1 and 5.2.2.1 of the Risk
Assessment Report, USEPA, 2007b). There is significant uncertainty in
simulating conditions associated with the implementation of emissions
reduction actions to meet a lower standard. There are a variety of
changes other than that represented by a proportional roll-down that
could result in air concentrations that just meet lower alternative
standards. For example, control measures might be targeted only at the
specific area exceeding the standard, resulting in a reduction of air
Pb concentrations to the alternate standard while concentrations in the
rest of the study area remain unchanged (at current conditions).
Consequently, there is significant uncertainty associated with
estimates for the alternate NAAQS scenarios.
Estimates of outdoor soil/dust Pb concentrations: Outdoor
soil Pb concentration for both the urban case studies and the primary
Pb smelter case study are based on empirical data (see Section 3.1.3 of
the Risk Assessment). To the extent that the underlying sampling data
included areas containing older structures, the impact of Pb paint
weathered from older structures on soil Pb levels will be reflected in
these empirical estimates. In the case of the urban case studies, a
mean value from a sample of houses built between 1940 and 1998 was used
to represent soil Pb levels (see Section 3.1.3.1 of the Risk
Assessment). Outdoor soil/dust Pb concentrations in all air quality
scenarios have been set equal to the values for the current conditions
scenarios. An impact of changes in air Pb concentrations on soil
concentrations, and the associated impact on dust concentrations, blood
Pb and risk estimates were not simulated. In areas where air
concentrations have been greater in the past, however, implementation
of a reduced NAAQS might be expected to yield reduced soil Pb levels
over the long term. As described in Section 2.3.3 of the Risk
Assessment Report (USEPA, 2007b), however, there is potentially
significant uncertainty associated with this specification,
particularly with regard to implications for areas in which a Pb source
may locate where one of comparable size had not been previously.
Additionally, it is possible that control measures implemented to meet
alternative NAAQS may result in changes to soil Pb concentrations;
these are not reflected in the assessment.
Estimates of indoor dust Pb concentrations for the urban
case studies (application of the hybrid model): The hybrid mechanistic-
empirical model for estimating indoor dust Pb for the urban case
studies (see Section 3.1.4.1 of the Risk Assessment Report, USEPA,
2007b) has several sources of uncertainty that could significantly
impact its estimates. These include: (a) Failure to consider house-to-
house variability in factors related to infiltration of outdoor ambient
air Pb indoors and subsequent buildup on indoor surfaces, (b)
limitations in data available on the rates and efficiency of indoor
dust cleaning and removal, (c) limitations in the method for converting
model estimates of dust Pb loading to dust Pb concentration needed for
blood Pb modeling, and (d) the approach employed to partition estimates
of dust Pb concentration into ``recent air'' and ``other'' components
(see Section 5.3.3.4 of the Risk Assessment Report, USEPA, 2007b).
These last two sources of uncertainty reduce our confidence in
estimates of apportionment of dust Pb between ``recent air'' and
``other''. In recognition of this limitation, in evaluating exposure
and risk reduction trends related to reducing ambient air Pb levels,
focus has been placed on changes in total blood Pb rather than on
estimates of ``recent air'' blood Pb.
Estimates of indoor dust Pb concentrations for the primary
Pb smelter case study (application of the site-specific regression
model): There is uncertainty associated with the site-specific
regression model applied in the remediation zone (see Section 3.1.4.2
of the Risk Assessment Report), and relatively greater uncertainty
associated with its application to air quality scenarios that simulate
notably lower air Pb levels. Limitations in the dataset from which the
model was derived limited its form to that of a simple regression that
predicts dust Pb concentration as a function of air Pb concentration
plus a constant (intercept). However there may be variables in addition
to air that influence dust Pb concentrations and their absence in the
regression contributes uncertainty to the resulting estimates. To the
extent that these unaccounted-for variables are spatially related to
the smelter facility Pb sources, our estimates could be biased, not
with regard to the absolute dust Pb concentration, but with regard to
differences in dust Pb concentration estimate between different air
quality scenarios. Those differences may be overestimated because of
potential overestimation of the air coefficient and underestimation of
the intercept in the regression model. Examples of such unaccounted-for
variables are roadside dust Pb and historical contributions to current
levels of indoor dust Pb (e.g., Pb that entered a house in the past and
continues to contribute to current dust Pb levels).
Characterizing interindividual variability using a GSD:
There is uncertainty associated with the GSD specified for each case
study (see Sections 3.2.3 and 5.2.2.3 of the Risk Assessment Report).
Two factors are described here as contributors to that uncertainty.
Interindividual variability in blood Pb levels for any study population
(as described by the GSD) will reflect, to a certain extent, spatial
variation in media concentrations, including outdoor ambient air Pb
levels and indoor dust Pb levels. For each case study, there is
significant uncertainty in the specification of spatial variability in
ambient air Pb levels and associated indoor dust Pb levels, as noted
above. In addition, there are a limited number of datasets for
different types of residential child populations from which a GSD can
be derived (e.g., NHANES datasets \38\ for more heterogeneous
populations and individual study datasets for likely more homogeneous
populations near specific industrial Pb sources). This uncertainty
associated with the GSDs introduces significant uncertainty in exposure
and risk estimates for the 95th population percentile.
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\38\ For example, the GSD for the urban case studies, in the
risk assessment described in this notice, was derived using NHANES
data for the years 1999-2000.
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Exposure pathway apportionment for higher percentile blood
Pb level and IQ loss estimates: Apportionment of blood Pb levels for
higher population percentiles is assumed to be the same as that
estimated using the central tendency estimate of blood Pb in an
exposure zone. This introduces significant uncertainty into projections
of pathway apportionment for higher population percentiles of blood Pb
and IQ loss. In reality, pathway apportionment may differ in higher
exposure percentiles. For example, paint and/or drinking water
exposures may increase in importance, with air-related contributions
decreasing as an overall percentage of blood Pb levels and associated
risk. Because of this uncertainty related to pathway apportionment, as
mentioned earlier, greater confidence is placed in estimates of total
Pb exposure and risk in evaluating the impact of the current NAAQS and
alternative NAAQS relative to current conditions.
Relating blood Pb levels to IQ loss: Specification of the
quantitative relationship between blood Pb level and
[[Page 71508]]
IQ loss is subject to significant uncertainty at lower blood Pb levels
(e.g., below 5 [mu]g/dL concurrent blood Pb). As discussed earlier,
there are limitations in the datasets and concentration-response
analyses available for characterizing the concentration-response
relationship at these lower blood Pb levels. For example, the pooled
international dataset analyzed by Lanphear and others (2005) includes
relatively few children with blood Pb levels below 5 [mu]g/dL and no
children with levels below 1 [mu]g/dL. In recognition of the
uncertainty in specifying a quantitative concentration-response
relationship at such levels, our core modeling approach involves the
application of four different functions to generate a range of risk
estimates (see Section 4.2.6 and Section 5.3.1 of the Risk Assessment
Report, USEPA, 2007b). The difference in absolute IQ loss estimates for
the four concentration-response functions for a given case study/air
quality scenario combination is typically close to a factor of 3.
Estimates of differences in IQ loss between air quality scenarios (in
terms of percent), however, are more similar across the four functions,
although the function producing higher overall risk estimates (the dual
linear function, stratified at 7.5 [mu]g/dL, peak blood Pb) also
produces larger absolute reductions in IQ loss compared with the other
three functions.
3. Summary of Results
This section presents blood Pb and IQ loss estimates generated in
the exposure and risk assessments. Blood Pb estimates are presented
first, followed by IQ loss estimates.
a. Blood Pb Estimates
This section presents blood Pb estimates for the median (Table 1)
and 95th (Table 2) population percentiles.\39\ Each table presents
estimates of blood Pb levels resulting from total Pb exposure across
all pathways (policy relevant and background), as well as estimates of
the percent contribution from ``recent air'' and ``recent plus past
air'' exposure categories. As noted in Sections 4.2.4 of the Staff
Paper and Section 3.4 of the Risk Assessment Report, given the various
limitations of our modeling tools, the contribution to blood Pb levels
from air-related exposure pathways and current levels of Pb emitted to
the air (including via resuspension) are likely to fall between
contributions attributed to ``recent air'' and those attributed to
``recent plus past air''. Key uncertainties regarding partitioning dust
Pb into ``recent air'' and ``other'' categories are summarized above
(and in Section 4.2.7 of the Staff Paper). The ``recent air'' component
of indoor dust Pb is the projected level associated with outdoor
ambient air Pb levels, with outdoor ambient air potentially including
resuspended, previously deposited Pb which may reflect the resuspension
of historic levels of Pb from gasoline and from exterior house and
building Pb paint. In presenting the 95th population percentile
estimates, it is recognized that 5 percent of the child study
population at each case study are estimated to have blood Pb levels
above these estimates. Due to technical limitations, however, we
believe that it is not possible at this point to reasonably predict the
distribution of blood Pb levels for that top 5 percent. Observations
regarding the blood Pb results presented in Tables 1 and 2 are
presented in Section 4.3 of the Staff Paper.
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\39\ Blood Pb level estimates for current conditions for these
cases studies differ from the national values associated with
NHANES. For example, median blood Pb levels presented in Table 1 for
the current conditions scenario for the urban case studies are
somewhat larger than the national median from the NHANES data for
2003-2004. Specifically, values for the three location-specific
urban case studies range from 1.7 to 1.8 [mu]g/dL with the general
urban case study having a value of 1.9 [mu]g/dL (current-conditions
mean) (see Table 1), while the median value from NHANES (2003-2004)
is 1.6 [mu]g/dL (http://www.epa.gov/envirohealth/children/body_burdens/b1-table.htm
). NHANES values for the 95th percentile were
not available for 2003-2004, precluding a comparison of modeled
estimates presented in Table 2 against NHANES data. We note,
however, that the 95th percentile value in 2001-2002 was 5.8 [mu]g/
dL (see footnote 7). However, NHANES values for the 90th percentile
(for 2003-2004) were identified and these values can be compared
against 90th percentile estimates generated for the urban case
studies (see Risk Assessment Report, Appendix O, Section O.3.2 for
the location-specific urban case study and Appendix N, Section
N.2.1.2 for the general urban case study). The 90th percentile blood
Pb levels for the current conditions scenario, for the three
location-specific urban case studies range from 4.5 to 4.6 [mu]g/dL,
while the estimate for the general urban case study is 5.0 [mu]g/dL.
These 90th percentile values for the case study populations are
larger than the 90th percentile value of 3.9 [mu]g/dL reported by
NHANES for all children in 2003-2004. It is noted that ambient air
levels reflected in the urban case studies are likely to differ from
those underlying the NHANES data.
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[[Page 71509]]
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\40\ As noted in footnote 39, median blood Pb levels generated
for the three location-specific urban case studies and the general
urban case study for the current conditions scenario are somewhat
larger than the median value from NHANES for 2003-2004.
\41\ As recognized in section III.B.2.d above, to simulate air
concentrations associated with the current NAAQS, a proportional
roll-up of concentrations from those for current conditions was
performed for the location-specific urban case studies. This was not
necessary for the primary Pb smelter case study in which air
concentrations currently exceed the current standard.
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\42\ As noted in footnote 39, 90th percentile blood Pb levels
generated for the three location specific urban case studies and the
general urban case study for the current conditions scenario are
larger than the 90th percentile value from NHANES for 2003-2004.
Note, 95th percentile values were not available for the NHANES 2003-
2004 dataset, preventing a direct comparison to modeled estimates
presented in Table 2. However, in 2001-2002, the 95th percentile
value was 5.8 [mu]g/dL (see footnote 7).
\43\ As recognized in section III.B.2.d above, to simulate air
concentrations associated with the current NAAQS, a proportional
roll-up of concentrations from those for current conditions was
performed for the location-specific urban case studies. This was not
necessary for the primary Pb smelter case study in which air
concentrations currently exceed the current standard.
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[[Page 71511]]
b. IQ Loss Estimates
This section presents IQ loss estimates in Tables 3 through 6.
These IQ loss estimates need to be understood in the context of the
broader and more comprehensive and detailed presentation provided Risk
Assessment Report (USEPA, 2007b). The tables presented here include
three types of risk estimates:
Estimates of IQ loss for all air quality scenarios (based
on total Pb exposure): Tables 3 and 4 present IQ loss estimates for
total Pb exposure for each of the air quality scenarios simulated for
each case study. Table 3 presents estimates for the population median
and Table 4 presents results for the 95th population percentile. These
results included both median and 95th population percentile estimates.
To reflect the variation in estimates derived from the four different
concentration-response functions included in the analysis, three
categories of estimates are considered including (a) IQ loss estimates
generated using the low concentration-response function (the model that
generated the lowest IQ loss estimates), (b) estimates generated using
the log-linear with low-exposure linearization (LLL) model, and (c) IQ
loss estimates generated using the high concentration-response function
(the model that generated the highest IQ loss estimates). For reasons
described above, estimates generated using the LLL model have been
given emphasis in the summary below.
Estimates of IQ loss under the current NAAQS air quality
scenario (with pathway apportionment): Tables 5 and 6 present IQ loss
estimates for total Pb exposure based on simulation of just meeting the
current NAAQS for the case studies to which the core modeling approach
was applied. Specifically, Table 5 presents estimates of the total Pb-
related IQ loss for the population median and Table 6 presents
estimates for the 95th population percentile. Both of these tables
present total IQ loss estimates for (a) total Pb exposure (including
both policy-relevant pathways and background sources) and (b) policy-
relevant exposures alone (bounded by estimates for ``recent air'' and
for ``recent plus past air'').
IQ loss incidence estimates for the three location-
specific urban case studies: Estimates of the number of children for
each location-specific urban case study projected to have total Pb-
related IQ loss greater than one point are summarized in Table 7, and
similar estimates for IQ loss greater than 7 points are summarized in
Table 8. Also presented are the changes in incidence of the current
NAAQS and alternative NAAQS scenarios compared to current conditions,
with emphasis placed on estimates generated using the LLL
concentration-response function. Estimates are presented for each of
the four concentration-response functions used in the core analysis.
The complete set of incidence results is presented in Risk Assessment
Report Appendix O, Section O.3.4.
The IQ loss results presented in Tables 3 through 8 need to be
understood in the context of the broader and more comprehensive and
detailed presentation provided in the Risk Assessment Report.
Observations regarding the IQ loss results presented in Tables 3
through 8 are presented in Section 4.4 of the Staff Paper.
It is important to point out that the range of absolute IQ loss
estimates generated using the four models for a given case study and
air quality scenario is typically around a factor of three. However,
the relative (proportional) change in IQ loss across air quality
scenarios (i.e., the pattern of IQ loss reduction across air quality
scenarios for the same case study) is fairly consistent across all four
models. This suggests uncertainty in estimates of absolute IQ loss for
a median or 95th percentile child with exposures related to a given
ambient air Pb level. Accordingly, we have greater confidence in
predicting incremental changes in IQ loss across air quality scenarios
and this is reflected in the observations presented in Section 4.4 of
the Staff Paper. As with the blood Pb estimates, 5 percent of the child
study population at each case study location is estimated to have IQ
loss above the 95th percentile estimates presented here, however, due
to technical limitations of our modeling tools, it is not feasible at
this point to reasonably predict the distribution of IQ loss levels for
that top 5 percent.
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\44\ As recognized in section III.B.2.d above, to simulate air
concentrations associated with the current NAAQS, a proportional
roll-up of concentrations from those for current conditions was
performed for the location-specific urban case studies. This was not
necessary for the primary Pb smelter case study in which air
concentrations currently exceed the current standard.
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[[Page 71513]]
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\45\ As recognized in section III.B.2.d above, to simulate air
concentrations associated with the current NAAQS, a proportional
roll-up of concentrations from those for current conditions was
performed for the location-specific urban case studies. This was not
necessary for the primary Pb smelter case study in which air
concentrations currently exceed the current standard.
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[[Page 71514]]
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\46\ As recognized in section III.B.2.d above, to simulate air
concentrations associated with the current NAAQS, a proportional
roll-up of concentrations from those for current conditions was
performed for the location-specific urban case studies. This was not
necessary for the primary Pb smelter case study in which air
concentrations currently exceed the current standard.
\47\ As recognized in section III.B.2.d above, to simulate air
concentrations associated with the current NAAQS, a proportional
roll-up of concentrations from those for current conditions was
performed for the location-specific urban case studies. This was not
necessary for the primary Pb smelter case study in which air
concentrations currently exceed the current standard.
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\48\ As recognized in section III.B.2.d above, to simulate air
concentrations associated with the current NAAQS, a proportional
roll-up of concentrations from those for current conditions was
performed for the location-specific urban case studies. This was not
necessary for the primary Pb smelter case study in which air
concentrations currently exceed the current standard.
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[[Page 71516]]
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\49\ As recognized in section III.B.2.d above, to simulate air
concentrations associated with the current NAAQS, a proportional
roll-up of concentrations from those for current conditions was
performed for the location-specific urban case studies. This was not
necessary for the primary Pb smelter case study in which air
concentrations currently exceed the current standard.
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[[Page 71517]]
C. Considerations in Review of the Standard
This section presents an integrative synthesis of information in
the Criteria Document together with EPA analyses and evaluations. EPA
notes that the final decision on retaining or revising the current
primary Pb standard is a public health policy judgment to be made by
the Administrator. The Administrator's final decision will draw upon
scientific information and analyses about health effects, population
exposure and risks, as well as judgments about the appropriate response
to the range of uncertainties that are inherent in the scientific
evidence and analyses. These judgments will be informed by a
recognition that the available health effects evidence generally
reflects a continuum consisting of ambient levels at which scientists
generally agree that health effects are likely to occur, through lower
levels at which the likelihood and magnitude of the response become
increasingly uncertain.
This approach is consistent with the requirements of the NAAQS
provisions of the Act and with how EPA and the courts have historically
interpreted the Act. These provisions require the Administrator to
establish primary standards that, in the Administrator's judgment, are
requisite to protect public health with an adequate margin of safety.
In so doing, the Administrator seeks to establish standards that are
neither more nor less stringent than necessary for this purpose. The
Act does not require that primary standards be set at a zero-risk level
but rather at a level that avoids unacceptable risks to public health,
including the health of sensitive groups.
The following discussion starts with background information on the
current standard (section III.C.1), including both the basis for
derivation of the current standard and considerations and conclusions
from the 1990 Staff Paper (USEPA, 1990b). This is followed by a summary
of the general approach for this current review (section III.C.2).
Considerations with regard to the adequacy of the current standard are
discussed in section III.C.3, with evidence and exposure-risk-based
considerations in subsections III.C.3.a and b, respectively, followed
by a summary of CASAC advice and recommendations (section III.C.3.c)
and, lastly, solicitation of comment on the broad range of policy
options (section III.C.3.d). Considerations with regard to elements of
alternative standards--indicator, averaging time and form, and level--
are discussed in sections III.C.4.a., III.C.4.b, and III.C.4.c,
respectively. The discussion with regard to level includes subsections
on evidence and exposure-risk-based considerations (sections III.C.4.a
and b), followed by a summary of CASAC advice and recommendations
(section III.C.4.c) and, lastly, solicitation of comment on the broad
range of policy options (section III.C.4.d).
1. Background on the Current Standard
a. Basis for Setting the Current Standard
The current primary standard is set at a level of 1.5 [mu]g/
m3, measured as Pb-TSP, not to be exceeded by the maximum
arithmetic mean concentration averaged over a calendar quarter. The
standard was set in 1978 to provide protection to the public,
especially children as the particularly sensitive population subgroup,
against Pb-induced adverse health effects (43 FR 46246). The basis for
selecting each of the elements of the standard is described below.
i. Level
EPA's objective in selecting the level of the current standard was
``to estimate the concentration of Pb in the air to which all groups
within the general population can be exposed for protracted periods
without an unacceptable risk to health'' (43 FR 46252). Consistent with
section 109 of the Clean Air Act, the Agency selected a level for the
current standard that was below the concentration that was at that time
identified as a threshold for adverse health effects (i.e., 40 [mu]g/dl
blood Pb), so as to provide an adequate margin of safety. As stated in
the notice of final rulemaking, ``This estimate was based on EPA's
judgment in four key areas:
(1) Determining the ``sensitive population'' as that group within
the general population which has the lowest threshold for adverse
effects or greatest potential for exposure. EPA concludes that young
children, aged 1 to 5, are the sensitive population.
(2) Determining the safe level of total lead exposure for the
sensitive population, indicated by the concentration of lead in the
blood. EPA concludes that the maximum safe level of blood lead for an
individual child is 30 [mu]g Pb/dl and that population blood lead,
measured as the geometric mean, must be 15 [mu]g Pb/dl in order to
place 99.5 percent of children in the United States below 30 [mu]g Pb/
dl.
(3) Attributing the contribution to blood lead from nonair
pollution sources. EPA concludes that 12 [mu]g Pb/dl of population
blood lead for children should be attributed to nonair exposure.
(4) Determining the air lead level which is consistent with
maintaining the mean population blood lead level at 15 [mu]g Pb/dl [the
maximum safe level]. Taking into account exposure from other sources
(12 [mu]g Pb/dl), EPA has designed the standard to limit air
contribution after achieving the standard to 3 [mu]g Pb/dl. On the
basis of an estimated relationship of air lead to blood lead of 1 to 2,
EPA concludes that the ambient air standard should be 1.5 [mu]g Pb/
m3.'' (43 FR 46252)
EPA's judgments in these key areas, as well as margin of safety
considerations, are discussed below.
The assessment of the science that was presented in the 1977
Criteria Document (USEPA, 1977), indicated young children, aged 1 to 5,
as the population group at particular risk from Pb exposure. Children
were recognized to have a greater physiological sensitivity than adults
to the effects of Pb and a greater exposure. In identifying young
children as the sensitive population, EPA also recognized the
occurrence of subgroups with enhanced risk due to genetic factors,
dietary deficiencies or residence in urban areas. Yet information was
not available to estimate a threshold for adverse effects for these
subgroups separate from that of all young children. Additionally, EPA
recognized both a concern regarding potential risk to pregnant women
and fetuses, and a lack of information to establish that these
subgroups are more at risk than young children. Accordingly, young
children, aged 1 to 5, were identified as the group which has the
lowest threshold for adverse effects of greatest potential for exposure
(i.e., the sensitive population) (43 FR 46252).
