National Ambient Air Quality Standards for Lead

Federal RegisterNov 12, 2008

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Parts 50, 51, 53 and 58

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

RIN 2060-AN83

National Ambient Air Quality Standards for Lead

AGENCY:

Environmental Protection Agency (EPA).

ACTION:

Final rule.

SUMMARY:

. EPA is retaining the current indicator of Pb in total suspended particles (Pb-TSP). EPA is revising the averaging time to a rolling 3-month period with a maximum (not-to-be-exceeded) form, evaluated over a 3-year period. EPA is revising the secondary standard to be identical in all respects to the revised primary standard.

EPA is also revising data handling procedures, including allowance for the use of Pb-PM

data in certain circumstances, and the treatment of exceptional events, and ambient air monitoring and reporting requirements for Pb, including those related to sampling and analysis methods, network design, sampling schedule, and data reporting. Finally, EPA is revising emissions inventory reporting requirements and providing guidance on its approach for implementing the revised primary and secondary standards for Pb.

DATES:

This final rule is effective on January 12, 2009.

ADDRESSES:

EPA has established a docket for this action under Docket ID No. EPA-HQ-OAR-2006-0735. All documents in the docket are listed on the

www.regulations.gov

Web site. Although listed in the index, some information is not publicly available, e.g., confidential business information or other information whose disclosure is restricted by statute. Certain other material, such as copyrighted material, will be publicly available only in hard copy form. Publicly available docket materials are available either electronically through

www.regulations.gov

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

FOR FURTHER INFORMATION CONTACT:

For further information in general or specifically with regard to sections I through III or VIII, contact Dr. Deirdre Murphy, Health and Environmental Impacts Division, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Mail code C504-06, Research Triangle Park, NC 27711;

telephone:

919-541-0729;

fax:

919-541-0237;

e-mail:

Murphy.deirdre@epa.gov.

With regard to section IV, contact Mr. Mark Schmidt, Air Quality Analysis Division, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Mail code C304-04, Research Triangle Park, NC 27711;

telephone:

919-541-2416;

fax:

919-541-1903;

e-mail:

Schmidt.mark@epa.gov.

With regard to section V, contact Mr. Kevin Cavender, Air Quality Analysis Division, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Mail code C304-06, Research Triangle Park, NC 27711;

telephone:

919-541-2364;

fax:

919-541-1903;

e-mail:

Cavender.kevin@epa.gov.

With regard to section VI, contact Mr. Larry Wallace, Ph.D., Air Quality Policy Division, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Mail code C539-01, Research Triangle Park, NC 27711;

telephone:

919-541-0906;

fax:

919-541-0824;

e-mail:

Wallace.larry@epa.gov.

With regard to section VII, contact Mr. Tom Link, Air Quality Policy Division, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Mail code C539-04, Research Triangle Park, NC 27711;

telephone:

919-541-5456;

e-mail:

Link.tom@epa.gov.

SUPPLEMENTARY INFORMATION:

Table of Contents

The following topics are discussed in this preamble:

I. Summary and Background

A. Summary of Revisions to the Lead NAAQS

B. Legislative Requirements

C. Review of Air Quality Criteria and Standards for Lead

D. Current Related Control Requirements

E. Summary of Proposed Revisions to the Lead NAAQS

F. Organization and Approach to Final Lead NAAQS Decisions

II. Rationale for Final Decisions on the Primary Lead Standard

A. Introduction

1. Overview of Multimedia, Multipathway Considerations and Background

2. Overview of Health Effects Information

a. Blood Lead

b. Array of Health Effects and At-risk Subpopulations

c. Neurological Effects in Children

3. Overview of Human Exposure and Health Risk Assessments

B. Need for Revision of the Current Primary Lead Standard

1. Introduction

2. Comments on the Need for Revision

3. Conclusions Regarding the Need for Revision

C. Conclusions on the Elements of the Primary Lead Standard

1. Indicator

a. Basis for Proposed Decision

b. Comments on Indicator

c. Conclusions on Indicator

2. Averaging Time and Form

a. Basis for Proposed Decision

b. Comments on Averaging Time and Form

c. Conclusions on Averaging Time and Form

3. Level

a. Basis for Proposed Range

b. Comments on Level

c. Conclusions on Level

D. Final Decision on the Primary Lead Standard

III. Secondary Lead Standard

A. Introduction

1. Overview of Welfare Effects Evidence

2. Overview of Screening Level Ecological Risk Assessment

B. Conclusions on the Secondary Lead Standard

1. Basis for Proposed Decision

2. Comments on the Proposed Secondary Standard

3. Administrator's Conclusions

C. Final Decision on the Secondary Lead Standard

IV. Appendix R—Interpretation of the NAAQS for Lead

A. Ambient Data Requirements

1. Proposed Provisions

2. Comments on Ambient Data Requirements

3. Conclusions on Ambient Data Requirements

B. Averaging Time and Procedure

1. Proposed Provisions

2. Comments on Averaging Time and Procedure

3. Conclusions on Averaging Time and Procedure

C. Data Completeness

1. Proposed Provisions

2. Comments on Data Completeness

3. Conclusions on Data Completeness

D. Scaling Factors to Relate Pb-TSP and Pb-PM

1. Proposed Provisions

2. Comments on Scaling Factors

3. Conclusions on Scaling Factors

E. Use of Pb-TSP and Pb-PM

Data

1. Proposed Provisions

2. Comments on Use of Pb-TSP and Pb-PM

Data

3. Conclusions on Use of Pb-TSP and Pb-PM

Data

F. Data Reporting and Rounding

1. Proposed Provisions

2. Comments on Data Reporting and Rounding

3. Conclusions on Data Reporting and Rounding

G. Other Aspects of Data Interpretation

V. Ambient Monitoring Related to Revised Lead Standards

A. Sampling and Analysis Methods

1. Pb-TSP Method

a. Proposed Changes

b. Comments on Pb-TSP Method

c. Decisions on Pb-TSP Method

2. Pb-PM

Method

a. Proposed FRM for Pb-PM

Monitoring

b. Comments on Proposed Pb-PM

FRM

c. Decisions on Pb-PM

FRM

3. FEM Requirements

a. Proposed FEM Requirements

b. Comments

c. Decisions on FEM Requirements

4. Quality Assurance Requirements

a. Proposed Changes

b. Comments

c. Decisions on Quality Assurance Requirements

B. Network Design

1. Proposed Changes

2. Comments on Network Design

a. Source-oriented monitoring

b. Non-source-oriented monitoring

c. Roadway Monitoring

d. Use of Pb-PM

Monitors

e. Required timeline for monitor installation and operation

3. Decisions on Network Design Requirements

C. Sampling Frequency

D. Monitoring for the Secondary Standard

E. Other Monitoring Regulation Changes

1. Reporting of Average Pressure and Temperature

2. Special Purpose Monitoring

3. Reporting of Pb-TSP Concentrations

VI. Implementation Considerations

A. Designations for the Lead NAAQS

1. Proposal

2. Comments and Responses

3. Final

B. Lead Nonattainment Area Boundaries

1. Proposal

2. Comments and Responses

3. Final

C. Classifications

1. Proposal

2. Comments and Responses

3. Final

D. Section 110(a)(2) Lead NAAQS Infrastructure Requirements

1. Proposal

2. Final

E. Attainment Dates

1. Proposal

2. Comments and Responses

3. Final

F. Attainment Planning Requirements

1. RACM/RACT for Lead Nonattainment Areas

a. Proposal

b. Comments and Responses

c. Final

2. Demonstration of Attainment for Lead Nonattainment Areas

a. Proposal

b. Final

3. Reasonable Further Progress (RFP)

a. Proposal

b. Comments and Responses

c. Final

4. Contingency Measures

a. Proposal

b. Comments and Responses

c. Final

5. Nonattainment New Source Review (NSR) and Prevention of Significant Deterioration (PSD) Requirements

a. Proposal

b. Comments and Responses

c. Final

6. Emissions Inventories

a. Proposal

b. Comments and Responses

c. Final

7. Modeling

a. Proposal

b. Comments and Responses

c. Final

G. General Conformity

1. Proposal

2. Final

H. Transition From the Current NAAQS to a Revised NAAQS for Lead

1. Proposal

2. Final

VII. Exceptional Events Information Submission Schedule for Lead NAAQS

A. Proposal

B. Comments and Responses

C. Final

VIII. Statutory and Executive Order Reviews

A. Executive Order 12866: Regulatory Planning and Review

B. Paperwork Reduction Act

C. Regulatory Flexibility Act

D. Unfunded Mandates Reform Act

E. Executive Order 13132: Federalism

F. Executive Order 13175: Consultation and Coordination With Indian Tribal Governments

G. Executive Order 13045: Protection of Children From Environmental Health & Safety Risks

H. Executive Order 13211: Actions That Significantly Affect Energy Supply, Distribution or Use

I. National Technology Transfer and Advancement Act

J. Executive Order 12898: Federal Actions to Address Environmental Justice in Minority Populations and Low-Income Populations

K. Congressional Review Act

References

I. Summary and Background

A. Summary of Revisions to the Lead NAAQS

Based on its review of the air quality criteria and national ambient air quality standards (NAAQS) for lead (Pb), EPA is making revisions to the primary and secondary NAAQS for Pb to provide requisite protection of public health and welfare, respectively. With regard to the primary standard, EPA is revising various elements of the standard to provide increased protection for children and other at-risk populations against an array of adverse health effects, most notably including neurological effects in children, including neurocognitive and neurobehavioral effects. EPA is revising the level to 0.15 μg/m

EPA is revising the secondary standard to be identical in all respects to the revised primary standard.

EPA is also revising data handling procedures, including allowance for the use of Pb-PM

B. Legislative Requirements

Two sections of the Clean Air Act (Act) govern the establishment and revision of the NAAQS. Section 108 (42 U.S.C. 7408) directs the Administrator to identify and list each air pollutant, emissions of which “in his judgment, cause or contribute to air pollution which may reasonably be anticipated to endanger public health and welfare” and whose “presence * * * in the ambient air results from numerous or diverse mobile or stationary sources” and to issue air quality criteria for those that are listed. Air quality criteria are to “accurately reflect the latest scientific knowledge useful in indicating the kind and extent of all identifiable effects on public health or welfare which may be expected from the presence of [the] pollutant in ambient air * * *”. Section 109 (42 U.S.C. 7409) directs the Administrator to propose and promulgate “primary” and “secondary” NAAQS for pollutants listed under section 108. Section 109(b)(1) defines a primary standard as one “the attainment and maintenance of which in the judgment of the Administrator, based on [air quality] criteria and allowing an adequate margin of safety, are requisite to protect the public health.”

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.”

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).

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.”

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

EPA,

647 F.2d 1130, 1154 (D.C. Cir 1980),

cert. denied,

449 U.S. 1042 (1980);

American Petroleum Institute

Costle,

665 F.2d 1176, 1186 (D.C. Cir. 1981),

cert. denied,

455 U.S. 1034 (1982). Both kinds of uncertainties are components of the risk associated with pollution at levels below those at which human health effects can be said to occur with reasonable scientific certainty. Thus, in selecting primary standards that include an adequate margin of safety, the Administrator is seeking not only to prevent pollutant levels that have been demonstrated to be harmful but also to prevent lower pollutant levels that may pose an unacceptable risk of harm, even if the risk is not precisely identified as to nature or degree. The CAA does not require the Administrator to establish a primary NAAQS at a zero-risk level or at background concentration levels, see

Lead Industries Association

EPA,

647 F.2d at 1156 n. 51, but rather at a level that reduces risk sufficiently so as to protect public health with an adequate margin of safety.

The selection of any particular approach to providing an adequate margin of safety is a policy choice left specifically to the Administrator's judgment.

Lead Industries Association

EPA,

647 F.2d at 1161-62. In addressing the requirement for an adequate margin of safety, EPA considers such factors as the nature and severity of the health effects involved, the size of the population(s) at risk, and the kind and degree of the uncertainties that must be addressed. In setting standards that are “requisite” to protect public health and welfare, as provided in section 109(b), EPA's task is to establish standards that are neither more nor less stringent than necessary for these purposes.

Whitman

American Trucking Associations,

531 U.S. 457, 473. Further the Supreme Court ruled that “[t]he text of § 109(b), interpreted in its statutory and historical context and with appreciation for its importance to the CAA as a whole, unambiguously bars cost considerations from the NAAQS-setting process * * *”

Id.

at 472.

In considering whether the CAA allowed for economic considerations to play a role in the promulgation of the NAAQS, the Supreme Court rejected arguments that because many more factors than air pollution might affect public health, EPA should consider compliance costs that produce health losses in setting the NAAQS.

Whitman

American Trucking Associations,

531 U.S. at 466. Thus, EPA may not take into account possible public health impacts from the economic cost of implementation.

Id.

Section 109(d)(1) of the Act requires that “[n]ot later than December 31, 1980, and at 5-year intervals thereafter, the Administrator shall complete a thorough review of the criteria published under section 108 and the national ambient air quality standards promulgated under this section and shall make such revisions in such criteria and standards and promulgate such new standards as may be appropriate in accordance with section 108 and subsection (b) of this section.” Section 109(d)(2)(A) requires that “The Administrator shall appoint an independent scientific review committee composed of seven members including at least one member of the National Academy of Sciences, one physician, and one person representing State air pollution control agencies.” Section 109(d)(2)(B) requires that, “[n]ot later than January 1, 1980, and at five-year intervals thereafter, the committee referred to in subparagraph (A) shall complete a review of the criteria published under section 108 and the national primary and secondary ambient air quality standards promulgated under this section and shall recommend to the Administrator any new national ambient air quality standards and revisions of existing criteria and standards as may be appropriate under section 108 and subsection (b) of this section.” Since the early 1980's, this independent review function has been performed by the Clean Air Scientific Advisory Committee (CASAC) of EPA's Science Advisory Board.

C. Review of Air Quality Criteria and Standards for Lead

On October 5, 1978, EPA promulgated primary and secondary NAAQS for Pb under section 109 of the Act (43 FR 46246). Both primary and secondary standards were set at a level of 1.5 micrograms per cubic meter (μg/m

), measured as Pb in total suspended particulate matter (Pb-TSP), not to be exceeded by the maximum arithmetic mean concentration averaged over a calendar quarter. This standard was based on the 1977

Air Quality Criteria for Lead

(USEPA, 1977).

