Vol. 80 Monday, 

No. 2 January 5, 2015 

Part II 

Environmental Protection Agency 

40 CFR Part 50 

National Ambient Air Quality Standards for Lead; Proposed Rule 

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278 Federal Register / Vol. 80, No. 2 / Monday, January 5, 2015 / Proposed Rules 

ENVIRONMENTAL PROTECTION 

AGENCY 

40 CFR Part 50 

[EPA–HQ–OAR–2010–0108; FRL–9915–57– 

OAR] 

RIN 2060–AQ44 

National Ambient Air Quality 

Standards for Lead 

AGENCY: Environmental Protection 

Agency. 

ACTION: Proposed rule. 

SUMMARY: Based on the Environmental 

Protection Agency’s (EPA’s) review of 

the air quality criteria and the national 

ambient air quality standards (NAAQS) 

for lead (Pb), the EPA is proposing to 

retain the current standards, without 

revision. 

DATES: Comments must be received on 

or before April 6, 2015. 

Public Hearings: If, by January 26, 

2015, the EPA receives a request from a 

member of the public to speak at a 

public hearing concerning the proposed 

decision, we will hold a public hearing, 

with information about the hearing 

provided in a subsequent notice in the 

Federal Register. 

ADDRESSES: Submit your comments, 

identified by Docket ID No. EPA–HQ– 

OAR–2010–0108 by one of the following 

methods: 

• Federal eRulemaking Portal: http:// 

www.regulations.gov: Follow the on-line 

instructions for submitting comments. 

• Email: a-and-r-Docket@epa.gov. 

Include docket ID No. EPA–HQ–OAR– 

2010–0108 in the subject line of the 

message. 

• Fax: 202–566–9744. 

• Mail: Docket No. EPA–HQ–OAR– 

2010–0108, Environmental Protection 

Agency, Mail Code 28221T, 1200 

Pennsylvania Ave. NW., Washington, 

DC 20460. 

• Hand Delivery: Docket No. EPA– 

HQ–OAR–2010–0108, Environmental 

Protection Agency, EPA WJC West 

Building, Room 3334, 1301 Constitution 

Ave. NW., Washington, DC. Such 

deliveries are only accepted during the 

Docket’s normal hours of operation, and 

special arrangements should be made 

for deliveries of boxed information. 

Instructions: Direct your comments to 

Docket ID No. EPA–HQ–OAR–2010– 

0108. The EPA’s policy is that all 

comments received will be included in 

the public docket without change and 

may be made available online at 

www.regulations.gov, including any 

personal information provided, unless 

the comment includes information 

claimed to be Confidential Business 

Information (CBI) or other information 

whose disclosure is restricted by statute. 

Do not submit information that you 

consider to be CBI or otherwise 

protected through www.regulations.gov 

or email. The www.regulations.gov Web 

site is an ‘‘anonymous access’’ system, 

which means the EPA will not know 

your identity or contact information 

unless you provide it in the body of 

your comment. If you send an email 

comment directly to the EPA without 

going through www.regulations.gov, 

your email address will be 

automatically captured and included as 

part of the comment that is placed in the 

public docket and made available on the 

Internet. If you submit an electronic 

comment, the EPA recommends that 

you include your name and other 

contact information in the body of your 

comment and with any disk or CD–ROM 

you submit. If the EPA cannot read your 

comment due to technical difficulties 

and cannot contact you for clarification, 

the EPA may not be able to consider 

your comment. Electronic files should 

avoid the use of special characters, any 

form of encryption, and be free of any 

defects or viruses. For additional 

information about the EPA’s public 

docket, visit the EPA Docket Center 

homepage at http://www.epa.gov/

epahome/dockets.htm. 

Public Hearing: To request a public 

hearing or information pertaining to a 

public hearing on this document, 

contact Ms. Eloise Shepherd, Health and 

Environmental Impacts Division, Office 

of Air Quality Planning and Standards 

(C504–02), U.S. Environmental 

Protection Agency, Research Triangle 

Park, NC 27711; telephone number (919) 

541–5507; fax number (919) 541–0804; 

email address: shepherd.eloise@epa.gov. 

See the SUPPLEMENTARY INFORMATION for 

further information about a possible 

public hearing. 

Docket: All documents in the docket 

are listed on the www.regulations.gov 

Web site. This includes documents in 

the rulemaking docket (Docket ID No. 

EPA–HQ–OAR–2010–0108) and a 

separate docket, established for the 

Integrated Science Assessment for this 

review (Docket ID No. EPA–HQ–ORD– 

2011–0051) that has been incorporated 

by reference into the rulemaking docket. 

All documents in these dockets are 

listed on the www.regulations.gov Web 

site. Although listed in the index, some 

information is not publicly available, 

e.g., CBI or other information whose 

disclosure is restricted by statute. 

Certain other material, such as 

copyrighted material, is not placed on 

the Internet and may be viewed, with 

prior arrangement, at the EPA Docket 

Center. Publicly available docket 

materials are available either 

electronically in www.regulations.gov or 

in hard copy at the Air and Radiation 

Docket Information Center, EPA/DC, 

WJC West Building, 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 Information 

Center is (202) 566–1742. 

FOR FURTHER INFORMATION CONTACT: Dr. 

Deirdre L. 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; email: 

murphy.deirdre@epa.gov. To request a 

public hearing or information pertaining 

to a public hearing on this document, 

contact Ms. Eloise Shepherd, Health and 

Environmental Impacts Division, Office 

of Air Quality Planning and Standards 

(C504–02), U.S. Environmental 

Protection Agency, Research Triangle 

Park, NC 27711; telephone number (919) 

541–5507; fax number (919) 541–0804; 

email address: shepherd.eloise@epa.gov. 