In identifying the maximum safe exposure, EPA relied upon the
measurement of Pb in blood (43 FR 46252-46253). The physiological
effect of Pb that had been identified as occurring at the lowest blood
Pb level was inhibition of an enzyme integral to the pathway by which
heme (the oxygen carrying protein of human blood) is synthesized, i.e.,
delta-aminolevulinic acid dehydratase ([delta]-ALAD). The 1977 Criteria
Document reported a threshold for inhibition of this enzyme in children
at 10 [mu]g Pb/dL. The 1977 Criteria Document also reported a threshold
of 15-20 [mu]g/dL for elevation of protoporphyrin (EP), which is an
indication of some disruption of the heme synthesis pathway. EPA
concluded that this effect on the heme synthesis pathway (indicated by
EP) was potentially adverse. EPA further described a range of blood
levels associated with a progression in
[[Page 71518]]
detrimental impact on the heme synthesis pathway. At the low end of the
range (15-20 [mu]g/dL), the initial detection of EP associated with
blood Pb was not concluded to be associated with a significant risk to
health. The upper end of the range (40 [mu]g/dL), the threshold
associated with clear evidence of heme synthesis impairment and other
effects contributing to clinical symptoms of anemia, was regarded as
clearly adverse to health. EPA also recognized the existence of
thresholds for additional adverse effects (e.g., nervous system
deficits) occurring for some children at just slightly higher blood Pb
levels (e.g., 50 [mu]g/dL). Additionally, EPA stated that the maximum
safe blood level should not be higher than the blood Pb level
recognized by the CDC as ``elevated'' (and indicative of the need for
intervention). In 1978, that level was 30 [mu]g/dL. \50\
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\50\ The CDC subsequently revised their advisory level for
children's blood Pb to 25 [mu]g/dL in 1985, and to 10 [mu]g/dL 1991.
In 2005, with consideration of a review of the evidence by their
advisory committee, CDC revised their statement on Preventing Lead
Poisoning in Young Children, specifically recognizing the evidence
of adverse health effects in children with blood Pb levels below 10
[mu]g/dL and the data demonstrating that no ``safe'' threshold for
blood Pb in children had been identified, and emphasizing the
importance of preventative measures (CDC, 2005a). Recently, CDC's
Advisory Committee on Childhood Lead Poisoning Prevention noted the
2005 CDC statements and reported on a review of the clinical
interpretation and management of blood Pb levels below 10 [mu]g/dL
(ACCLPP, 2007). More details on this level are provided in Section
III.A.1.
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Having identified the maximum safe blood level in individual
children, EPA next made a public health policy judgment regarding the
target mean blood level for the U.S. population of young children (43
FR 46252-46253). With this judgment, EPA identified a target of 99.5
percent of this population to be brought below the maximum safe blood
Pb level. This judgment was based on consideration of the size of the
sensitive subpopulation, and the recognition that there are special
high-risk groups of children within the general population. The
population statistics available at the time (the 1970 U.S. Census)
indicated a total of 20 million children younger than 5 years of age,
with 15 million residing in urban areas and 5 million in center cities
where Pb exposure was thought likely to be ``high''. Concern about
these high-risk groups influenced EPA's determination of 99.5 percent,
deterring EPA from selecting a population percentage lower than 99.5
(43 FR 46253). EPA then used standard statistical techniques to
calculate the population mean blood Pb level that would place 99.5
percent of the population below the maximum safe level. Based on the
then available data, EPA concluded that blood Pb levels in the
population of U.S. children were normally distributed with a GSD of
1.3. Based on standard statistical techniques, EPA determined that a
thus described population in which 99.5 percent of the population has
blood Pb levels below 30 [mu]g/dL would have a geometric mean blood
level of 15 [mu]g/dL. EPA described 15 [mu]g/dL as ``the maximum safe
blood lead level (geometric mean) for a population of young children''
(43 FR 46247).
When setting the current NAAQS, EPA recognized that the air
standard needed to take into account the contribution to blood Pb
levels from Pb sources unrelated to air pollution. Consequently, the
calculation of the current NAAQS included the subtraction of Pb
contributed to blood Pb from nonair sources from the estimate of a safe
mean population blood Pb level. Without this subtraction, EPA
recognized that the combined exposure to Pb from air and nonair sources
would result in a blood Pb concentration exceeding the safe level (43
FR 46253). In developing an estimate of this nonair contribution, EPA
recognized the lack of detailed or widespread information about the
relative contribution of various sources to children's blood Pb levels,
such that an estimate could only be made by inference from other
empirical or theoretical studies, often involving adults. Additionally,
EPA recognized the expectation that the contribution to blood Pb levels
from nonair sources would vary widely, was probably not in constant
proportion to air Pb contribution, and in some cases may alone exceed
the target mean population blood Pb level (43 FR 46253-46254). The
amount of blood Pb attributed to nonair sources was selected based
primarily on findings in studies of blood Pb levels in areas where air
Pb levels were low relative to other locations in U.S. The air Pb
levels in these areas ranged from 0.1 to 0.7 [mu]g/m\3\. The average of
the reported blood Pb levels for children of various ages in these
areas was on the order of 12 [mu]g/dL. Thus, 12 [mu]g/dL was identified
as the nonair contribution, and subtracted from the population mean
target level of 15 [mu]g/dL to yield a value of 3 [mu]g/dL as the limit
on the air contribution to blood Pb.
In determining the air Pb level consistent with an air contribution
of 3 [mu]g Pb/dL, EPA reviewed studies assessed in the 1977 Criteria
Document that reported changes in blood Pb with different air Pb
levels. These studies included a study of children exposed to Pb from a
primary Pb smelter, controlled exposures of adult men to Pb in fine
particulate matter, and a personal exposure study involving several
male cohorts exposed to Pb in a large urban area in the early 1970s (43
FR 46254). Using all three studies, EPA calculated an average slope or
ratio over the entire range of data. That value was 1.95 (rounded to 2
[mu]g/dL blood Pb concentration to 1 [mu]g/m\3\ air Pb concentration),
and is recognized to fall within the range of values reported in the
1977 Criteria Document. On the basis of this 2-to-1 relationship, EPA
concluded that the ambient air standard should be 1.5 [mu]g Pb/m\3\ (43
FR 46254).
In consideration of the appropriate margin of safety during the
development of the current NAAQS, EPA identified the following factors:
(1) The 1977 Criteria Document reported multiple biological effects of
Pb in practically all cell types, tissues and organ systems, of which
the significance for health had not yet been fully studied; (2) no
beneficial effects of Pb at then current environmental levels were
recognized; (3) data were incomplete as to the extent to which children
are indirectly exposed to air Pb that has moved to other environmental
media, such as water, soil and dirt, and food; (4) Pb is chemically
persistent and with continued uncontrolled emissions would continue to
accumulate in human tissue and the environment; and (5) the possibility
that exposure associated with blood Pb levels previously considered
safe might influence neurological development and learning abilities of
the young child (43 FR 46255). Recognizing that estimating an
appropriate margin of safety for the air Pb standard was complicated by
the multiple sources and media involved in Pb exposure, EPA chose to
use margin of safety considerations principally in establishing a
maximum safe blood Pb level for individual children (30 [mu]g Pb/dL)
and in determining the percentage of children to be placed below this
maximum level (about 99.5 percent). Additionally, in establishing other
factors used in calculating the standard, EPA used margin of safety
considerations in the sense of making careful judgment based on
available data, but these judgments were not considered to be at the
precautionary extreme of the range of data available at the time (43 FR
46251).
EPA further recognized that, because of the variability between
individuals in a population experiencing a given level of Pb exposure,
it was considered impossible to provide the same margin
[[Page 71519]]
of safety for all members in the sensitive population or to define the
margin of safety in the standard as a simple percentage. EPA believed
that the factors it used in designing the standards provided an
adequate margin of safety for a large proportion of the sensitive
population. The Agency did not believe that the margin was excessively
large or on the other hand that the air standard could protect everyone
from elevated blood Pb levels (43 FR 46251).
ii. Averaging Time, Form, and Indicator
The averaging time for the current standard is a calendar quarter.
In the decision for this aspect of the standard, the Agency also
considered a monthly averaging period, but concluded that ``a
requirement for the averaging of air quality data over calendar quarter
will improve the validity of air quality data gathered without a
significant reduction in the protectiveness of the standards.'' As
described in the notice for this decision (43 FR 46250), this
conclusion was based on several points, including the following:
An analysis of ambient measurements available at the time
indicated that the distribution of air Pb levels was such that there
was little possibility that there could be sustained periods greatly
above the average value in situations where the quarterly standard was
achieved.
A recognition that the monitoring network may not actually
represent the exposure situation for young children, such that it
seemed likely that elevated air Pb levels when occurring would be close
to Pb air pollution sources where young children would typically not
encounter them for the full 24-hour period reported by the monitor.
Medical evidence available at the time indicated that
blood Pb levels re-equilibrate slowly to changes in air exposure, a
finding that would serve to dampen the impact of short-term period of
exposure to elevated air Pb.
Direct exposure to air is only one of several routes of
total exposure, thus lessening the impact of a change in air Pb on
blood Pb levels.
The statistical form of the current standard is as a not-to-be-
exceeded or maximum value. EPA set the standard as a ceiling value with
the conclusion that this air level would be safe for indefinite
exposure for young children (43 FR 46250).
The indicator is total airborne Pb collected by a high volume
sampler (43 FR 46258). EPA's selection of Pb-TSP as the indicator for
the standard was based on explicit recognition both of the significance
of ingestion as an exposure pathway for Pb that had deposited from the
air and of the potential for Pb deposited from the air to become re-
suspended in respirable size particles in the air and available for
human inhalation exposure. As stated in the final rule, ``a significant
component of exposure can be ingestion of materials contaminated by
deposition of lead from the air,'' and that, ``in addition to the
indirect route of ingestion and absorption from the gastrointestinal
tract, non-respirable Pb in the environment may, at some point become
respirable through weathering or mechanical action'' (43 FR 46251).
b. Policy Options Considered in the Last Review
During the 1980s, EPA initiated a review of the air quality
criteria and NAAQS for Pb. CASAC and the public were fully involved in
this review, which led to the publication of a criteria document with
associated addendum and a supplement (USEPA, 1986a, 1986b, 1990a), an
exposure analysis methods document (USEPA, 1989) and a staff paper
(USEPA, 1990b).
Total emissions to air were estimated to have dropped by 94 percent
between 1978 and 1987, with the vast majority of it attributed to the
reduction of Pb in gasoline. Accordingly, the focus of the last review
was on areas near stationary sources of Pb emissions. Although such
sources were not considered to have made a significant contribution (as
compared to Pb in gasoline) to the overall Pb pollution across large,
urban or regional areas, Pb emissions from such sources were considered
to have the potential for a significant impact on a local scale. Air Pb
concentrations, and especially soil and dust Pb concentrations had been
associated with elevated levels of Pb absorption in children and adults
in numerous Pb point source community studies. Exceedances of the
current NAAQS were found at that time only in the vicinity of
nonferrous smelters or other point sources of Pb.
In summarizing and interpreting the health evidence presented in
the 1986 Criteria Document and associated documents, the 1990 Staff
Paper described the collective impact on children of the effects at
blood Pb levels above 15 [mu]g/dL as representing a clear pattern of
adverse effects worthy of avoiding. This is in contrast to EPA's
identification of 30 [mu]g/dL as a safe blood Pb level for individual
children when the NAAQS was set in 1978. The Staff Paper further stated
that at blood Pb levels of 10-15 [mu]g/dL, there was a convergence of
evidence of Pb-induced interference with a diverse set of physiological
functions and processes, particularly evident in several independent
studies showing impaired neurobehavioral function and development.
Further, the available data did not indicate a clear threshold in this
blood Pb range. Rather, it suggested a continuum of health risks down
to the lowest levels measured.\51\
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\51\ In 1991, the CDC reduced their advisory level for
children's blood Pb from 25 [mu]g/dL to 10 [mu]g/dL.
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For the purposes of comparing the relative protectiveness of
alternative Pb NAAQS, the staff conducted analyses to estimate the
percentages of children with blood Pb levels above 10 [mu]g/dL and
above 15 [mu]g/dL for several air quality scenarios developed for a
small set of stationary source exposure case studies. The results of
the analyses of child populations living near two Pb smelters indicated
that substantial reductions in Pb exposure could be achieved through
just meeting the current Pb NAAQS. According to the best estimate
analyses, over 99.5% of children living in areas significantly affected
by the smelters would have blood Pb levels below 15 [mu]g/dL if the
current standard was achieved. Progressive changes in this number were
estimated for the alternative monthly Pb NAAQS levels evaluated in
those analyses, which ranged from 1.5 [mu]g/m\3\ to 0.5 [mu]g/m\3\.
In light of the health effects evidence available at the time, the
1990 Staff Paper presented air quality, exposure, and risk analyses,
and other policy considerations, as well as the following staff
conclusions with regard to the primary Pb NAAQS (USEPA, 1990b, pp. xii
to xiv):
(1) ``The range of standards * * * should be from 0.5 to 1.5 [mu]g/
m\3\.''
(2) ``A monthly averaging period would better capture short-term
increases in lead exposure and would more fully protect children's
health than the current quarterly average.''
(3) ``The most appropriate form of the standard appears to be the
second highest monthly averages {sic{time} in a 3-year span. This form
would be nearly as stringent as a form that does not permit any
exceedances and allows for discounting of one ``bad'' month in 3 years
which may be caused, for example, by unusual meteorology.''
(4) ``With a revision to a monthly averaging time more frequent
sampling is needed, except in areas, like roadways remote from lead
point sources, where the standard is not expected to be violated. In
those situations, the current 1-in-6 day sampling schedule would
sufficiently reflect air quality and trends.''
[[Page 71520]]
(5) ``Because exposure to atmospheric lead particles occurs not
only via direct inhalation, but via ingestion of deposited particles as
well, especially among young children, the hi-volume sampler provides a
reasonable indicator for determining compliance with a monthly standard
and should be retained as the instrument to monitor compliance with the
lead NAAQS until more refined instruments can be developed.''
Based on its review of a draft Staff Paper, which contained the
above recommendations, the CASAC strongly recommended to the
Administrator that EPA should actively pursue a public health goal of
minimizing the Pb content of blood to the extent possible, and that the
Pb NAAQS is an important component of a multimedia strategy for
achieving that goal (CASAC, 1990, p. 4). In noting the range of levels
recommended by staff, CASAC recommended consideration of a revised
standard that incorporates a ``wide margin of safety, because of the
risk posed by Pb exposures, particularly to the very young whose
developing nervous system may be compromised by even low level
exposures'' (id., p. 3). More specifically, CASAC judged that a
standard within the range of 1.0 to 1.5 [mu]g/m\3\ would have
``relatively little, if any, margin of safety;'' that greater
consideration should be given to a standard set below 1.0 [mu]g/m\3\;
and, to provide perspective in setting the standard, it would be
appropriate to consider the distribution of blood Pb levels associated
with meeting a monthly standard of 0.25 [mu]g/m\3\, a level below the
range considered by staff (id.).
After consideration of the documents developed during the review,
EPA chose not to propose revision of the NAAQS for Pb. During the same
time period, the Agency published and embarked on the implementation of
a broad, multi-program, multi-media, integrated national strategy to
reduce Pb exposures (USEPA, 1991). As part of implementing this
integrated Pb strategy, the Agency focused efforts primarily on
regulatory and remedial clean-up actions aimed at reducing Pb exposures
from a variety of non-air sources judged to pose more extensive public
health risks to U.S. populations, as well as on actions to reduce Pb
emissions to air, particularly near stationary sources. This focus
reflected in part the dramatic reduction of Pb in gasoline that
occurred since the standard was set in 1978, which resulted in orders-
of-magnitude reductions in airborne emissions of Pb, and a significant
shift in the types of sources with the greatest Pb emissions. EPA
established standards for Pb-based paint hazards and Pb dust cleanup
levels in most pre-1978 housing and child-occupied facilities.
Additionally, EPA has developed standards for the management of Pb in
solid and hazardous waste, oversees the cleanup of Pb contamination at
Superfund sites, and has issued regulations to reduce Pb in drinking
water (http://www.epa.gov/lead/regulation.htm). Beyond these specific
regulatory actions, the Agency's Lead Awareness Program has continued
to work to protect human health and the environment against the dangers
of Pb by conducting research and designing educational outreach
activities and materials (http://www.epa.gov/lead/). Actions to reduce
Pb emissions to air during the 1990s included enforcement of the NAAQS,
as well as the promulgation of regulations under Section 112 of the
Clean Air Act, including national emissions standards for hazardous air
pollutants at primary and secondary Pb smelters, as well as other Pb
sources.
2. Approach for Current Review
To evaluate whether it is appropriate to consider retaining the
current primary Pb standard, or whether consideration of revisions is
appropriate, EPA is considering an approach in this review like that
used in the Staff Paper. As discussed below, this approach builds upon
the general approach used in the initial setting of the standard, as
well as that used in the last review, and reflects the broader body of
evidence and information now available.
This approach is based on an integration of information on health
effects associated with exposure to ambient Pb; expert judgment on the
adversity of such effects on individuals; and policy judgments as to
when the standard is requisite to protect public health with an
adequate margin of safety, which are informed by air quality and
related analyses, quantitative exposure and risk assessments when
possible, and qualitative assessment of impacts that could not be
quantified.
In conducting this assessment, EPA is aware of the dramatic
reductions in air Pb emissions in the U.S. in recent decades.\52\ In
addition to the dramatic reduction of Pb in gasoline, an additional
circumstance that has changed since the standard was set is the
enactment of the Clean Air Act Amendments of 1990, which amended Clean
Air Act Section 112 to list Pb compounds as hazardous air pollutants
(HAP) and to require technology-based and risk-based standards, as
appropriate, for major stationary sources of HAP.\53\ EPA is also aware
that these significantly changed circumstances have raised the question
in this review of whether it is still appropriate to maintain a NAAQS
for Pb or to retain Pb on the list of criteria pollutants. As a result,
this evaluation will consider the status of Pb as a criteria pollutant
and assesses whether revocation of the standard is an appropriate
option for the Administrator to consider.
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\52\ Detailed information on air Pb emissions, and temporal
trends in emissions since 1980 is provided in Section 2.2 of the
Staff Paper.
\53\ The use of Pb paint in new houses has declined
substantially over the 20\th\ century. For example ``an estimated
68% of U.S. homes built before 1940 have Pb hazards, as do 43% of
those built during 1940-1959 and 8% of those built during 1960-
1977'' (ACCLPP, 2007). We are uncertain of the implications of these
reductions for ambient air.
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As discussed below, in conducting this evaluation, EPA will take
into account both evidence-based and quantitative exposure- and risk-
based considerations. To the extent that the available information
suggests that revision of the current standard may be appropriate to
consider, EPA will also evaluate the currently available information to
determine the extent to which it supports consideration of a revised
standard. In this evaluation, EPA will consider the specific elements
of the standard to identify options (in terms of an indicator,
averaging time, level, and form) for consideration in making public
health policy judgments, based on the currently available information,
as to the degree of protection that is requisite to protect public
health with an adequate margin of safety.
To help inform the Agency's consideration of the quantitative
exposure and risk assessments, summarized above in section III.B, EPA
solicits comment on the appropriate weight to be placed on the results
from these assessments in evaluating the adequacy of the current
primary standard and in considering alternative standards.
Specifically, we solicit comment on a number of aspects of the design
of the assessments and interpretation of the assessment results,
including in particular: (1) The appropriateness of rolling up ambient
Pb concentrations to simulate just meeting the current standard for
areas in which current concentrations are well below the level of the
current standard; \54\ (2) the use of a proportional
[[Page 71521]]
method to roll-up and roll-down Pb concentrations to simulate just
meeting the current and alternative standards; \55\ (3) the
categorization and apportionment of policy-relevant exposure pathways
and policy-relevant background, particularly with regard to exposures
related to historically deposited Pb from leaded gasoline and from Pb
paint; and (4) the weight to be given to risk estimates derived using
various concentration-response functions. More broadly, we also solicit
comment on the approach of considering exposures and risks resulting
from the ingestion of historically emitted Pb that may now be present
in indoor dust and outdoor soil (e.g., that associated with past use of
Pb in gasoline or Pb paint) impacted by ambient air Pb as being policy-
relevant for the purpose of setting a NAAQS.
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\54\ We have not in the past used such an approach in developing
risk assessments for other NAAQS reviews since other risk
assessments (i.e., for ozone and PM) included a number of areas that
did not meet the current NAAQS such that rolling up ambient
pollutant concentrations was not needed to characterize risks
associated with just meeting the current standard.
\55\ There are other methods that might be used.
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3. Adequacy of the Current Standard
In considering the adequacy of the current standard, EPA will first
consider whether it is appropriate to maintain a NAAQS for Pb or to
retain Pb on the list of criteria pollutants. As noted above, this
question has arisen in this review as a result of the dramatic
alteration in the basic patterns of air Pb emissions in the U.S. since
the standard was set, that primarily reflects the dramatic reduction of
Pb in gasoline, which resulted in orders-of-magnitude reductions in
airborne emissions of Pb and a significant shift in the types of
sources with the greatest Pb emissions. In addition, Section 112 of the
Clean Air Act was amended in 1990 to include Pb compounds on the list
of HAP and to require EPA to establish technology-based emission
standards for those listed major source categories emitting Pb
compounds, and to establish risk-based standards, as appropriate, for
those categories of sources.
EPA notes that CASAC specifically examined several scientific
issues and related public health (and public welfare) policy issues
that the CASAC Lead Review Panel \56\ judged to be essential in
determining whether delisting Pb or revoking the Pb NAAQS would be
appropriate options for the Administrator to consider. In its letter to
the Administrator of March 27, 2007, based on its review of the first
draft Staff Paper (Henderson, 2007a; Attachment A of the Staff Paper),
CASAC's examination of these issues was framed by the following series
of questions:
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\56\ This Lead Panel includes the statutorily defined seven-
member CASAC and additional subject-matter experts needed to provide
an appropriate breadth of expertise for this review of the Pb NAAQS.