A review of the Pb standards was initiated in the mid-1980s. The scientific assessment for that review is described in the 1986

Air Quality Criteria for Lead

(USEPA, 1986a), the associated Addendum (USEPA, 1986b) and the 1990 Supplement (USEPA, 1990a). As part of the review, the Agency designed and performed human exposure and health risk analyses (USEPA, 1989), the results of which were presented in a 1990 Staff Paper (USEPA, 1990b). Based on the scientific assessment and the human exposure and health risk analyses, the 1990 Staff Paper presented options for the Pb NAAQS level in the range of 0.5 to 1.5 μg/m

, and suggested the second highest monthly average in three years for the form and averaging time of the standard (USEPA, 1990b). After consideration of the documents developed during the review and the significantly changed circumstances since Pb was listed in 1976, the Agency did not propose any revisions to the 1978 Pb NAAQS. In a parallel effort, the Agency developed the broad, multi-program, multimedia, integrated

U.S. Strategy for Reducing Lead Exposure

(USEPA, 1991). As part of implementing this strategy, the Agency focused efforts primarily on regulatory and remedial clean-up actions aimed at reducing Pb exposures from a variety of nonair sources judged to pose more extensive public health risks to U.S. populations, as well as on actions to reduce Pb emissions to air, such as bringing more areas into compliance with the existing Pb NAAQS (USEPA, 1991).

EPA initiated the current review of the air quality criteria for Pb on November 9, 2004 with a general call for information (69 FR 64926). A project work plan (USEPA, 2005a) for the preparation of the Criteria Document was released in January 2005 for CASAC and public review. EPA held a series of workshops in August 2005, inviting recognized scientific experts to discuss initial draft materials that dealt with various lead-related issues being addressed in the Pb air quality criteria document. In February 2006, EPA released the

Plan for Review of the National Ambient Air Quality Standards for Lead

(USEPA 2006c) that described Agency plans and a timeline for reviewing the air quality criteria, developing human exposure and risk

assessments and an ecological risk assessment, preparing a policy assessment, and developing the proposed and final rulemakings.

The first draft of the Criteria Document (USEPA, 2005b) was released for CASAC and public review in December 2005 and discussed at a CASAC meeting held on February 28-March 1, 2006. A second draft Criteria Document (USEPA, 2006b) was released for CASAC and public review in May 2006, and discussed at the CASAC meeting on June 28, 2006. A subsequent draft of

Chapter 7—Integrative Synthesis

(chapter 8 in the final Criteria Document), released on July 31, 2006, was discussed at an August 15, 2006 CASAC teleconference. The final Criteria Document was released on September 30, 2006 (USEPA, 2006a; cited throughout this preamble as CD). While the Criteria Document focuses on new scientific information available since the last review, it integrates that information with scientific information from previous reviews.

In May 2006, EPA released for CASAC and public review a draft

Analysis Plan for Human Health and Ecological Risk Assessment for the Review of the Lead National Ambient Air Quality Standards

(USEPA, 2006d), which was discussed at a June 29, 2006 CASAC meeting (Henderson, 2006). The May 2006 assessment plan discussed two assessment phases: A pilot phase and a full-scale phase. The pilot phase of both the human health and ecological risk assessments was presented in the draft

Lead Human Exposure and Health Risk Assessments and Ecological Risk Assessment for Selected Areas

(ICF, 2006; henceforth referred to as the first draft Risk Assessment Report) which was released for CASAC and public review in December 2006. The first draft Staff Paper, also released in December 2006, discussed the pilot assessments and the most policy-relevant science from the Criteria Document. These documents were reviewed by CASAC and the public at a public meeting on February 6-7, 2007 (Henderson, 2007a).

Subsequent to that meeting, EPA conducted full-scale human exposure and health risk assessments, although no further work was done on the ecological assessment due to resource limitations. A second draft Risk Assessment Report (USEPA, 2007a), containing the full-scale human exposure and health risk assessments, was released in July 2007 for review by CASAC at a meeting held on August 28-29, 2007. Taking into consideration CASAC comments (Henderson, 2007b) and public comments on that document, we conducted additional human exposure and health risk assessments. A final Risk Assessment Report (USEPA, 2007b) and final Staff Paper (USEPA, 2007c) were released on November 1, 2007.

The final Staff Paper presents OAQPS staff's evaluation of the public health and welfare policy implications of the key studies and scientific information contained in the Criteria Document and presents and interprets results from the quantitative risk/exposure analyses conducted for this review. Further, the Staff Paper presents OAQPS staff recommendations on a range of policy options for the Administrator to consider concerning whether, and if so how, to revise the primary and secondary Pb NAAQS. Such an evaluation of policy implications is intended to help “bridge the gap” between the scientific assessment contained in the Criteria Document and the judgments required of the EPA Administrator in determining whether it is appropriate to retain or revise the NAAQS for Pb. In evaluating the adequacy of the current standard and a range of alternatives, the Staff Paper considered the available scientific evidence and quantitative risk-based analyses, together with related limitations and uncertainties, and focused on the information that is most pertinent to evaluating the basic elements of national ambient air quality standards: Indicator,

averaging time, form,

and level. These elements, which together serve to define each standard, must be considered collectively in evaluating the public health and welfare protection afforded by the Pb standards. The information, conclusions, and OAQPS staff recommendations presented in the Staff Paper were informed by comments and advice received from CASAC in its reviews of the earlier draft Staff Paper and drafts of related risk/exposure assessment reports, as well as comments on these earlier draft documents submitted by public commenters.

The “indicator” of a standard defines the chemical species or mixture that is to be measured in determining whether an area attains the standard.

The “form” of a standard defines the air quality statistic that is to be compared to the level of the standard in determining whether an area attains the standard.

Subsequent to completion of the Staff Paper, EPA issued an advance notice of proposed rulemaking (ANPR) that was signed by the Administrator on December 5, 2007 (72 FR 71488). The ANPR is one of the key features of the new NAAQS review process that EPA has instituted over the past two years to help to improve the efficiency of the process the Agency uses in reviewing the NAAQS while ensuring that the Agency's decisions are informed by the best available science and broad participation among experts in the scientific community and the public. The ANPR provided the public an opportunity to comment on a wide range of policy options that could be considered by the Administrator.

A public meeting of CASAC was held on December 12-13, 2007 to provide advice and recommendations to the Administrator based on its review of the ANPR and the previously released final Staff Paper and Risk Assessment Report. Transcripts of the meeting and CASAC's letter to the Administrator (Henderson, 2008a) are in the docket for this review and CASAC's letter is also available on the EPA Web site (

http://www.epa.gov/sab

A public comment period for the ANPR extended through January 16, 2008 and comments received are in the docket for this review. Comments were received from nearly 9000 private citizens (roughly 200 of them were not part of one of several mass comment campaigns), 13 State and local agencies, one federal agency, three regional or national associations of government agencies or officials, 15 nongovernmental environmental or public health organizations (including one submission on behalf of a coalition of 23 organizations) and five businesses or industry organizations.

The proposed decision (henceforth “proposal”) on revisions to the Pb NAAQS was signed on May 1, 2008 and published in the

Federal Register

on May 20, 2008. Public teleconferences of the CASAC Pb Panel were held on June 9 and July 8, 2008 to provide advice and recommendations to the Administrator based on its review of the proposal notice. CASAC's letter to the Administrator (Henderson, 2008b) is in the docket for this review and also available on the EPA Web site (

http://www.epa.gov/sab

The EPA held two public hearings to provide direct opportunities for oral testimony by the public on the proposal. The hearings were held concurrently on June 12, 2008 in Baltimore, Maryland and St. Louis, Missouri. At these public hearings, EPA heard testimony from 33 individuals representing themselves or specific interested organizations. Transcripts from these hearings and written testimony provided at the hearings are in the docket for this review. Additionally, a large number of written comments were received from various commenters during the public comment period on the proposal. Comments were received from EPA's

Children's Health Protection Advisory Committee, the American Academy of Pediatrics, the American Medical Association, the American Thoracic Society, two organizations of state and local air agencies (National Association of Clean Air Agencies and Northeast States for Coordinated Air Use Management), approximately 40 State, Tribal and local government agencies, approximately 20 environmental or public health organizations or coalitions, approximately 20 industry organizations or companies, and approximately 6200 private citizens (roughly 150 of whom were not part of one of several mass comment campaigns). Significant issues raised in the public comments are discussed throughout the preamble of this final action. A summary of all other significant comments, along with EPA's responses (henceforth “Response to Comments”), can be found in the docket for this review.

The schedule for completion of this review has been governed by a judicial order in

Missouri Coalition for the Environment

EPA

(No. 4:04CV00660 ERW, Sept. 14, 2005). The court-ordered schedule governing this review, entered by the court on September 14, 2005 and amended on April 29, 2008 and July 1, 2008, requires EPA to sign, for publication, a notice of final rulemaking concerning its review of the Pb NAAQS no later than October 15, 2008.

Some commenters have referred to and discussed individual scientific studies on the health effects of Pb that were not included in the Criteria Document (EPA, 2006a) (“ ‘new’ studies”). In considering and responding to comments for which such “new” studies were cited in support, EPA has provisionally considered the cited studies in conjunction with other relevant “new” studies published since the completion of the Criteria Document in the context of the findings of the Criteria Document.

As in prior NAAQS reviews, EPA is basing its decision in this review on studies and related information included in the Criteria Document and Staff Paper, which have undergone CASAC and public review. In this Pb NAAQS review, EPA also prepared an ANPR, consistent with the Agency's new NAAQS process. The ANPR discussed studies that were included in the Criteria Document and Staff Paper. The studies assessed in the Criteria Document and Staff Paper, and the integration of the scientific evidence presented in them, have undergone extensive critical review by EPA, CASAC, and the public. The rigor of that review makes these studies, and their integrative assessment, the most reliable source of scientific information on which to base decisions on the NAAQS, decisions that all parties recognize as of great import. NAAQS decisions can have profound impacts on public health and welfare, and NAAQS decisions should be based on studies that have been rigorously assessed in an integrative manner not only by EPA but also by the statutorily mandated independent advisory committee, as well as the public review that accompanies this process. EPA's provisional consideration of these studies did not and could not provide that kind of in-depth critical review.

This decision is consistent with EPA's practice in prior NAAQS reviews and its interpretation of the requirements of the CAA. Since the 1970 amendments, the EPA has taken the view that NAAQS decisions are to be based on scientific studies and related information that have been assessed as a part of the pertinent air quality criteria, and has consistently followed this approach. This longstanding interpretation was strengthened by new legislative requirements enacted in 1977, which added section 109(d)(2) of the Act concerning CASAC review of air quality criteria.

See

71 FR 61144, 61148 (October 17, 2006) (final decision on review of PM NAAQS) for a detailed discussion of this issue and EPA's past practice.

As discussed in EPA's 1993 decision not to revise the NAAQS for ozone, “new” studies may sometimes be of such significance that it is appropriate to delay a decision on revision of a NAAQS and to supplement the pertinent air quality criteria so the studies can be taken into account (58 FR at 13013-13014, March 9, 1993). In the present case, EPA's provisional consideration of “new” studies concludes that, taken in context, the “new” information and findings do not materially change any of the broad scientific conclusions regarding the health effects and exposure pathways of ambient air Pb made in the air quality criteria. For this reason, reopening the air quality criteria review would not be warranted even if there were time to do so under the court order governing the schedule for this rulemaking.

Accordingly, EPA is basing the final decisions in this review on the studies and related information included in the Pb air quality criteria that have undergone CASAC and public review. EPA will consider the “new” studies for purposes of decision-making in the next periodic review of the Pb NAAQS, which EPA expects to begin soon after the conclusion of this review and which will provide the opportunity to fully assess these studies through a more rigorous review process involving EPA, CASAC, and the public. Further discussion of these “new” studies can be found in the Response to Comments document.

D. Current Related Lead Control Programs

States are primarily responsible for ensuring attainment and maintenance of national ambient air quality standards once EPA has established them. Under section 110 of the Act (42 U.S.C. 7410) and related provisions, States are to submit, for EPA approval, State implementation plans (SIPs) that provide for the attainment and maintenance of such standards through control programs directed to sources of the pollutants involved. The States, in conjunction with EPA, also administer the prevention of significant deterioration program (42 U.S.C. 7470-7479) for these pollutants. In addition, Federal programs provide for nationwide reductions in emissions of these and other air pollutants through the Federal Motor Vehicle Control Program under Title II of the Act (42 U.S.C. 7521-7574), which involves controls for automobile, truck, bus, motorcycle, nonroad engine, and aircraft emissions; the new source performance standards under section 111 of the Act (42 U.S.C. 7411); and the national emission standards for hazardous air pollutants under section 112 of the Act (42 U.S.C. 7412).

As Pb is a multimedia pollutant, a broad range of Federal programs beyond those that focus on air pollution control provide for nationwide reductions in environmental releases and human exposures. In addition, the Centers for Disease Control and Prevention (CDC) programs provide for the tracking of children's blood Pb levels nationally and provide guidance on levels at which medical and environmental case management activities should be implemented (CDC, 2005a; ACCLPP, 2007).

In 1991, the Secretary of the Health and Human Services (HHS) characterized Pb poisoning as the “number one environmental threat to the health of children in the United States” (Alliance to End Childhood Lead Poisoning, 1991). In 1997, President Clinton created, by Executive Order 13045, the President's Task Force on Environmental Health Risks and Safety Risks to Children in response to

increased awareness that children face disproportionate risks from environmental health and safety hazards (62 FR 19885).

By Executive Orders issued in October 2001 and April 2003, President Bush extended the work for the Task Force for an additional three and a half years beyond its original charter (66 FR 52013 and 68 FR 19931). The Task Force set a Federal goal of eliminating childhood Pb poisoning by the year 2010 and reducing Pb poisoning in children was identified as the Task Force's top priority.

As described in section II.A.2.a below the CDC stated in 2005 that no “safe” threshold for blood Pb levels in young children has been identified (CDC, 2005a).

Co-chaired by the Secretary of the HHS and the Administrator of the EPA, the Task Force consisted of representatives from 16 Federal departments and agencies.

Federal abatement programs provide for the reduction in human exposures and environmental releases from in-place materials containing Pb (

e.g.

, Pb-based paint, urban soil and dust, and contaminated waste sites). Federal regulations on disposal of Pb-based paint waste help facilitate the removal of Pb-based paint from residences (68 FR 36487). Further, in 1991, EPA lowered the maximum levels of Pb permitted in public water systems from 50 parts per billion (ppb) to 15 ppb measured at the consumer's tap (56 FR 26460).

Federal programs to reduce exposure to Pb in paint, dust, and soil are specified under the comprehensive federal regulatory framework developed under the Residential Lead-Based Paint Hazard Reduction Act (Title X). Under Title X and Title IV of the Toxic Substances Control Act (TSCA), EPA has established regulations and associated programs in the following five categories: (1) Training and certification requirements for persons engaged in lead-based paint activities; accreditation of training providers; authorization of State and Tribal lead-based paint programs; and work practice standards for the safe, reliable, and effective identification and elimination of lead-based paint hazards; (2) ensuring that, for most housing constructed before 1978, lead-based paint information flows from sellers to purchasers, from landlords to tenants, and from renovators to owners and occupants; (3) establishing standards for identifying dangerous levels of Pb in paint, dust and soil; (4) providing grant funding to establish and maintain State and Tribal lead-based paint programs, and to address childhood lead poisoning in the highest-risk communities; and (5) providing information on Pb hazards to the public, including steps that people can take to protect themselves and their families from lead-based paint hazards.