SUPPLEMENTARY INFORMATION: 

General Information 

Preparing Comments for the EPA 

1. Submitting CBI. Do not submit this 

information to the EPA through 

www.regulations.gov or email. Clearly 

mark the part or all of the information 

that you claim to be CBI. For CBI 

information in a disk or CD–ROM that 

you mail to the EPA, mark the outside 

of the disk or CD–ROM as CBI and then 

identify electronically within the disk or 

CD–ROM the specific information that 

is claimed as CBI. In addition to one 

complete version of the comment that 

includes information claimed as CBI, a 

copy of the comment that does not 

contain the information claimed as CBI 

must be submitted for inclusion in the 

public docket. Information so marked 

will not be disclosed except in 

accordance with procedures set forth in 

40 CFR part 2. 

2. Tips for Preparing Your Comments. 

When submitting comments, remember 

to: 

• Identify the rulemaking by docket 

number and other identifying 

information (subject heading, Federal 

Register date and page number). 

• Follow directions—the agency may 

ask you to respond to specific questions 

or organize comments by referencing a 

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Federal Register / Vol. 80, No. 2 / Monday, January 5, 2015 / Proposed Rules 279 

1The 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.’’ See 

S. Rep. No. 91–1196, 91st Cong., 2d Sess. 10 (1970). 

2Welfare 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, manmade materials, animals, wildlife, weather, 

visibility and climate, damage to and deterioration 

of property, and hazards to transportation, as well 

as effects on economic values and on personal 

comfort and well-being.’’ 

Code of Federal Regulations (CFR) part 

or section number. 

• Explain why you agree or disagree, 

suggest alternatives, and substitute 

language for your requested changes. 

• Describe any assumptions and 

provide any technical information and/ 

or data that you used. 

• Provide specific examples to 

illustrate your concerns, and suggest 

alternatives. 

• Explain your views as clearly as 

possible, avoiding the use of profanity 

or personal threats. 

• Make sure to submit your 

comments by the comment period 

deadline identified. 

Availability of Information Related to 

This Action 

A number of the documents that are 

relevant to this action are available 

through the EPA’s Office of Air Quality 

Planning and Standards (OAQPS) 

Technology Transfer Network (TTN) 

Web site at http://www.epa.gov/ttn/

naaqs/standards/pb/s_pb_index.html. 

These documents include the Plan for 

Review of the National Ambient Air 

Quality Standards for Lead (USEPA, 

2011a), available at http://www.epa.gov/ 

ttn/naaqs/standards/pb/s_pb_2010_

pd.html, the Integrated Science 

Assessment for Lead (USEPA, 2013a), 

available at http://www.epa.gov/ttn/

naaqs/standards/pb/s_pb_2010_

isa.html, the Review of the National 

Ambient Air Quality Standards for 

Lead: Risk and Exposure Assessment 

Planning Document (USEPA, 2011b), 

available at http://www.epa.gov/ttn/

naaqs/standards/pb/s_pb_2010_

pd.html, and the Policy Assessment for 

the Review of the Lead National 

Ambient Air Quality Standards (USEPA, 

2014), available at http://www.epa.gov/

ttn/naaqs/standards/pb/s_pb_2010_

pa.html. These and other related 

documents are also available for 

inspection and copying in the EPA 

docket identified above. 

Information About a Possible Public 

Hearing 

To request a public hearing or 

information pertaining to a public 

hearing on this document, contact Ms. 

Eloise Shepherd, Health and 

Environmental Impacts Division, Office 

of Air Quality Planning and Standards 

(C504–02), U.S. Environmental 

Protection Agency, Research Triangle 

Park, NC 27711; telephone number (919) 

541–5507; fax number (919) 541–0804; 

email address: shepherd.eloise@epa.gov. 

Table of Contents 

The following topics are discussed in 

this preamble: 

I. Background 

A. Legislative Requirements 

B. Related Lead Control Programs 

C. Review of the Air Quality Criteria and 

Standards for Lead 

D. Multimedia, Multipathway Aspects of 

Lead 

E. Air Quality Monitoring 

II. Rationale for Proposed Decision on the 

Primary Standard 

A. General Approach 

1. Approach in the Last Review 

2. Approach for the Current Review 

B. Health Effects Information 

1. Array of Effects 

2. Critical Periods of Exposure 

3. Nervous System Effects in Children 

4. At-Risk Populations 

5. Potential Impacts on Public Health 

C. Blood Lead as a Biomarker of Exposure 

and Relationships With Air Lead 

D. Summary of Risk and Exposure 

Assessment Information 

1. Overview 

2. Summary of Design Aspects 

3. Key Limitations and Uncertainties 

4. Summary of Risk Estimates and Key 

Observations 

E. Conclusions on Adequacy of the Current 

Primary Standard 

1. Evidence-Based Considerations in the 

Policy Assessment 

2. Exposure/Risk-Based Considerations in 

the Policy Assessment 

3. CASAC Advice 

4. Administrator’s Proposed Conclusions 

on the Adequacy of the Current Primary 

Standard 

III. Rationale for Proposed Decision on the 

Secondary Standard 

A. General Approach 

1. Approach in the Last Review 

2. Approach for the Current Review 

B. Welfare Effects Information 

C. Summary of Risk Assessment 

Information 

D. Conclusions on Adequacy of the Current 

Secondary Standard 

1. Evidence- and Risk-Based 

Considerations in the Policy Assessment 

2. CASAC Advice 

3. Administrator’s Proposed Conclusions 

on the Adequacy of the Current Standard 

IV. Statutory and Executive Order Reviews 

A. Executive Order 12866: Regulatory 

Planning and Review and Executive 

Order 13563: Improving Regulation and 

Regulatory 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 

and 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. Determination Under Section 307(d) 

References 

I. Background 

A. Legislative Requirements 

Two sections of the Clean Air Act 

(CAA or the Act) govern the 

establishment and revision of the 

NAAQS. Section 108 (42 U.S.C. 7408) 

directs the Administrator to identify and 

list certain air pollutants and then to 

issue air quality criteria for those 

pollutants. The Administrator is to list 

those air pollutants that in her 

‘‘judgment, cause or contribute to air 

pollution which may reasonably be 

anticipated to endanger public health or 

welfare;’’ ‘‘the presence of which in the 

ambient air results from numerous or 

diverse mobile or stationary sources;’’ 

and ‘‘for which . . . [the Administrator] 

plans to issue air quality criteria . . .’’ 