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(1) Does new scientific information accumulated since EPA's
promulgation of the current primary Lead NAAQS of 1.5 [mu]g/m\3\ in
1978 suggest that science previously overstated the toxicity of lead?
(2) Have past regulatory and other controls on lead decreased PbB
[blood lead] concentrations in human populations so far below levels of
concern as to suggest there is now an adequate margin of safety
inherent in those PbB levels?
(3) Have the activities that produced emissions and atmospheric
redistribution of lead in the past changed to such an extent that
society can have confidence that emissions will remain low even in the
absence of NAAQS controls?
(4) Are airborne concentrations and amounts of lead sufficiently
low throughout the United States that future regulation of lead
exposures can be effectively accomplished by regulation of lead-based
products and allowable amounts of lead in soil and/or water?
(5) If lead were de-listed as a criteria air pollutant, would it be
appropriately regulated under the Agency's Hazardous Air Pollutants
(HAP) program?
For the reasons presented in its March 2007 letter, the CASAC Lead
Review Panel judged that the answer to each of these questions was
``no,'' leading the Panel to conclude that ``the existing state of
science is consistent with continuing to list ambient lead as a
criteria pollutant for which fully-protection NAAQS are required'' (id,
p. 5). Further, in a subsequent letter to the Administrator of
September 27, 2007, based on its review of the second draft Risk
Assessment Report (Henderson, 2007b; Attachment B of the Staff Paper),
CASAC strongly reiterated its opposition to any considered delisting of
Pb, and expressed its unanimous support for maintaining fully-
protective NAAQS (id., p. 2). The EPA seeks comment and supporting
information on the issue of whether it would be appropriate for EPA to
determine that emissions of Pb no longer contribute to air pollution
that may reasonably be anticipated to endanger public heath. EPA also
solicits comment and supporting information on the extent to which
reductions in the ambient air Pb standard would benefit public health.
In considering the adequacy of the current standard, EPA will
consider the available evidence and quantitative exposure- and risk-
based information, summarized below.
a. Evidence-Based Considerations
In considering the broad array of health effects evidence assessed
in the Criteria Document with respect to the adequacy of the current
standard, EPA will focus on those health endpoints associated with the
Pb exposure and blood levels most pertinent to ambient exposures.
Additionally, we will give particular weight to evidence available
today that differs from that available at the time the standard was set
with regard to its support of the current standard.
First, with regard to the sensitive population, the susceptibility
of young children to the effects of Pb is well recognized, in addition
to more recent recognition of effects of chronic exposure to low level
Pb with advancing age (CD, Sections 5.3.7 and pp. 8-73 to 8-75). The
prenatal period and early childhood are periods of increased
susceptibility to Pb exposures, with evidence of adverse effects on the
developing nervous system that generally appear to persist into later
childhood and adolescence (CD, Section 6.2).\57\ Thus, while the
sensitivity of the elderly and other particular subgroups is
recognized, as at the time the standard was set, young children
continue to be recognized as the key sensitive population for Pb
exposures.
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\57\ For example, the following statement is made in the
Criteria Document ``Negative Pb impacts on neurocognitive ability
and other neurobehavioral outcomes are robust in most recent studies
even after adjustment for numerous potentially confounding factors
(including quality of care giving, parental intelligence, and
socioeconomic status). These effects generally appear to persist
into adolescence and young adulthood.'' (CD, p.E-9)
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With regard to the exposure levels at which adverse health effects
occur, the current evidence demonstrates the occurrence of adverse
health effects at appreciably lower blood Pb levels than those
demonstrated by the evidence at the time the standard was set. This
change in the evidence since the time the standard was set is reflected
in changes made by the CDC in their advisory level for Pb in children's
blood, and changes they have made in their characterization of that
level. Although CDC recognized a level of 30 [mu]g/dL blood Pb as
warranting individual intervention in 1978 when the Pb NAAQS was set,
in 2005 they recognized the evidence of adverse health effects in
children with blood Pb levels below 10 [mu]g/dL and the data
demonstrating that no ``safe'' threshold for blood Pb had been
identified (CDC, 1991; CDC, 2005).
The Criteria Document describes current evidence regarding the
occurrence of a variety of adverse health
[[Page 71522]]
effects, including those on the developing nervous system, associated
with blood Pb levels extending well below 10 [mu]g/dL to 5 [mu]g/dL and
possibly lower (CD, Sections 8.4 and 8.5).\58\ With regard to the
evidence of effects on the developing nervous system at these low
levels, EPA notes, in particular, the international pooled analysis by
Lanphear and others (2005), studies of individual cohorts such as the
Rochester, Boston, and Mexico City cohorts (Canfield et al., 2003a;
Canfield et al., 2003b; Bellinger and Needleman, 2003; Tellez-Rojo et
al., 2006), the study of African-American inner-city children from
Detroit (Chiodo et al., 2004), and the cross-sectional analysis of a
nationally representative sample from the NHANES III (conducted from
1988-1994), in which the mean blood Pb level was 1.9 [mu]g/dL (Lanphear
et al., 2000). Further, current evidence does not indicate a threshold
for the more sensitive health endpoints such as adverse effects on the
developing nervous system (CD, pp. 5-71 to 5-74 and Section 6.2.13).
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\58\ For context, it is noted that the 2001-2004 median blood
level for children aged 1-5 of all races and ethnic groups is 1.6
[mu]g/dL, the median for the subset living below the poverty level
is 2.3 [mu]g/dL and 90th percentile values for these two groups are
4.0 [mu]g/dL and 5.4 [mu]g/dL, respectively. Similarly, the 2001-
2004 median blood level for black, non-hispanic children aged 1-5 is
2.5 [mu]g/dL, while the median level for the subset of that group
living below the poverty level is 2.9 [mu]g/dL and the median level
for the subset living in a household with income more than 200% of
the poverty level is 1.9 [mu]g/dL. Associated 90th percentile values
for 2001-2004 are 6.4 [mu]g/dL (for black, non-hispanic children
aged 1-5), 7.7 [mu]g/dL (for the subset of that group living below
the poverty level) and 4.1 [mu]g/dL (for the subset living in a
household with income more than 200% of the poverty level). (http://www.epa.gov/envirohealth/children/body_burdens/b1-table.htm_then
click on ``Download a universal spreadsheet file of the Body Burdens
data tables'').
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As when the standard was set in 1978, EPA recognizes that there
remain today contributions to blood Pb levels from nonair sources.
Estimating contributions from nonair sources are complicated by the
persistent nature of Pb. For example, Pb that is a soil or dust
contaminant today may have been airborne yesterday or many years ago.
The studies currently available and reviewed in the Criteria Document
that evaluate the multiple pathways of Pb exposure do not usually
distinguish between outdoor soil/dust Pb resulting from historical
emissions and outdoor soil/dust Pb resulting from recent emissions.
Further, while indoor dust Pb has been identified as being a
predominant contributor to children's blood Pb, available studies do
not distinguish the different pathways (air-related and other)
contributing to indoor dust Pb. As recognized in Section III.A. above
(including footnote 13), some studies have found that dietary intake of
Pb may be a predominant source of Pb exposure among adults, greater
than consumption of water and beverages or inhalation (CD, p. 3-43).
The exposure assessment for children performed for this review has
employed available data and methods to develop estimates intended to
inform a characterization of these pathways.
Consistent with reductions in air Pb concentrations \59\ which
contribute to blood Pb, nonair contributions have also been reduced.
For example, the use of Pb paint in new houses has declined
substantially over the 20th century, such that ``an estimated 68% of
U.S. homes built before 1940 have Pb hazards, as do 43% of those built
during 1940-1959 and 8% of those built during 1960-1977'' (ACCLPP,
2007). Additionally, Pb contributions to diet have been reported to
have declined significantly since 1978, perhaps as much as 70% or more
between then and 1990 (WHO, 1995) and the 2006 Criteria Document
identifies a drop in dietary Pb intake by 2 to 5 year olds of 96%
between the early 1980s and mid 1990s. The 1977 Criteria Document
included a dietary Pb intake estimate for the general population of 100
to 350 [mu]g Pb/day (USEPA 1977, p. 1-2) and the 2006 Criteria Document
cites recent studies indicating a dietary intake ranging from 2 to 10
[mu]g Pb/day (CD, Section 3.4 and p. 8-14). Reductions in elevated
blood Pb levels in urban areas indicate that other nonair contributions
to blood Pb (e.g., drinking water distribution systems, and Pb-based
paint) have also been reduced since the late 1970s. In their March 2007
letter to the Administrator, the CASAC Pb Panel recommended that 1.0-
1.4 [mu]g/dL or lower be considered as an estimate of the nonair
component of blood Pb.
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\59\ Air Pb concentrations nationally are estimated to have
declined more than 90% since the early 1980s.
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As in 1978, the evidence demonstrates that Pb in ambient air
contributes to Pb in blood, with the pertinent exposure routes
including both inhalation and ingestion (CD, Sections 3.1.3.2, 4.2 and
4.4; Hilts et al., 2003). In 1978, the evidence indicated a
quantitative relationship between ambient air Pb and blood Pb--i.e.,
the ratio describing the increase in blood Pb per unit of air Pb--that
ranged from 1:1 to 1:2 (USEPA, 1977). In setting the standard, the
Agency relied on a ratio of 1:2, i.e., 2 [mu]g/dL blood Pb per 1 [mu]g/
m\3\ air Pb (43 FR 46252). The evidence now and in the past on this
relationship is limited by the circumstances in which the data are
collected. Specific measurements of Pb in blood that derived from Pb
that had been in the air are not available. Rather, estimates are
available for the relationship between Pb concentrations in air and Pb
levels in blood, developed from populations in differing Pb exposure
circumstances, which inform this issue. Many of the currently available
reviews of estimates for air-to-blood ratios, which include air
contributions from both inhalation and ingestion exposure pathways,
indicate that such ratios generally fall between 1:3 to 1:5, with some
higher \60\ (USEPA 1986a, pp. 11-99 to 11-100 and 11-106; Brunekreef,
1984). Findings of a recent study of changes in children's blood Pb
levels associated with reduced Pb emissions and associated air
concentrations near a Pb smelter in Canada indicates a ratio on the
order of 1:7 (CD, pp. 3-23 to 3-24; Hilts et al., 2003). In their
advice to the Agency, CASAC identified values of 1:5 as used by the
World Health Organization (2000) and 1:10 as supported by an empirical
analysis of changes in air Pb and changes in blood Pb between 1976 and
the time when the phase-out of Pb from gasoline was completed
(Henderson, 2007a).\61\ While there is uncertainty in the absolute
value of the air-to-blood relationship, the current evidence indicates
a notably greater ratio, with regard to increase in blood Pb, than the
1978 1:2 relationship e.g., on the order of 1:3 to 1:5 with some higher
estimates (see footnote 60) and some lower estimates (down to 1:1).
EPA's consideration of this issue in 1986 indicated that ratios which
consider both inhalation and ingestion pathways are ``necessarily
higher than those estimates for inhaled air lead alone'' (USEPA, 1986a,
p. 11-106). We solicit comment on data or studies that may help inform
our understanding of this important parameter.
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\60\ For example, adjusted ratios from Brunekreef (1984, Table
1) ranged up to 1:8.5 and unadjusted ratios extended above 1:10.
\61\ The CASAC Panel stated ``The Schwartz and Picher analysis
showed that in 1978, the midpoint of the National Health and
Nutrition Examination Survey (NHANES) II, gasoline lead was
responsible for 9.1 [mu]g/dL of blood lead in children. Their
estimate is based on their coefficient of 2.14 [mu]g/dL per 100
metric tons (MT) per day of gasoline use, and usage of 426 MT/day in
1976. Between 1976 and when the phase-out of lead from gasoline was
completed, air lead concentrations in U.S. cities fell a little less
than 1 [mu]g/m\3\ (24). These two facts imply a ratio of 9-10 [mu]g/
dL per [mu]g/m\3\ reduction in air lead, taking all pathways into
account.'' (Henderson, 2007a, page D-2 to D-3).
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Based on this information, the Staff Paper concluded that young
children remain the sensitive population of primary focus in this
review, there is now no recognized safe level of Pb in
[[Page 71523]]
children's blood, and studies appear to show adverse effects at mean
concurrent blood Pb levels as low as 2 ug/dL (CD, pp. 6-31 to 6-32;
Lanphear et al., 2000). Further, while the nonair contribution to blood
Pb has declined, perhaps to a range of 1.0-1.4 [mu]g/dL, the air-to-
blood ratio appears to be higher at today's lower blood Pb levels than
the estimates at the time the standard was set, with current estimates
on the order of 1:3 to 1:5 and perhaps up to 1:10. Using the framework
employed in setting the standard in 1978, the more recently available
evidence and more recently available estimates may suggest a level for
the standard that is lower by an order of magnitude or more.
b. Exposure- and Risk-Based Considerations
In addition to the evidence-based considerations, EPA will also
consider exposures and health risks estimated to occur upon meeting the
current Pb standard to help inform judgments about the extent to which
exposure and risk estimates may be judged to be important from a public
health perspective, taking into account key uncertainties associated
with the estimated exposures and risks.
As discussed above, young children are the sensitive population of
primary focus in this review. The exposure and risk assessment
estimates Pb exposure for children (less than 7 years of age), and
associated risk of neurocognitive effects in terms of IQ decrements. In
addition to the risks (IQ decrement) that were quantitatively
estimated, EPA recognizes that there may be long-term adverse
consequences of such deficits over a lifetime, that there is evidence
of other health effects occurring at similar or higher exposures for
young children, and that other health evidence demonstrates
associations between Pb exposure and adverse health effects in adults.
As noted in section III.B above, the risk assessment results focus
predominantly on risk estimates derived using the log-linear with low-
exposure linearization (LLL) concentration-response function, with the
range associated with the other three functions also being noted.
As noted in the Criteria Document, a modest change in the mean for
a health index at the individual level can have substantial
implications at the population level (CD, p. 8-77, Sections 8.6.1 and
8.6.2; Bellinger, 2004; Needleman et al., 1982; Weiss, 1988; Weiss,
1990)). For example, for an individual functioning in the low range of
IQ due to the influence of risk factors other than Pb, a Pb-associated
IQ decline of a few points might be sufficient to drop that individual
into the range associated with increased risk of educational,
vocational, and social handicap (CD, p. 8-77). Further, given a
somewhat uniform manifestation of Pb-related decrements across the
range of IQ scores in a population, a downward shift in the mean IQ
value is not associated only with a substantial increase in the
percentage of individuals achieving very low scores, but also with
substantial decreases in percentages achieving very high scores (CD, p.
8-81). The CASAC Pb Panel has advised on this point that ``a population
loss of 1-2 IQ points is highly significant from a public health
perspective'' (Henderson, 2007a, p. 6).
In this section, risk estimates for the median and for an upper
percentile, the 95th are discussed. In setting the standard in 1978,
EPA accorded risk management significance to the 99.5th percentile by
selecting a mean blood Pb level intended to bring 99.5 percent of the
population to or below the then described maximum safe blood Pb level.
Similarly, in their advice to EPA in this review, CASAC stated that
``the primary lead standard should be set so as to protect 99.5% of the
population'' (Henderson, 2007a, p. 6). In considering estimates from
the quantitative assessment that will inform conclusions consistent
with this objective, however, EPA and CASAC also recognize
uncertainties in the risk estimates at the edges of the distribution
and consequently the 95th percentile is reported as the estimate of the
high end of the risk distribution (Henderson, 2007b, p. 3). In so
doing, however, EPA notes that there are individuals in the population
expected to have higher risk, the consideration of which is important
given the risk management objectives for the current standard when set
in 1978 with regard to the 99.5th percentile.
In addition to estimating IQ loss associated with the combined
exposure to Pb from all exposure pathways, EPA estimated IQ loss for
two policy-relevant categories of exposure pathways. These are ``recent
air'', which conceptually is intended to include contributions to blood
Pb associated with Pb that has recently been in the air, and ``past
air'', intended to include contributions to blood Pb associated with Pb
that was in the air in the past but not in the air recently. In the
exposure modeling conducted for the risk assessment, the exposure
pathways assigned to the recent air category were inhalation of ambient
air Pb and ingestion of the component of indoor dust Pb that is
predicted to be associated with ambient air concentrations. The
exposure pathways assigned to the past air category were ingestion of
outdoor soil/dust Pb and ingestion of the component of indoor dust Pb
not assigned to recent air. There are various limitations associated
with our modeling tools that affected the estimates for these two
categories. As a result, blood Pb levels and associated risks of
greatest interest in this review--those associated with exposure
pathways involving ambient air Pb and current levels of Pb emitted to
the air (including via resuspension)--are likely to fall between
estimates for recent air and those for the sum of recent plus past
air.\62\ Accordingly, this notice presents these two sets of estimates
as providing a range of interest, with regard to policy-relevant Pb,
for this review.
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\62\ Comparisons of blood Pb levels estimated for individual
case study populations (from all exposure sources in current
conditions scenarios) to national population values from NHANES are
noted in footnote 39 in Section III.B.3.a.
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In considering the adequacy of the current standard, it is
important to note that the standard is currently met throughout the
country with very few exceptions. The national composite average
maximum quarterly mean based on 198 active monitoring sites during
2003-2005 is 0.17 [mu]g/m\3\, an order of magnitude below the current
standard, indicating that most of the monitored areas of the country
are well below the standard. Review of the current monitoring network
in light of current information on Pb sources and emissions, however,
indicated that monitors are not located near many of the larger
sources. Therefore, the assessment may be underestimating Pb
concentrations.
Using the current monitoring data, EPA estimated exposure and risk
associated with current conditions in a general urban case study and in
three location-specific urban case studies in areas where air
concentrations fall significantly below the current standard.\63\ Two
current conditions scenarios were assessed for the general urban case
study, one based on the 95th percentile of levels in large urban areas
(0.87 [mu]g/m\3\, maximum quarterly mean) and one based on mean levels
in such
[[Page 71524]]
areas (0.14 [mu]g/m\3\, maximum quarterly. Levels in the three
location-specific case studies ranged from 0.09 to 0.35 [mu]g/m\3\, in
terms of maximum quarterly average. For the general urban case study,
which is a simplified representation of urban areas, median estimates
of total Pb-related IQ loss range from 1.5 to 6.3 points (across all
four concentration-response functions), with estimates based on the LLL
function of 4.5 and 4.7 points, for the mean and high-end current
conditions scenarios, respectively. Associated estimates for exposure
pathway contributions to total IQ loss (LLL estimate) at the population
median in these two scenarios indicate that IQ loss associated with
policy-relevant Pb falls somewhere between 1.3 and 3.6 points. At the
95th percentile for total IQ loss (LLL estimate), IQ loss associated
with policy-relevant Pb is estimated to fall somewhere between 2.2 and
6.0 points (Risk Assessment Report, Table 5-9).
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\63\ Comparisons of median and 90th percentile blood Pb levels
estimated for individual case study populations (from all exposure
sources in current conditions scenarios) to national population
values from NHANES are noted in footnote 39 in Section III.B.3.a.
That comparison suggests that modeled estimates generated for the
location-specific urban case studies for both population percentiles
are somewhat larger than values cited in NHANES (for 2003-2004).
However, as mentioned earlier, factors related to Pb exposure,
including ambient air levels, are likely to differ for the urban
case study populations compared with the national population
underlying NHANES.
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For the three location-specific areas, median estimates of total
Pb-related IQ loss for current conditions range from 1.4 to 5.2 points
(across all four concentration-response functions), with estimates
based on the LLL function all being 4.2 points.\64\ Median IQ loss
associated with policy-relevant Pb (LLL function) is estimated to fall
between 0.6 to 2.9 points IQ loss. The 95th percentile estimates for
total Pb-related IQ loss across the three location-specific urban case
studies range from 4.1 to 11.4 points (across all four concentration-
response functions), with estimates based on the LLL function ranging
from 7.5 to 7.6 points. At the 95th percentile for the three location-
specific urban case studies, IQ loss associated with policy-relevant Pb
(LLL function) is estimated to fall between 1.2 to 5.2 points IQ loss
(Risk Assessment Report, Tables 5-9 and 5-10).
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\64\ Although the maximum quarterly average concentration for
the highest monitor in each study area differs among the three areas
by a factor of 4 (0.09 to 0.36 [mu]g/m\3\), the population weighted
air Pb concentrations for these three study areas are more similar
and differ by approximately a factor of 2, with the study area with
highest maximum quarterly average concentration having a lower
population-weighted air concentration that is more similar to the
other two areas. This similarity in population weighted
concentrations explains the finding of similar total IQ loss across
the three study areas.
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In order to consider exposure and risk associated with the current
standard, EPA developed estimates for a case study based on air quality
projected to just meet the standard in a location of the country where
air concentrations do not meet the current standard (the primary Pb
smelter case study). In so doing, we consider it extremely unlikely
that air concentrations in urban areas across the U.S. that are
currently well below the current standard would increase to just meet
the standard. However, we recognize the potential for air Pb
concentrations in some areas currently well below the standard to
increase to just meet the standard by way of, for example, expansion of
existing sources (e.g., facilities operating as secondary smelters may
exercise previously used capabilities as primary smelters) or by the
congregation of multiple Pb sources in adjacent locations. We have
simulated this scenario (increased Pb concentrations to just meet the
current standard) in a general urban case study and three location-
specific urban case studies. In this scenario, we note substantial
uncertainty in simulating how the profile of Pb concentrations might
change in the hypothetical case where concentrations increase to just
meet the current standard.
Turning first to the estimates of total blood Pb for the current
NAAQS scenario simulated for the location-specific urban case studies,
we note the extent to which exposures associated with increased air Pb
concentrations that simulate just meeting the current standard are
estimated to increase blood Pb levels in young children. The magnitude
of this for the median total blood Pb ranges from 0.3 [mu]g/dL (an
increase of 20 percent) in the case of the Cleveland study area for
which current conditions are estimated to be approximately one fourth
of the current NAAQS, up to approximately 1 [mu]g/dL (an increase of 50
to 70%) for the Chicago and Los Angeles study areas for which current
conditions are estimated to be at or below one tenth of the current
NAAQS.