Under Title IV of TSCA, EPA established standards identifying hazardous levels of lead in residential paint, dust, and soil in 2001. This regulation supports the implementation of other regulations which deal with worker training and certification, Pb hazard disclosure in real estate transactions, Pb hazard evaluation and control in Federally-owned housing prior to sale and housing receiving Federal assistance, and U.S. Department of Housing and Urban Development grants to local jurisdictions to perform Pb hazard control. The TSCA Title IV term “lead-based paint hazard” implemented through this regulation identifies lead-based paint and all residential lead-containing dust and soil regardless of the source of Pb, which, due to their condition and location, would result in adverse human health effects. One of the underlying principles of Title X is to move the focus of public and private decision makers away from the mere presence of lead-based paint, to the presence of lead-based paint hazards, for which more substantive action should be undertaken to control exposures, especially to young children. In addition the success of the program will rely on the voluntary participation of States and Tribes as well as counties and cities to implement the programs and on property owners to follow the standards and EPA's recommendations. If EPA were to set unreasonable standards (

e.g.

, standards that would recommend removal of all Pb from paint, dust, and soil), States and Tribes may choose to opt out of the Title X Pb program and property owners may choose to ignore EPA's advice believing it lacks credibility and practical value. Consequently, EPA needed to develop standards that would not waste resources by chasing risks of negligible importance and that would be accepted by States, Tribes, local governments and property owners. In addition, a separate regulation establishes, among other things, under authority of TSCA section 402, residential Pb dust cleanup levels and amendments to dust and soil sampling requirements (66 FR 1206).

On March 31, 2008, the Agency issued a new rule (Lead: Renovation, Repair and Painting [RRP] Program, 73 FR 21692) to protect children from lead-based paint hazards. This rule applies to renovators and maintenance professionals who perform renovation, repair, or painting in housing, child-care facilities, and schools built prior to 1978. It requires that contractors and maintenance professionals be certified; that their employees be trained; and that they follow protective work practice standards. These standards prohibit certain dangerous practices, such as open flame burning or torching of lead-based paint. The required work practices also include posting warning signs, restricting occupants from work areas, containing work areas to prevent dust and debris from spreading, conducting a thorough cleanup, and verifying that cleanup was effective. The rule will be fully effective by April 2010. The rule contains procedures for the authorization of States, territories, and Tribes to administer and enforce these standards and regulations in lieu of a federal program. In announcing this rule, EPA noted that almost 38 million homes in the United States contain some lead-based paint, and that this rule's requirements were key components of a comprehensive effort to eliminate childhood Pb poisoning. To foster adoption of the rule's measures, EPA also intends to conduct an extensive education and outreach campaign to promote awareness of these new requirements.

Programs associated with the Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA or Superfund) and Resource Conservation Recovery Act (RCRA) also implement abatement programs, reducing exposures to Pb and other pollutants. For example, EPA determines and implements protective levels for Pb in soil at Superfund sites and RCRA corrective action facilities. Federal programs, including those implementing RCRA, provide for management of hazardous substances in hazardous and municipal solid waste (see,

e.g.

, 66 FR 58258). Federal regulations concerning batteries in municipal solid waste facilitate the collection and recycling or proper disposal of batteries containing Pb.

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/

See, e.g.

, “Implementation of the Mercury-Containing and Rechargeable Battery Management Act”

http://www.epa.gov/epaoswer/hazwaste/recycle/battery.pdf

and “Municipal Solid Waste Generation, Recycling, and Disposal in the United States: Facts and Figures for 2005”

http://www.epa.gov/epaoswer/osw/conserve/resources/msw-2005.pdf.

A variety of federal nonregulatory programs also provide for reduced environmental release of Pb-containing materials through more general encouragement of pollution prevention, promotion of reuse and recycling, reduction of priority and toxic chemicals in products and waste, and

conservation of energy and materials. These include the Resource Conservation Challenge (

http://www.epa.gov/epaoswer/osw/conserve/index.htm

), the National Waste Minimization Program (

http://www.epa.gov/epaoswer/hazwaste/minimize/leadtire.htm

), “Plug in to eCycling” (a partnership between EPA and consumer electronics manufacturers and retailers;

http://www.epa.gov/epaoswer/hazwaste/recycle/electron/crt.htm#crts

), and activities to reduce the practice of backyard trash burning (

http://www.epa.gov/msw/backyard/pubs.htm

As a result of coordinated, intensive efforts at the national, state and local levels, including those programs described above, blood Pb levels in all segments of the population have dropped significantly from levels observed around 1990. In particular, blood Pb levels for the general population of children 1 to 5 years of age have dropped to a median level of 1.6 μg/dL and a level of 3.9 μg/dL for the 90th percentile child in the 2003-2004 National Health and Nutrition Examination Survey (NHANES) as compared to median and 90th percentile levels in 1988-1991 of 3.5 μg/dL and 9.4 μg/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

are at the low end of the historic range of blood Pb levels for general population of children aged 1-5 years. However, as recognized in section II.A.2.b, levels have been found to vary among children of different socioeconomic status and other demographic characteristics (CD, p. 4-21) and racial/ethnic and income disparities in blood Pb levels in children persist. The Agency has continued to grapple with soil and dust Pb levels from the historical use of Pb in paint and gasoline and from other sources.

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

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

http://www.epa.gov/ord/researchaccomplishments/index.html

E. Summary of Proposed Revisions to the Lead NAAQS

For reasons discussed in the proposal, the Administrator proposed to revise the current primary and secondary Pb standards. With regard to the primary Pb standard, the Administrator proposed to revise the level of the Pb standard to a level within the range of 0.10 μg/m

to 0.30 μg/m

, in conjunction with retaining the current indicator of Pb in total suspended particles (Pb-TSP) but with allowance for the use of Pb-PM

data. With regard to the averaging time and form, the Administrator proposed two options: to retain the current averaging time of a calendar quarter and the current not-to-be-exceeded form, revised to apply across a 3-year span; and to revise the averaging time to a calendar month and the form to the second-highest monthly average across a 3-year span. With regard to the secondary standard for Pb, the Administrator proposed to revise the standard to make it identical to the proposed primary standard.

F. Organization and Approach to Final Lead NAAQS Decisions

This action presents the Administrator's final decisions regarding the need to revise the current primary and secondary Pb standards. Revisions to the primary standard for Pb are addressed below in section II. The secondary Pb standard is addressed below in section III. Related data completeness, data handling, data reporting and rounding conventions are addressed in section IV, and related ambient monitoring methods and network design are addressed below in section V. Implementation of the revised NAAQS is discussed in section VI, and the exceptional events information submission schedule is described in section VII. A discussion of statutory and executive order reviews is provided in section VIII.

Today's final decisions are based on a thorough review in the Criteria Document of scientific information on known and potential human health and welfare effects associated with exposure to Pb in the environment. These final decisions also take into account: (1) Assessments in the Staff Paper and ANPR of the most policy-relevant information in the Criteria Document as well as quantitative exposure and risk assessments based on that information; (2) CASAC Panel advice and recommendations, as reflected in its letters to the Administrator, its discussions of drafts of the Criteria Document and Staff Paper, and of the ANPR and the notice of proposed rulemaking at public meetings; (3) public comments received during the development of these documents, either in connection with CASAC Panel meetings or separately; and (4) public comments received on the proposed rulemaking.

II. Rationale for Final Decision on the Primary Standard

A. Introduction

This section presents the rationale for the Administrator's final decision that the current primary standard is not requisite to protect public health with an adequate margin of safety, and that the existing Pb primary standard should be revised. In developing this rationale, EPA has drawn upon an integrative synthesis in the Criteria Document of the entire body of evidence published through late 2006 on human health effects associated with Pb exposure. Some 6000 studies were considered in this review. This body of evidence addresses a broad range of health endpoints associated with exposure to Pb (EPA, 2006a, chapter 8), and includes hundreds of epidemiologic studies conducted in the U.S., Canada, and many countries around the world since the time of the last review (EPA, 2006a, chapter 6).

As discussed below, a significant amount of new research has been conducted since the last review, with important new information coming from epidemiological, toxicological, controlled human exposure, and dosimetric studies. Moreover, the newly available research studies evaluated in the Criteria Document have undergone intensive scrutiny through multiple layers of peer review, with extended opportunities for review and comment by the CASAC Panel and the public. As with virtually any policy-relevant scientific research, there is uncertainty

in the characterization of health effects attributable to exposure to ambient Pb. While important uncertainties remain, the review of the health effects information has been extensive and deliberate. In the judgment of the Administrator, this intensive evaluation of the scientific evidence provides an adequate basis for regulatory decision making at this time. This review also provides important input to EPA's research plan for improving our future understanding of the relationships between exposures to ambient Pb and health effects.

The health effects information and quantitative exposure and health risk assessment were summarized in sections II.B and II.C of the proposal (73 FR at 29193-29220) and are only briefly outlined below in sections II.A.2 and II.A.3. Responses to public comments specific to the material presented in sections II.A.1 through II.A.3 below are provided in the Response to Comments document.

Subsequent sections of this preamble provide a more complete discussion of the Administrator's rationale, in light of key issues raised in public comments, for concluding that the current standard is not requisite to protect public health with an adequate margin of safety and that it is appropriate to revise the current primary Pb standard to provide additional public health protection (section II.B), as well as a more complete discussion of the Administrator's rationale for retaining or revising the specific elements of the primary Pb standards (section II.C), namely the indicator (section II.C.1), averaging time and form (section II.C.2), and level (section II.C.3). A summary of the final decisions on revisions to the primary Pb standards is presented in section II.D.

1. Overview of Multimedia, Multipathway Considerations and Background

This section briefly summarizes the information presented in section II.A of the proposal and chapter 2 of the Staff Paper on multimedia, multipathway and background considerations of the Pb NAAQS review. As was true in the setting of the current standard, multimedia distribution of and multipathway exposure to Pb that has been emitted into the ambient air play a key role in the Agency's consideration of the Pb NAAQS. Some key multimedia and multipathway considerations in the review include:

(1) Lead is emitted into the air from many sources encompassing a wide variety of stationary and mobile source types. Lead emitted to the air is predominantly in particulate form, with the particles occurring in various sizes. Once emitted, the particles can be transported long or short distances depending on their size, which influences the amount of time spent in aerosol phase. In general, larger particles tend to deposit more quickly, within shorter distances from emissions points, while smaller particles will remain in aerosol phase and travel longer distances before depositing. As summarized in sections II.A.1 and II.E.1 of the proposal, airborne concentrations of Pb at sites near sources are much higher, and the representation of larger particles is greater, than at sites not known to be directly influenced by sources.

(2) Once deposited out of the air, Pb can subsequently be resuspended into the ambient air and, because of the persistence of Pb, Pb emissions contribute to media concentrations for some years into the future.

(3) Exposure to Pb emitted into the ambient air (air-related Pb) can occur directly by inhalation, or indirectly by ingestion of Pb-contaminated food, water or other materials including dust and soil.

This occurs as Pb emitted into the ambient air is distributed to other environmental media and can contribute to human exposures via indoor and outdoor dusts, outdoor soil, food and drinking water, as well as inhalation of air. These exposure pathways are described more fully in the proposal.

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

(4) Air-related exposure pathways are affected by changes to air quality, including changes in concentrations of Pb in air and changes in atmospheric deposition of Pb. Further, because of its persistence in the environment, Pb deposited from the air may contribute to human and ecological exposures for years into the future. Thus, because of the roles of both air concentration and air deposition in human exposure pathways, and because of the persistence of Pb once deposited, some pathways respond more quickly to changes in air quality than others. Pathways most directly involving Pb in ambient air and exchanges of ambient air with indoor air respond more quickly while pathways involving exposure to Pb deposited from ambient air into the environment generally respond more slowly.

Additionally, as when the standard was set, human exposures to Pb include nonair or background contributions in addition to air-related pathways. Some key aspects of the consideration of air and nonair pathways in the review (described in more detail in the proposal) are summarized here:

(1) Human exposure pathways that are not air-related are those in which Pb does not pass through ambient air. These pathways as well as air-related human exposure pathways that involve natural sources of Pb to air are considered “policy-relevant background” in this review.

(2) The pathways of human exposure to Pb that are not air-related include ingestion of indoor Pb paint,

Pb in diet as a result of inadvertent additions during food processing, and Pb in drinking water attributable to Pb in distribution systems, as well as other generally less prevalent pathways, as described in the proposal (73 FR 29192) and Criteria Document (CD, pp. 3-50 to 3-51).

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

(3) Some amount of Pb in the air derives from background sources, such as volcanoes, sea salt, and windborne soil particles from areas free of anthropogenic activity and may also derive from anthropogenic sources of airborne Pb located outside of North America (which would also be considered policy-relevant background). In considering contributions from policy-relevant background to human exposures and associated health effects, however, policy-relevant background in air is likely insignificant in comparison to the contributions from exposures to nonair media.

(4) The relative contribution of Pb from different exposure media to human exposure varies, particularly for different age groups. For example, some studies have found that dietary intake of Pb may be a predominant source of Pb exposure among adults, greater than consumption of water and beverages or inhalation, while for young children, ingestion of indoor dust can be a significant Pb exposure pathway (e.g., via hand-to-mouth activity of very young children).

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

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

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

(6) Relative contributions to a child's total Pb exposure from air-related exposure pathways compared to other (nonair-related) Pb exposures depends on many factors including ambient air concentrations and air deposition in the area where the child resides (as well as in the area from which the child's food derives) and access to other sources of Pb exposure such as Pb paint, tap water affected by plumbing containing Pb, and lead-tainted products. Studies indicate that in the absence of paint-related exposures, Pb from other sources such as stationary sources of Pb emissions may dominate a child's Pb exposures. In other cases, such as children living in older housing with peeling paint or where renovations have occurred, the dominant source of Pb exposure may be lead paint used in the house in the past. Depending on Pb levels in a home's tap water, drinking water can sometimes be a significant source. In still other cases, there may be more of a mixture of contributions from multiple sources, with no one source dominating.

2. Overview of Health Effects Information

This section summarizes information presented in section II.B of the proposal pertaining to health endpoints associated with the range of exposures considered to be most relevant to current exposure levels. In recognition of the role of multiple exposure pathways and routes and the use of an internal exposure or dose metric in evaluating health risk for Pb, the following section summarizes key aspects of the internal disposition or distribution of Pb, the use of blood Pb as an internal exposure or dose metric, and the evidence with regard to the quantitative relationship between air Pb and blood Pb levels (section II.A.2.a). This is followed first by a summary of the broad array of Pb-induced health effects and recognition of at-risk subpopulations (section II.A.2.b) and then by a summary of neurological effects in children and quantitative concentration-response relationships for blood Pb and IQ (section II.A.2.c).

a. Blood Lead

(i) Internal Disposition of Lead

Lead enters the body via the respiratory system and gastrointestinal tract, from which it is quickly absorbed into the blood stream and distributed throughout the body.