Air quality criteria are intended to 

‘‘accurately reflect the latest scientific 

knowledge useful in indicating the kind 

and extent of all identifiable effects on 

public health or welfare which may be 

expected from the presence of [a] 

pollutant in the ambient air . . .’’ 42 

U.S.C. 7408(b). Section 109 (42 U.S.C. 

7409) directs the Administrator to 

propose and promulgate ‘‘primary’’ and 

‘‘secondary’’ NAAQS for pollutants for 

which air quality criteria are issued. 

Section 109(b)(1) defines a primary 

standard as one ‘‘the attainment and 

maintenance of which in the judgment 

of the Administrator, based on such 

criteria and allowing an adequate 

margin of safety, are requisite to protect 

the public health.’’ 1 A secondary 

standard, as defined in section 

109(b)(2), must ‘‘specify a level of air 

quality the attainment and maintenance 

of which, in the judgment of the 

Administrator, based on such criteria, is 

requisite to protect the public welfare 

from any known or anticipated adverse 

effects associated with the presence of 

[the] pollutant in the ambient air.’’ 2

The requirement that primary 

standards provide an adequate margin 

of safety was intended to address 

uncertainties associated with 

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3As used here and similarly throughout this 

notice, the term population (or group) refers to 

persons having a quality or characteristic in 

common, such as a specific pre-existing illness or 

a specific age or life stage. As discussed more fully 

in section II.B.4 below, the identification of 

sensitive groups (called at-risk groups or at-risk 

populations) involves consideration of 

susceptibility and vulnerability. 

4Lists of CASAC members and of members of the 

CASAC Lead Review Panel are available at: http:// 

yosemite.epa.gov/sab/sabproduct.nsf/WebCASAC/

CommitteesandMembership?OpenDocument. 

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. See Lead 

Industries Association v. EPA, 647 F.2d 

1130, 1154 (D.C. Cir 1980), cert. denied, 

449 U.S. 1042 (1980); American 

Petroleum Institute v. Costle, 665 F.2d 

1176, 1186 (D.C. Cir. 1981), cert. denied, 

455 U.S. 1034 (1982); American Farm 

Bureau Federation v. EPA, 559 F.3d 

512, 533 (D.C. Cir. 2009); Association of 

Battery Recyclers v. EPA, 604 F.3d 613, 

617–18 (D.C. Cir. 2010). 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 provide 

an adequate margin of safety, the 

Administrator is seeking not only to 

prevent pollution levels that have been 

demonstrated to be harmful but also to 

prevent lower pollutant levels that may 

pose an unacceptable risk of harm, even 

if the risk is not precisely identified as 

to nature or degree. 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 v. EPA, 647 F.2d at 1156 

n.51, but rather at a level that reduces 

risk sufficiently so as to protect public 

health with an adequate margin of 

safety. 

In addressing the requirement for an 

adequate margin of safety, the EPA 

considers such factors as the nature and 

severity of the health effects involved, 

the size of sensitive population(s) at 

risk,3 and the kind and degree of the 

uncertainties that must be addressed. 

The selection of any particular approach 

to providing an adequate margin of 

safety is a policy choice left specifically 

to the Administrator’s judgment. See 

Lead Industries Association v. EPA, 647 

F.2d at 1161–62. 

In setting primary and secondary 

standards that are ‘‘requisite’’ to protect 

public health and welfare, respectively, 

as provided in section 109(b), the EPA’s 

task is to establish standards that are 

neither more nor less stringent than 

necessary for these purposes. In so 

doing, the EPA may not consider the 

costs of implementing the standards. 

See generally, Whitman v. American 

Trucking Associations, 531 U.S. 457, 

465–472, 475–76 (2001). Likewise, 

‘‘[a]ttainability and technological 

feasibility are not relevant 

considerations in the promulgation of 

national ambient air quality standards.’’ 

American Petroleum Institute v. Costle, 

665 F.2d at 1185. 

Section 109(d)(1) requires that ‘‘not 

later than December 31, 1980, and at 5- 

year intervals thereafter, the 

Administrator shall complete a 

thorough review of the criteria 

published under section 108 and the 

national ambient air quality standards 

. . . and shall make such revisions in 

such criteria and standards and 

promulgate such new standards as may 

be appropriate. . . .’’ Section 109(d)(2) 

requires that an independent scientific 

review committee ‘‘shall complete a 

review of the criteria . . . and the 

national primary and secondary ambient 

air quality standards . . . and shall 

recommend to the Administrator any 

new . . . standards and revisions of 

existing criteria and standards as may be 

appropriate. . . .’’ Since the early 

1980s, this independent review function 

has been performed by the Clean Air 

Scientific Advisory Committee 

(CASAC).4

B. Related Lead Control Programs 

States are primarily responsible for 

ensuring attainment and maintenance of 

the NAAQS. 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 the EPA, also 

administer the Prevention of Significant 

Deterioration program (42 U.S.C. 7470– 

7479) for these pollutants. 

The NAAQS is only one component 

of the EPA’s programs to address Pb in 

the environment. Federal programs 

additionally provide for nationwide 

reductions in air 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); 

emissions standards for solid waste 

incineration units and the national 

emission standards for hazardous air 

pollutants (NESHAP) under sections 

129 (42 U.S.C. 7429) and 112 (42 U.S.C. 