Estimates of IQ loss (for child with median total IQ loss estimate)
associated with recent air plus past air Pb at exposures allowed by
just meeting the current NAAQS in the primary Pb smelter case study
differ when considering the full study area (10 km radius) or the 1.5
km radius subarea. Estimates for median IQ loss associated with the
recent air plus past air categories of exposure pathways for the full
study area range from 0.6 point to 2.3 points (for the range of
concentration-response functions), while these estimates for the
subarea range from 3.2 points to 9.4 points IQ loss. The estimates
(recent plus past) for the median based on the LLL concentration-
response function are 1.9 points IQ loss for the full study area and
6.0 points for the subarea. The 95th percentile estimates of total IQ
loss in the subarea range from 5.0 to 12.4 points, with an associated
range for the recent air plus past air of 4.2 to 10.4 points.
For the current NAAQS scenario in the three location-specific case
studies, estimates of IQ loss associated with policy-relevant Pb for
the median total IQ loss range from 0.6 points loss (recent air
estimate using low-end concentration-response function) to 7.4 points
loss (recent plus past air estimate using the high-end concentration-
response function). The corresponding estimates based on the LLL
concentration-response function range from 2.7 points (lowest location-
specific recent air estimate) to 4.7 points IQ loss (highest location-
specific recent plus past air estimate). The comparable estimates of IQ
loss for children at the 95th percentile range from 2.6 to 7.6 points
for the LLL concentration-response function.
Further, in comparing current NAAQS scenario estimates to current
conditions estimates for the three location-specific urban case
studies, the estimated difference in total Pb-related IQ loss for the
median is about 0.5 to 1.4 points using the LLL concentration-response
function and a similar magnitude of difference is estimated for the
95th percentile. The corresponding estimate for the general urban case
study is 1.1 to 1.3 points higher total Pb-related IQ loss for the
current NAAQS scenario compared to the two current conditions
scenarios.
Estimates of median and 95th percentile IQ loss associated with
policy-relevant Pb exposure for air quality scenarios under current
conditions (which meet the current NAAQS) and, particularly those
reflecting conditions simulated to just meet the current standard,\65\
indicate levels of IQ loss that some may reasonably consider to be
significant from a public health perspective. Further, for the three
location-specific urban case studies, the estimated differences in
incidences of children with IQ loss greater than one point and with IQ
loss greater than seven points in comparing current conditions to those
associated with the current NAAQS indicate the potential for
significant numbers of children to be negatively affected if air Pb
concentrations increased to levels just meeting the
[[Page 71525]]
current standard. Estimates of the additional number of children with
IQ loss greater than one point (based on the LLL concentration-response
function) in these three study areas with the current NAAQS scenario
compared to current conditions range from 100 to 6,000 across the three
locations. The corresponding estimates for the additional number of
children with IQ loss greater than seven points, for the current NAAQS
as compared to the current conditions scenario range from 600 to
35,000. These latter values for the change in incidence of children
with greater than seven points Pb-related IQ loss represent 5 to 17
percent of the children (aged less than 7 years of age) in these study
areas. This increase corresponds to approximately a doubling in the
number of children with this magnitude of Pb-related IQ loss in the
study area most affected.
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\65\ As recognized in section III.B.2.d above, to simulate air
concentrations associated with the current NAAQS, a proportional
roll-up of concentrations from those for current conditions was
performed for the location-specific urban case studies. This was not
necessary for the primary Pb smelter case study in which air
concentrations currently exceed the current standard.
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While the risk assessment has quantified risks associated with IQ
impacts in childhood, there are other, unquantified adverse
neurocognitive effects that may occur at similarly low exposures which
might additionally contribute to reduced academic performance, which
may have adverse consequences over a lifetime (CD, pp. 8-29 to 8-30).
Additional impacts at low levels of childhood exposure that were not
quantified in the risk assessment include: other neurological effects
(sensory, motor, cognitive and behavioral), immune system effects
(including some related to allergic responses and asthma), and early
effects related to anemia.
c. CASAC Advice and Recommendations
Beyond the evidence- and risk/exposure-based information discussed
above, in considering the adequacy of the current standard, EPA will
also consider the advice and recommendations of CASAC, based on their
review of the Criteria Document and the drafts of the Staff Paper and
the related technical support document, as well as comments from the
public on drafts of the Staff Paper and related technical support
document.\66\ With regard to the public comments, those that addressed
adequacy of the current standard concluded that the current standard is
inadequate and should be revised, suggesting appreciable reductions in
the level. No comments were received expressing the view that the
current standard is adequate. One comment was received arguing not that
the standard was inadequate but rather that conditions justified that
it should be revoked. In both the 1990 review and this review of the
standard set in 1978, CASAC, has recommended consideration of more
health protective NAAQS. In CASAC's review of the 1990 Staff Paper, as
discussed in Section 5.2.2, they generally recommended consideration of
levels below 1.0 [mu]g/m\3\, specifically recommended analyses of a
standard set at 0.25 [mu]g/m\3\, and also recommended a monthly
averaging time (CASAC, 1990). In two letters to the Administrator
during the current review, CASAC has consistently recommended that the
primary NAAQS should be ``substantially lowered'' from the current
level of 1.5 [mu]g/m\3\ to a level of ``0.2 [mu]g/m\3\ or less''
(Henderson, 2007a, b). CASAC drew support for this recommendation from
the current evidence, described in the Criteria Document, of health
effects occurring at dramatically lower blood Pb levels than those
indicated by the evidence available when the standard was set.
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\66\ All written comments submitted to the Agency will be
available in the docket for this rulemaking, as will be transcripts
of the public meeting held in conjunction with CASAC's review of the
first draft of the Staff Paper and the first draft of the related
technical support document, and of draft and final versions of the
Criteria Document.
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CASAC concluded that the current Pb NAAQS ``are totally inadequate
for assuring the necessary decreases of lead exposures in sensitive
U.S. populations below those current health hazard markers identified
by a wealth of new epidemiological, experimental and mechanistic
studies'', and stated that ``Consequently, it is the CASAC Lead Review
Panel's considered judgment that the NAAQS for Lead must be decreased
to fully-protect both the health of children and adult populations''
(Henderson, 2007a, p. 5).
d. Policy Options
In considering the adequacy of the current standard, EPA first
notes the dramatic changes in the basic patterns of air Pb emissions in
the U.S. since the standard was set, reflecting the phase-out of Pb in
gasoline, as well as changes to the CAA related to the inclusion of Pb
compounds on the list of HAPs and associated requirements for
technology- and risk-based standards for major stationary sources. We
are aware that questions have been raised about the appropriateness of
retaining Pb on the list of criteria pollutants and/or maintaining a
NAAQS for Pb in light of these changed circumstances. We take note of
the views of CASAC, summarized above, and the conclusions and
recommendations in the OAQPS Staff Paper on these questions, which do
not support delisting Pb or revoking the Pb NAAQS. We recognize,
however, that there may be differing views on interpreting or weighing
the available information. Thus, EPA solicits comment related to the
questions of delisting and revocation. The EPA also solicits comment on
whether the broad range of current multimedia Federal and State Pb
control programs, summarized above in section II.C, are sufficient to
provide appropriate public health protection in lieu of a Pb NAAQS.
In further considering the adequacy of the current standard, EPA
will focus on the body of available evidence (summarized above in
section III.A and discussed in the Criteria Document) that is much
expanded from that available when the current standard was set. The
presentation of the evidence in the Criteria Document describes the
occurrence of adverse health effects at appreciably lower blood Pb
levels than those demonstrated by the evidence at the time the standard
was set. We recognize that the current health effects evidence together
with findings from the exposure and risk assessments (summarized above
in section III.B), like the information available at the time the
standard was set, supports the conclusion that air-related Pb exposure
pathways (by inhalation and ingestion) contribute to blood Pb levels in
young children. Furthermore, we take note of the information that
suggests that the air-to-blood relationship (i.e., the air-to-blood
ratio), is likely larger, with regard to increase in blood Pb per unit
air concentration, when air inhalation and ingestion are considered
than that estimated when the standard was set using only inhalation and
may be several times larger. EPA recognizes there is uncertainty in
estimates of this relationship and solicits comment on on ratios
supported by the current evidence.
In areas projected to just meet the current standard, the
quantitative estimates of risk (for IQ decrement) associated with
policy-relevant Pb indicate risk of a magnitude that some may consider
to be significant from a public health perspective.\67\ Further,
although the current monitoring data indicate few areas with airborne
Pb near or just exceeding the current standard, we recognize
significant limitations with the current monitoring network and thus
the potential that the prevalence of such levels of Pb
[[Page 71526]]
concentrations may be underestimated by currently available data.
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\67\ As recognized in section III.B.2.d above, to simulate air
concentrations associated with the current NAAQS, a proportional
roll-up of concentrations from those for current conditions was
performed for the location-specific urban case studies. This was not
necessary for the primary Pb smelter case study in which air
concentrations currently exceed the current standard.
---------------------------------------------------------------------------
As summarized above, CASAC conclusions and recommendations and
recommendations presented in the OAQPS Staff Paper reflect the view
that the current standard is not adequate and support consideration of
a revised standard to provide an adequate margin of safety for
sensitive groups. Taking these views into account, we recognize that
one approach is to consider a revised standard. We also recognize that
there may be differing interpretations of the available information.
Thus, EPA solicits comment on delisting, revocation, and the adequacy
of the current standard and the rationale upon which such views are
based.
4. Elements of the Standard
The four elements of the standard--indicator, averaging time, form
and level serve to define the standard and must be considered
collectively in evaluating the health and welfare protection afforded
by the standard. In considering revisions to the current primary Pb
standard, as discussed in the following sections, EPA will consider
each of the four elements of the standard as to how they might be
revised to provide a primary standard for Pb that is requisite to
protect public health with an adequate margin of safety.
a. Indicator
The indicator for the current standard is Pb-TSP. When the standard
was set, the Agency considered identifying Pb in particles less than or
equal to 10 [mu]m in diameter (Pb-PM10) as the indicator in
response to comments expressing concern that because only a fraction of
airborne particulate matter is respirable, an air standard based on
total air Pb is unnecessarily stringent. The Agency responded that
while it agreed that some Pb particles are too small or too large to be
deposited in the respiratory system, a significant component of
exposures can be ingestion of materials contaminated by deposition of
Pb from the air. In addition to the route of ingestion and absorption
from the gastrointestinal tract, nonrespirable Pb in the environment
may, at some point, become respirable through weathering or mechanical
action. EPA concluded that total airborne Pb, both respirable and
nonrespirable fractions should be addressed by the air standard.
More recently, in the 1990 Staff Paper, this issue was reconsidered
in light of information regarding limitations of the high-volume
sampler used for the Pb-TSP measurements and the continued use of total
suspended particulate matter (TSP) as the indicator was supported by
OAQPS staff (USEPA, 1990).
Given that exposure to lead occurs not only via direct
inhalation, but via ingestion of deposited particles as well,
especially among young children, the hi-vol provides a more complete
measure of the total impact of ambient air lead. * * * Despite its
shortcomings, the staff believes the high-volume sampler will
provide a reasonable indicator for determination of compliance * * *
In the current review, CASAC has recommended that EPA consider a
change in the indicator to utilize low-volume PM10 sampling
(Henderson, 2007a, b). In so doing, CASAC recognized that a scaling of
the NAAQS level would be needed to accommodate the loss of very large
coarse-mode Pb particles and concurrent Pb-PM10 and Pb-TSP
sampling would be needed to inform development of scaling factors. The
September 2007 CASAC letter states that the CASAC Lead Panel ``strongly
encourages the Agency to consider revising the Pb reference method to
allow sample collection by PM10, rather than TSP samplers,
accompanied by analysis with low-cost multi-elemental techniques like
X-Ray Fluorescence (XRF) or Inductively Coupled Plasma-Mass
Spectroscopy (ICP-MS).'' While recognizing the importance of coarse
dust contributions to total Pb exposure via the ingestion route and
acknowledging that TSP sampling is likely to capture additional very
coarse particles which are excluded by PM10 samplers, the
Panel raised some concerns. The concerns were regarding the precision
and variability of TSP samplers, and the inability to efficiently
capture the non-homogeneity of very coarse particles in a national
monitoring network, which the Panel indicated may need to be addressed
in implementing additional monitoring sites and an increased frequency
of sample collection that might be required with the substantial
reduction in the level of the standard and shorter averaging time that
they recommend (Henderson, 2007b).
In considering the appropriate indicator, EPA takes note of and
solicits comment on previous Agency conclusions that the health
evidence indicates that Pb in all particle size fractions, not just
respirable Pb, contributes to Pb in blood and to associated health
effects. Additionally, the current information does not support the
derivation of a single scaling factor, which might be used to relate a
level for Pb-TSP to a monitoring result using Pb-PM10 on a
national scale. The EPA recognizes, however, that an indicator that
exhibits low spatial variability is desirable such that it facilitates
implementation of an effective monitoring network, i.e., one that
assures identification of areas with the potential to exceed the NAAQS.
To the extent that Pb-PM10 exhibits less spatial
variability and that a ``crosswalk'' can be developed between a level
in terms of Pb-TSP, EPA recognizes that it is appropriate to consider
moving to a Pb-PM10 indicator in the future. One of the
issues to consider when moving to a Pb-PM10 indicator is
whether regulating concentrations of Pb-PM10 will lead to
appropriate controls on Pb emissions from sources with a large
percentage of Pb in the greater than 10 micron size range (e.g.,
fugitive dust emissions from Pb smelters). It is reasonable to believe
that Pb-PM10/Pb-TSP ratios are sensitive to distance from
emissions sources (due to faster deposition of larger particles). As
such, the use of a Pb-PM10 indicator may have a significant
influence on the degree of Pb controls needed from emission sources.
The EPA will consider several options that might improve the
available database and facilitate such a move in the future, while
retaining Pb-TSP as the indicator for the NAAQS at this time,
consistent with the recommendations in the Staff Paper. For example, we
might consider describing a FEM in terms of PM10 that might
be acceptably applied on a site-by-site basis where an appropriate
relationship between Pb-TSP and Pb-PM10 can be developed
based on site-specific data. Alternatively, use of such an FEM might be
approved, in combination with more limited Pb-TSP monitoring, in areas
where the Pb-TSP data indicate ambient Pb levels are well below the
NAAQS level.
These examples were intended purely for purposes of illustrating
the types of options the Agency might consider. Specific details of any
options would need to be supported by appropriate data analyses. We
solicit information and comments that would help inform such analyses
and the Agency's views on the indicator for the primary Pb NAAQS.
b. Averaging Time and Form
The basis for the averaging time of the current standard reflects
consideration of the evidence available when the Pb NAAQS were
promulgated in 1978. At that time, the Agency had concluded that the
level of the standards, 1.5 [mu]g/m\3\, would be a ``safe ceiling for
indefinite exposure of young children'' (43 FR 46250), and that the
slightly greater possibility of elevated air Pb levels within the
quarterly averaging
[[Page 71527]]
period as contrasted to the monthly averaging period proposed in 1977
(43 FR 63076), was not significant for health. These conclusions were
based in part on the Agency's interpretation of the health effects
evidence as indicating that 30 [mu]g/dL was the maximum safe level of
blood Pb for an individual child.
As discussed above, the currently available health effects evidence
\68\ indicates a variety of neurological effects, as well as immune
system and hematological effects, associated with levels below 10
[mu]g/dL as a central tendency metric of study cohorts of young
children. Further, EPA recognizes that today ``there is no level of Pb
exposure that can yet be identified, with condfidence, as clearly not
being associated with some risk of deleterious health effects'' (CD, p.
8-63). Accordingly, to the extent that air Pb contributes to variation
in blood Pb, we currently cannot identify a safe ceiling for indefinite
exposure of young children.
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\68\ The differing evidence and associated strength of the
evidence for these different effects is described in detail in the
Criteria Document.
---------------------------------------------------------------------------
Additionally, several aspects of the current health effects
evidence for Pb pertain to the consideration of averaging time:
Children are exposed to ambient Pb via inhalation and
ingestion, with Pb taken into the body absorbed through the lungs and
through the gastrointestinal tract. Studies on Pb uptake, elimination
and distribution show that Pb is absorbed into peripheral tissues in
adults within a few days (USEPA 1986a; USEPA 1990b, p. IV-2).
Absorption of Pb from the gastrointestinal tract appears to be greater
and faster in children as compared to adults (CD, Section 4.2.1). Once
absorbed, it is quickly distributed from plasma to red blood cells and
throughout the body.
Lead accumulates in the body and is only slowly removed,
with bone Pb serving as a blood Pb source for years after exposure and
as a source of fetal Pb exposure during pregnancy (CD, Sections 4.3.1.4
and 4.3.1.5).
Blood Pb levels, including levels of the toxicologically
active fraction, respond quickly to increased Pb exposure, such that an
abrupt increase in Pb uptake rapidly changes blood Pb levels, with the
time to reach a new quasi-steady state with the total body burden after
such an occurrence projected to be approximately 75 to 100 days (CD, p.
4-27).
The elimination half-life, which describes the time for
blood Pb levels to stabilize after a reduction in exposure, for the
dominant phase for blood Pb responses to changes in exposure is on the
order of 20 to 30 days for adults (CD, p. 4-25). Blood elimination
half-lives are influenced by contributions from bone. Given the tighter
coupling in children of bone stores with blood levels, children's blood
Pb is expected to respond more quickly than adults (CD, pp. 4-20 and 4-
27).
Data from NHANES II and an analysis of the temporal
relationship between gasoline consumption data and blood lead data
generally support the inference of a prompt response of children's
blood Pb levels to changes in exposure in that children's blood Pb
levels and the number of children with elevated blood Pb levels appear
to respond to monthly variations in Pb emissions from Pb in gasoline
(EPA, 1986a, p. 11-39; Rabinowitz and Needleman, 1983; Schwartz and
Pitcher, 1989).
The evidence with regard to sensitive neurological effects
is limited in what it indicates regarding the specific duration of
exposure associated with effect, although it indicates both the
sensitivity of the first 3 years of life and a sustained sensitivity
throughout the lifespan as the human central nervous system continues
to mature and be vulnerable to neurotoxicants (CD, Section 8.4.2.7).
The animal evidence supports our understanding of periods of
development with increased vulnerability to specific types of effect
(CD, Section 5.3), and indicates a potential importance of exposures on
the order of months.
Evidence of a differing sensitivity of the immune system
to Pb across and within different periods of life stages indicates a
potential importance of exposures as short as weeks to months duration.
For example, the animal evidence suggests that the gestation period is
the most sensitive life stage followed by early neonatal stage, and
within these life stages, critical windows of vulnerability are likely
to exist (CD, Section 5.9 and p. 5-245).
Further, evidence described in the Criteria Document and the risk
assessment indicate that ingestion of dust can be a predominant
exposure pathway for young children to policy-relevant Pb, and that
there is a strong association between indoor dust Pb levels and
children's blood Pb levels. As stated in the Criteria Document, ``given
the large amount of time people spend indoors, exposure to Pb in dusts
and indoor air can be significant'' (CD, p. 3-27). The Criteria
Document further describes studies that evaluated the influence of dust
Pb exposure on children's blood Pb: ``Using a structural equation
model, Lanphear and Roghmann (1997) also found the exposure pathway
most influential on blood Pb was interior dust Pb loading, directly or
through its influence on hand Pb. Both soil and paint Pb influenced
interior dust Pb; with the influence of paint Pb greater than that of
soil Pb. Interior dust Pb loading also showed the strongest influence
on blood Pb in a pooled multivariate regression analysis (Lanphear et
al., 1998).'' (CD, p. 4-134).
While some of these aspects of the health effects evidence would be
consistent with a quarterly averaging time, taken as a whole, and in
combination with information on potential response time for indoor dust
Pb levels, EPA recognizes that there is also support for consideration
of an averaging time shorter than a calendar quarter.
When the standard was set in 1978, an analysis of ambient
measurements available at the time indicated that the distribution of
air Pb levels was such that there was little possibility that there
could be sustained periods greatly above the average value in
situations where the quarterly standard was achieved. This may have
been related to the pattern of Pb emissions at the time the standard
was set, which differed from the pattern today in that, due to
emissions from cars and trucks at that time, emissions were more
spatially distributed. In this review, based on data from 2003-2005,
the air quality analysis in Chapter 2 of the Staff Paper indicates the
presence of areas in the U.S. currently where temporal variability does
create differences between average quarterly levels and levels
sustained for shorter than quarterly periods. For example, four percent
of the monitoring sites in the three-year analysis dataset that meet
the current standard as an average over a calendar quarter exceed the
level of the current standard when considering an average for any
individual month. The same analysis indicates that this number is as
high as ten percent for some alternate lower levels.
In further considering the appropriate form of the standard that
might accompany a shorter averaging time, EPA will take into account
analyses using air quality data for 2003-2005 that characterize maximum
quarterly average and various monthly statistics for each year across
the three year Pb-TSP dataset and also across the three year period.
The latter time period is consistent with the three calendar year
attainment period that has been adopted for the ozone and particulate
matter
[[Page 71528]]
NAAQS subsequent to the promulgation of the Pb NAAQS. For the three
year period, the monthly statistics derived are maximum monthly mean,
second maximum monthly mean, average of three overall highest monthly
means, and average of three annual maximum monthly means; these
statistical forms were also considered in the 1990 Staff paper.
Additionally, the maximum and 2nd maximum monthly means for each year
of the three year data set was derived, as well as the averages of
these individual year statistics.
With regard to comparison of monthly forms with the maximum
quarterly mean, the average Pb-TSP maximum monthly mean among all 189
sites in the analysis is notably higher (nearly a factor of two) than
the average of the average maximum quarterly mean among these sites.
Further, this difference is slightly greater for source-oriented sites
than non source-oriented sites or urban sites (e.g., a factor of
approximately 1.8 as compared to one of approximately 1.6), indicating
perhaps an influence of variability in emissions. The alternate forms
of a monthly averaging time that were analyzed yield an across-site
average that is similar although slightly higher than the quarterly
average (e.g., Figure 2-8 in Chapter 2 of the Staff Paper).