Lead bioaccumulates in the body, with the bone serving as a large, long-term storage compartment; soft tissues (e.g., kidney, liver, brain, etc.) serve as smaller compartments, in which Pb may be more mobile (CD, sections 4.3.1.4 and 8.3.1). During childhood development, bone represents approximately 70% of a child's body burden of Pb, and this accumulation continues through adulthood, when more than 90% of the total Pb body burden is stored in the bone (CD, section 4.2.2). Throughout life, Pb in the body is exchanged between blood and bone, and between blood and soft tissues (CD, section 4.3.2), with variation in these exchanges reflecting “duration and intensity of the exposure, age and various physiological variables” (CD, p. 4-1).

Additionally, Pb freely crosses the placenta resulting in continued fetal exposure throughout pregnancy, with that exposure increasing during the latter half of pregnancy (CD, section 6.6.2).

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

(ii) Use of Blood Pb as Dose Metric

Blood Pb levels are extensively used as an index or biomarker of exposure by national and international health agencies, as well as in epidemiological (CD, sections 4.3.1.3 and 8.3.2) and toxicological studies of Pb health effects and dose-response relationships (CD, chapter 5). The U.S. Centers for Disease Control and Prevention (CDC), and its predecessor agencies, have for many years used blood Pb level as a metric for identifying children at risk of adverse health effects and for specifying particular public health recommendations (CDC, 1991; CDC, 2005a). Most recently, in 2005, with consideration of a review of the evidence by their advisory committee, CDC revised their statement on Preventing Lead Poisoning in Young Children, specifically recognizing the evidence of adverse health effects in children with blood Pb levels below 10 μg/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).

As described by the Advisory Committee on Childhood Lead Poisoning Prevention, “In 1991, CDC defined the blood lead level (BLL) that should prompt public health actions as 10 μg/dL. Concurrently, CDC also recognized that a BLL of 10 μg/dL did not define a threshold for the harmful effects of lead. Research conducted since 1991 has strengthened the evidence that children's physical and mental development can be affected at BLLS <10 μg/dL” (ACCLPP, 2007).

With the 2005 statement, CDC did not lower the 1991 level of concern and identified a variety of reasons, reflecting both scientific and practical considerations, for not doing so, including a lack of effective clinical or public health interventions to reliably and consistently reduce blood Pb levels that are below 10 μg/dL, the lack of a demonstrated threshold for adverse effects, and concerns for deflecting resources from children with higher blood Pb levels (CDC, 2005a, pp. 2-3). The preface for the CDC statement included the following: “Although there is evidence of adverse health effects in children with blood lead levels below 10 μg/dL, CDC has not changed its level of concern, which remains at levels >10 μg/dL. We believe it critical to focus available resources where the potential adverse effects remain the greatest. If no threshold level exists for adverse health effects, setting a new BLL of concern somewhere below 10 μg/dL would be based on an arbitrary decision. In addition, the feasibility and effectiveness of individual interventions to further reduce BLLs below 10 μg/dL has not been demonstrated.” [CDC, 2005a, p. ix] CDC further stated “Nonetheless, the sources of lead exposure and the population-based interventions that can be expected to reduce lead exposure are similar in children with BLLs <10 μg/ dL and >10 μg/dL, so preventive lead hazard control measures need not be deferred pending further research findings or consensus.” [CDC, 2005a, p. 2] CDC's Advisory Committee on Childhood Lead Poisoning Prevention recently provided recommendations regarding interpreting and managing blood Pb levels below 10 μg/dL in children and reducing childhood exposures to Pb (ACCLPP, 2007).

Since 1976, the CDC has been monitoring blood Pb levels in multiple age groups nationally through the National Health and Nutrition Examination Survey (NHANES).

The NHANES information has documented the dramatic decline in mean blood Pb levels in the U.S. population that has occurred since the 1970s and that coincides with regulations regarding leaded fuels, leaded paint, and Pb-containing plumbing materials that have reduced Pb exposure among the general population (CD, sections 4.3.1.3 and 8.3.3; Schwemberger

et al.

, 2005). The

Criteria Document summarizes related information as follows (CD, p. E-6).

This information documents a variation in mean blood Pb levels across the various age groups monitored. For example, mean blood Pb levels in 2001-2002 for ages 1-5, 6-11, 12-19 and greater than or equal to 20 years of age, are 1.70, 1.25, 0.94, and 1.56 μg/dL, respectively (CD, p. 4-22).

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

While blood Pb levels in the U.S. general population, including geometric mean levels in children aged 1-5, have declined significantly, levels have been found to vary among children of different socioeconomic status (SES) and other demographic characteristics (CD, p. 4-21), and racial/ethnic and income disparities in blood Pb levels in children persist. For example, as described in the proposal, blood Pb levels for lower income and African American children are higher than those for the general population. The recently released RRP rule (discussed above in section I.C) is expected to contribute to further reductions in blood Pb levels for children living in houses with Pb paint.

(iii) Air-to-Blood Relationships

As described in section II.A.1 above and discussed in section II.A of the proposal, Pb in ambient air contributes to Pb in blood by multiple pathways, with the pertinent exposure routes including both inhalation and ingestion (CD, sections 3.1.3.2, 4.2 and 4.4; Hilts, 2003). The quantitative relationship between ambient air Pb and blood Pb (discussed in section II.B.1.c of the proposal), which is often termed a slope or ratio, describes the increase in blood Pb (in μg/dL) estimated to be associated with each unit increase of air Pb (in μg/m

Ratios are presented in the form of 1:x, with the 1 representing air Pb (in μg/m

) and x representing blood Pb (in μg/dL). Description of ratios as higher or lower refers to the values for x (i.e., the change in blood Pb per unit of air Pb). Slopes are presented as simply the value of x.

The evidence on this quantitative relationship is now, as in the past, limited by the circumstances in which the data are collected. These estimates are generally developed from studies of populations in various Pb exposure circumstances. The 1986 Criteria Document discussed the studies available at that time that addressed the relationship between air Pb and blood Pb,

recognizing that there is significant variability in air-to-blood ratios for different populations exposed to Pb through different air-related exposure pathways and at different exposure levels.

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

In discussing the available evidence, the 1986 Criteria Document observed that estimates of air-to-blood ratios that included air-related ingestion pathways in addition to the inhalation pathway are “necessarily higher”, in terms of blood Pb response, than those estimates based on inhalation alone (USEPA 1986a, p. 11-106). Thus, the extent to which studies account for the full set of air-related inhalation and ingestion exposure pathways affects the magnitude of the resultant air-to-blood estimates, such that fewer pathways included as “air-related” yields lower ratios. The 1986 Criteria Document also observed that ratios derived from studies focused only on inhalation pathways (e.g., chamber studies, occupational studies) have generally been on the order of 1:2 or lower, while ratios derived from studies including more air-related pathways were generally higher (USEPA, 1986a, p. 11-106). Further, the current evidence appears to indicate higher ratios for children as compared to those for adults (USEPA, 1986a), perhaps due to behavioral differences between the age groups.

Reflecting these considerations, the 1986 Criteria Document identified a range of air-to-blood ratios for children that reflected both inhalation and ingestion-related air Pb contributions as generally ranging from 1:3 to 1:5 based on the information available at that time (USEPA 1986a, p. 11-106). Table 11-36 (p. 11-100) in the 1986 Criteria Document (drawn from Table 1 in Brunekreef, 1984) presents air-to-blood ratios from a number of studies in children (i.e., those with identified air monitoring methods and reliable blood Pb data). For example, air-to-blood ratios from the subset of those studies that used quality control protocols and presented adjusted slopes

include adjusted ratios of 3.6 (Zielhuis

et al.

, 1979), 5.2 (Billick

et al.

, 1979, 1980); 2.9 (Billick

et al.

, 1983), and 8.5 (Brunekreef et al., 1983).

Brunekreef

et al.

(1984) discusses potential confounders to the relationship between air Pb and blood Pb, recognizing that ideally all possible confounders should be taken into account in deriving an adjusted air-to-blood relationship from a community study. The studies cited here adjusted for parental education (Zielhuis

et al.

, 1979), age and race (Billick

et al.

, 1979, 1980) and additionally measuring height of air Pb (Billick

et al.

, 1983); Brunekreef

et al.

(1984) used multiple regression to control for several confounders. The authors conclude that “presentation of both unadjusted and (stepwise) adjusted relationships is advisable, to allow insight in the range of possible values for the relationship” (p. 83). Unadjusted ratios were presented for two of these studies, including ratios of 4.0 (Zielhuis

et al.

, 1979) and 18.5 (Brunekreef

et al.

, 1983). The proposal noted that the Brunekreef

et al.

, 1983 study is subject to a number of sources of uncertainty that could result in air-to-blood Pb ratios that are biased high, including the potential for underestimating ambient air Pb levels due to the use of low volume British Smoke air monitors and the potential for higher historical ambient air Pb levels to have influenced blood Pb levels (see Section V.B.1 of the 1989 Pb Staff Report for the Pb NAAQS review, EPA, 1989). In addition, the 1989 Staff Report notes that the higher air-to-blood ratios obtained from this study could reflect the relatively lower blood Pb levels seen across the study population (compared with blood Pb levels reported in other studies from that period).

Additionally, the 1986 Criteria Document noted that ratios derived from studies involving higher blood and air Pb levels are generally smaller than ratios from studies involving lower blood and air Pb levels (USEPA, 1986a. p. 11-99). In consideration of this factor, the proposal observed that the range of 1:3 to 1:5 in air-to-blood ratios for children noted in the 1986 Criteria Document generally reflected study populations with blood Pb levels in the range of approximately 10-30 μg/dL (USEPA 1986a, pp. 11-100; Brunekreef, 1984), much higher than those common in today's population. This observation suggests that air-to-blood ratios relevant for today's population of children would likely extend higher than the 1:3 to 1:5 range identified in the 1986 Criteria Document.

More recently, a study of changes in children's blood Pb levels associated with reduced Pb emissions and associated air concentrations near a Pb smelter in Canada (for children through age six in age) reports a ratio of 1:6, and additional analysis of the data by EPA for the initial time period of the study resulted in a ratio of 1:7 (CD, pp. 3-23 to 3-24; Hilts, 2003).

Ambient air and blood Pb levels associated with the Hilts (2003) study range from 1.1 to 0.03 μg/m

, and associated population mean blood Pb levels range from 11.5 to 4.7 μg/dL, which are lower than levels associated with the older studies cited in the 1986 Criteria Document (USEPA, 1986).

This study considered changes in ambient air Pb levels and associated blood Pb levels over a five-year period which included closure of an older Pb smelter and subsequent opening of a newer facility in 1997 and a temporary (3 month) shutdown of all smelting activity in the summer of 2001. The author observed that the air-to-blood ratio for children in the area over the full period was approximately 1:6. The author noted limitations in the dataset associated with exposures in the second time period, after the temporary shutdown of the facility in 2001, including sampling of a different age group at that time and a shorter time period (3 months) at these lower ambient air Pb levels prior to collection of blood Pb levels. Consequently, EPA calculated an alternate air-to-blood Pb ratio based on consideration for ambient air Pb and blood Pb reductions in the first time period (after opening of the new facility in 1997).

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

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

In addition to the study by Hilts (2003), we are aware of two other studies published since the 1986 Criteria Document that report air-to-blood ratios for children (Tripathi

et al.

, 2001 and Hayes

et al.

, 1994). These studies were not cited in the 2006 Criteria Document, but were referenced in public comments received by EPA during this review.

The study by Tripathi

et al.

(2001) reports an air-to-blood ratio of approximately 1:3.6 for an analysis of children aged six through ten in India. The ambient air and blood Pb levels in this study (geometric mean blood Pb levels generally ranged from 10 to 15 μg/dL) are similar to levels reported in older studies reviewed in the 1986 Criteria Document and are much higher than current conditions in the U.S. The study by Hayes

et al.

(1994) compared patterns of ambient air Pb reductions and blood Pb reductions for large numbers of children in Chicago between 1971 and 1988, a period when significant reductions occurred in both measures. The study reports an air-to-blood ratio of 1:5.6 associated with ambient air Pb levels near 1 μg/m

and a ratio of 1:16 for ambient air Pb levels in the range of 0.25 μg/m

, indicating a pattern of higher ratios with lower ambient air Pb and blood Pb levels consistent with conclusions in the 1986 Criteria Document.

EPA is not basing its decisions on these two studies, but notes that these estimates are consistent with other studies that were included in the 1986 and 2006 Criteria Documents and considered by CASAC and the public.

As with all studies, we note that there are strengths and limitations for these two studies which may affect the specific magnitudes of the reported ratios, but that the studies' findings and trends are generally consistent with the conclusions from the 1986 Criteria Document.

In their advice to the Agency prior to the proposal, CASAC identified air-to-blood ratios of 1:5, as used by the World Health Organization (2000), and 1:10, as supported by an empirical analysis of changes in air Pb and changes in blood Pb between 1976 and the time when the phase-out of Pb from gasoline was completed (Henderson, 2007a).

The CASAC Panel stated “The Schwartz and Pitcher analysis showed that in 1978, the midpoint of the National Health and Nutrition Examination Survey (NHANES) II, gasoline Pb was responsible for 9.1 μg/dL of blood Pb in children. Their estimate is based on their coefficient of 2.14 μg/dL per 100 metric tons (MT) per day of gasoline use, and usage of 426 MT/day in 1976. Between 1976 and when the phase-out of Pb from gasoline was completed, air Pb concentrations in U.S. cities fell a little less than 1 μg/m

(24). These two facts imply a ratio of 9-10 μg/dL per μg/m

reduction in air Pb, taking all pathways into account.” (Henderson, 2007a, pp. D-2 to D-3).

In the proposal, beyond considering the evidence presented in the published literature and that reviewed in Pb Criteria Documents, we also considered air-to-blood ratios derived from the exposure assessment for this review (summarized below in section II.A.3 and described in detail in USEPA, 2007b). In that assessment, current modeling tools and information on children's activity patterns, behavior and physiology (e.g., CD, section 4.4) were used to estimate blood Pb levels associated with multimedia and multipathway Pb exposure. The results from the various case studies included in this assessment, with consideration of the context in which they were derived (e.g., the extent to which the range of air-related pathways were simulated), are also informative to our understanding of air-to-blood ratios.

For the general urban case study, air-to-blood ratios ranged from 1:2 to 1:9 across the alternative standard levels assessed, which ranged from the current standard of 1.5 μg/m

down to a level of 0.02 μg/m

. This pattern of model-derived ratios generally supports the range of ratios obtained from the literature and also supports the observation that lower ambient air Pb levels are associated with higher air-to-blood ratios. There are a number of sources of uncertainty associated with these model-derived ratios. The hybrid indoor dust Pb model, which is used in estimating indoor dust Pb levels for the urban case studies, uses a U.S. Department of Housing and Urban Development (HUD) survey dataset reflecting housing constructed before 1980 in establishing the relationship between dust loading and concentration, which is a key component in the hybrid dust model (as described in the Risk Assessment Report, Volume II, Appendix G, Attachment G-1). Given this application of the HUD dataset, there is the potential that the nonlinear relationship between indoor dust Pb loading and concentration (which is reflected in the structure of the hybrid dust model) could be driven more by the presence of indoor Pb paint than contributions from outdoor ambient air Pb. We also note that only recent air pathways were adjusted in modeling the impact of ambient air Pb reductions on blood Pb levels in the urban case studies, which could have implications for the air-to-blood ratios.