7412) of the Act, respectively. 

The EPA has taken a number of 

actions associated with these air 

pollution control programs since the last 

review of the Pb NAAQS, including 

completion of several regulations which 

will result in reduced Pb emissions from 

stationary sources regulated under the 

CAA sections 112 and 129. For example, 

in January 2012, the EPA updated the 

NESHAP for the secondary lead 

smelting source category (77 FR 555, 

January 5, 2012). These amendments to 

the original maximum achievable 

control technology standards apply to 

facilities nationwide that use furnaces to 

recover Pb from Pb-bearing scrap, 

mainly from automobile batteries (15 

existing facilities, one under 

construction). By the effective date in 

2014, this action is estimated to result 

in a Pb emissions reduction of 13.6 tons 

per year (tpy) across the category (a 68% 

reduction). Somewhat lesser Pb 

emissions reductions are also expected 

from regulations completed in 2013 for 

commercial and industrial solid waste 

incineration units (78 FR 9112, February 

7, 2013), as well as several other 

regulations since 2007 (72 FR 73179, 

December 26, 2007; 72 FR 74088, 

December 28, 2007; 73 FR 225, 

November 20, 2008; 78 FR 10006, 

February 12, 2013; 76 FR 15372, March 

21, 2011; 78 FR 7138, January 31, 2013; 

74 FR 51368, October 6, 2009; Policy 

Assessment, Appendix 2A). 

The presentation below briefly 

summarizes additional ongoing 

activities that, although not directly 

pertinent to the review of the NAAQS, 

are associated with controlling 

environmental Pb levels and human Pb 

exposures more broadly. Among those 

identified are the EPA programs 

intended to encourage exposure 

reduction programs in other countries. 

Reducing Pb exposures has long been 

recognized as a federal priority as 

environmental and public health 

agencies continue to grapple with soil 

and dust Pb levels from the historical 

use of Pb in paint and gasoline and from 

other sources (Alliance to End 

Childhood Lead Poisoning, 1991; 62 FR 

19885, April 23, 1997; 66 FR 52013, 

October 11, 2001; 68 FR 19931, April 

23, 2003). A broad range of federal 

programs beyond those that focus on air 

pollution control provide for 

nationwide reductions in environmental 

releases and human exposures. For 

example, pursuant to section 1412 of the 

Safe Drinking Water Act (SDWA), the 

EPA regulates Pb in public drinking 

water systems through corrosion control 

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5Effective in January 2014, the amount of Pb 

permitted in pipes, fittings, and fixtures was 

lowered (see ‘‘Summary of the Reduction of Lead 

in Drinking Water Act and Frequently Asked 

Questions’’ at http://water.epa.gov/drink/info/lead/ 

index.cfm). 

6See, e.g., ‘‘Implementation of the MercuryContaining and Rechargeable Battery Management 

Act’’ at http://www.epa.gov/epawaste/hazard/

recycling/battery.pdf and ‘‘Municipal Solid Waste 

Generation, Recycling, and Disposal in the United 

States: Facts and Figures for 2005 http://

www.epa.gov/epawaste/nonhaz/municipal/pubs/

msw-2005.pdf. 

and other utility actions which work 

together to minimize Pb levels at the tap 

(40 CFR 141.80–141.91). Under section 

1417 of the SDWA, pipes, fittings and 

fixtures for potable water applications 

may not be used or introduced into 

commerce unless they are considered 

‘‘lead free’’ as defined by that Act (40 

CFR 141.43).5 Additionally, federal Pb 

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, June 18, 2003). 

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 (codified as Title IV of the Toxic 

Substances Control Act [TSCA]), the 

EPA has established regulations and 

associated programs in six categories: 

(1) Training, certification and work 

practice requirements for persons 

engaged in Pb-based paint activities 

(abatement, inspection and risk 

assessment); accreditation of training 

providers; and authorization of state and 

tribal Pb-based paint programs; (2) 

training, certification, and work practice 

requirements for persons engaged in 

home renovation, repair and painting 

(RRP) activities; accreditation of RRP 

training providers; and authorization of 

state and tribal RRP programs; (3) 

ensuring that, for most housing 

constructed before 1978, information 

about Pb-based paint and Pb-based paint 

hazards flows from sellers to 

purchasers, from landlords to tenants, 

and from renovators to owners and 

occupants; (4) establishing standards for 

identifying dangerous levels of Pb in 

paint, dust and soil; (5) providing grant 

funding to establish and maintain state 

and tribal Pb-based paint programs; and 

(6) providing information on Pb hazards 

to the public, including steps that 

people can take to protect themselves 

and their families from Pb-based paint 

hazards. The most recent rule issued 

under Title IV of TSCA is for the Lead 

Renovation, Repair and Painting 

Program (73 FR 21692, April 22, 2008), 

which became fully effective in April 

2010 and which applies to compensated 

renovators and maintenance 

professionals who perform RRP 

activities in housing and child-care 

facilities built prior to 1978. To foster 

adoption of the rule’s measures, the EPA 

has been conducting an extensive 

education and outreach campaign to 

promote awareness of these new 

requirements among both the regulated 

entities and the consumers who hire 

them (http://www2.epa.gov/lead/

renovation-repair-and-paintingprogram). In addition, the EPA is 

investigating whether Pb hazards are 

also created by RRP activities in public 

and commercial buildings, in which 

case the EPA plans to issue RRP 

requirements, where appropriate, for 

this class of buildings (79 FR 31072, 

May 30, 2014). 

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, the EPA 

determines and implements protective 

levels for Pb in soil at Superfund sites 

and RCRA corrective action facilities. 