The analyses described in Chapter 2 of the Staff Paper consider
both a period of three calendar years and one of an individual calendar
year (with the form of the current standard being the maximum quarterly
mean in any one year). These analyses indicate that with regard to
either single-year or 3-year statistics for the 2003-2005 dataset, a
2nd maximum monthly mean yields very similar, although just slightly
greater, numbers of sites exceeding various alternate levels as a
maximum quarterly mean, with both yielding fewer exceedances than a
maximum monthly mean.
In their advice to the Agency, CASAC has recommended that
consideration be given to changing from a calendar quarter to a monthly
averaging time (Henderson, 2007a, b). In making that recommendation,
CASAC emphasizes support from studies that suggest that blood Pb
concentrations respond at shorter time scales than would be captured
completely by quarterly values, as indicated by their description of
their recommendation for adoption of a monthly averaging time as ``more
protective of human health in light of the response of blood lead
concentrations that occur at sub-quarterly time scales'' (Henderson,
2007b).
With regard to form of the standard, CASAC stated that one could
``consider having the lead standards based on the second highest
monthly average, a form that appears to correlated well with using the
maximum quarterly value'', while also indicating that ``the most
protective form would be the highest monthly average in a year.''
The following observations support consideration of a monthly
averaging time: (1) The health evidence indicates that very short
exposures can lead to increases in blood Pb Pb levels, (2) the time
period of response of indoor dust Pb to airborne Pb can be on the order
of weeks and, (3) the health evidence indicates that adverse effects
may occur with exposures during relatively short windows of
susceptibility, such as prenatally and in developing infants. EPA also
recognizes the limited available evidence specific to the consideration
of the particular duration of sustained airborne Pb levels having the
potential to contribute to the adverse health effects identified as
most relevant to this review.
Based on the information and air quality analyses discussed above,
EPA is requesting comment on a range of options, including the
recommendations in the Staff Paper that include changing the averaging
time to monthly, with a form of maximum or second maximum, as well as
retaining the quarterly averaging time. The EPA is also requesting
comment on, the options of changing the form to apply to a three-year
period as well as retaining a single-year period. We solicit comments
on these ranges of averaging times and forms as well as views and
related rationales that might support alternative options.
c. Level
At this time, the Agency is interested in soliciting comment on a
wide range of possible options for consideration when making a proposed
decision on the level of the primary Pb NAAQS. These policy options
range from lowering the standard, to the levels recommended by CASAC
and the OAQPS Staff paper or lower, as well as on other alternative
levels, up to and including the current level, and the rationale upon
which such views are based.
i. Evidence-Based Considerations
The EPA recognizes that there are several aspects to the body of
epidemiological evidence available in this review that complicate
efforts to translate the evidence into the basis for selecting an
appropriate level for an ambient air quality standard. As an initial
matter, as summarized above and discussed in greater depth in the
Criteria Document (CD, Sections 4.3 and 6.1.3), the epidemiological
evidence that associates Pb exposures with health effects uses blood Pb
as the dose metric, not ambient air concentrations. Further, for the
health effects receiving greatest emphasis in this review (neurological
effects on the developing nervous system), no threshold levels can be
discerned from the evidence. As was recognized at the time of the last
review, estimating a threshold for toxic effects of Pb on the central
nervous system entails a number of difficulties (CD, pp. 6-10 to 6-11).
The task is made still more complex by support in the evidence for a
nonlinear rather than linear relationship of blood Pb with
neurocognitive decrement, with greater risk of decrement-associated
changes in blood Pb at the lower levels of blood Pb in the exposed
population (Section 3.3.7; CD, Section 6.2.13).
In considering how this evidence can help inform the selection of
the level of the standard, EPA will consider how the framework applied
in the establishment of the standard may be applied to the much
expanded body of evidence that is now available. This consideration
builds upon the evidence-based considerations of the adequacy of the
current standard, discussed above in Section III.C.3.a.
As noted above, this review focuses on young children as the key
sensitive population for Pb exposures, the same population identified
in 1978. In this sensitive population, the current evidence
demonstrates the occurrence of adverse health effects, including those
on the developing nervous system, associated with blood Pb levels
extending well below 10 [mu]g/dL to 5 [mu]g/dL and possibly lower. Some
studies indicate Pb effects on intellectual attainment of young
children at blood Pb levels ranging from 2 to 8 [mu]g/dL (CD, Sections
6.2, 8.4.2 and 8.4.2.6), including findings of similar Pb-related
effects in a study of a nationally representative sample of children in
which the mean blood Pb level was 1.9 [mu]g/dL (CD, pp. 6-31 to 6-32;
Lanphear et al., 2000).\69\ Further, the current evidence does not
indicate a threshold for the more sensitive health endpoints such as
adverse effects on the
[[Page 71529]]
developing nervous system (CD, pp. 5-71 to 5-74 and Section 6.2.13).
This differs from the Agency's inference in the 1978 rulemaking of a
threshold of 40 [mu]g/dL blood Pb for effects of Pb considered clearly
adverse to health at that time, i.e., impairment of heme synthesis and
other effects which result in anemia. Thus, the level of Pb in
children's blood associated with adverse health effect has dropped
substantially.
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\69\ These findings include significant associations in the
study sample subsets of children with blood Pb levels less than 10
[mu]g/dL, less than 7.5 [mu]g/dL and less than 5 [mu]g/dL. A
positive, but not statistically significant association, was
observed in the less than 2.5 [mu]g/dL subset, although the effect
estimate for this subset was largest among all the subsets. The lack
of statistical significance for this subset may be due to the
smaller sample size of this subset which would lead to lower
statistical power.
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As when the standard was set in 1978, EPA recognizes that there
remain today contributions to blood Pb levels from nonair sources. As
discussed above, these contributions have been reduced since 1978, with
estimates of reduction in the dietary component of 70 to 95 percent
(CD, Section 3.4). The evidence is limited with regard to the aggregate
reduction since 1978 of all nonair sources to blood Pb. However, the
available evidence and some preliminary analysis led CASAC to recommend
consideration of 1.0 to 1.4 [mu]g/dL or lower as an estimate of the
nonair component of blood Pb (Henderson, 2007a). The value of 1.4
[mu]g/dL was the mean blood Pb level derived from a simulation of
current nonair exposures using the IEUBK model (Henderson, 2007a, pp.
F-60 to F-61). These current estimates are roughly an order of
magnitude lower than the value of 12 [mu]g/dL that was used in setting
the 1978 standard.
Regarding the relationship between air and blood, while the
evidence demonstrates that airborne Pb influences blood Pb
concentrations through a combination of inhalation and ingestion
exposure pathways, estimates of the precise quantitative relationship
(i.e., air-to-blood ratio) available in the evidence vary (USEPA,
1986a; Brunekreef, 1984) and there is uncertainty as to the values that
pertain to current exposures. Studies summarized in the 1986 Criteria
Document typically yield estimates in the range of 1:3 to 1:5, with
some as high as 1:10 or higher (USEPA, 1986a; Brunekreef, 1984).
Findings in a more recent study identified in the Criteria Document of
blood Pb response to reduced air concentrations indicate a ratio on the
order of 1:7 (CD, pp. 3-23 to 3-24; Hilts et al., 2003). A value of 1:5
has been used by the World Health Organization (2000). These ratios are
appreciably higher than the ratio of 1:2 that was used in setting the
1978 standard.
A standard setting approach being considered is to apply the
framework relied upon in setting the standard in 1978 to the currently
available information. In applying that framework, however, EPA
recognizes that today ``there is no level of Pb exposure that can yet
be identified, with confidence, as clearly not being associated with
some risk of deleterious health effects'' (CD, p. 8-63). However, there
is increasing uncertainty with regard to the magnitude and type of
effects at levels below 5 [mu]g/dL \70\. This is in contrast to the
situation in 1978 when the Agency judged that the maximum safe blood Pb
level (geometric mean) for a population of young children was 15 [mu]g/
dL based on its conclusion that the maximum safe blood Pb level of an
individual child was 30 [mu]g/dL. \71\
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\70\ As stated in the Criteria Document ``Some recent studies of
Pb neurotoxicity in infants have observed effects at population
average blood-Pb levels of only 1 or 2 [mu]g/dL; and some
cardiovascular, renal, and immune outcomes have been reported at
blood-Pb levels below 5 [mu]g/dL.'' (CD, p. E-16).
\71\ More specifically, the 1978 target of 15 [mu]g/dL was
described as the geometric mean level associated with a 99.5
percentile of 30 [mu]g/dL which the Agency described as a ``safe
level'' for an individual child (43 FR 46247-49).
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In illustrating the application of the 1978 framework, two blood Pb
levels are used here for illustrative purposes. A level of 2 [mu]g/dL
was used because it represents some of the lowest population levels
associated with adverse effect in the current evidence (e.g., CD, p. E-
9; Lanphear et al., 2000). In addition, a level of 5 [mu]g/dL has been
used. This level has been associated with adverse health effects with a
higher degree of certainty in the published literature, and is a level
where cognitive deficits were identified with statistical significance
(Lanphear et al., 2000).
Using a blood Pb target of 2 [mu]g/dL as a substitute for the 1978
target of 15 [mu]g/dL for the child population geometric mean, then
subtracting 1 to 1.4 [mu]g/dL for background, yields 0.6 to 1 [mu]g/dL
as a target for the air contribution to blood Pb. Dividing the air
target by 5, consistent with currently available information on the
ratio of air Pb to blood Pb, yields a potential standard level of 0.1
to 0.2 [mu]g/m\3\. Alternatively, using the same approach substituting
5 [mu]g/dL for the child population geometric mean and subtracting 1 to
1.4 [mu]g/dL for background, yields 3.6 to 4 [mu]g/dL as a target for
the air contribution to blood Pb. Dividing the air target by 5,
consistent with currently available information on the ratio of air Pb
to blood Pb, yields a level of 0.7 to 0.8 [mu]g/m\3\. Similarly,
substitution of other blood Pb targets would result in still other
levels.
In light of the current CDC blood Pb ``level of concern'' of 10
[mu]g/dL, some might consider a blood Pb value of 10 [mu]g/dL as a
target blood Pb value for this calculation to derive a level for the
primary standard. EPA notes, however, that the CDC does not consider
this level of concern as a safe blood Pb level or one without evidence
of adverse effects (CDC, 2005a). Rather, it is used by CDC to identify
children with elevated blood Pb levels for follow-up activities \72\ at
the individual level and to trigger communitywide prevention activities
(CDC, 2005a). The level of concern has been frequently misinterpreted
as a definitive toxicologic threshold (CDC, 2005a). As summarized in
Section III.A and above, and as described in detail in the Criteria
Document, various adverse effects have been associated with children's
blood Pb levels below 10 [mu]g/dL. For example, the Criteria Document
states that the currently available toxicologic and epidemiologic
information ``includes assessment of new evidence substantiating risks
of deleterious effects on certain health endpoints beng induced by
distinctly lower than previously demonstrated Pb exposures indexed by
blood-Pb levels extending well below 10 [mu]g/dL in children and/or
adults'' (CD, p. 8-25). Accordingly, EPA has not used a mean or an
individual target blood Pb value of 10 [mu]g/dL as the basis for an
illustrative example of deriving a standard that is intended to protect
public health with an adequate margin of safety. In recognition of
differing views on this subject, however, we solicit comment on the
appropriateness of using a mean or individual target blood Pb value of
10 [mu]g/dL as the foundation for deriving a level for the primary Pb
standard.
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\72\ Activities such as taking an environmental history,
educating parents about Pb and conducting follow-up blood Pb
monitoring were among those suggested for children with blood Pb
levels greater than or equal to 10 [mu]g/dL (CDC, 2005a). Recently,
CDC's Advisory Committee on Childhood Lead Poisoning Prevention has
also provided information and recommendations relevant to clinical
management of children with blood Pb levels below 10 [mu]g/dL
(ACCLPP, 2007).
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The above examples focus on the mean target blood Pb level for the
sensitive population by way of illustrating application of the 1978
framework. The EPA solicits comment on mean target blood Pb levels as
well as other factors that would be important in applying the 1978
framework. For example, the distribution of blood Pb levels within the
sensitive population is an important aspect of the 1978 framework. When
the standard was set in 1978, the Agency stated that the population
mean, measured as the geometric mean, must be 15 [mu]g/dL in order to
ensure that 99.5 percent of children in the United States would
[[Page 71530]]
have a blood Pb level below 30 [mu]g/dL, which was identified as the
maximum safe blood Pb level for individual children based on the
information available at that time (43 FR 46252). Target values for the
mean of the population necessarily imply higher values for individuals
associated with the upper percentiles of the blood Pb distribution. For
example, the 2001-2002 NHANES information indicates that a geometric
mean blood level of 1.7 [mu]g/dL for children nationally, aged 1-5
years, is associated with a 95th percentile blood Pb level of 5.8
[mu]g/dL (CDC, 2005b).
Additionally, the nonair (background) contribution to total blood
Pb is an important input to the framework and we solicit comment on the
definition and appropriate values for this parameter.\73\ In the
assessment presented in this notice, contributions attributed to
``recent air'' and to ``recent plus past air'' may include some Pb from
the historic use of Pb in paint and gasoline and other sources.
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\73\ As noted above, in 2001 when establishing standards for
lead-based paint hazards in most pre-1978 housing and child-occupied
facilities (66 FR 1206), the Agency grappled with the uncertainties
in what environmental levels of historic Pb in soil and dust (from
the historical use of Pb in paint and gasoline) in which specific
medium may cause blood Pb levels that are associated with adverse
effects (see Section II.C).
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Further, there are a range of estimates for the air-to-blood ratio
that include estimates higher than that used in 1978 when the standard
was set. We solicit comment and supporting information regarding the
air-to-blood ratio and differences in the available estimates. All of
these factors are important in applying a framework such as that used
in 1978, and we solicit comment, along with supporting information, on
all of these factors.
Beyond the 1978 framework illustrated above, EPA recognizes a
variety of approaches can be used in translating the current evidence
to a level for the standard. With this notice, EPA solicits comment on
the 1978 standard setting framework and on alternate approaches and the
factors that are relevant to those approaches.
ii. Exposure- and Risk-Based Considerations
To inform judgments about a range of levels for the standard that
could provide an appropriate degree of public health protection, in
addition to considering the health effects evidence, EPA will also
consider the quantitative estimates of exposure and health risks
attributable to policy-relevant Pb upon meeting specific alternative
levels of alternative Pb standards and the uncertainties in the
estimated exposures and risks, as discussed above in Section III.B. As
discussed above, the risk assessment conducted by EPA is based on
exposures that have been estimated for children of less than 7 years of
age in six case studies. The assessment estimated the risk of adverse
neurocognitive effects in terms of IQ decrements associated with total
and policy-relevant Pb exposures, including incidence of different
levels of IQ loss in three of the six case studies. In so doing, EPA is
mindful of the important uncertainties and limitations that are
associated with the exposure and risk assessments. For example, with
regard to the risk assessment important uncertainties include those
related to estimation of blood Pb concentration-response functions,
particularly for blood Pb concentrations at and below the lower end of
those represented in the epidemiological studies characterized in the
Criteria Document.
EPA also recognizes important limitations in the design of, and
data and methods employed in, the exposure and risk analyses. For
example, the available monitoring data for Pb, relied upon for
estimating current conditions for the urban case studies is quite
limited, in that monitors are not located near some of the larger known
Pb sources, which provides the potential for underestimation of current
conditions, and there is uncertainty about the proximity of existing
monitors to other Pb sources potentially influencing exposures, such as
old urban roadways and areas where housing with Pb paint has been
demolished. All of these limitations raise uncertainty as to whether
these data adequately capture the magnitude of ambient Pb
concentrations to which the target population is currently exposed.
Additionally, EPA recognizes that there is not sufficient information
available to evaluate all relevant sensitive groups (e.g., adults with
chronic kidney disease) or all Pb-related adverse health effects (e.g.,
neurological effects other than IQ decrement, immune system effects,
adult cardiovascular or renal effects), and the scope of our analyses
was generally limited to estimating exposures and risks in six case
studies intended to illustrate a variety of Pb exposure situations
across the U.S., with three of them focused on specific areas in three
cities. As noted above, however, coordinated intensive efforts over the
last 20 years have yielded a substantial decline in blood Pb levels in
the United States. Recent NHANES data (2003-2004) yield blood lead
level estimates for children age 1 to 5 years of 1.6 [mu]g/dL (median)
and 3.9 [mu]g/dL (90th percentile). These median and 90th percentile
national-level data are lower than modeled values generated for the
three location-specific urban case studies current conditions scenarios
(see footnote 39). It is noted, however, that the urban case studies
and the NHANES study are likely to differ with regard to factors
related to Pb exposure, including ambient air levels.
EPA also recognizes limitations in our ability to characterize the
contribution of policy-relevant Pb to total Pb exposure and Pb-related
health risk. For example, given various limitations of our modeling
tools, blood Pb levels associated with air-related exposure pathways
and current levels of Pb emitted to the air (including via
resuspension) may fall between the estimates for ``recent air'' and
those for ``recent'' plus ``past air''. However, there are limitations
associated with the indoor dust Pb models that affect our ability to
discern differences in the recent air category among different
alternate air quality scenarios and both categories may include Pb in
soil and dust from the historical use of Pb in paint.
With these limitations in mind, EPA will consider the estimates of
IQ loss associated with policy-relevant Pb at air Pb concentrations
near those currently occurring in urban areas as illustrated by
conditions in the three cities chosen for the location-specific urban
case studies, e.g., 0.09 to 0.36 [mu]g/m\3\ as a maximum quarterly
average or 0.17 to 0.56 [mu]g/m\3\ as a maximum monthly average.
Recognizing, as described above, that estimates of IQ loss associated
with air-related exposure pathways and current levels of Pb emitted to
the air (including via resuspension) may fall between the estimates for
``recent air'' and those for ``recent'' plus ``past air'', EPA will
consider ranges reflecting those two categories. Further, as noted
above, we will focus on risk estimates derived using the LLL (log-
linear with low exposure linearization) concentration-response
function.
The ambient air Pb related IQ loss (based on LLL function)
associated with the median IQ loss for current conditions in the three
location-specific case studies (see Tables 5-9 and 5-10 of the Risk
Assessment Report)--estimated to fall between the estimates for recent
air (0.6-0.7 points) and those for recent plus past air (2.9 points)--
appears to be of a magnitude in the range that CASAC considered to be
highly significant from a public health perspective (e.g., a
[[Page 71531]]
population IQ loss of 1-2 points). Comparable estimates for the current
conditions scenarios in the general urban case study are still more
significant with estimates for the general urban case study ranging
from 1.3-1.8 for recent air and 3.2-3.6 for recent plus past air. For
the primary Pb smelter case study, in which air quality exceeds the
current NAAQS, IQ loss reductions in the recent plus past air category
associated with the alternate NAAQS levels of 0.2 and 0.5 [mu]g/m\3\
ranging from 4.0 to 4.9 points IQ loss for the subarea.
Focusing only on the recent air estimates, estimates of IQ loss
(based on the LLL function) associated with policy-relevant Pb at the
95th percentile of population total IQ loss are greater than 1 point
for all current conditions scenarios in all three urban case studies
for which the lowest air Pb concentrations are 0.09 [mu]g/m\3\ maximum
quarterly average, and 0.17 [mu]g/m\3\ maximum monthly average.
EPA will also consider the extent to which alternative standard
levels below current conditions are estimated to reduce blood Pb levels
and associated health risk in young children (Tables 4-1 through 4-4 in
the Staff Paper), looking first to the estimates of total blood Pb. In
the general urban case study, blood Pb levels for the median of the
population associated with the lowest alternative NAAQS (0.02 [mu]g/
m\3\) are estimated to be reduced from levels in the two current
conditions scenarios by 14% (0.3 [mu]g/dL) and 24% (0.5 [mu]g/dL),
respectively. For the 95th percentile of the population, the estimated
reductions are similar in terms of percentage, but are higher in
absolute values (1.7 and 1.0 [mu]g/dL). For the three location-specific
urban case studies, median blood Pb estimates associated with the
lowest alternative standard are reduced from those associated with
current conditions by approximately 10% in the Chicago and Cleveland
study areas and 6% in the Los Angeles study area; similar percent
reductions are estimated at the 95th percentile total blood Pb. For the
localized subarea of the primary Pb smelter case study, a 65% reduction
in both median and 95th percentile blood Pb (3 and 8.1 [mu]g/dL,
respectively) is estimated for the lowest alternative NAAQS as compared
to the current NAAQS.\74\
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\74\ This can be compared to reductions in blood Pb, for the
primary Pb smelter case study subarea estimated to be associated
with a change in the level from the current standard to the 0.2
[mu]g/m\3\ level (either averaging time) which are approximately 45-
50% for both the median and 95th percentile values.
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EPA will also consider the extent to which specific levels of
alternative Pb standards reduce the estimated risks in terms of IQ loss
attributable to policy-relevant exposures to Pb (Tables 4-3 and 4-4 in
the Staff Paper). For the general urban case study, estimated
reductions in median Pb-related IQ loss associated with reduced
exposures at the lowest alternative NAAQS level (0.02 [mu]g/m\3\) were
0.5 and 0.7 points (LLL function) for the two current conditions
scenarios. Reductions at the 95th percentile were of a similar
magnitude. Among the three location-specific case study areas,
estimated reductions in median Pb-related IQ loss associated with
reduced exposures at the lowest alternate NAAQS as compared to current
conditions range from 0.4 to 0.6 points for the high-end concentration-
response function to 0.1 to 0.2 points for the low-end concentration-
response functions, with estimates for the LLL function ranging from
0.2 to 0.3 points. The reduction at the 95th percentile, based on the
LLL function, is 0.3-0.4 points. Reduced exposures associated with the
lowest alternative NAAQS in the primary Pb smelter case study subarea
as compared with the current NAAQS (which is not currently met by this
area) were more substantial, ranging from 2.8 points at the median and
3 points at the 95th percentile (based on LLL function).
Based on estimated reductions in Pb-associated IQ loss discussed
above, EPA observes that estimates for the 95th percentile of the
population are quite similar to (for the LLL concentration-response
function) or smaller (for the high- and low-end concentration-response
functions) than those at the median for all case studies. This is
because of the nonlinear relationship between IQ decrement and blood Pb
level such that relatively smaller IQ decrement is associated with
changes in blood Pb at higher blood Pb levels.