For the primary Pb smelter (subarea) case study, air-to-blood ratios ranged from 1:10 to 1:19 across the same range of alternative standard levels, from 1.5 down to 0.02 μg/m

Because these ratios are based on regression modeling developed using empirical data, there is the potential for these ratios to capture more fully the impact of ambient air on indoor dust Pb, and ultimately blood Pb, including longer timeframe impacts resulting from changes in outdoor deposition. Therefore, given that these ratios are higher than ratios developed for the general urban case study using the hybrid indoor dust Pb model (which only considers reductions in recent air), the ratios estimated for the primary Pb smelter (subarea) support the evidence-based observation discussed above that consideration of more of the exposure pathways relating ambient air Pb to blood Pb, may result in higher air-to-blood Pb ratios. In considering this case study, some have suggested, however, that the regression modeling fails to accurately reflect the temporal relationship between reductions in ambient air Pb and indoor dust Pb, which could result in an over-estimate

of the degree of dust Pb reduction associated with a specified degree of ambient air Pb reduction, which in turn could produce air-to-blood Pb ratios that are biased high.

Air-to-blood ratios for the full study area of the primary Pb smelter range from 1:3 to 1:7 across the range of alternative standard levels from 1.5 down to 0.02 μg/m

(USEPA, 2007b).

In summary, EPA's view in the proposal was that the current evidence in conjunction with the results and observations drawn from the exposure assessment, including related uncertainties, supports consideration of a range of air-to-blood ratios for children ranging from 1:3 to 1:7, reflecting multiple air-related pathways beyond simply inhalation and the lower air and blood Pb levels pertinent to this review. EPA invited comment on this range as well as the appropriate weight to place on specific ratios within this range. Advice from CASAC and comments from the public on this issue are discussed below in section II.C.3.

b. Array of Health Effects and At-Risk Subpopulations

Lead has been demonstrated to exert “a broad array of deleterious effects on multiple organ systems via widely diverse mechanisms of action” (CD, p. 8-24 and section 8.4.1). This array of health effects includes effects on heme biosynthesis and related functions; neurological development and function; reproduction and physical development; kidney function; cardiovascular function; and immune function. The weight of evidence varies across this array of effects and is comprehensively described in the Criteria Document. There is also some evidence of Pb carcinogenicity, primarily from animal studies, together with limited human evidence of suggestive associations (CD, sections 5.6.2, 6.7, and 8.4.10).

Lead has been classified as a probable human carcinogen by the International Agency for Research on Cancer (inorganic lead compounds), based mainly on sufficient animal evidence, and as reasonably anticipated to be a human carcinogen by the U.S. National Toxicology Program (lead and lead compounds) (CD, Section 6.7.2). U.S. EPA considers Pb a probable carcinogen (

http://www.epa.gov/iris/subst/0277.htm;

CD, p. 6-195).

This review is focused on those effects most pertinent to ambient exposures, which, given the reductions in ambient Pb levels over the past 30 years, are generally those associated with individual blood Pb levels in children and adults in the range of 10 μg/dL and lower. These key effects include neurological, hematological and immune

effects for children, and hematological, cardiovascular and renal effects for adults (CD, Tables 8-5 and 8-6, pp. 8-60 to 8-62). As evident from the discussions in chapters 5, 6 and 8 of the Criteria Document, “neurotoxic effects in children and cardiovascular effects in adults are among those best substantiated as occurring at blood Pb concentrations as low as 5 to 10 μg/dL (or possibly lower); and these categories are currently clearly of greatest public health concern” (CD, p. 8-60).

28 29

The toxicological and epidemiological information available since the time of the last review “includes assessment of new evidence substantiating risks of deleterious effects on certain health endpoints being induced by distinctly lower than previously demonstrated Pb exposures indexed by blood Pb levels extending well below 10 μg/dL in children and/or adults” (CD, p. 8-25). Some health effects associated with individual blood Pb levels extend below 5 μg/dL, and some studies have observed these effects at the lowest blood levels considered. With regard to population mean levels, the Criteria Document points to studies reporting “Pb effects on the intellectual attainment of preschool and school age children at population mean concurrent blood-Pb levels ranging down to as low as 2 to 8 μg/dL” (CD, p. E-9).

At mean blood Pb levels, in children, on the order of 10 μg/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).

With regard to blood Pb levels in individual children associated with particular neurological effects, the Criteria Document states “Collectively, the prospective cohort and cross-sectional studies offer evidence that exposure to Pb affects the intellectual attainment of preschool and school age children at blood Pb levels <10 μg/dL (most clearly in the 5 to 10 μg/dL range, but, less definitively, possibly lower).” (p. 6-269)

Epidemiological studies have consistently demonstrated associations between Pb exposure and enhanced risk of deleterious cardiovascular outcomes, including increased blood pressure and incidence of hypertension. A meta-analysis of numerous studies estimates that a doubling of blood-Pb level (

e.g.

, from 5 to 10 μg/dL) is associated with ~1.0 mm Hg increase in systolic blood pressure and ~0.6 mm Hg increase in diastolic pressure (CD, p. E-10).

We note that many studies over the past decade, in investigating effects at lower blood Pb levels, have utilized the CDC advisory level or level of concern for individual children (10 μg/dL)

as a benchmark for assessment, and this is reflected in the numerous references in the Criteria Document to 10 μg/dL. Individual study conclusions stated with regard to effects observed below 10 μg/dL are usually referring to individual blood Pb levels. In fact, many such study groups have been restricted to individual blood Pb levels below 10 μg/dL or below levels lower than 10 μg/dL. We note that the mean blood Pb level for these groups will necessarily be lower than the blood Pb level they are restricted below.

This level has variously been called an advisory level or level of concern (

http://www.atsdr.cdc.gov/csem/lead/pb_standards2.html

). In addressing children's blood Pb levels, CDC has stated “Specific strategies that target screening to high-risk children are essential to identify children with BLLs ≥ 10 μg/dL.” (CDC, 2005, p.1)

Threshold levels, in terms of blood Pb levels in individual children, for neurological effects cannot be discerned from the currently available studies (CD, pp. 8-60 to 8-63). The Criteria Document states “There is no level of Pb exposure that can yet be identified, with confidence, as clearly not being associated with some risk of deleterious health effects” (CD, p. 8-63). As discussed in the Criteria Document, “a threshold for Pb neurotoxic effects may exist at levels distinctly lower than the lowest exposures examined in these epidemiologic studies” (CD, p. 8-67).

In consideration of the evidence from experimental animal studies with regard to the issue of threshold for neurotoxic effects, the CD notes that there is little evidence that allows for clear delineation of a threshold, and that “blood-Pb levels associated with neurobehavioral effects appear to be reasonably parallel between humans and animals at reasonably comparable blood-Pb concentrations; and such effects appear likely to occur in humans ranging down at least to 5-10 μg/dL, or possibly lower (although the possibility of a threshold for such neurotoxic effects cannot be ruled out at lower blood-Pb concentrations)” (CD, p. 8-38).

As described in the proposal, physiological, behavioral and demographic factors contribute to increased risk of Pb-related health effects. Potentially at-risk subpopulations, also referred to as sensitive sub-populations, include those with increased susceptibility (

i.e.

, physiological factors contributing to a greater response for the same exposure), as well as those with greater vulnerability (

i.e.

, those with increased exposure such as through exposure to higher media concentrations or resulting from behavior leading to increased contact with contaminated media), or those affected by socioeconomic factors, such as reduced access to health care or low socioeconomic status.

While adults are susceptible to Pb effects at lower blood Pb levels than previously understood (

e.g.

, CD, p. 8-25), the greater influence of past exposures on their current blood Pb levels (as summarized above in section II.A.2.a) leads us to give greater prominence to children as the sensitive subpopulation in this review. Children are at increased risk of Pb-related health effects due to various factors that enhance their exposures (

e.g.

, via the hand-to-mouth activity that is prevalent in very young children, CD, section 4.4.3) and susceptibility. While children are considered to be at a period of

maximum exposure around 18-27 months, the current evidence has found even stronger associations between blood Pb at school age and IQ at school age. The evidence “supports the idea that Pb exposure continues to be toxic to children as they reach school age, and [does] not lend support to the interpretation that all the damage is done by the time the child reaches 2 to 3 years of age” (CD, section 6.2.12). The following physiological and demographic factors can further affect risk of Pb-related effects in some children.

• Children with particular genetic polymorphisms (

e.g.

, presence of the δ-aminolevulinic acid dehydratase-2 [ALAD-2] allele) have increased sensitivity to Pb toxicity, which may be due to increased susceptibility to the same internal dose and/or to increased internal dose associated with same exposure (CD, p. 8-71, sections 6.3.5, 6.4.7.3 and 6.3.6).

• Some children may have blood Pb levels higher than those otherwise associated with a given Pb exposure (CD, section 8.5.3) as a result of nutritional status (e.g., iron deficiency, calcium intake), as well as genetic and other factors (CD, chapter 4 and sections 3.4, 5.3.7 and 8.5.3).

• Situations of elevated exposure, such as residing near sources of ambient Pb, as well as socioeconomic factors, such as reduced access to health care or low socioeconomic status (SES) (USEPA, 2003, 2005c) can also contribute to increased blood Pb levels and increased risk of associated health effects from air-related Pb.

• As described in the proposal (sections II.B.1.b and II.B.3), children in poverty and black, non-Hispanic children have notably higher blood Pb levels than do economically well-off children and white children, in general.

c. Neurological Effects in Children

Among the wide variety of health endpoints associated with Pb exposures, there is general consensus that the developing nervous system in children is among the, if not the, most sensitive. While blood Pb levels in U.S. children have decreased notably since the late 1970s, newer studies have investigated and reported associations of effects on the neurodevelopment of children with these more recent blood Pb levels (CD, chapter 6). Functional manifestations of Pb neurotoxicity during childhood include sensory, motor, cognitive and behavioral impacts. Numerous epidemiological studies have reported neurocognitive, neurobehavioral, sensory, and motor function effects in children with blood Pb levels below 10 μg/dL (CD, sections 6.2 and 8.4).

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).

Further, neurological effects in general 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 and 8.4.2.3), and deficits in neuromotor function (CD, p. 8-36).

Cognitive effects associated with Pb exposures that have been observed in epidemiological studies have included decrements in intelligence test results, such as the widely used IQ score, and in academic achievement as assessed by various standardized tests as well as by class ranking and graduation rates (CD, section 6.2.16 and pp 8-29 to 8-30). As noted in the Criteria Document with regard to the latter, “Associations between Pb exposure and academic achievement observed in the above-noted studies were significant even after adjusting for IQ, suggesting that Pb-sensitive neuropsychological processing and learning factors not reflected by global intelligence indices might contribute to reduced performance on academic tasks” (CD, pp 8-29 to 8-30).

With regard to potential implications of Pb effects on IQ, the Criteria Document recognizes the “critical” distinction between population and individual risk, identifying issues regarding declines in IQ for an individual and for the population. The Criteria Document further states that a “point estimate indicating a modest mean change on a health index at the individual level can have substantial implications at the population level” (CD, p. 8-77).

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).

For an individual functioning in the low IQ range due to the influence of developmental risk factors other than Pb, a Pb-associated IQ decline of several points might be sufficient to drop that individual into the range associated with increased risk of educational, vocational, and social failure (CD, p. 8-77).

As an example, the Criteria Document states “although an increase of a few mmHg in blood pressure might not be of concern for an individual's well-being, the same increase in the population mean might be associated with substantial increases in the percentages of individuals with values that are sufficiently extreme that they exceed the criteria used to diagnose hypertension” (CD, p. 8-77).

For example, for a population mean IQ of 100 (and standard deviation of 15), 2.3% of the population would score above 130, but a shift of the population to a mean of 95 results in only 0.99% of the population scoring above 130 (CD, pp. 8-81 to 8-82).

Other cognitive effects observed in studies of children have included effects on attention, executive functions, language, memory, learning and visuospatial processing (CD, sections 5.3.5, 6.2.5 and 8.4.2.1), with attention and executive function effects associated with Pb exposures indexed by blood Pb levels below 10 μg/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 (CD, section 5.3.5), as well as associated mechanistic findings.

The persistence of such Pb-induced effects is described in the proposal and the Criteria Document (e.g., CD, sections 5.3.5, 6.2.11, and 8.5.2). The persistence or irreversibility of such effects can be the result of damage occurring without adequate repair offsets or of the persistence of Pb in the body (CD, section 8.5.2). It is additionally important to note that there may be long-term consequences of such deficits over a lifetime. Poor academic skills and achievement can have “enduring and important effects on objective parameters of success in real life”, as well as increased risk of antisocial and delinquent behavior (CD, section 6.2.16).

Multiple epidemiologic studies of Pb and child development have demonstrated inverse associations between blood Pb concentrations and children's IQ and other cognitive-related outcomes at successively lower Pb exposure levels over the past 30 years (as discussed in the CD, section 6.2.13). For example, the overall weight of the available evidence, described in the Criteria Document, provides clear substantiation of neurocognitive decrements being associated in children with mean blood Pb levels in the range of 5 to 10 μg/dL, and some analyses indicate Pb effects on intellectual attainment of children for which population mean blood Pb levels in the analysis ranged from 2 to 8 μg/dL (CD, sections 6.2, 8.4.2 and 8.4.2.6). Thus, while blood Pb levels in U.S. children have decreased notably since the late 1970s, newer studies have investigated and reported associations of effects on the neurodevelopment of children with blood Pb levels similar to the more recent, lower blood Pb levels (CD,

chapter 6; and as discussed in section II.B.2.b of the proposal).

The current evidence reviewed in the Criteria Document with regard to the quantitative relationship between neurocognitive decrement, such as IQ, and blood Pb levels indicates that the slope for Pb effects on IQ is nonlinear and is steeper at lower blood Pb levels, such that each μg/dL increase in blood Pb may have a greater effect on IQ at lower blood Pb levels (

e.g.,

below 10 μg/dL) than at higher levels (CD, section 6.2.13; pp. 8-63 to 8-64; Figure 8-7). As stated in the CD, “the most compelling evidence for effects at blood Pb levels <10 μg/dL, as well as a nonlinear relationship between blood Pb levels and IQ, comes from the international pooled analysis of seven prospective cohort studies (n=1,333) by Lanphear et al. (2005)” (CD, pp. 6-67 and 8-37 and section 6.2.3.1.11). Using the full pooled dataset with concurrent blood Pb level as the exposure metric and IQ as the response from the pooled dataset of seven international studies, Lanphear and others (2005) employed mathematical models of various forms, including linear, cubic spline, log-linear, and piece-wise linear, in their investigation of the blood Pb concentration-response relationship (CD, p. 6-29; Lanphear et al., 2005). They observed for this pooled dataset that the shape of the concentration-response relationship is nonlinear and the log-linear model provides a better fit over the full range of blood Pb measurements

than a linear one (CD, p. 6-29 and pp. 6-67 to 6-70; Lanphear et al., 2005). In addition, they found that no individual study among the seven was responsible for the estimated nonlinear relationship between Pb and deficits in IQ (CD p. 6-30). Others have also analyzed the same dataset and similarly concluded that, across the range of the dataset's blood Pb levels, a log-linear relationship was a significantly better fit than the linear relationship (p=0.009) with little evidence of residual confounding from included model variables (CD, section 6.2.13; Rothenberg and Rothenberg, 2005).