Federal programs, including those 

implementing RCRA, provide for 

management of hazardous substances in 

hazardous and municipal solid waste 

(e.g., 66 FR 58258, November 20, 2001). 

Federal regulations concerning batteries 

in municipal solid waste facilitate the 

collection and recycling or proper 

disposal of batteries containing Pb.6

Similarly, federal programs provide for 

the reduction in environmental releases 

of hazardous substances such as Pb in 

the management of wastewater (http://

www.epa.gov/owm/). 

A variety of federal nonregulatory 

programs also provide for reduced 

environmental release of Pb-containing 

materials by encouraging 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 the 

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). 

The EPA’s research program 

identifies, encourages and conducts 

research needed to locate and assess 

serious risks and to develop methods 

and tools to characterize and help 

reduce risks related to Pb exposure. For 

example, the EPA’s Integrated Exposure 

Uptake Biokinetic Model for Lead in 

Children (IEUBK model) is widely used 

and accepted as a tool that informs the 

evaluation of site-specific data. More 

recently, in recognition of the need for 

a single model that predicts Pb 

concentrations in tissues for children 

and adults, the EPA has been 

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 (USEPA, 2006a, 

sections 4.4.5 and 4.4.8; USEPA, 2013a, 

section 3.6). The EPA’s research 

activities on substances including Pb, 

such as those identified here, focus on 

improving our characterization of health 

and environmental effects, exposure, 

and control or management of 

environmental releases (see http://

www.epa.gov/research/). 

Other federal agencies also participate 

in programs intended to reduce Pb 

exposures. For example, programs of the 

Centers for Disease Control and 

Prevention (CDC) provide for the 

tracking of children’s blood Pb levels in 

the U.S. and provide guidance on levels 

at which medical and environmental 

case management activities should be 

implemented (CDC, 2012; ACCLPP, 

2012). 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 continued to decline from levels 

observed in the past. For example, blood 

Pb levels for the general population of 

children 1 to 5 years of age have 

dropped to a geometric mean level of 

1.17 mg/dL in the 2009–2010 National 

Health and Nutrition Examination 

Survey (NHANES) as compared to the 

geometric mean in 1999–2000 of 2.23 

mg/dL and in 1988–1991 of 3.6 mg/dL 

(USEPA, 2013a, section 3.4.1; USEPA, 

2006a, AX4–2). Similarly, blood Pb 

levels in non-Hispanic black, Mexican 

American and lower socioeconomic 

groups, which are generally higher than 

those for the general population, have 

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7 International programs in which the U.S. 

participates, including those identified here, are 

described at: http://epa.gov/international/air/

pcfv.html, http://www.unep.org/transport/pcfv/, 

http://www.unep.org/hazardoussubstances/Home/

tabid/197/hazardoussubstances/LeadCadmium/

PrioritiesforAction/GAELP/tabid/6176/

Default.aspx. 

8The CEC was established to support cooperation 

among the North American Free Trade Agreement 

partners to address environmental issues of 

continental concern, including the environmental 

challenges and opportunities presented by 

continent-wide free trade. 

9 In the current review, these two documents have 

been combined in the Integrated Review Plan for 

the National Ambient Air Quality Standards for 

Lead (USEPA, 2011a). 

also declined (USEPA, 2013a, sections 

3.4.1, 5.2.3 and 5.2.4; Jones et al., 2009). 

The EPA also participates in a broad 

range of international programs focused 

on reducing environmental releases and 

human exposures in other countries. For 

example, the Partnership for Clean 

Fuels and Vehicles program engages 

governments and stakeholders in 

developing countries to eliminate Pb in 

gasoline globally.7 From 2007 to 2011, 

the number of countries known to still 

be using leaded gasoline was reduced 

from just over 20 to six, with three of 

the six also offering unleaded fuel. All 

six were expected to eliminate Pb from 

fuel in the near future (USEPA, 2011c). 

The EPA is a contributor to the Global 

Alliance to Eliminate Lead Paint, a 

cooperative initiative jointly led by the 

World Health Organization and the 

United Nations Environment 

Programme (UNEP) to focus and 

catalyze the efforts to achieve 

international goals to prevent children’s 

Pb exposure from paints containing Pb 

and to minimize occupational exposures 

to Pb paint. This alliance has the broad 

objective of promoting a phase-out of 

the manufacture and sale of paints 

containing Pb and eventually to 

eliminate the risks that such paints 

pose. The UNEP is also engaged on the 

problem of managing wastes containing 

Pb, including Pb-containing batteries. 

The Governing Council of the UNEP, of 

which the U.S. is a member, has 

adopted decisions focused on promoting 

the environmentally sound management 

of products, wastes and contaminated 

sites containing Pb and reducing risks to 

human health and the environment 

from Pb and cadmium throughout the 

life cycles of those substances (UNEP 

Governing Council, 2011, 2013). The 

EPA is also engaged in the issue of 

environmental impacts of spent Pb-acid 

batteries internationally through the 

Commission for Environmental 

Cooperation (CEC), where the EPA 

Administrator along with the cabinetlevel or equivalent representatives of 

Mexico and Canada comprise the CEC’s 

senior governing body (CEC Council).8

C. Review of the Air Quality Criteria and 

Standards for Lead 

Unlike pollutants such as particulate 

matter and carbon monoxide, air quality 

criteria had not been issued for Pb as of 

the enactment of the CAA of 1970, 

which first set forth the requirement to 

set NAAQS based on air quality criteria. 

In the years just after enactment of the 

CAA, the EPA did not list Pb under 

Section 108 of the Act, having 

determined to control Pb air pollution 

through regulations to phase out the use 

of Pb additives in gasoline (See 41 FR 

14921, April 8, 1976). However, the 

decision not to list Pb under Section 108 

was challenged by environmental and 

public health groups, and the U.S. 