Reductions in air Pb concentrations from current conditions to meet
the lower alternative NAAQS (0.02 and 0.05 [mu]g/m\3\, maximum monthly
mean) are estimated to reduce the number of children having Pb-related
IQ loss greater than one point by one half to one percent in each of
the three location-specific urban case studies. More specifically,
within the three study areas this corresponds to a range of
approximately 100 to 3,000 fewer children having total IQ loss greater
than 1.0 for an alternative standard of 0.02 [mu]g/m\3\, maximum
monthly mean. Further, just meeting the lowest alternative standard in
these three study areas is estimated to reduce the number of children
having an IQ loss greater than seven points by one to two percent. This
corresponds to a range of approximately 350 (for the Cleveland study
area) up to 8,000 (for the Chicago study area) fewer children with
total Pb-related IQ loss greater than 7.0.
As discussed above, CASAC considered a population IQ loss of 1-2
points to be highly significant from a public health perspective.
Estimates of IQ loss associated with policy-relevant Pb are of a
magnitude that appears to fall near or within this range for air
quality scenarios involving levels at or above 0.09 [mu]g/m\3\, maximum
quarterly mean, or 0.17 [mu]g/m\3\, maximum monthly mean. Estimated
reductions in risk associated with reducing air Pb concentrations from
current conditions (in the urban case studies) to the two lower
alternative levels evaluated (0.02 and 0.05 [mu]g/m\3\) appear to range
from a few tenths to just below one IQ point (for the LLL
concentration-response function) (and up to 1.5 IQ points for the
highest concentration-response function). Based on estimated changes in
risk across the population associated with the two lower alternative
levels (as compared to current conditions), reductions in the number of
children with total Pb-related IQ loss greater than 1 or greater than 7
are estimated to be on the order of hundreds to thousands of children
in the three location-specific urban case studies.
In considering the exposure and risk information with regard to a
level for the standard, EPA notes that at the time the standard was
set, the Agency recognized a particular blood Pb level as ``safe''.
Today, current evidence does not support the recognition of a ``safe''
level. This is generally reflected in the concentration-response
functions used in the risk assessment and in CASAC recommendations on
these functions with regard to a lack of a threshold. EPA will
therefore consider a different approach in this review.
In considering these risk estimates, EPA is mindful of CASAC's
recommendation regarding the public health significance of a population
loss of 1 to 2 IQ points, the significant implications of potential
shifts in the distribution of IQ for the exposed population, and other
unquantified Pb-related health effects. Based on these factors and the
range of estimates summarized above for IQ loss associated with policy-
relevant Pb for the current conditions scenarios of the location-
specific case studies, we recognize that some may consider reducing the
NAAQS as important from a public health perspective (from air-related
ambient Pb) relative to that afforded by the current standard.
[[Page 71532]]
In considering the public health significance of IQ loss beyond
CASAC's recommendation on this issue, we note that some may consider
that any IQ loss at the population level is of potential public health
significance. That is, there is no amount of IQ loss at the population
level that is clearly recognized as being of no importance from a
public health perspective. On the other hand, we also recognize that
some may hold different views. Thus, the magnitude of IQ loss that
could be allowed by a standard that protects public health with an
adequate margin of safety is clearly a public health policy judgment to
be made by the Administrator.
In considering the magnitudes of IQ loss estimated in our
assessment for the lowest alternative levels considered, EPA will focus
on total IQ loss and on the contribution to total IQ loss from policy-
relevant pathways. In so doing, we recognize that nonair contributions
to total Pb-related IQ loss are estimated to reach and exceed an IQ
loss of 1-2 points, and we also recognize that air Pb contributions are
generally of a much smaller magnitude. Thus, we recognize that it may
be appropriate to consider smaller estimates of IQ loss from air Pb
contributions (e.g., less than 1 point IQ loss) in identifying the
appropriate target for the policy-relevant component.
Placing weight on incremental changes in policy-relevant Pb-related
IQ loss of less than one point IQ would lead to consideration of the
lower standard levels evaluated in the risk assessment as part of a
judgment as to what standard would protect public health with an
adequate margin of safety. EPA recognizes, however, the significant
uncertainties in the quantitative risk estimates and that uncertainty
in the estimates increases with increasing difference of the air
quality scenarios from current conditions. Thus, to the extent that
incremental exposure reductions achieved through lowering the NAAQS
might contribute to incremental reductions in children's blood Pb and
to associated reductions in health effects, consideration of NAAQS
levels below 0.1 [mu]g/m\3\ (e.g., the lower levels included in the
risk assessment of 0.02 and 0.05 [mu]g/m\3\) may be appropriate. On the
other hand, to the extent that the uncertainties and limitations in the
exposure and risk assessments are judged to be so great as to prevent
meaningful conclusions from being drawn for these low alternative
standard levels, consideration of such low levels may not be
appropriate.
If the policy goal for the Pb NAAQS was to be defined, for example,
so as to provide protection that limited estimates of IQ loss from
policy-relevant exposures to no more than 1-2 points IQ loss at the
population-level, EPA notes that standard levels in the range of 0.1 to
0.2 [mu]g/m\3\ may achieve that goal. We also note that even with lower
levels of the standard evaluated, while the range of policy-relevant IQ
loss estimates is lower, the upper end of the range still extends up to
and in some cases above 1 point IQ loss. We note, however, appreciably
greater uncertainty associated with these estimates that increases with
increasing difference of the alternative standards from current
conditions.
Alternatively, if the policy goal was to be defined so as to
provide somewhat greater public health protection by limiting the air-
related component of risk to somewhat less than 1 point IQ loss at the
population level, this would suggest greater consideration for
standards in the lower part of the range evaluated (0.02-0.05 [mu]g/
m\3\). Such a goal might reflect recognition that nonair sources, in
and of themselves, are estimated to contribute 1-2 points or more of IQ
loss, such that the incremental risk for policy-relevant Pb is adding
to a level of total Pb exposure that is already in a range that can be
reasonably judged to be highly significant from a public health
perspective. We note, however that considering standards in this lower
range places greater weight on the more highly uncertain risk estimates
and thus would be more precautionary in nature.
iii. CASAC Advice and Recommendations
Beyond the evidence- and risk/exposure-based information discussed
above, EPA's consideration of the level for the NAAQS will also take
into account the advice and recommendations of CASAC, based on their
review of the Criteria Document and drafts of the Staff Paper and the
related technical support document, as well as comments from the public
on drafts of the Staff Paper and related technical support document.
Public comments pertaining to the level of the standard recommended
appreciable reductions in the level, e.g., setting it at 0.2 [mu]g/m\3\
or less.
In their advice to the Agency during this review CASAC has
recognized the importance of both the health effects evidence and the
exposure and risk information in selecting the level for the standard
(Henderson, 2007a,b). In two separate letters, CASAC has stated that it
is the unanimous judgement of the CASAC Lead Panel that the primary
NAAQS should be ``substantially lowered'' to ``a level of about 0.2
[mu]g/m\3\ or less'', reflecting their view of the health effects
evidence (Henderson, 2007a,b). In their March 2007 letter conveying
comments on the pilot phase risk assessment, CASAC based their
recommendation as to level on consideration of the health effects
evidence they provided initial recommendations that the level should be
substantially lower, reflecting their view of the evidence itself.
The CASAC Pb Panel also provided advice regarding how the Agency
should consider IQ loss estimates derived from the risk assessment in
selecting a level for the standard. The Panel stated that they consider
a population loss of 1-2 IQ points to be ``highly significant from a
public health perspective.'' Further they recommended that ``the
primary Pb standard should be set so as to protect 99.5% of the
population from exceeding that IQ loss.'' The Agency anticipates
further advice from CASAC with regard to level at the time of their
review of this ANPR.
iv. Policy Options
In considering alternative levels of the primary Pb standard, EPA
will consider the health effects evidence and the exposure and risk
assessment, as well as the important uncertainties and limitations in
the evidence and the assessment results. To help inform public health
policy judgments, we specifically solicit comment on levels of IQ loss
considered to be significant from a public health perspective.
Additionally, we solicit comment on the magnitude of IQ loss associated
with exposures to ambient Pb by the pathways categorized as ``recent
air'' in the risk assessment described in this notice that are
considered to be significant from a public health perspective. We also
solicit comment on the approach of adopting a public health policy goal
of limiting policy-relevant air exposure such that the incremental
blood Pb level (and the associated resulting IQ loss) are below a
specified level (e.g., to a magnitude of 0.5 or 1 [mu]g/dL, or other
alternative values).
The EPA takes note of the views of CASAC on these matters,
summarized above, the conclusions and recommendations in the OAQPS
Staff Paper,\75\ and the views of public commenters. We also note other
views,
[[Page 71533]]
including retaining the current standard level or a range of
alternative levels that includes the upper end of the alternative
standards considered in the risk assessment (i.e., 0.5 [mu]g/m\3\ as a
maximum monthly average). The EPA recognizes that there may be
differing interpretations of the available evidence, the public health
significance of various changes in population IQ loss, and various
aspects of the evidence and exposure and risk assessments, including
important uncertainties and limitations associated with the evidence
and assessments. Thus, EPA solicits comment on the range of alternative
standard levels identified above, as well as on other alternative
levels, up to and including the current level, and the rationale upon
which such views are based.
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\75\ The OAQPS Staff Paper recommends consideration of a range
of alternative standard levels from as high as 0.1 to 0.2 [mu]g/m\3\
down to the lower levels evaluated in the risk assessment of 0.02 to
0.05 [mu]g/m\3\.
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IV. The Secondary Standard
This section presents information relevant to the review of the
secondary Pb NAAQS, including information on the welfare effects
associated with Pb exposures, results of the screening-level ecological
risk assessment, and considerations related to evaluating the adequacy
of the current standard and alternative standards that might be
appropriate for the Administrator to consider.
A. Welfare Effects Information
Welfare effects addressed by the secondary NAAQS include, but are
not limited to, effects on soils, water, crops, vegetation, manmade
materials, animals, wildlife, weather, visibility and climate, damage
to and deterioration of property, and hazards to transportation, as
well as effects on economic values and on personal comfort and well-
being. A qualitative assessment of welfare effects evidence related to
ambient Pb is summarized in this section, drawing from Chapter 6 of the
Staff Paper. The presentation here first recognizes several key aspects
of the welfare evidence for Pb. Lead is persistent in the environment
and accumulates in soils, aquatic systems (including sediments), and
some biological tissues of plants, animals and other organisms, thereby
providing long-term, multipathway exposures to organisms and
ecosystems. Additionally, EPA recognizes that there have been a number
of uses of Pb, especially as an ingredient in automobile fuel but also
in other products such as paint, lead-acid batteries, and some
pesticides, which have significantly contributed to widespread
increases in Pb concentrations in the environment, a portion of which
remains today (e.g., CD, Chapters 2 and 3).
Ecosystems near smelters, mines and other industrial sources of Pb
have demonstrated a wide variety of adverse effects including decreases
in species diversity, loss of vegetation, changes to community
composition, decreased growth of vegetation, and increased number of
invasive species. Apportioning these effects between Pb and other
stressors is complicated because these point sources also emit a wide
variety of other heavy metals and sulfur dioxide which may cause toxic
effects. There are no field studies which have investigated effects of
Pb additions alone but some studies near large point sources of Pb have
found significantly reduced species composition and altered community
structures. While these effects are significant, they are spatially
limited: The majority of contamination occurs within 20 to 50 km of the
emission source (CD, AX7.1.4.2).
By far, the majority of Pb found in terrestrial ecosystems was
deposited in the past during the use of Pb additives in gasoline. This
gasoline-derived Pb was emitted predominantly in small size particles
which were widely dispersed and transported across large distances.
Many sites receiving Pb predominantly through such long-range transport
have accumulated large amounts of Pb in soils (CD, p.l AX7-98). There
is little evidence that terrestrial sites exposed as a result of this
long range transport of Pb have experienced significant effects on
ecosystem structure or function (CD, AX7.1.4.2, p. AX7-98). Strong
complexation of Pb by soil organic matter may explain why few
ecological effects have been observed (CD, p. AX7-98). Studies have
shown decreasing levels of Pb in vegetation which seems to correlate
with decreases in atmospheric deposition of Pb resulting from the
removal of Pb additives to gasoline (CD, AX7.1.4.2).
Terrestrial ecosystems remain primarily sinks for Pb but amounts
retained in various soil layers vary based on forest type, climate, and
litter cycling (CD, Section 7.1). Once in the soil, the migration and
distribution of Pb is controlled by a multitude of factors including
pH, precipitation, litter composition, and other factors which govern
the rate at which Pb is bound to organic materials in the soil (CD,
Section 2.3.5).
Like most metals the solubility of Pb is increased at lower pH.
However, the reduction of pH may in turn decrease the solubility of
dissolved organic material (DOM). Given the close association between
Pb mobility and complexation with DOM, a reduced pH does not
necessarily lead to increased movement of Pb through terrestrial
systems and into surface waters. In areas with moderately acidic soil
(i.e., pH of 4.5 to 5.5) and abundant DOM, there is no appreciable
increase in the movement of Pb into surface waters compared to those
areas with neutral soils (i.e., pH of approximately 7.0). This appears
to support the theory that the movement of Pb in soils is limited by
the solubilization and transport of DOM. In sandy soils without
abundant DOM, moderate acidification appears likely to increase outputs
of Pb to surface waters (CD, AX7.1.4.1).
Lead exists in the environment in various forms which vary widely
in their ability to cause adverse effects on ecosystems and organisms.
Current levels of Pb in soil also vary widely depending on the source
of Pb but in all ecosystems Pb concentrations exceed natural background
levels. The deposition of gasoline-derived Pb into forest soils has
produced a legacy of slow moving Pb that remains bound to organic
materials despite the removal of Pb from most fuels and the resulting
dramatic reductions in overall deposition rates. For areas influenced
by point sources of air Pb, concentrations of Pb in soil may exceed by
many orders of magnitude the concentrations which are considered
harmful to laboratory organisms. Adverse effects associated with Pb
include neurological, physiological and behavioral effects which may
influence ecosystem structure and functioning. Ecological soil
screening levels (Eco-SSLs) have been developed for Superfund site
characterizations to indicate concentrations of Pb in soils below which
no adverse effects are expected to plants, soil invertebrates, birds
and mammals. Values like these may be used to identify areas in which
there is the potential for adverse effects to any or all of these
receptors based on current concentrations of Pb in soils.
Atmospheric Pb enters aquatic ecosystems primarily through the
erosion and runoff of soils containing Pb and deposition (wet and dry).
While overall deposition rates of atmospheric Pb have decreased
dramatically since the removal of Pb additives from gasoline, Pb
continues to accumulate and may be re-exposed in sediments and water
bodies throughout the United States (CD, Section 2.3.6).
Several physical and chemical factors govern the fate and
bioavailability of Pb in aquatic systems. A significant portion of Pb
remains bound to suspended particulate matter in the water column and
eventually settles into the substrate. Species, pH, salinity,
temperature,
[[Page 71534]]
turbulence and other factors govern the bioavailability of Pb in
surface waters (CD, Section 7.2.2).
Lead exists in the aquatic environment in various forms and under
various chemical and physical parameters which determine the ability of
Pb to cause adverse effects either from dissolved Pb in the water
column or Pb in sediment. Current levels of Pb in water and sediment
also vary widely depending on the source of Pb. Conditions exist in
which adverse effects to organisms and thereby ecosystems may be
anticipated given experimental results. It is unlikely that dissolved
Pb in surface water constitutes a threat to ecosystems that are not
directly influenced by point sources. For Pb in sediment, the evidence
is less clear. It is likely that some areas with long-term historical
deposition of Pb to sediment from a variety of sources as well as areas
influenced by point sources have the potential for adverse effects to
aquatic communities. The long residence time of Pb in sediment and its
ability to be resuspended by turbulence make Pb likely to be a factor
for the foreseeable future. Criteria have been developed to indicate
concentrations of Pb in water and sediment below which no adverse
effects are expected to aquatic organisms. These values may be used to
identify areas in which there is the potential for adverse effects to
receptors based on current concentrations of Pb in water and sediment.
B. Screening Level Ecological Risk Assessment
This section presents a brief summary of the screening-level
ecological risk assessment conducted by EPA for this review. The
assessment is described in detail in Lead Human Exposure and Health
Risk Assessments and Ecological Risk Assessment for Selected Areas,
Pilot Phase (ICF, 2006). Funding constraints have precluded performance
of a full-scale ecological risk assessment. The discussion here is
focused on the screening level assessment performed in the pilot phase
(ICF, 2006) and takes into consideration CASAC recommendations with
regard to interpretation of this assessment (Henderson, 2007a, b). The
following summary focuses on key features of the approach used in the
assessment and presents only a brief summary of the results of the
assessment. A complete presentation of results is provided in the pilot
phase Risk Assessment Report (ICF, 2006) and summarized in Chapter 6 of
the Staff Paper.
1. Design Aspects of Assessment and Associated Uncertainties
The screening level risk assessment involved several location-
specific case studies and a national-scale surface water and sediment
screen. The case studies included areas surrounding a primary Pb
smelter and a secondary Pb smelter, as well as a location near a
nonurban roadway. An additional case study for an ecologically
vulnerable location was identified and described (ICF, 2006), but
resource constraints have precluded risk analysis for this location.
The case study analyses were designed to estimate the potential for
ecological risks associated with exposures to Pb emitted into ambient
air. Soil, surface water, and/or sediment concentrations were estimated
from available monitoring data or modeling analysis, and then compared
to ecological screening benchmarks to assess the potential for
ecological impacts from Pb that was emitted into the air. Results of
these comparisons are not definitive estimates of risk, but rather
serve to identify those locations at which there is the greatest
likelihood for adverse effect. Similarly, the national-scale screening
assessment evaluated surface water and sediment monitoring locations
across the United States for the potential for ecological impacts
associated with atmospheric deposition of Pb. The reader is referred to
the pilot phase Risk Assessment Report (ICF, 2006) for details on the
use of this information and models in the screening assessment.
The measures of exposure for these analyses are total Pb
concentrations in soil, dissolved Pb concentrations in fresh surface
waters (water column), and total Pb concentrations in freshwater
sediments. The hazard quotient (HQ) approach was then used to compare
Pb media concentrations with ecological screening values. The exposure
concentrations were estimated for the three case studies and the
national-scale screening analyses as described below:
For the primary Pb smelter case study, measured
concentrations of total Pb in soil, dissolved Pb in surface waters, and
total Pb in sediment were used to develop point estimates for sampling
clusters thought to be associated with atmospheric Pb deposition,
rather than Pb associated with nonair sources, such as runoff from
waste storage piles.
For the secondary Pb smelter case study, concentrations of
Pb in soil were estimated using fate and transport modeling based on
EPA's MPE methodology (USEPA, 1998) and data available from similar
locations.
For the near roadway nonurban case study, measured soil
concentration data collected from two interstate sampling locations,
one with fairly high-density development (Corpus Christi, Texas) and
another with medium-density development (Atlee, Virginia), were used to
develop estimates of Pb in soils for each location.
For the national-scale surface water and sediment
screening analyses, measurements of dissolved Pb concentrations in
surface water and total Pb in sediment for locations across the United
States were compiled from available databases (USGS, 2004). Air
emissions, surface water discharge, and land use data for the areas
surrounding these locations were assessed to identify locations where
atmospheric Pb deposition may be expected to contribute to potential
ecological impacts. The exposure assessment focused on these locations.
The ecological screening values used in this assessment were
developed from the Eco-SSLs methodology, EPA's recommended ambient
water quality criteria, and sediment screening values developed by
MacDonald and others (2000, 2003). Soil screening values were derived
for this assessment using the Eco-SSL methodology with the toxicity
reference values for Pb (USEPA, 2005d, 2005e) and consideration of the
inputs on diet composition, food intake rates, incidental soil
ingestion, and contaminant uptake by prey (details are presented in
Section 7.1.3.1 and Appendix L, of ICF, 2006). Hardness-specific
surface water screening values were calculated for each site based on
EPA's recommended ambient water quality criteria for Pb (USEPA, 1984).
For sediment screening values, the assessment relied on sediment
``threshold effect concentrations'' and ``probable effect
concentrations'' developed by MacDonald et al. (2000). The methodology
for these sediment criteria is described more fully in section 7.1.3.3
and Appendix M of the pilot phase Risk Assessment Report (ICF, 2006).
The HQ is calculated as the ratio of the media concentration to the
ecotoxicity screening value, and represented by the following equation:
HQ = (estimated Pb media concentration) / (ecotoxicity screening value)
For each case study, HQ values were calculated for each location
where either modeled or measured media concentrations were available.
Separate soil HQ values were calculated for each
[[Page 71535]]
ecological receptor group for which an ecotoxicity screening value has
been developed (i.e., birds, mammals, soil invertebrates, and plants).
HQ values less than 1.0 suggest that Pb concentrations in a specific
medium are unlikely to pose significant risks to ecological receptors.
HQ values greater than 1.0 indicate that the expected exposure exceeds
the ecotoxicity screening value and that there is a potential for
adverse effects.
There are several uncertainties that apply across case studies
noted below:
The ecological risk screen is limited to specific case
study locations and other locations for which dissolved Pb data were
available and evaluated in the national-scale surface water and
sediment screens. In identifying sites for inclusion in the assessment,
efforts were made to ensure that the Pb exposures assessed were
attributable to airborne Pb and not dominated by nonair sources.
However, there is uncertainty as to whether other sources might have
actually contributed to the Pb exposure estimates.
A limitation to using the selected ecotoxicity screening
values is that they might not be sufficient to identify risks to some
threatened or endangered species or unusually sensitive aquatic
ecosystems (e.g., CD, p. AX7-110).
The methods and database from which the surface water
screening values (i.e., the AWQC for Pb) were derived is somewhat
dated. New data and approaches (e.g., use of pH as indicator of
bioavailability) may now be available to estimated the aquatic toxicity
of Pb (CD, Sections AX7.2.1.2 and AX7.2.1.3).