The median of the concurrent blood Pb levels modeled was 9.7 μg/dL; the 5th and 95th percentile values were 2.5 and 33.2 μg/dL, respectively (Lanphear

et al.,

2005).

As noted in the Criteria Document, a number of examples of non- or supralinear dose-response relationships exist in toxicology (CD, pp. 6-76 and 8-38 to 8-39). With regard to the effects of Pb on neurodevelopmental outcome such as IQ, the Criteria Document suggests that initial neurodevelopmental effects at lower Pb levels may be disrupting very different biological mechanisms (

e.g.

, early developmental processes in the central nervous system) than more severe effects of high exposures that result in symptomatic Pb poisoning and frank mental retardation (CD, p. 6-76). The Criteria Document describes this issue in detail with regard to Pb (summarized in CD at p. 8-39). Various findings within the toxicological evidence, presented in the Criteria Document (described in the proposal), provide biologic plausibility for a steeper IQ loss at low blood levels, with a potential explanation being that the predominant mechanism at very low blood-Pb levels is rapidly saturated and that a different, less-rapidly-saturated process, becomes predominant at blood-Pb levels greater than 10 μg/dL.

The current evidence includes multiple studies that have examined the quantitative relationship between IQ and blood Pb level in analyses of children with individual blood Pb concentrations below 10 μg/dL. In comparing across the individual epidemiological studies and the international pooled analysis, the Criteria Document observed that at higher blood Pb levels (

e.g.

, above 10 μg/dL), the slopes (for change in IQ with blood Pb) derived for log-linear and linear models are almost identical, and for studies with lower blood Pb levels, the slopes appear to be steeper than those observed in studies involving higher blood Pb levels (CD, p. 8-78, Figure 8-7). In making these observations, the Criteria Document focused on the curves from the models from the 10th percentile to the 90th percentile saying that the “curves are restricted to that range because log-linear curves become very steep at the lower end of the blood Pb levels, and this may be an artifact of the model chosen”.

The quantitative relationship between IQ and blood Pb level has been examined in the Criteria Document using studies where all or the majority of study subjects had blood Pb levels below 10 μg/dL and also where an analysis was performed on a subset of children whose blood Pb levels have never exceeded 10 μg/dL (CD, Table 6-1).

The datasets for three of these studies included concurrent blood Pb levels above 10 μg/dL; the concentration-response (C-R) relationship reported for one of the three was linear while it was log-linear for the other two. For the one study among these three that reported a linear C-R relationship, the highest blood Pb level was just below 12 μg/dL and the population mean was 7.9 μg/dL (Kordas

et al.

, 2006). Of the two studies with log-linear functions, one reported 69% of the children with blood Pb levels below 10 μg/dL and a population mean blood Pb level of 7.44 μg/dL (Al-Saleh

et al.

, 2001), and the second reported a population median blood Pb level of 9.7 μg/dL and a 95th percentile of 33.2 μg/dL (Lanphear

et al.

, 2005). In order to compare slopes across all of these studies (linear and log-linear) in the Criteria Document, EPA estimated, for each, the average slope of change in IQ with change in blood Pb between the 10th percentile

blood Pb level and 10 μg/dL (CD, Table 6-1). The resultant group of reported and estimated average linear slopes for IQ change with blood Pb levels up to 10 μg/dL range from -0.4 to -1.8 IQ points per μg/dL blood Pb (CD, Tables 6-1 and 8-7), with a median of -0.9 IQ points per μg/dL blood Pb (CD, p. 8-80).

These slopes from

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

The tests for cognitive function in these studies include age-appropriate Wechsler intelligence tests (Lanphear

et al.

, 2005; Bellinger and Needleman, 2003), the Stanford-Binet intelligence test (Canfield

et al.

, 2003), the Test of Non-Verbal Intelligence (Al-Saleh

et al.

, 2001), an abbreviated form of the Wechsler tests (Kordas

et al.

, 2006) and the Bayley Scales of Infant Development (Tellez-Rojo

et al.

, 2006). The Wechsler and Stanford-Binet tests are widely used to assess neurocognitive function in children and adults, however, these tests are not appropriate for children under age three. For such children, studies generally use the age-appropriate Bayley Scales of Infant Development as a measure of cognitive development.

In the Criteria Document analysis, the 10th percentile was chosen as a common point of comparison for the loglinear (and linear) models at a point prior to the lowest end of the blood Pb levels.

One of these slopes (CD, Table 6-1) is for the IQ-blood Pb (concurrent) relationship for children whose peak blood Pb levels are below 10 μg/dL in the international pooled dataset studied by Lanphear and others (2005); these authors reported this slope along with the companion slope, from the same (piece-wise) model, for the remaining children whose peak blood Pb level equals or is above 10 μg/dL (Lanphear

et al.

, 2005). In the economic analysis for EPA's recent Lead Renovation, Repair and Painting (RRP) Program rule (described above in section I.C) for children living in houses with lead-based paint, changes in IQ were estimated as a function of changes in lifetime average blood Pb level using the corresponding piece-wise model for lifetime average blood Pb derived from the pooled dataset (USEPA, 2008; USEPA, 2007d). The piecewise models that gave greater weight to impacts in this blood Pb range were chosen because peak blood Pb levels are likely to be less than 10 μg/dL for the vast majority of children exposed to Pb during renovation activities. Further, while Lanphear

et al.

(2005) used peak blood Pb concentrations to determine which segment of a model to apply, for the hypothetical children to whom the approach is discussed in the RRP Program rule, only lifetime averages were used (in the RRP analysis). To counter the impact of assigning additional hypothetical RRP children to the steeper of the two slopes than would have been the case if they could be assigned based on peak blood Pb levels (as a child's lifetime average blood Pb is lower than peak blood Pb), the RRP analysis

used the piece-wise model with node at 10 μg/dL, for which the steeper of the two slopes is less steep than it is for the model with node at 7.5 μg/dL. As stated in the RRP economic analysis document, “[s]electing a model with a node, or changing one segment to the other, at a lifetime average blood Pb concentration of 10 μg/dL rather than at 7.5 μg/dL, is a small protection against applying an incorrectly rapid change (steep slope with increasingly smaller effect as concentrations lower) to the calculation” (USEPA, 2008). We note here that the slope for the less-than-10-μg/dL portion of the model used in the RRP analysis (-0.88) is similar to the median for the slopes included in the Criteria Document analysis of quantitative relationships for studies in which the majority of blood Pb levels were below 10 μg/dL.

Among this group of quantitative IQ-blood Pb relationships examined in the Criteria Document (CD, Tables 6-1 and 8-7), the steepest slopes for change in IQ with change in blood Pb level are those derived for the subsets of children in the Rochester and Boston cohorts for which peak blood Pb levels were <10 μg/dL; these slopes, in terms of IQ points per μg/dL blood Pb, are −1.8 (for concurrent blood Pb influence on IQ) and −1.6 (for 24-month blood Pb influence on IQ), respectively. The mean blood Pb levels for children in these subsets of the Rochester and Boston cohorts are 3.32 (Canfield, 2008) and 3.8 μg/dL (Bellinger, 2008), respectively, which are the lowest population mean levels among the datasets included in the table. Other studies with analyses involving similarly low blood Pb levels (

e.g.

, mean levels below 4 μg/dL) also had slopes steeper than −1.5 points per μg/dL blood Pb. These include the slope of −1.71 points per μg/dL blood Pb

for the subset of 24-month old children in the Mexico City cohort with blood Pb levels less than 5 μg/dL (n=193), for which the mean concurrent blood Pb level was 2.9 μg/dL (Tellez-Rojo

et al.

2006, 2008),

and the slope of −2.94 points per μg/dL blood Pb for the subset of 6-10 year old children whose peak blood Pb levels never exceeded 7.5 μg/dL (n=112), and for which the mean concurrent blood Pb level was 3.24 μg/dL (Lanphear

et al.

2005; Hornung 2008a). Thus, from these subset analyses, the slopes range from −1.71 to −2.94 IQ points per μg/dL of concurrent blood Pb, as shown in the first set of slopes in Table 1. In this first set are studies that included quantitative relationships for IQ and blood Pb that focused on lower individual blood Pb levels (below 7.5 μg/dL). We also note that for blood Pb levels up to approximately 3.7 μg/dL, the slope of the nonlinear C-R function in which greatest confidence is placed in estimating IQ loss in the quantitative risk assessment (the LLL function)

falls intermediate between these two values.

This slope reflects effects on cognitive development in this cohort of 24-month old children based on the age-appropriate test described earlier, and is similar in magnitude to slopes for the cohorts of older children described here. The strengths and limitations of this age-appropriate test, the Mental Development Index (MDI) of the Bayley Scales of Infant Development (BSID), were discussed in a letter to the editor by Black and Baqui (2005). The letter states that “the MDI is a well-standardized, psychometrically strong measure of infant mental development.” The MDI represents a complex integration of empirically-derived cognitive skills, for example, sensory/perceptual acuities, discriminations, and response; acquisition of object constancy; memory learning and problem solving; vocalization and beginning of verbal communication; and basis of abstract thinking. Black and Baqui additionally state that although the MDI is one of the most well-standardized, widely used assessment of infant mental development, evidence indicates low predictive validity of the MDI for infants younger than 24 months to subsequent measures of intelligence. They explain that the lack of continuity may be partially explained by “the multidimensional and rapidly changing aspects of infant mental development and by variations in performance during infancy, variations in tasks used to measure intellectual functioning throughout childhood, and variations in environmental challenges and opportunities that may influence development.” Martin and Volkmar (2007) also noted that correlations between BSID performance and subsequent IQ assessments were variable, but they also reported high test-retest reliability and validity, as indicated by the correlation coefficients of 0.83 to 0.91, as well as high interrater reliability, correlation coefficient of 0.96, for the MDI. Therefore, the BSID has been found to be a reliable indicator of current development and cognitive functioning of the infant. Martin and Volkmar (2007) further note that “for the most part, performance on the BSID does not consistently predict later cognitive measures, particularly when socioeconomic status and level of functioning are controlled”.

In this study, the slope for blood Pb levels between 5 and 10 μg/dL (population mean blood Pb of 6.9 μg/dL; n=101) was −0.94 points per μg/dL blood Pb but was not statistically significant, with a p value of 0.12. The difference in the slope between the <5 μg/dL and the 5-10 μg/dL groups was not statistically significant (Tellez-Rojo

et al.

, 2006; Tellez-Rojo, 2008).

The LLL function is the loglinear function from Lampshear

et al.

(2005), with linearization at low exposures (as described in sections 2.1.5 and 4.1.1.2 ofthe Risk Assessment Report).

Table 1—Summary of Quantitative Relationships of IQ and Blood P

for Two Sets of Studies Discussed Above

Study/analysis

Study cohort

Analysis dataset

Range BLL

(μg/dL)

Geometric mean BLL

(μg/dL)

Form of model from which

average slope

derived

Average linear slope

(points per μg/dL)

Set of studies from which steeper slopes are drawn in the proposal

Tellez-Rojo <5 subgroup

Mexico City, age 24 mo

Children—BLL<5 μg/dL

193

0.8-4.9

2.9

Linear

−1.71

based on Lanphear et al 2005

, Log-linear with low-exposure linearization (LLL)

Dataset from which the log-linear function is derived is the pooled International dataset of 1333 children, age 6-10 yr, having median blood Pb of 9.7 μg/dL and 5th-95th percentile of 2.5-33.2 μg/dL.

LLL

: −2.29 at 2 μg/dL

−1.89 at 3 μg/dL

Lanphear et al. 2005

, <7.5 peak subgroup

Pooled International, age 6-10 yr

Children—peak BLL <7.5 μg/dL

103

0.9-7.4

3.24

Linear

−2.94

Set of studies with shallower slopes (Criteria Document Table 6-1) presented in the proposal

Canfield et al 2003

, <10 peak subgroup

Rochester, age 5 yr

Children—peak BLL <10 μg/dL

0.5-8.4

3.32

Linear

−1.79

Bellinger and Needleman 2003

Boston

Children—peak BLL <10 μg/dL

1-9.3

3.8

Linear

−1.56

Tellez-Rojo et al. 2006

Mexico City, age 24 mo

Full dataset

294

0.8-9.8

4.28

Linear

−1.04

Tellez-Rojo et al. 2006 full—loglinear

Mexico City, age 24 mo

Full dataset

294

0.8-9.8

4.28

Log-linear

−0.94

Lanphear et al. 2005

, <10 peak

subgroup

Pooled International, age 6-10 yr

Children—peak BLL <10 μg/dL

244

0.1-9.8

4.30

Linear

−0.80

Al-Saleh et al 2001 full—loglinear

Saudi Arabia, age 6-12 yr

Full dataset

533

2.3-27.36

7.44

Log-linear

−0.76

Kordas et al 2006, <12 subgroup

Torreon, Mexico, age 7 yr

Children—BLL <12 μg/dL

377

2.3-<12

7.9

Linear

−0.40

Lanphear et al 2005

full—loglinear

Pooled International, age 6-10 yr

Full dataset

1333

0.1-71.7

9.7 (median)

Log-linear

−0.41

Median value

−0.9

Blood Pb level (BLL) information provided here is drawn from publications listed in table, in some cases augmented by study authors (Bellinger, 2008; Canfield, 2008a,b; Hornung, 2008a,b; Kordas, 2008; Tellez-Rojo, 2008).

Average linear slope estimates here are for relationship between IQ and concurrent blood Pb levels (BLL), except for Bellinger & Needleman which used 24 month BLLs with 10 year old IQ.

The Lanphear et al. 2005 pooled International study includes blood Pb data from the Rochester and Boston cohorts, although for different ages (6 and 5 years, respectively) than the ages analyzed in Canfield et al 2003 and Bellinger and Needleman 2003.

The LLL function (described in section II.C.2.b) was developed from Lanphear et al 2005 loglinear model with a linearization of the slope at BLL below 1 μg/dL. In estimating IQ loss with this function in the risk assessment (section II.A.3) the nonlinear form of the model with varying slope was used for all BLL above 1 μg/dL. The slopes shown are the average slopes (IQ points per μg/dL blood Pb) associated with application of the LLL functions from zero to the blood Pb levels identified (2 and 3 μg/dL).

These studies and quantitative relationships are discussed in the Criteria Document (CD, sections 6.2, 6.2.1.3 and 8.6.2).

The BLL for Bellinger and Needleman (2003) are for age 24 months.