District Court for the Southern District 

of New York concluded that the EPA 

was required to list Pb under Section 

108. Natural Resources Defense Council 

v. EPA, 411 F. Supp. 864 21 (S.D. N.Y. 

1976), affirmed, 545 F.2d 320 (2d Cir. 

1978). Accordingly, on April 8, 1976, 

the EPA published a notice in the 

Federal Register that Pb had been listed 

under Section 108 as a criteria pollutant 

(41 FR 14921, April 8, 1976) and on 

October 5, 1978, the EPA promulgated 

primary and secondary NAAQS for Pb 

under Section 109 of the Act (43 FR 

46246, October 5, 1978). Both primary 

and secondary standards were set at a 

level of 1.5 micrograms per cubic meter 

(mg/m3), measured as Pb in total 

suspended particles (Pb–TSP), not to be 

exceeded by the maximum arithmetic 

mean concentration averaged over a 

calendar quarter. These standards were 

based on the 1977 Air Quality Criteria 

for Lead (USEPA, 1977). 

The first 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; 

henceforth referred to as the 1986 CD), 

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 

recommendations for consideration by 

the Administrator (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, multiprogram, 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). The EPA 

continues this broad, multi-program, 

multimedia approach to reducing Pb 

exposures today, as described in section 

I.B above. 

The last review of the Pb air quality 

criteria and standards was initiated in 

November 2004 (69 FR 64926, 

November 9, 2004); the agency’s plans 

for preparation of the Air Quality 

Criteria Document and conduct of the 

NAAQS review were presented in 

documents completed in 2005 and early 

2006 (USEPA, 2005a; USEPA 2006b).9

The schedule for completion of the 

review was governed by a judicial order 

in Missouri Coalition for the 

Environment v. EPA (No. 4:04CV00660 

ERW, September 14, 2005; and amended 

on April 29, 2008 and July 1, 2008). 

The scientific assessment for the 

review is described in the 2006 Air 

Quality Criteria for Lead (USEPA, 

2006a; henceforth referred to as the 

2006 CD), multiple drafts of which 

received review by CASAC and the 

public. The EPA also conducted human 

exposure and health risk assessments 

and a pilot ecological risk assessment 

for the review, after consultation with 

CASAC and receiving public comment 

on a draft analysis plan (USEPA, 2006c). 

Drafts of these quantitative assessments 

were reviewed by CASAC and the 

public. The pilot ecological risk 

assessment was released in December 

2006 (ICF International, 2006), and the 

final health risk assessment report was 

released in November 2007 (USEPA, 

2007a). The policy assessment, based on 

both of these assessments, air quality 

analyses and key evidence from the 

2006 CD, was presented in the Staff 

Paper (USEPA, 2007b), a draft of which 

also received CASAC and public review. 

The final Staff Paper presented OAQPS 

staff’s evaluation of the public health 

and welfare policy implications of the 

key studies and scientific information 

contained in the 2006 CD and presented 

and interpreted results from the 

quantitative risk/exposure analyses 

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10The ANPR, one of the features of the revised 

NAAQS review process that EPA instituted in 2006, 

was replaced by reinstatement of the Policy 

Assessment prepared by OAQPS staff (previously 

termed the OAQPS Staff Paper) in 2009 (Jackson, 

2009). 

conducted for this review. Based on this 

evaluation, the Staff Paper presented 

OAQPS staff recommendations that the 

Administrator give consideration to 

substantially revising the primary and 

secondary standards to a range of levels 

at or below 0.2 mg/m3. 

Immediately subsequent to 

completion of the Staff Paper, the EPA 

issued an advance notice of proposed 

rulemaking (ANPR) that was signed by 

the Administrator on December 5, 2007 

(72 FR 71488, December 17, 2007).10

CASAC provided advice and 

recommendations to the Administrator 

with regard to the Pb NAAQS based on 

its review of the ANPR and the 

previously released final Staff Paper and 

risk assessment reports. In 2008, the 

proposed decision on revisions to the Pb 

NAAQS was signed on May 1 and 

published in the Federal Register on 

May 20 (73 FR 29184, May 20, 2008). 

Members of the public provided 

comments and the CASAC Pb Panel also 

provided advice and recommendations 

to the Administrator based on its review 

of the proposal notice. The final 

decision on revisions to the Pb NAAQS 

was signed on October 15, 2008, and 

published in the Federal Register on 

November 12, 2008 (73 FR 66964, 

November 12, 2008). 

The November 2008 notice described 

the EPA’s decision to revise the primary 

and secondary NAAQS for Pb, as 

discussed more fully in section II.A.1 

below. In consideration of the muchexpanded health effects evidence on 

neurocognitive effects of Pb in children, 

the EPA substantially revised the 

primary standard from a level of 1.5 mg/ 

m3 to a level of 0.15 mg/m3. The 

averaging time was revised to a rolling 

3-month period with a maximum (notto-be-exceeded) form, evaluated over a 

3-year period. The indicator of Pb–TSP 

was retained, reflecting the evidence 

that Pb particles of all sizes pose health 

risks. The secondary standard was 

revised to be identical in all respects to 

the revised primary standard (40 CFR 

50.16). Revisions to the NAAQS were 

accompanied by revisions to the data 

handling procedures, the treatment of 

exceptional events and the ambient air 

monitoring and reporting requirements, 

as well as emissions inventory reporting 

requirements. One aspect of the revised 

data handling requirements is the 

allowance for the use of monitoring for 

particulate matter with mean diameter 

below 10 microns (Pb–PM10) for Pb 

NAAQS attainment purposes in certain 

limited circumstances at non-sourceoriented sites. Subsequent to the 2008 

rulemaking, additional revisions were 

made to the monitoring network 

requirements (75 FR 81126, December 

27, 2010). Guidance on the approach for 

implementation of the new standards 

was described in the Federal Register 

notices for the proposed and final rules 

(73 FR 29184, May 20, 2008; 73 FR 

66964, November 12, 2008). 