No adjustments were made for sediment-specific
characteristics that might affect the bioavailability of Pb in
sediments in the derivation of the sediment quality criteria used for
this ecological risk screen (CD, Sections 7.2.1 and AX7.2.1.4; Appendix
M, ICF, 2006). Similarly, characteristics of soils for the case study
locations were not evaluated for measures of bioavailability.
Although the screening value for birds used in this
analysis is based on reasonable estimates for diet composition and
assimilation efficiency parameters, it was based on a conservative
estimate of the relative bioavailability of Pb in soil and natural
diets compared with water soluble Pb added to an experimental pellet
diet (Appendix L, ICF, 2006).
2. Summary of Results
The following is a brief summary of key observations related to the
results of the screening-level ecological risk assessment. A more
complete discussion of the results is provided in Chapter 6 of the
Staff Paper and the complete presentation of the assessment and results
is presented in the pilot phase Risk Assessment Report (ICF, 2006).
The national-scale screen of surface water data initial
identified some 42 sample locations of which 15 were then identified as
unrelated to mining sites and having water column levels of dissolved
Pb that were greater than hardness adjusted chronic criteria for the
protection of aquatic life (with one location having a HQ of 15),
indicating a potential for adverse effect if concentrations were
persistent over chronic periods. Acute criteria were not exceeded at
any of these locations. The extent to which air emissions of Pb have
contributed to these surface water Pb concentrations is unclear.
In the national-scale screen of sediment data associated
with the 15 surface water sites described above, threshold effect
concentration-based HQs at nine of these sites exceeded 1.0.
Additionally, HQs based on probable effect concentrations exceeded 1.0
at five of the sites, indicating probable adverse effects to sediment
dwelling organisms. Thus, sediment Pb concentrations at some sites are
high enough that there is a likelihood that they would cause adverse
effects to sediment dwelling organisms. However, the contribution of
air emissions to these concentrations is unknown.
In the primary Pb smelter case study, all three of the
soil sampling clusters (including the ``reference areas'') had HQs that
exceeded 1.0 for birds. Samples from one cluster also had HQs greater
than 1.0 for plants and mammals. The surface water sampling clusters
all had measurements below the detection limit of 3.0 [mu]g/L. However,
three sediment sample clusters had HQs greater than 1.0. In summary,
the concentrations of Pb in soil and sediments exceed screening values
for these media indicating potential for adverse effects to terrestrial
organisms (plants, birds and mammals) and to sediment dwelling
organisms. While the contribution to these Pb concentrations from air
as compared to nonair sources is not quantified, air emissions from
this facility are substantial (see Appendix D, USEPA 2007b; ICF 2006).
In the secondary Pb smelter case study, the soil
concentrations, developed from soil data for similar locations,
resulted in avian HQs greater than 1.0 for all distance intervals
evaluated. The scaled soil concentrations within 1 km of the facility
also showed HQs greater than 1.0 for plants, birds, and mammals. These
estimates indicate a potential for adverse effect to those receptor
groups.
In the nonurban, near roadway case study, HQs for birds
and mammals were greater than 1.0 at all but one of the distances from
the road. Plant HQs were greater than 1.0 at the closest distance. In
summary, HQs above one were estimated for plants, birds and mammals,
indicating potential for adverse effect to these receptor groups.
C. Considerations in Review of the Standard
This section presents an integrative synthesis of information in
the Criteria Document together with EPA analyses and evaluations. EPA
notes that the final decision on retaining or revising the current
secondary Pb standard is a public policy judgment to be made by the
Administrator. The Administrator's final decision will draw upon
scientific information and analyses about welfare effects, exposure and
risks, as well as judgments about the appropriate response to the range
of uncertainties that are inherent in the scientific evidence and
analyses.
The NAAQS provisions of the Act require the Administrator to
establish secondary standards that, in the judgment of the
Administrator, are requisite to protect the public welfare from any
known or anticipated adverse effects associated with the presence of
the pollutant in the ambient air. In so doing, the Administrator seeks
to establish standards that are neither more nor less stringent than
necessary for this purpose. The Act does not require that secondary
standards be set to eliminate all risk of adverse welfare effects, but
rather at a level requisite to protect public welfare from those
effects that are judged by the Administrator to be adverse.
The following discussion starts with background information on the
current standard (Section IV.C.1). The general approach for this
current review is summarized in Section IV.C.2. Considerations with
regard to the adequacy of the current standard are discussed in section
IV.C.3, with evidence and exposure-risk-based considerations in
subsections IV.C.3.a and b, respectively, followed by a summary of
CASAC advice and recommendations (section IV.C.3.c) and, lastly,
solicitation of comment on the broad range of policy options (section
IV.C.3.d). Considerations with regard to elements of alternative
standards are discussed in Section IV.C.4.
[[Page 71536]]
1. Background on the Current Standard
The current standard was set in 1978 to be identical to the primary
standard (1.5 [mu]g Pb/m\3\, as a maximum arithmetic mean averaged over
a calendar quarter), the basis for which is summarized in Section
III.C.1. At the time the standard was set, the Agency concluded that
the primary air quality standard would adequately protect against known
and anticipated adverse effects on public welfare, as the Agency stated
that it did not have evidence that a more restrictive secondary
standard was justified. In the rationale for this conclusion, the
Agency stated that the available evidence cited in the 1977 Criteria
Document indicated that ``animals do not appear to be more susceptible
to adverse effects from lead than man, nor do adverse effects in
animals occur at lower levels of exposure than comparable effects in
humans'' (43 FR 46256). The Agency recognized that Pb may be deposited
on the leaves of plants and present a hazard to grazing animals. With
regard to plants, the Agency stated that Pb is absorbed but not
accumulated to any great extent by plants from soil, and that although
some plants may be susceptible to Pb, it is generally in a form that is
largely nonavailable to them. Further the Agency stated that there was
no evidence indicating that ambient levels of Pb result in significant
damage to manmade materials and Pb effects on visibility and climate
are minimal.
The secondary standard was subsequently considered during the 1980s
in development of the 1986 Criteria Document (USEPA, 1986a) and the
1990 Staff Paper (USEPA, 1990). In summarizing OAQPS staff conclusions
and recommendations at that time, the 1990 Staff Paper stated that a
qualitative assessment of available field studies and animal
toxicological data suggested that ``domestic animals and wildlife are
as susceptible to the effects of lead as laboratory animals used to
investigate human lead toxicity risks.'' Further, the 1990 Staff Paper
highlighted concerns over potential ecosystem effects of Pb due to its
persistence, but concluded that pending development of a stronger
database that more accurately quantifies ecological effects of
different Pb concentrations, consideration should be given to retaining
a secondary standard at or below the level of the then-current
secondary standard of 1.5 [mu]g/m\3\.
2. Approach for Current Review
To evaluate whether it is appropriate to consider retaining the
current secondary Pb standard, or whether consideration of revisions is
appropriate, EPA is considering an approach in this review like that
used in the Staff Paper that considers the evidence and risk analyses.
This approach recognizes that the available welfare effects evidence
generally reflects laboratory-based evidence of toxicological effects
on specific organisms exposed to concentrations of Pb at which
scientists generally agree that adverse effects are likely to occur. It
is widely recognized, however, that environmental exposures are likely
to be at lower concentrations and/or accompanied by significant
confounding factors (e.g., other metals, acidification), which
increases our uncertainty about the likelihood and magnitude of the
organism and ecosystem response.
3. Adequacy of the Current Standard
a. Evidence-Based Considerations
In considering the welfare effects evidence with respect to the
adequacy of the current standard, EPA will consider not only the array
of evidence newly assessed in the Criteria Document but also that
assessed in the 1986 Criteria Document and summarized in the 1990 Staff
Paper. As discussed extensively in the latter two documents, there was
a significantly improved characterization of environmental effects of
Pb in the ten years after the Pb NAAQS was set. And, in the subsequent
nearly 20 years, many additional studies on Pb effects in the
environment are now available (2006 Criteria Document). Some of the
more relevant aspects of the evidence available since the standard was
set include the following:
A more quantitative determination of the mobility,
distribution, uptake, speciation, and fluxes of atmospherically
delivered Pb in terrestrial ecosystems shows that the binding of Pb to
organic materials in the soil slows its mobility through soil and may
prevent uptake by plants (CD, Sections 7.1.2, 7.1.5, AX7.1.4.1,
AX7.1.4.2, AX7.1.4.3 and AX7.1.2 ). Therefore, while atmospheric
deposition of Pb has decreased, Pb may be more persistent in some
ecosystems than others and may remain in the active zone of the soil,
where exposure may occur, for decades (CD, Sections 7.1.2, AX7.1.2 and
AX7.1.4.3).
Plant toxicity may occur at lower levels than previously
identified as determined by data considered in development of Eco-SSLs
(CD, pp. 7-11 to 7-12, AX7-16 and Section AX7.1.3.2), although the
range of reported soil Pb effect levels is large (tens to thousands of
mg/kg soil).
Avian and mammalian toxicity may occur at lower levels
than those previously identified, although the range of Pb effect
levels is large (<1 to >1,000 mg Pb/kg bw-day) (CD, p. 7-12, Section
AX7.1.3.3).
There is an expanded understanding of the fate and effects
of Pb in aquatic ecosystems and of the distribution and concentrations
of Pb in surface waters throughout the United States (CD, Section
AX7.2.2).
New methods for assessing the toxicity of metals to water
column and sediment-dwelling organisms and data collection efforts (CD,
Sections 7.2.1, 7.2.2, AX7.2.2, and AX7.2.2.2) have improved our
understanding of Pb aquatic toxicity and findings include an indication
that in some estuarine systems Pb deposited during historic usage of
leaded gasoline may remain in surface sediments for decades. (CD, p. 7-
23).
A larger dataset of aquatic species assessed with regard
to Pb toxicity, and findings of lower effect levels for previously
untested species (CD, p. AX7-176 and Section AX7.2.4.3).
Currently available studies have also shown effects on
community structure, function and primary productivity, although some
confounders (such as co-occurring pollutants) have not been well
addressed (CD, Section AX7.1.4.2).
Evidence in ecological research generally indicates the
value of a critical loads approach; however, current information on Pb
critical loads is lacking for many processes and interactions involving
Pb in the environment and work is ongoing (CD, Section 7.3).
Given the full body of current evidence, despite wide variations in
Pb concentrations in soils throughout the country, Pb concentrations
are likely in excess of concentrations expected from geologic or other
non-anthropogenic forces. In particular, the deposition of gasoline-
derived Pb into forest soils has produced a legacy of slow moving Pb
that remains bound to organic materials despite the removal of Pb from
most fuels and the resulting dramatic reductions in overall deposition
rates (CD, Section AX7.1.4.3). For areas influenced by point sources of
air Pb that meet the current standard, concentrations of Pb in soil may
exceed by many orders of magnitude the concentrations which are
considered harmful to laboratory organisms (CD, Section 3.2 and
AX7.1.2.3).
There are several difficulties in quantifying the role of current
ambient Pb in the environment: Some Pb deposited before the standard
was
[[Page 71537]]
enacted is still present in soils and sediments; historic Pb from
gasoline continues to move slowly through systems as does current Pb
derived from both air and nonair sources. Additionally, the evidence of
adversity in natural systems is very sparse due in no small part to the
difficulty in determining the effects of confounding factors such as
multiple metals or factors influencing bioavailability in field
studies. However, the evidence summarized above and in Section 4.2 of
the Staff Paper and described in detail in the Criteria Document
informs our understanding of Pb in the environment today and evidence
of environmental Pb exposures of potential concern.
Conditions exist in which Pb-associated adverse effects to aquatic
organisms and thereby ecosystems may be anticipated given experimental
results. While the evidence does not indicate that dissolved Pb in
surface water constitutes a threat to those ecosystems that are not
directly influenced by point sources, the evidence regarding Pb in
sediment is less clear (CD, Sections AX7.2.2.2.2 and AX7.2.4). It is
likely that some areas with long term historical deposition of Pb to
sediment from a variety of sources as well as areas influenced by point
sources have the potential for adverse effects to aquatic communities.
The long residence time of Pb in sediment and its ability to be
resuspended by turbulence make Pb contamination likely to be a factor
for the foreseeable future. Based on this information, the Staff Paper
concluded that the evidence suggests that the environmental levels of
Pb occurring under the current standard, set nearly thirty years ago,
may pose risk of adverse environmental effect.
b. Risk-based Considerations
In addition to the evidence-based considerations described in the
previous section, the screening level ecological risk assessment is
informative, taking into account key limitations and uncertainties
associated with the analyses.
The screening level risk assessment involved a comparison of
estimates of environmental media concentrations of Pb to ecological
screening levels to assess the potential for ecological impacts from Pb
that was emitted into the air. Results of these comparisons are not
considered to be definite predictors of risk, but rather serve to
identify those locations at which there is greatest likelihood for
adverse effect. Similarly, the national-scale screening assessment
evaluated the potential for ecological impacts associated with the
atmospheric deposition of Pb released into ambient air at surface water
and sediment monitoring locations across the United States.
The ecological screening levels employed in the screening level
risk assessment for different media are drawn from different sources.
Consequently there are somewhat different limitations and uncertainties
associated with each. In general, their use here recognizes their
strength in identifying media concentrations with the potential for
adverse effect and their relative nonspecificity regarding the
magnitude of risk of adverse effect.
As discussed in the previous section, as a result of its
persistence, Pb emitted in the past remains today in aquatic and
terrestrial ecosystems of the United States. Consideration of the
environmental risks associated with the current standard is complicated
by the environmental burden associated with air Pb concentrations that
exceeded the current standard, predominantly in the past.
Concentrations of Pb in soil and sediments associated with the
primary Pb smelter case study exceeded screening values for those media
indicating potential for adverse effect in terrestrial organisms
(plants, birds and mammals) and in sediment dwelling organisms. While
the contribution to these Pb concentrations from air as compared to
nonair sources has not been quantified, air emissions from this
facility are substantial (see Appendix D, USEPA 2007b; ICF 2006).
Additionally, estimates of Pb concentration in soils associated with
the nonurban near roadway case study and the secondary Pb smelter case
study were also associated with HQs above 1 for plants, birds and
mammals, indicating potential for adverse effect to those receptor
groups. The industrial facility in the secondary Pb smelter case study
is much younger than the primary Pb smelter and apparently became
active less than ten years prior to the establishment of the current
standard.
The national-scale screens, which are not focused on particular
point source locations, indicate the ubiquitous nature of Pb in aquatic
systems of the United States today. Further the magnitude of Pb
concentrations in several aquatic systems exceeded screening values. In
the case of the national-scale screen of surface water data, 15
locations were identified with water column levels of dissolved Pb that
were greater than hardness adjusted chronic criteria for the protection
of aquatic life (with one location having a HQ as high as 15),
indicating a potential for adverse effect if concentrations were
persistent over chronic periods. Further, sediment Pb concentrations at
some sites in the national-scale screen were high enough that the
likelihood that they would cause adverse effects to sediment dwelling
organisms may be considered ``probable''.
A complicating factor in interpreting the findings for the
national-scale screening assessments is the lack of clear apportionment
of Pb contributions from air as compared to nonair sources, such as
industrial and municipal discharges. While the contribution of air
emissions to the elevated concentrations has not been quantified,
documentation of historical trends in the sediments of many water
bodies has illustrated the sizeable contribution that airborne Pb can
have on aquatic systems (e.g., Section 2.8.1). This documentation also
indicates the greatly reduced contribution in many systems as compared
to decades ago (presumably reflecting the banning of Pb-additives from
gasoline used by cars and trucks). However, the timeframe for removal
of Pb from surface sediments into deeper sediment varies across
systems, such that Pb remains available to biological organisms in some
systems for much longer than in others (Section 2.8, CD, pages AX7-141
to AX7-145).
The case study locations included in the screening assessment, with
the exception of the primary Pb smelter site, are currently meeting the
current Pb standard, yet Pb occurs in some locations at concentrations,
particularly in soil, and aquatic sediment above the screening levels,
indicative of a potential for harm to some terrestrial and sediment
dwelling organisms. While the role of airborne Pb in determining these
Pb concentrations is unclear, the historical evidence indicates that
airborne Pb can create such concentrations in sediments and soil.
Further, environmental concentrations may be related to emissions prior
to establishment of the current standard and such concentrations appear
to indicate a potential for harm to ecological receptors today.
c. CASAC Advice and Recommendations
In the CASAC letter transmitting advice and recommendations
pertaining to the review of the first draft Staff Paper and draft Pb
Exposure and Risk Assessments, the CASAC Pb panel provided
recommendations regarding the need for a Pb NAAQS, and the adequacy of
the current Pb NAAQS, as well as comments on the draft documents. With
regard to the need for a Pb NAAQS and adequacy of the current NAAQS,
the CASAC letter said:
[[Page 71538]]
The unanimous judgment of the Lead Panel is that lead should not
be delisted as a criteria pollutant, as defined by the Clean Air
Act, for which primary (public health based) and secondary (public
welfare based) NAAQS are established, and that both the primary and
secondary NAAQS should be substantially lowered.
Specifically with regard to the secondary NAAQS, the CASAC Pb Panel
stated that the December 2006 draft documents presented ``compelling
scientific evidence that current atmospheric Pb concentrations and
deposition--combined with a large reservoir of historically deposited
Pb in soils, sediments and surface waters--continue to cause adverse
environmental effects in aquatic and/or terrestrial ecosystems,
especially in the vicinity of large emissions sources.'' The Panel went
on to state that ``These effects persist in some cases at locations
where current airborne lead concentrations are below the level of the
current primary and secondary lead standards'' and ``Thus, from an
environmental perspective, there are convincing reasons to both retain
lead as a regulated criteria air pollutant and to lower the level of
the current secondary standard.''
In making this recommendation, the CASAC Pb Panel also cites the
persistence of Pb in the environment, the possibility of some of the
large amount of historically deposited Pb becoming resuspended by
natural events, and the expectation that humans are not uniquely
sensitive among the many animal and plant species in the environment.
In summary, with regard to the recommended level of a revised secondary
standard, the CASAC panel stated that:
Therefore, at a minimum, the level of the secondary Lead NAAQS
should be at least as low as the lowest-recommended primary lead
standard.
CASAC provided further advice and recommendations on the Agency's
consideration of the secondary standard in this review in their letter
of September 2007 (Henderson, 2007b). In that letter they recognized
the role of the secondary standard in influencing the long-term
environmental burden of Pb and a need for environmental monitoring to
assess the success of the standard in this role.
d. Policy Options
In considering the adequacy of the current secondary standard, EPA
will consider, for reasons discussed above in III.C.3.d on the primary
standard, whether it is appropriate to maintain a NAAQS for Pb or to
retain Pb on the list of criteria pollutants. We take note of the views
of CASAC, summarized above, the conclusions and recommendations in the
OAQPS Staff Paper, and the views of public commenters on these
questions. We recognize that there may be differing views on
interpreting or weighing the available information. Thus, EPA solicits
comment related to the questions of delisting and revocation.
In further considering the adequacy of the current standard in
providing requisite protection from Pb-related adverse effects on
public welfare, EPA will focus on the body of available evidence
(briefly summarized above in Section IV.A). Depending on the
interpretation, the available data and evidence, primarily qualitative,
may suggest the potential for adverse environmental impacts under the
current standard. Given the limited data on Pb effects in ecosystems,
it is necessary to look at evidence of Pb effects on organisms and
extrapolate to ecosystem effects. Therefore, taking into account the
available evidence and current media concentrations in a wide range of
areas, EPA seeks comment on whether the evidence suggests that adverse
effects are occurring, particularly near point sources, under the
current standard. While the role of current airborne emissions is
difficult to apportion, it is conclusive that deposition of Pb from air
sources is occurring and that this ambient Pb is likely to be
persistent in the environment. Historically deposited Pb has persisted,
although location-specific dynamics of Pb in soil result in differences
in the timeframe during which Pb is retained in surface soils or
sediments where it may be available to ecological receptors (USEPA,
2007b, section 2.3.3). EPA seeks comment on the role of deposition of
Pb from current sources and the availability of this Pb to ecological
receptors.
There is only very limited information available pertinent to
assessing whether groups of organisms which influence ecosystem
function are subject to similar effects as those in humans. The
screening-level risk information, while limited and accompanied by
various uncertainties, also suggests occurrences of environmental Pb
concentrations existing under the current standard that could have
adverse environmental effects. Environmental Pb levels today are
associated with atmospheric Pb concentrations and deposition that have
combined with a large reservoir of historically deposited Pb in
environmental media.
The EPA takes note of the views of CASAC, summarized above, the
conclusions and recommendations in the OAQPS Staff Paper, and views of
public commenters on the adequacy of the current standard. EPA solicits
comment on the adequacy of the current standard and the rationale upon
which such views are based.
4. Elements of the Standard
The secondary standard is defined in terms of four basic elements:
indicator, averaging time, level and form, which serve to define the
standard and must be considered collectively in evaluating the welfare
protection afforded by the standards. In considering a revision to the
current standard, EPA will consider the four elements of the standard,
the information available and advice and recommendations from CASAC
regarding how the elements might be revised to provide a secondary
standard for Pb that protects against adverse environmental effect.
With regard to the pollutant indicator for use in a secondary NAAQS
that provides protection for public welfare from exposure to Pb, EPA
notes that Pb is a persistent pollutant to which ecological receptors
are exposed via multiple pathways. While the evidence indicates that
the environmental mobility and ecological toxicity of Pb are affected
by various characteristics of its chemical form, and the media in which
it occurs, information are insufficient to identify an indicator other
than total Pb that would provide protection against adverse
environmental effect in all ecosystems nationally.
Lead is a cumulative pollutant with environmental effects that can
last many decades. In considering the appropriate averaging time for
such a pollutant the concept of critical loads may be useful (CD,
Section 7.3). However, information is currently insufficient for such
use in this review.