For nonlinear models, this is the estimated average slope for change in IQ with change in blood Pb over the range from the 10th percentile blood Pb value in study to 10 μg/dL (CD, p. 6-65). The shape of these models is such that the average slopes from the 10th percentiles to a value lower than 10 μg/dL are larger negative values than those shown here (e.g., the slopes to 5 μg/dL are 50% larger negative values).

69% of children in Al-Saleh

et al.

(2001) study had BLL<10 μg/dL.

3. Overview of Human Exposure and Health Risk Assessments

To put judgments about risk associated with exposure to air-related Pb in a broader public health context, EPA developed and applied models to estimate human exposures to air-related Pb and associated health risk for various air quality scenarios and alternative standards. The design and implementation of the risk assessment needed to address significant limitations and complexity that go far beyond the situation for similar assessments typically performed for other criteria pollutants. The multimedia and persistent nature of Pb and the role of multiple exposure pathways add significant complexity as compared with other criteria pollutants that focus only on the inhalation exposure. Not only was the risk assessment constrained by the timeframe allowed for this review in the context of the breadth of information to address, it was also constrained by significant limitations in data and modeling tools for the assessment, as described in section II.C.2.h of the proposal.

The scope and methodology for this assessment were developed over the last few years with considerable input from the CASAC Pb Panel and the public, as described in the proposal (section II.C.2.a).

The following sections provide a brief summary of the quantitative exposure and risk assessment and key findings. The complete full-scale assessment, including the associated uncertainties, is more fully summarized in section II.C of the proposal and described in detail in the Risk Assessment Report (USEPA, 2007b).

In their review of the final risk assessment, CASAC expressed strong support, stating that “[t]he Final Risk Assessment report captures the breadth of issues related to assessing the potential public health risk associated with lead exposures; it competently documents the universe of knowledge and interpretations of the literature on lead toxicity, exposures, blood lead modeling and approaches for conducting risk assessments for lead” (Henderson, 2008a, p. 4).

a. Design Aspects and Associated Uncertainties

As discussed in section II.C.2 of the proposal, EPA conducted exposure and risk analyses to estimate blood Pb and associated IQ loss in children exposed to air-related Pb. As recognized in section II.A.2 above and discussed in the proposal notice and Criteria Document, among the wide variety of health endpoints associated with Pb exposures, there is general consensus

that the developing nervous system in children is among, if not, the most sensitive, and that neurobehavioral effects (specifically neurocognitive deficits), including IQ decrements, appear to occur at lower blood Pb levels than previously believed. 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).

CASAC advice on the design of the risk assessment is summarized in section II.C.2.a of the proposal.

The brief summary provided here focuses on blood Pb and risk estimates for five case studies

that generally represent two types of population exposures: (1) More highly air-pathway exposed children (as described below) residing in small neighborhoods or localized residential areas with air concentrations somewhat near the standard being evaluated, and (2) location-specific urban populations with a broader range of air-related exposures.

A sixth case study (the secondary Pb smelter case study) is also described in the Risk Assessment Report. However, as discussed in Section 4.3.1 of that document (USEPA, 2007a), significant limitations in the approaches have contributed to large uncertainties in the corresponding estimates.

The case studies representing the more highly air-pathway exposed children are the general urban case study and the primary Pb smelter case study. The general urban case study case study is not based on a specific geographic location and reflects several simplifications in representing exposure including uniform ambient air Pb levels associated with the standard of interest across the hypothetical study area and a uniform study population. Additionally, the method for simulating temporal variability in air Pb concentrations in this case study relied on national average estimates of the relationships between air concentrations in terms of the statistics considered for different forms of the standard being assessed and the annual ambient air concentrations required for input to the blood Pb model.

Thus, while this case study provides characterization of risk to children that are relatively more highly air pathway exposed (as compared to the location-specific case studies), this case study is not considered to represent a high-end scenario with regard to the characterization of ambient air Pb levels and associated risk. The primary Pb smelter case study provides risk estimates for children living in a specific area that is currently not in attainment with the current NAAQS. We have focused on a subarea within 1.5 km of the facility where airborne Pb concentrations are closest to the current standard and where children's air-related exposures are most impacted by emissions associated with the Pb smelter from which air Pb concentrations were estimated.

As the blood Pb model used in the risk assessment was limited in that it did not accept inputs of a temporal time step shorter than annual average, ratios of relationships in the available air monitoring data between different statistical forms being considered for the standard and an annual average were employed for the urban case studies (that did not rely on dispersion modeling) as a method of simulating the temporal variability in air Pb concentrations that occurs as a result of meteorology, source and emissions characteristics.

The three location-specific urban case studies focus on specific residential areas within Cleveland, Chicago, and Los Angeles to provide representations of urban populations with a broader range of air-related exposures due to spatial gradients in both ambient air Pb levels and population density. For example, the highest air concentrations in these case studies (

i.e.

, those closest to the standard being assessed) are found in very small parts of the study areas, while a large majority of the case study populations reside in areas with much lower air concentrations.

Based on the nature of the population exposures represented by the two categories of case study, the first category (the general urban and primary Pb smelter case studies) relates more closely to the air-related IQ loss evidence-based framework described in the proposal (sections II.D.2.a.ii and II.E.3.a) with regard to estimates of air-related IQ loss. As mentioned above, these case studies, as compared to the other category of case studies, include populations that are relatively more highly exposed by way of air pathways to air Pb concentrations somewhat near the standard level evaluated.

The air quality scenarios assessed include (a) the current NAAQS (for all five case studies);

(b) current conditions for the location-specific

and general urban case studies (which are below the current NAAQS); and (c) a range of alternate standard levels (for all case studies). The alternative NAAQS scenarios included levels of 0.50, 0.20, 0.05 and 0.02 μg/m

, with a form of maximum monthly average, as well as a level of 0.20 μg/m

, with a form of maximum quarterly average. Details of the assessment scenarios, including the Pb concentrations for other media are presented in Sections 2.3 and 5.1.1 of the Risk Assessment Report (USEPA, 2007b).

The current NAAQS scenario for the urban case studies assumes ambient air Pb concentrations higher than those currently occurring in nearly all urban areas nationally. 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 roll-up procedure used for the location-specific urban case studies (as described in Section II.C.2.h of the proposal), this scenario was included for those case studies to provide perspective on potential risks associated with raising levels to the point that the highest level across the study area just meets the current NAAQS. This scenario was simulated for the location-specific urban case studies using a proportional roll-up procedure. For the general urban case study, the maximum quarterly average ambient air concentration was set equal to the current NAAQS.

Current conditions for the three location-specific urban case studies in terms of maximum quarterly average air Pb concentrations were 0.09, 0.14 and 0.36 μg/m

for the study areas in Los Angeles, Chicago and Cleveland, respectively.

Exposure and associated blood Pb levels were simulated using the IEUBK model, as more fully described and presented in the Risk Assessment Report (USEPA, 2007b). Because of the nonlinear response of blood Pb to exposure and also the nonlinearity reflected in the C-R functions for estimation of IQ loss, this assessment first estimated total blood Pb and risk (air- and nonair-related), and then separated out those estimates of blood Pb and associated risk associated with the pathways of interest in this review. We separated out the estimates of total (all-pathway) blood Pb and IQ loss into a background category and two air-related categories (referred to as “recent air” and “past air”). However, significant limitations in our modeling tools and data resulted in an inability to parse specific risk estimates into specific pathways, such that we have approximated estimates for the air-related and background categories.

Those Pb exposure pathways tied most directly to ambient air, which consequently have the potential to respond relatively more quickly to changes in air Pb (

i.e.

, inhalation and ingestion of indoor dust Pb derived from the infiltration of ambient air Pb indoors), were placed into the “recent air” category. The other air-related Pb exposure pathways, all of which are associated with atmospheric deposition, were placed into the “past air” category. These include ingestion of Pb in outdoor dust/soil and ingestion of the portion of Pb in indoor dust that after deposition from ambient air outdoors is carried indoors with humans (as noted in section II.A.1 above).

Among the limitations affecting our estimates for the air-related and background categories is the apportionment of background (nonair) pathways. For example, while conceptually indoor Pb paint

contributions to indoor dust Pb would be considered background and included in the “background” category for this assessment, due to technical limitations related to indoor dust Pb modeling, dust from Pb paint was included as part of “other” indoor dust Pb (

i.e.

, as part of past air exposure). The inclusion of indoor paint Pb as a component of “other” indoor dust Pb (and consequently as a component of the “past air” category) represents a source of potential high bias in our prediction of exposure and risk associated with the “past air” category because conceptually, exposure to indoor paint Pb is considered part of background exposure. At the same time, Pb in ambient air does contribute to the exposure pathways included in the “background” category (drinking water and diet), and is likely a substantial contribution to diet (CD, p. 3-48). We could not separate the air contribution from the nonair contributions, and the total contribution from both the drinking water and diet pathways are categorized as “background” in this assessment. As a result, our “background” risk estimate includes some air-related risk representing a source of potential low bias in our predictions of air-related risk.

Further, we note that 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) only the exposure pathways categorized as “recent air” (inhalation and ingestion of that portion of indoor dust associated with outdoor ambient air) were varied with changes in air concentration. The assessment did not simulate decreases in “past air” 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).

These exposures were held constant across all air quality scenarios.

Similarly, since dietary Pb was included within “background”, reductions in dietary Pb,

e.g.

, as a result of reduced deposition to crops, were also not simulated.

In comparing total risk estimates between alternate NAAQS scenarios, 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.

In summary, because of limitations in the assessment design, data and modeling tools, our risk estimates for the “past air” category include both risks that are truly air-related and potentially, some background risk. Because we could not sharply separate Pb linked to ambient air from Pb that is background, some of the three categories of risk are underestimated and others overestimated. On balance, we believe this limitation leads to a slight overestimate of the risks in the “past air” category. At the same time, as discussed above, the “recent air” category does not fully represent the risk associated with all air-related pathways. Thus, we consider the risk attributable to air-related exposure pathways to be 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.

As discussed in the proposal notice and in greater detail in the Staff Paper and Risk Assessment Report, exposure and risk modeling conducted for this analysis was complex and subject to significant uncertainties due to limitations, data, models and time available. Key assumptions, limitations and uncertainties, which were recognized in various ways in the assessment and presentation of results, are listed here, beginning with those related to design of the assessment or case studies, followed by those related to estimation of Pb concentrations in ambient air, indoor dust, outdoor soil/dust, and blood, and estimation of Pb-related IQ loss.

•

Temporal Aspects:

During the 7-year exposure period, media concentrations remain fixed and the simulated child remains at the same residence (while exposure factors and physiological parameters are adjusted to match the age of the child).

•

General Urban Case Study:

The design for this case study employs assumptions regarding uniformity that are reasonable in the context of a small neighborhood population, but would contribute significant uncertainty to extrapolation of these estimates to a specific urban location, particularly a relatively large one. Thus, the risk estimates for this general urban 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 large urban population.

•

Location-Specific Urban Case Studies:

Limitations in the ambient air monitoring network limit our characterization of spatial gradients of ambient air Pb levels in these case studies.

•

Air Quality Simulation:

The proportional roll-up and roll-down procedures used in some case studies to simulate current NAAQS and alternate NAAQS levels, respectively, assume proportional changes in air concentrations across the study area in those scenarios for those case studies. EPA recognizes that it is extremely unlikely that Pb concentrations would rise to just meet the current NAAQS in urban areas nationwide and that there is substantial uncertainty with our simulation of such conditions in the urban location-specific case studies. There is also significant uncertainty in simulation conditions associated with the implementation of emissions reduction actions to meet a lower standard.

• Outdoor Soil/Dust Pb Concentrations:

Uncertainty regarding soil/dust Pb levels and the inability to simulate the influence of changing air Pb levels related to lowering the NAAQS contributes uncertainty to air-related risk estimates.

• Indoor Dust Pb Concentrations:

Limitations and uncertainty in modeling of indoor dust Pb levels, including the impact of reductions in ambient air Pb levels, contributes uncertainty to air-related risk estimates.

•

Interindividual Variability in Blood Pb Levels:

Uncertainty related to population variability in blood Pb levels and limitations in modeling of this introduces significant uncertainty into blood Pb and IQ loss estimates for the 95th percentile of the population.

•

Pathway Apportionment for Higher Percentile Blood Pb and IQ Loss:

Limitations in data, modeling tools and assessment design introduce uncertainty into estimates of air-related blood Pb and IQ loss for the upper ends of population distribution.

•

IQ Loss Concentration-Response Functions:

Specification of the quantitative relationship between blood Pb level and IQ loss is subject to significant uncertainty at lower blood Pb levels (

e.g.

, below 5 μg/dL concurrent blood Pb).

b. Summary of Blood Pb Estimates

Key observations regarding the blood Pb estimates from this analysis are noted here:

• As shown in Table 2 of the proposal (73 FR 29215), median blood Pb levels for the current conditions air quality scenario in the urban case studies ranged from 1.7-1.8 μg/dL for the location-specific case studies up to 1.9 μg/dL for the general urban case study. These values are slightly larger than the median value from NHANES for children aged 1-5 years old in 2003-2004 of 1.6 μg/dL (

http://www.epa.gov/envirohealth/children/body_burdens/

b1-table.htm

). Blood Pb level estimates for the 90th percentile in the urban case studies are also higher than the NHANES 90th percentile blood Pb levels. We note, however, that ambient air Pb levels in the urban case studies are higher than those at most monitoring sites in the U.S., as described in section II.C.3.a of the proposal.

• With regard to air-to-blood ratios, estimates for the general urban case study ranged from 1:2 to 1:9 with the majority of the estimates ranging from 1:4 to 1:6.

Because the risk assessment only reflects the impact of reductions on recent air-related pathways in predicting changes in indoor dust Pb for the general urban case study (as noted in section II.C.3.a of the proposal), however, the ratios generated are lower than they would be if they had also reflected other air-related pathways (

e.g.

, changes in outdoor surface soil/dust and dietary Pb with changes in ambient air Pb).

The ratios increase as the level of the alternate standard decreases. This reflects the nonlinearity in the Pb response, which is greater on a per-unit basis for lower ambient air Pb levels.

• Air-to-blood ratios estimated for the primary Pb smelter subarea ranged from 1:10 and higher.

One reason for these estimates being higher than those for the urban case study may be that the dust Pb model used may somewhat reflect ambient air-related pathways other than that of ambient air infiltrating a home.

For the primary Pb smelter (full study area), for which limitations are noted in section II.C.2.c of the proposal, the air-to-blood ratio estimates, presented in section 5.2.5.2 of the Risk Assessment Report (USEPA, 2007b), ranged from 1:3 to 1:7. As in the other case studies, ratios are higher at lower ambient air Pb levels. It is noted that the underlying changes in both ambient air Pb and blood Pb across standard levels are extremely small, introducing uncertainty into ratios derived using these data.

c. Summary of IQ Loss Estimates

As described more fully in the proposal notice and in the Risk Assessment Report (USEPA, 2007b, section 5.3.1), four sets of IQ loss estimates were derived from the blood Pb estimates, one for each of four concentration-response functions derived from the international pooled analysis by Lanphear and others (2005). Each of these four functions utilizes a different approach for characterizing low-exposure IQ loss, thereby providing a range of estimates intended to reflect the uncertainty in this key aspect of the risk assessment. As described in section II.C.2.b of the proposal (and in more detail in section 2.1.5 of the Risk Assessment Report), we have placed greater confidence in the log-linear function with low-exposure linearization (LLL) and present risk estimates based on that function here.