On February 26, 2010, the EPA 

formally initiated its current review of 

the air quality criteria and standards for 

Pb, requesting the submission of recent 

scientific information on specified 

topics (75 FR 8934, February 26, 2010). 

Soon after this, the EPA held a 

workshop to discuss the policy-relevant 

science, which informed identification 

of key policy issues and questions to 

frame the review of the Pb NAAQS (75 

FR 20843, April 21, 2010). Drawing 

from the workshop discussions, the EPA 

developed the draft Integrated Review 

Plan (draft IRP, USEPA, 2011d). The 

draft IRP was made available in late 

March 2011 for consultation with the 

CASAC Pb Review Panel and for public 

comment (76 FR 20347, April 12, 2011). 

This document was discussed by the 

Panel via a publicly accessible 

teleconference consultation on May 5, 

2011 (76 FR 21346, April 15, 2011; Frey, 

2011a). The final Integrated Review Plan 

for the National Ambient Air Quality 

Standards for Lead (IRP), developed in 

consideration of the CASAC 

consultation and public comment, was 

released in November 2011 (USEPA, 

2011a; 76 FR 76972, December 9, 2011). 

In developing the Integrated Science 

Assessment (ISA) for this review, the 

EPA held a workshop in December 2010 

to discuss with invited scientific experts 

preliminary draft materials and released 

the first external review draft of the 

document for CASAC review and public 

comment in May 2011 (USEPA, 2011e; 

76 FR 26284, May 6, 2011; 76 FR 36120, 

June 21, 2011). The CASAC Pb Review 

Panel met at a public meeting on July 

20, 2011, to review the draft ISA (76 FR 

36120, June 21, 2011). The CASAC 

provided comments in a December 9, 

2011, letter to the EPA Administrator 

(Frey and Samet, 2011). The second 

external review draft ISA was released 

for CASAC review and public comment 

in February 2012 (USEPA, 2012a; 77 FR 

5247, February 2, 2012) and was the 

subject of a public meeting on April 10– 

11, 2012 (77 FR 14783, March 13, 2012). 

The CASAC provided comments in a 

July 20, 2012, letter (Samet and Frey, 

2012). The third external review draft 

was released for CASAC review and 

public comment in November 2012 

(USEPA, 2012b; 77 FR 70776, November 

27, 2012) and was the subject of a public 

meeting on February 5–6, 2013 (78 FR 

938, January 7, 2013). The CASAC 

provided comments in a June 4, 2013, 

letter (Frey, 2013a). The final ISA was 

released in late June 2013 (USEPA, 

2013a, henceforth referred to as the ISA; 

78 FR 38318, June 26, 2013). 

In June 2011, the EPA developed and 

released the Risk and Exposure 

Assessment Planning Document (REA 

Planning Document) for consultation 

with CASAC and public comment 

(USEPA, 2011b; 76 FR 58509). This 

document presented a critical 

evaluation of the information related to 

Pb human and ecological exposure and 

risk (e.g., data, modeling approaches) 

newly available in this review, with a 

focus on consideration of the extent to 

which new or substantially revised 

REAs for health and ecological risk 

might be warranted by the newly 

available evidence. Evaluation of the 

newly available information with regard 

to designing and implementing health 

and ecological REAs for this review led 

us to conclude that the currently 

available information did not provide a 

basis for developing new quantitative 

risk and exposure assessments that 

would have substantially improved 

utility for informing the agency’s 

consideration of health and welfare 

effects and evaluation of the adequacy 

of the current primary and secondary 

standards, respectively (REA Planning 

Document, sections 2.3 and 3.3, 

respectively). The CASAC Pb Review 

Panel provided consultative advice on 

that document and its conclusions at a 

public meeting on July 21, 2011 (76 FR 

36120, June 21, 2011; Frey, 2011b). 

Based on their consideration of the REA 

Planning Document analysis, the 

CASAC Pb Review Panel generally 

concurred with the conclusion that a 

new REA was not warranted in this 

review (Frey, 2011b; Frey, 2013b). In 

consideration of the conclusions 

reached in the REA Planning Document 

and CASAC’s consultative advice, the 

EPA has not developed REAs for health 

and ecological risk for this review. 

Accordingly, we consider the risk 

assessment findings from the last review 

for human exposure and health risk 

(USEPA, 2007a, henceforth referred to 

as the 2007 REA) and ecological risk 

(ICF International, 2006; henceforth 

referred to as the 2006 REA) with regard 

to any appropriate further interpretation 

in light of the evidence newly available 

in this review. 

A draft of the Policy Assessment (PA) 

was released for public comment and 

review by CASAC in January 2013 

(USEPA, 2013b; 77 FR 70776, November 

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27, 2012) and was the subject of a public 

meeting on February 5–6, 2013 (78 FR 

938, January 7, 2013). Comments 

provided by the CASAC in a June 4, 

2013 letter (Frey, 2013b), as well as 

public comments received on the draft 

PA were considered in preparing the 

final PA, which was released in May 

2014 (USEPA, 2014; 79 FR 26751, May 

9, 2014). 

D. Multimedia, Multipathway Aspects of 

Lead 

Since Pb distributes from air to other 

media and is persistent, our review of 

the NAAQS for Pb considers the 

protection provided against such effects 

associated both with exposures to Pb in 

ambient air and with exposures to Pb 

that makes its way into other media 

from ambient air. Additionally, in 

assessing the adequacy of protection 

afforded by the current NAAQS, we are 

mindful of the long history of greater 

and more widespread atmospheric 

emissions that occurred in previous 

years (both before and after 

establishment of the 1978 NAAQS) and 

that contributed to the Pb that exists in 

human populations and ecosystems 

today. Likewise, we also recognize the 

role of other, nonair sources of Pb now 

and in the past that also contribute to 

the Pb that exists in human populations 

and ecosystems today. 