There is a general lack of data that would indicate the appropriate
level of Pb in environmental media that may be associated with adverse
effects. The EPA notes the influence of airborne Pb on Pb in aquatic
systems and of changes in airborne Pb on aquatic systems, as
demonstrated by historical patterns in sediment cores from lakes and Pb
measurements (Section 2.8.1; CD, Section AX7.2.2; Yohn et al., 2004;
Boyle et al., 2005), as well as the comments of the CASAC Pb panel that
a significant change to current air concentrations (e.g., via a
significant change to the standard) is likely to have significant
beneficial effects on the magnitude of Pb exposures in the environment
and Pb toxicity impacts on natural and managed terrestrial and aquatic
ecosystems in various regions of
[[Page 71539]]
the U.S., the Great Lakes and also U.S. territorial waters of the
Atlantic Ocean (Henderson, 2007a, Appendix E). We concur with CASAC's
conclusion that the Agency lacks the relevant data to provide a clear,
quantitative basis for setting a secondary Pb NAAQS that differs from
the primary in indicator, averaging time, level or form. Thus, EPA
solicits comment on the option of a reduction in the secondary standard
consistent with any reduction of the primary standard that would
provide increased protection against adverse environmental effect.
Beyond the views noted above, EPA recognizes that there may be
differing interpretations of the available evidence and various aspects
of the evidence and exposure and risk information, including on the
important uncertainties and limitations associated with the evidence
and assessment. Thus, EPA solicits additional information pertaining to
and comment on the considerations described above, as well as on other
views with regard to the elements of a secondary standard for Pb, and
the rationale upon which such views are based.
V. Considerations for Ambient Monitoring
A determination of compliance with the Pb NAAQS for any given area
is made based on ambient air monitoring data collected by State and
local monitoring agencies. This section discusses aspects of the Pb
surveillance monitoring requirements with regards to the adequacy under
the current primary Pb NAAQS as well as under options being considered
for a revised primary Pb NAAQS. These aspects include the sampling and
analysis methods, network design, sampling schedule, and data handling
methods. In addition, this section discusses the need for monitoring in
support of the secondary Pb NAAQS.
A. Sampling and Analysis Methods
To be used in determination of compliance with the Pb NAAQS, the Pb
data must be collected and analyzed using a Federal Reference Method
(FRM), or a Federal Equivalent Method (FEM). The current FRM for Pb
sampling and analyses is based on the use of a high-volume TSP sampler
to collect the sample and the use of atomic absorption for the analysis
of Pb in the sample (40 CFR 50 Appendix G). There are 21 FEMs currently
approved for Pb-TSP (http://www.epa.gov/ttn/amtic/criteria.html). All
21 FEMs are based on the use of high-volume TSP samplers, but with a
variety of different analysis methods (e.g., XRF and ICP/MS).
Concerns have been raised over the use of high-volume TSP samplers.
CASAC has commented that TSP samplers have poor precision, that the
upper particle cut size varies widely as a function of wind speed and
direction, and that the spatial non-homogeneity of very coarse
particles cannot be efficiently captured by a national monitoring
network (Henderson, 2007b). For these reasons, CASAC recommended
considering a revision to the Pb reference method to allow sample
collection using PM10 samplers. CASAC suggested that it may
be possible to develop a single quantitative adjustment factor from a
short period of collocated sampling at multiple sites, or a Pb-
PM10/Pb-TSP equivalency ratio could be determined on a
regional or site-specific basis.
The EPA evaluated the precision and bias of the high-volume Pb-TSP
sampler based on data reported to AQS for collocated samplers and
results of in-field sampler flow audits and laboratory audits for Pb
(Camalier and Rice, 2007). In this evaluation, we found that the
average precision of the high-volume Pb-TSP sampler was approximately
12%, with a standard deviation of 19%, and average sampling bias (based
on flow audits) was -0.7%, with a standard deviation of 4.2%. We also
estimated the average bias for the lab analyses at -1.1% (with a
standard deviation of 5.5%) based on spiked filter audits. Total bias,
which includes bias from both sampling and laboratory analysis, was
estimated at -1.7%, with a standard deviation of 3.4%. This level of
precision and bias is comparable to the goal of the FRM and FEM for
other criteria pollutants (e.g., within 10% for PM2.5, 40
CFR 58 Appendix A). We attempted to look at the precision of low-volume
Pb-PM10 samplers based on data reported to AQS, however, we
did not have enough data (18 paired data points for one site) to make
any conclusions on the precision of this sampler.
Evaluations of the high-volume TSP sampler have demonstrated that
the sampler's cutpoint can vary between 25 and 50 [mu]m depending on
wind speed and direction (Wedding et al., 1977, McFarland and Rodes,
1979). A study was conducted during the last Pb NAAQS review to
evaluate the effect of wind speed and direction on sampler efficiency
(Purdue, 1988). This demonstration showed that the Pb collection
efficiency of the high-volume TSP sampler ranged from 80% to 90% over a
wide range of wind speeds and directions. In comparison, a study
conducted near a primary Pb smelter indicated that the ratio of Pb-
PM10 to Pb-TSP ranged from 17% to 186% for 22 collocated
samples (Brion, 1988). We believe that the variability of the
collection efficiency of the high-volume TSP sampler does not warrant
the discontinuation of its use. However, with this notice, we are
soliciting comments on this issue.
We analyzed data from a number of monitoring sites where collocated
Pb-TSP and Pb-PM10 data have been collected in order to
evaluate the appropriateness of using Pb-PM10 data as a
surrogate for Pb-TSP (Cavender, 2007). From this analysis it is clear
that a single relationship can not be made that would allow one to
accurately estimate Pb-TSP concentrations from Pb-PM10
measurements at all sites. However, at many locations it does appear a
strong linear relationship can be shown between Pb-TSP and Pb-PM10
concentrations. As such, it may be feasible for a monitoring agency to
develop a site-specific relationship, using conservative assumptions,
to estimate Pb-TSP based on Pb-PM10 measurements. We invite
comments on the appropriateness of using Pb-PM10 data as a
surrogate for Pb-TSP.
While all current FRM and FEM are based on the high-volume TSP
sampler, several vendors market low-volume TSP samplers. These samplers
are identical to low-volume PM10 samplers with the exception
of the sampling head and corresponding cut size. These samplers have a
number of advantages over the high-volume TSP sampler including the
capability of sequential sampling (i.e., the ability to collect more
than one sample between operator visits). Sequential sampling would be
highly desirable if the sampling frequency is increased as part of a
change to a monthly averaging period. Currently, the FEM demonstration
requirements [40 CFR 53.33(i)] dictate that the FEM testing must be
performed with an ambient Pb-TSP concentration between 0.5 [mu]g/m\3\
to 4.0 [mu]g/m\3\. Due to the dramatic decrease in ambient Pb
concentrations, there are few (if any) areas in the country where a
vendor could be assured that the average ambient Pb-TSP concentrations
would meet the FEM demonstration requirements during the field testing
period. If the Pb NAAQS is lowered, we believe it is appropriate to
lower the FEM requirement to a level more consistent with current
ambient Pb concentrations and the lowered NAAQS to allow for continued
development and approval of Pb-TSP FEM. We invite comment on the
appropriate range of concentrations for an FEM demonstration.
[[Page 71540]]
We also reviewed the method detection capabilities of the current
lab methods for the FRM and FEM to ensure that these methods had the
necessary sensitivity to accurately measure Pb-TSP at the low
concentrations considered in the Risk Assessment Report and Staff
Paper. Based on data submitted to AQS, the method detection limits for
these methods are all 0.01 [mu]g/m\3\ or less (Rice, 2007). From these
findings, we request comment on whether the current lab analysis
methods are adequate for continued use even at the lowest alternative
NAAQS levels considered in the Risk Assessment Report and Staff Paper.
B. Network Design
The existing Pb-TSP network has decreased substantially over the
last few decades. In 1980 there were over 900 Pb-TSP sites, this number
has been reduced to approximately 200 sites. These reductions were made
because of substantially reduced ambient Pb concentrations and shifting
priorities to other criteria pollutants. Now several states have no Pb-
TSP monitors resulting in large portions of the country with no data on
current ambient Pb-TSP concentrations. In addition, many of the largest
Pb emitting sources in the country do not have nearby monitors, and
there is substantial uncertainty about ambient air Pb levels resulting
from historic Pb deposits near roadways. For these reasons, we request
comment on whether the existing Pb-TSP network may not be adequate, and
that additional monitoring sites may be needed to determine compliance
with either the current or revised Pb NAAQS.
The minimum network design requirements are given in 40 CFR 58
Appendix D. The current network design requirements are for 2 FRM or
FEM sites in any area where Pb concentrations exceed or have exceeded
the NAAQS in the most recent 2 years. These requirements may make it
difficult to persuade state and local monitoring agencies to add
monitors in areas without existing monitors. As such, we believe that
these requirements are not adequate and should be modified (as part of
this rulemaking) to ensure monitoring is conducted in areas where NAAQS
violations may occur.
We request comment on options for improving the coverage of the Pb
network. One option would be to adopt network requirements similar to
those recently promulgated for PM2.5 and ozone which tie the
number of required monitors to the population of the urban area and
ambient Pb concentrations (40 CFR 58 Appendix D). Under this approach,
more monitoring sites would be required in areas with larger
populations and higher Pb concentrations. This approach would result in
improved network coverage in urban areas. However, large Pb emitting
sources that are not in urban areas may still not be monitored.
A second option would be to require one or more monitors near large
Pb emitting sources. For example, a monitor could be required at the
point near the maximum predicted concentrations for sources with a
potential Pb emission rate of 1 ton per year or more (as provided by
the most recent National Emissions Inventory, or permit data). Clearly,
some effort would be necessary to identify an appropriate emissions
threshold to ensure that all emission sources with the potential to
exceed the NAAQS are monitored without creating undue burden where
there is no potential to exceed the NAAQS. This option would ensure
coverage of the highest Pb emitting sources, but may not provide
adequate coverage in many populated areas where a combination of
smaller emissions sources and re-entrained dust may result in Pb
concentrations in excess of the NAAQS.
A third option could be created by the combination of the first two
options discussed above: Establish a minimum number of required
monitors in urban areas based on population and ambient Pb
concentrations and require monitors near large Pb emission sources.
This option would provide good monitoring coverage in urban areas and
near Pb emissions sources. Again, care would need to be taken in
establishing an emissions threshold.
A fourth option would be to utilize the current PM10
network if an acceptable regional or site-specific correlation of Pb-
TSP and Pb-PM10 can be made. This option would provide a
substantial increase in monitoring coverage without requiring a large
investment in new monitoring stations. The current PM10
network has been carefully established to include both rural and urban
ambient levels, though it was not designed to monitor near large Pb
emitting sources. We invite comments on these options as well as
suggestions for additional options to consider for improving the Pb
network.
C. Sampling Schedule
The current sampling frequency requirement is for one 24-hour
sample every six days [40 CFR 58.12(b)]. For the current NAAQS, which
is based on a quarterly average, the 1-in-6 sampling schedule yields 15
samples per quarter on average with 100% completeness, or 12 samples
with 75% completeness. A change to a monthly averaging period would
result in between 4 and 6 samples per month at the current sampling
frequency. If we change the averaging time to a monthly average, we
would likely need to increase the sampling frequency as 4 samples would
not result in a statistically valid estimate of the actual air quality
for the period.
Incomplete sampling results in increased uncertainty in the
estimate of actual ambient air quality. While some degree of
uncertainty is unavoidable due to the precision and bias inherent to
the sampling technique, it is important to understand the level of
uncertainty for each sampling option being considered and to select a
sampling frequency which achieves an acceptable level of uncertainty.
We plan to go through the Data Quality Objectives (DQO) process in
order to help us select an appropriate sampling option. The DQO process
is a series of logical steps that guides decision makers to a plan for
the resource-effective acquisition of environmental data. The DQO
process is used to establish performance and acceptance criteria, which
serve as the basis for designing a plan for collecting data of
sufficient quality and quantity to support the goals of the study (EPA,
2006e, EPA/240/B-06/001).
We are considering several options for sampling frequency. These
options include maintaining the current 1-in-6 day sampling schedule,
increasing the sampling frequency to 1-in-3 day, or increasing the
sampling frequency to 1-in-1 day sampling (i.e., complete sampling). In
addition, we will be considering an option that relates sampling
frequency to recent ambient Pb-TSP concentrations, such that an
increased sampling frequency is required as the recent ambient Pb-TSP
concentrations approach the NAAQS level. Other options that we will be
considering include--
Increasing sampling time duration (e.g., changing from a
24 hour sampling time duration to a 48 or 72 hour sampling time
duration).
Allowing for compositing of samples (i.e., analyzing
sequential samples together).
Allowing for multiple samplers at one site.
We invite comments on the appropriateness of these sampling options
and suggestions for additional options for consideration.
D. Data Handling
A number of data handling conventions and computations are
necessary when using ambient monitoring data to determine attainment
[[Page 71541]]
or non-attainment of the NAAQS. Recently, we have been codifying these
data handling conventions and computations into a separate appendix for
each NAAQS. As such, we intend to create an appendix for the
interpretation of the Pb NAAQS as part of this rule making. Specific
conventions we are considering and invite comments on at this time
include the following--
Design values will be developed based on the most recent 3
calendar year period.
Design values will be rounded to two significant figures
using conventional rounding methodology.
75% of the expected number of samples is needed for a
quarter to be considered complete, or 50% for a month.
Only one period (i.e., one month or one quarter depending
on the final form of the standard) is needed to demonstrate non-
attainment. Two periods would be needed if the NAAQS is based on the
2nd maximum.
Three full consecutive years of complete data are needed
to re-designate an area attainment from non-attainment.
Incomplete periods can be used to demonstrate non-
attainment, but not attainment.
E. Monitoring for the Secondary NAAQS
Currently, the secondary NAAQS is set equal to the primary NAAQS
(1.5 [mu]g/m\3\, maximum quarterly average). We do not expect there to
be ambient air concentrations in excess of the secondary NAAQS in rural
areas that are not associated with a Pb emission source. If the
secondary standard remains equal to the primary standard at the
completion of the current review, we request comment on the option of
developing Pb surveillance monitoring requirements for the primary
NAAQS that will be sufficient to determine compliance with the
secondary NAAQS.
While additional monitoring may not be necessary to demonstrate
compliance with the secondary NAAQS, CASAC has recommended additional
monitoring to gather information to better inform consideration of the
secondary NAAQS in the next and future reviews. Specifically, CASAC
stated that ``the EPA needs to initiate new measurement activities in
rural areas--which quantify and track changes in lead concentrations in
the ambient air, soils, deposition, surface waters, sediments and
biota, along with other information as may be needed to calculate and
apply a critical loads approach for assessing environmental lead
exposures and risks in the next review cycle'' (Henderson, 2007b).
We currently monitor ambient Pb in PM2.5 as part of the
IMPROVE network. There are 110 formally designated IMPROVE sites
located in or near national parks and other Class I visibility areas,
virtually all of these being rural. Approximately 80 additional sites
at various urban and rural locations, requested and funded by various
parties, are also informally treated as part of the network. While we
believe it may not be appropriate to rely on either Pb-PM10
or Pb-PM2.5 monitoring to demonstrate compliance with a Pb-
TSP NAAQS, we believe the Pb-PM2.5 measurements provided by
the IMPROVE network can be used as a useful indicator to track changes
in ambient Pb concentrations and resulting Pb deposition in rural areas
that are not directly impacted by a Pb emission source. It may also be
desirable to augment the IMPROVE network with a small ``sentinel''
network of collocated Pb-TSP monitors for a period of time in order to
develop a better understanding of how Pb-PM2.5 and Pb-TSP
relate in these rural areas. Alternatively, since it is likely that at
rural locations nearly all Pb is in the less than 10 [mu]m size range,
we could analyze the PM10 mass samples (which are already
being collected) for Pb for a period of time to develop a better
understanding of how Pb-PM2.5 and Pb-PM10 relate
in these rural areas. We welcome comments on the value and
appropriateness of use of the IMPROVE Pb-PM2.5 data for
assessing trends in ambient air concentrations of Pb, and the need to
collocate a small network of Pb-TSP or Pb-PM10 monitors at
IMPROVE sites.
The National Water-Quality Assessment (NAWQA), conducted by the
United States Geological Survey, contains data on Pb concentrations in
surface water, bed sediment, and animal tissue for more than 50 river
basins and aquifers throughout the country (CD, AX7.2.2.2). NAWQA data
are collected during long-term, cyclical investigations wherein study
units undergo intensive sampling for 3 to 4 years, followed by low-
intensity monitoring and assessment of trends every 10 years.
Similarly, the USGS is collaborating with Canadian and Mexican
government agencies on a multi-national project called ``Geochemical
Landscapes'' that has as its long-term goal a soil geochemical survey
of North America (http://minerals.cr.usgs.gov/projects/geochemical_landscapes/index.html
). The Geochemical Landscapes project has the
potential to fill the need for periodic Pb soil sampling. We note the
value of the NAWQA and Geochemical Landscapes data in the assessment of
trends in Pb concentrations in both soil and aquatic systems, and
support the continued collection of this data by the USGS.
VI. Solicitation of Comment
With the issuance of this ANPR, the Agency is soliciting broad
public input to inform the Agency's proposed rulemaking related to the
review of the Pb NAAQS. As noted in Section I above, this ANPR, as a
consequence of the timing of the Pb NAAQS review relative to the
Agency's initiation of the new NAAQS process, summarizes information
from the OAQPS Staff Paper, and from the Agency's risk assessment and
Criteria Document. In so doing, this notice presents OAQPS staff views
on the adequacy of the current standard and on a range of policy
options for the Administrator's consideration, together with the views
of CASAC and the public as reflected in their comments on the related
documents that have been previously made available for review. The
Agency is soliciting comment on the range of views discussed above as
well as any broader range of options that members of the public feel
appropriate for the Administrator to consider. Comments are solicited
together with the rationales for the views expressed in those comments.
The Agency is also soliciting further advice from CASAC on the issues
discussed in this notice at an upcoming public meeting (announced in a
separate Federal Register notice).
In soliciting public comment in advance of reaching proposed
decisions on whether to retain or revise the NAAQS under review, the
Agency is interested in general, specific, and technical comments on
all aspects of the rulemaking discussed in this notice and the related
documents. These aspects generally include characterization of Pb in
the ambient environment, characterization of the health effects
evidence and the assessment of human exposure and health risk,
characterization of the environmental effects evidence and
consideration of environmental exposure and risk, as well as an
assessment of the adequacy of the current primary and secondary
standards and of alternative standards for the Administrator's
consideration in reaching proposed decisions in this review of the Pb
NAAQS. We solicit broad comment on these aspects of this rulemaking,
informed by the discussion presented in this notice as well as the more
comprehensive discussion in the Criteria Document, the Staff Paper, and
related risk assessment reports.
Several types of information pertinent to the characterization of
Pb in the
[[Page 71542]]
ambient environment are considered for this review. These include
characterization of sources of Pb, including source distribution within
the U.S. and associated estimates of the magnitude of air emissions.
The currently available information on the magnitude, geographic
distribution and variability of Pb levels in the ambient air is also
considered. Further, given that Pb is a multimedia pollutant,
characterization of Pb includes consideration of atmospheric deposition
and Pb in ambient soil, surface waters and sediment. Comments,
including information and views, are solicited in all of these areas as
well as any other areas related to the characterization of Pb in the
ambient environment that are relevant to this review.
The current health effects evidence for Pb, evaluated in the
Agency's Criteria Document, encompasses a broad range of information
regarding human exposure to ambient Pb, toxicokinetics of Pb,
biological markers and models of Pb burden in humans, toxicological
effects of Pb in laboratory animals and in vitro test systems, and
epidemiologic studies of human health effects associated with Pb
exposure. In addition, based on the information in the Criteria
Documents, quantitative assessments of human exposures to Pb and
associated health risks as well as environmental exposures and related
risks have been conducted and are presented in related risk assessment
reports. We are soliciting comments, including information and views,
informed by the Criteria Document, Staff Paper, and risk assessment
reports, on characterization of the health effects evidence and
consideration of human exposure and health risk associated with Pb
exposures. Similarly, the Agency is soliciting comment on the
characterization of the environmental effects evidence and
environmental risks of Pb relevant to this review.
With regard to the primary and secondary standards, a wide range of
views have been expressed, reflecting differing conclusions about the
scientific evidence and quantitative risk assessments and differing
public health and welfare policy judgments about appropriate standards.
These views range from asserting the need for significant strengthening
of the standards to a recommendation in public comments that the Pb
NAAQS should be revoked and/or Pb should be delisted as a criteria
pollutant. We solicit comment on these views as well as on any other
views that are thought to be appropriate for the Agency to consider,
together with rationales for the views expressed. More specifically, we
solicit comment, including views and associated rationale, informed by
the Criteria Document, Staff Paper and related risk assessment reports,
on the adequacy of the current primary and secondary standards. We also
solicit comment on the range of alternative primary and secondary
standards the Agency should consider, with a focus on the four basic
elements of the standards, including indicator, averaging time, level,
and form. Further, we are soliciting comment on the view that it is
appropriate to revoke the NAAQS for Pb or to remove Pb from the list of
criteria pollutants.
Issues related to Pb surveillance monitoring requirements relevant
to this review are also discussed in this notice. These issues fall
into several areas, including sampling and analysis methods related to
Pb-TSP and Pb-PM10 measurements, monitoring network design,
sampling schedule, and data handling. Specific aspects of monitoring in
support of the secondary standard are also discussed. We are soliciting
comments on the issues related to Pb surveillance monitoring
requirements identified in this notice as well as on other issues
relevant to these requirements in this review.
The Agency will consider comments received in response to this
notice in reaching proposed decisions in this rulemaking. As noted
above, the public will have an additional opportunity for comment on
the proposed rulemaking, which will further inform the Administrator's
final decisions on the Pb NAAQS.
VII. Statutory and Executive Order Reviews
Executive Order 12866: Regulatory Planning and Review
Under Executive Order (EO) 12866 (58 FR 51735, October 4, 1993),
this action is a ``significant regulatory action.'' Accordingly, EPA
submitted this action to the Office of Management and Budget (OMB) for
review under EO 12866 and any changes made in response to OMB
recommendations have been documented in the docket for this action.
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List of Subjects in 40 CFR Part 50
Environmental protection, Air pollution control, Carbon monoxide,
Lead, Nitrogen dioxide, Ozone, Particulate matter, Sulfur oxides.
Dated: December 5, 2007.
Stephen L. Johnson,
Administrator.
[FR Doc. E7-23884 Filed 12-14-07; 8:45 am]
BILLING CODE 6560-50-P