As shown in the presentation in the Staff Paper (section 4.4), risk estimates for the LLL function are generally bounded by estimates based on the other three C-R functions included in the assessment.

The risk estimates summarized here are those considered most relevant to the review in considering whether the current NAAQS and potential alternative NAAQS provide protection of public health with an adequate margin of safety (i.e., estimates of IQ loss associated with air-related Pb exposure). In considering these estimates, we note that IQ loss associated with air-related Pb is bounded on the low end by risk associated with the

recent air

category of exposure pathways and on the upper end by the

recent plus past air

categories of pathways (as described above in section II.A.3.a). Key observations regarding the median estimates

of air-related risk for the current NAAQS and alternative standards include:

Because of greater uncertainty in characterizing high-end population risk, and specifically related to pathway apportionment of IQ loss estimates for high-end percentiles, results discussed here focus on those for the population median.

• As shown in Table 2 below (Table 3 in the proposal), in all five case studies, the lower bound of population median air-related risk associated with the current NAAQS exceeds 2 points IQ loss, and the upper bound is near or above 4 points.

As noted in Table 2 below and sections II.C.2.d and II.C.2.h of the proposal, with regard to associated limitations and uncertainties, a proportional roll-up procedure was used to estimate air Pb concentrations in this scenario for the location-specific case studies.

• Alternate standards provide substantial reduction in estimates of air-related risk across the full set of alternative NAAQS considered, particularly for the lower bound of air-related risk which includes only the pathways that were varied with changes in air concentrations (as shown in Table 2).

• In the general urban case study, the estimated population median air-related risk falls between 1.9 and 3.6 points IQ loss for an alternative NAAQS of 0.50 μg/m

, maximum monthly average, between 1.2 and 3.2 points IQ loss for an alternative NAAQS of 0.20 μg/m

and between 0.5 and 2.8 points IQ loss for an alternate NAAQS of 0.05 μg/m

, maximum monthly average, (as shown in Table 2). Higher risk estimates are associated with a maximum quarterly averaging time (USEPA, 2007b).

• At each NAAQS level assessed, the upper bound of population median air-related risk for the primary Pb smelter subarea, which due to limitations in modeling is the only air-related risk estimate for this case study, is generally higher than that for the general urban case study, likely due to differences in the indoor dust models used for the two case studies (as discussed in section II.C.3.b of the proposal).

• Compared to the other case studies, the air-related risk for the location-specific case studies is smaller because of the broader range of air-related exposures and the population distribution. For example, the majority of the populations in each of the location-specific case studies resides in areas with ambient air Pb levels well below each standard level assessed, particularly for standard levels above 0.05 μg/m

, maximum monthly average. Consequently, risk estimates for these case studies indicate little response to alternative standard levels above 0.05 μg/m

maximum monthly average (as shown in Table 2).

Table 2—Summary of Risk Attributable to Air-related P

Exposure

NAAQS level simulated

(μg/m

max monthly, except as noted below)

Median air-related IQ loss

General urban case study

Primary Pb smelter (subarea) case study

B C

Location-specific urban case studies

Cleveland

(0.56 μg/m

)

Chicago

(0.31 μg/m

)

Los Angeles

(0.17 μg/m

)

1.5 max quarterly

3.5-4.8

(1.5-7.7)

<(3.2-9.4)

2.8-3.9

(0.6-4.6)

3.4-4.7

(1.4-7.4)

2.7-4.2

(1.1-6.2)

0.5

1.9-3.6

(0.7-4.8)

<4.5

<(2.1-7.7)

0.6-2.9

(0.2-3.9)

(

)

(

)

0.2

1.2-3.2

(0.4-4.0)

<3.7

<(1.2-5.1)

0.6-2.8

(0.1-3.2)

0.6-2.9

(0.3-3.6)

0.7-2.9

(0.2-3.5)

0.05

0.5-2.8

(0.2-3.3)

<2.8

<(0.9-3.4)

0.1-2.6

(<0.1-3.1)

0.2-2.6

(0.1-3.2)

0.3-2.7

(0.1-3.2)

0.02

0.3-2.6

(0.1-3.1)

<2.9

<(0.9-3.3)

<0.1-2.6

(<0.1-3.0)

0.1-2.6

(<0.1-3.1)

0.1-2.6

(<0.1-3.1)

—Air-related risk is bracketed by “recent air” (lower bound of presented range) and “recent” plus “past air” (upper bound of presented range). While differences between standard levels are better distinguished by differences in the “recent” plus “past air” estimates (upper bounds shown here), these differences are inherently underestimates. The term “past air” includes contributions from the outdoor soil/dust contribution to indoor dust, historical air contribution to indoor dust, and outdoor soil/dust pathways; “recent air” refers to contributions from inhalation of ambient air Pb or ingestion of indoor dust Pb predicted to be associated with outdoor ambient air Pb levels, with outdoor ambient air also potentially including resuspended, previously deposited Pb (see section II.C.2.e of the proposal). Boldface values are estimates generated using the log-linear with low-exposure linearization function. Values in parentheses reflect the range of estimates associated with all four concentration-response functions.

—In the case of the primary Pb smelter case study, only recent plus past air estimates are available.

—Median air-related IQ loss estimates for the primary Pb smelter (full study area) range from <1.7 to <2.9 points, with no consistent pattern across simulated NAAQS levels. This lack of a pattern reflects inclusion of a large fraction of the study population with relatively low ambient air impacts such that there is lower variation (at the population median) across standard levels (see section 4.2 of the Risk Assessment, Volume 1).

—This corresponds to roughly 0.7-1.0 μg/m

maximum monthly mean, across the urban case studies.

—A “roll-up” was performed so that the highest monitor in the study area is increased to just meet this level.

—A “roll-up” to this level was not performed.

—A “roll-up” to this level was not performed; these estimates are based on current conditions in this area.

B. Need for Revision of the Current Primary Standard

The initial issue to be addressed in the current review of the primary Pb standard is whether, in view of the advances in scientific knowledge reflected in the Criteria Document and Staff Paper, the existing standard should be revised. In evaluating whether it is appropriate to revise the current standard, the Administrator builds on 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. The approach used 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. The Administrator has taken into account both evidence-based and quantitative exposure- and risk-based considerations in developing conclusions on the adequacy of the current primary Pb standard.

The Administrator's proposed conclusions on the adequacy of the current primary standard are summarized below in the Introduction (section II.B.1), followed by consideration of comments received on the proposal (section II.B.2) and the Administrator's final decision with regard to the need for revision of the current primary standard (II.B.3).

1. Introduction

As described in section II.D.1.a of the proposal, the current 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 standard was set to provide protection against anemia (as well as effects associated with higher exposures), with consideration of impacts on the heme synthesis pathway leading to anemia (43 FR 46252-46253). In setting the standard, EPA determined that “the maximum safe level of blood lead for an individual child” should be no higher than 30 μg/dL, and described 15 μg/dL Pb as “the maximum safe blood lead level (geometric mean) for a population of young children” (43 FR 46247, 46253). The basis for the level, averaging time, form and indicator are described in section II.D.1.a of the proposal.

As noted in the proposal, the body of available evidence today, summarized above in section II.A.2 and in section II.B of the proposal, and discussed in the Criteria Document, is substantially expanded from that available when the current standard was set three decades ago. The Criteria Document presents evidence of the occurrence of health effects at appreciably lower blood Pb levels than those demonstrated by the evidence at the time the standard was set. Further, subsequent to the setting of the standard, the Pb NAAQS criteria review during the 1980s and the current review have provided “(a) increasingly stronger evidence that substantiatied still lower fetal and/or postnatal Pb-exposure levels (indexed by blood-Pb levels extending to as low as 10 to 15 μg/dL or, possibly, below) as being associated with slowed physical and neurobehavioral development, lower IQ, impaired learning, and/or other indicators of adverse neurological impacts; and (b) other pathophysiological effects of Pb on cardiovascular function, immune system components, calcium and vitamin D metabolism and other selected health endpoints” (CD, pp. 8-24 to 8-25). This evidence is discussed fully in the Criteria Document.

In the proposal, EPA explained its evidence-based considerations regarding the adequacy of the current standard. With regard to the sensitive population, while the sensitivity of the elderly and other particular subgroups is recognized, as at the time the current standard was set, young children continue to be recognized as a key sensitive population for Pb exposures.

With regard to the exposure levels at which adverse health effects occur, the proposal noted that 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 evidence is reflected in

changes over the intervening years in the CDC's identification and description of their advisory level for Pb in individual children's blood (as described above in section II.A.2.a). The current evidence indicates the occurrence of a variety of health effects, including neurological effects in children, associated with blood Pb levels extending well below 10 μg/dL (CD, sections 6.2, 8.4 and 8.5). For example, as noted in the Criteria Document with regard to the neurocognitive effects in children, the “weight of overall evidence strongly substantiates likely occurrence of [this] type of effect in association with blood-Pb concentrations in range of 5-10 μg/dL, or possibly lower * * * Although no evident threshold has yet been clearly established for those effects, the existence of such effects at still lower blood-Pb levels cannot be ruled out based on available data.” (CD, p. 8-61). The Criteria Document further notes that any such threshold may exist “at levels distinctly lower than the lowest exposures examined in these epidemiological studies” (CD, p. 8-67).

In considering the adequacy of the current standard, the Staff Paper considered the evidence in the context of the framework used to determine the standard in 1978, as adapted to reflect the current evidence. In so doing, the Staff Paper recognized that the health effects evidence with regard to characterization of a threshold for adverse effects has changed since the standard was set in 1978, as have the Agency's views on the characterization of a safe blood Pb level. As summarized in the proposal (73 FR 29237-38) and described in the Staff Paper (section 5.4.1), parameters for this framework include estimates for average nonair blood Pb level, and air-to-blood ratio, as well as a maximum safe individual and/or geometric mean blood Pb level. For this last parameter, the Staff Paper for the purposes of this evaluation considered the lowest population mean blood Pb levels with which some neurocognitive effects have been associated in the evidence.

Based on the current evidence, the Staff Paper first concluded that young children remain the sensitive population of primary focus in this review and that “there is now no recognized safe level of Pb in children's blood and studies appear to show adverse effects at population mean concurrent blood Pb levels as low as approximately 2 μg/dL (CD, pp. 6-31 to 6-32; Lanphear

et al.

, 2000)” (USEPA, 2007c). The Staff Paper further stated that “while the nonair contribution to blood Pb has declined, perhaps to a range of 1.0-1.4 μg/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” (USEPA, 2007c). Adapting the framework employed in setting the standard in 1978, the Staff Paper concluded that “the more recently available evidence suggests a level for the standard that is lower by an order of magnitude or more” (USEPA, 2007c, p. 5-17).

Since completion of the Staff Paper and ANPR, the Agency further considered the evidence with regard to adequacy of the current standard using an approach other than the adapted 1978 framework considered in the Staff Paper. This alternative evidence-based

framework, referred to as the air-related IQ loss framework, shifts focus from identifying an appropriate target population mean blood lead level and instead focuses on the magnitude of effects of air-related Pb on neurocognitive functions. This framework builds on a recommendation by the CASAC Pb Panel to consider the evidence in a more quantitative manner, and is discussed in more detail in section II.E.3.a.ii of the proposal.

The term “evidence-based” as used here refers to the drawing of information directly from published studies, with specific attention to those reviewed and described in the Criteria Document, and is distinct from considerations that draw from the results of the quantitative exposure and risk assessment.

In this air-related IQ loss framework, EPA draws from the entire body of evidence as a basis for concluding that there are causal associations between air-related Pb exposures and population IQ loss.

We also draw more quantitatively from the evidence by using evidence-based C-R functions to quantify the association between air Pb concentrations and air-related population mean IQ loss. Thus, this framework more fully considers the evidence with regard to the concentration-response relationship for the effect of Pb on IQ than does the adapted 1978 framework, and it also draws from estimates for air-to-blood ratios.

For example, as stated in the Criteria Document, “Fortunately, there exists a large database of high quality studies on which to base inferences regarding the relationship between Pb exposure and neurodevelopment. In addition, Pb has been extensively studied in animal models at doses that closely approximate the human situation. Experimental animal studies are not compromised by the possibility of confounding by such factors as social class and correlated environmental factors. The enormous experimental animal literature that proves that Pb at low levels causes neurobehavioral deficits and provides insights into mechanisms must be considered when drawing causal inferences (Bellinger, 2004; Davis

et al.

, 1990; U.S. Environmental Protection Agency, 1986a, 1990).” (CD, p. 6-75).

In the proposal, while we noted the evidence of steeper slope for the C-R relationship for blood Pb concentration and IQ loss at lower blood Pb levels (described above in sections II.A.2.c), we stated that for purposes of consideration of the adequacy of the current standard we were concerned with the C-R relationship for blood Pb levels that would be associated with exposure to air-related Pb at the level of the current standard. For this purpose, we focused on a median linear estimate of the slope of the C-R function from study populations for which most blood Pb levels were below 10 μg/dL and for which a linear slope restricted to blood Pb levels below about 10 μg/dL could be estimated (described in CD, pp. 6-65 to 6-66 and summarized in section II.B.2.b of the proposal). The median slope estimate is −0.9 IQ points per μg/dL blood Pb (CD, p. 8-80). Applying estimates of air-to-blood ratios ranging from 1:3 to 1:5, drawing from the discussion of air-to-blood ratios in section II.B.1.c of the proposal, to a population of children exposed at the current level of the standard is estimated to result in an average air-related blood Pb level above 4 μg/dL.

Multiplying these blood Pb levels by the slope estimate, identified above, for blood Pb levels extending up to 10 μg/dL (−0.9 IQ points per μg/dL), would imply an average air-related IQ loss for such a group of children on the order of 4 or more IQ points.

This is based on the calculation in which 1.5 μg/m

is multiplied by a ratio of 3 μg blood Pb per 1 μg/m

air Pb to yield an air-related blood Pb estimates of 4.5 μg/dL; using a 1:5 ratio yields an estimate of 7.5 μg/dL. As with the 1978 framework considered in the Staff Paper, the context for use of the air-to-blood ratio here is a population being exposed at the level of the standard.

In the proposal, EPA also explained its exposure- and risk-based considerations regarding the adequacy of the current standard. EPA estimated exposures and health risks associated with air quality that just meets the current standard (as described in the Risk Assessment Report) to help inform judgments about whether or not the current standard provides adequate protection of public health, taking into account key uncertainties associated with the estimated exposures and risks (summarized above in section II.C of the proposal and more fully in the Risk

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