Lead emitted to ambient air is 

transported through the air and is also 

distributed from air to other media. This 

multimedia distribution of Pb emitted 

into ambient air (air-related Pb) 

contributes to multiple air-related 

pathways of human and ecosystem 

exposure (ISA, sections 3.1.1 and 3.7.1). 

Air-related pathways may also involve 

media other than air, including indoor 

and outdoor dust, soil, surface water 

and sediments, vegetation and biota. 

Air-related Pb exposure pathways for 

humans include inhalation of ambient 

air or ingestion of food, water or other 

materials, including dust and soil, that 

have been contaminated through a 

pathway involving Pb deposition from 

ambient air (ISA, section 3.1.1.1). 

Ambient air inhalation pathways 

include both inhalation of air outdoors 

and inhalation of ambient air that has 

infiltrated into indoor environments. 

The air-related ingestion pathways 

occur as a result of Pb passing through 

the ambient air, being distributed to 

other environmental media and 

contributing to human exposures via 

contact with and ingestion of indoor 

and outdoor dusts, outdoor soil, food 

and drinking water. 

Lead exposures via the various 

inhalation and ingestion air-related 

pathways may vary with regard to the 

time in which they respond to changes 

in air Pb concentrations. For example, 

exposures resulting from human 

exposure pathways most directly 

involving Pb in ambient air and 

exchanges of ambient air with indoor air 

(e.g., inhalation) can respond most 

quickly, while those for pathways 

involving exposure to Pb deposited from 

ambient air into the environment (e.g., 

diet) may be expected to respond more 

slowly. The extent of this will be 

influenced by the magnitude of change, 

as well as—for deposition-related 

pathways—the extent of prior 

deposition and environment 

characteristics influencing availability 

of prior deposited Pb. 

Lead currently occurring in nonair 

media may also derive from sources 

other than ambient air (nonair Pb 

sources) (ISA, sections 2.3 and 3.7.1). 

For example, Pb in dust inside some 

houses or outdoors in some urban areas 

may derive from the common past usage 

of leaded paint, while Pb in drinking 

water may derive from the use of leaded 

pipe or solder in drinking water 

distribution systems (ISA, section 

3.1.3.3). We also recognize the history of 

much greater air emissions of Pb in the 

past, such as that associated with leaded 

gasoline usage and higher industrial 

emissions which have left a legacy of Pb 

in other (nonair) media. 

The relative importance of different 

pathways of human exposure to Pb, as 

well as the relative contributions from 

Pb resulting from recent and historic air 

emissions and from nonair sources, vary 

across the U.S. population as a result of 

both extrinsic factors, such as a home’s 

proximity to industrial Pb sources or its 

history of leaded paint usage, and 

intrinsic factors, such as a person’s age 

and nutritional status (ISA, sections 5.1, 

5.2, 5.2.1, 5.2.5 and 5.2.6). Thus, the 

relative contributions from specific 

pathways is situation specific (ISA, p. 

1–11), although a predominant Pb 

exposure pathway for very young 

children is the incidental ingestion of 

indoor dust by hand-to-mouth activity 

(ISA, section 3.1.1.1). For adults, 

however, diet may be the primary Pb 

exposure pathway (2006 CD, section 

3.4). Similarly, the relative importance 

of air-related and nonair-related Pb also 

varies with the relative magnitudes of 

exposure by those pathways, which may 

vary with different circumstances. 

The distribution of Pb from ambient 

air to other environmental media also 

influences the exposure pathways for 

organisms in terrestrial and aquatic 

ecosystems. Exposure of terrestrial 

animals and vegetation to air-related Pb 

can occur by contact with ambient air or 

by contact with soil, water or food items 

that have been contaminated by Pb from 

ambient air (ISA, section 6.2). Transport 

of Pb into aquatic systems similarly 

provides for exposure of biota in those 

systems, and exposures may vary among 

systems as a result of differences in 

sources and levels of contamination, as 

well as characteristics of the systems 

themselves, such as salinity, pH and 

turbidity (ISA, section 2.3.2). In 

addition to Pb contributed by current 

atmospheric deposition, Pb may occur 

in aquatic systems as a result of nonair 

sources such as industrial discharges or 

mine-related drainage, of historical air 

Pb emissions (e.g., contributing to 

deposition to a water body or via runoff 

from soils near historical air sources) or 

combinations of different types of 

sources (e.g., resuspension of sediments 

contaminated by urban runoff and 

surface water discharges). 

The persistence of Pb contributes an 

important temporal aspect to lead’s 

environmental pathways, and the time 

(or lag) associated with realization of the 

impact of air Pb concentrations on 

concentrations in other media can vary 

with the media (e.g., ISA, section 6.2.2). 

For example, exposure pathways most 

directly involving Pb in ambient air or 

surface waters can respond more 

quickly to changes in ambient air Pb 

concentrations while pathways 

involving exposure to Pb in soil or 

sediments generally respond more 

slowly. An additional influence on the 

response time for nonair media is the 

environmental presence of Pb associated 

with past, generally higher, air 

concentrations. For example, after a 

reduction in air Pb concentrations, the 

time needed for sediment or surface soil 

concentrations to indicate a response to 

reduced air Pb concentrations might be 

expected to be longer in areas of more 

substantial past contamination than in 

areas with lesser past contamination. 

Thus, considering the Pb concentrations 

occurring in nonair environmental 

media as a result of air quality 

conditions that meet the current 

NAAQS is a complexity of this review, 

as it also was, although to a lesser 

degree, with regard to the prior standard 

in the last review. 

E. Air Quality Monitoring 

Lead emitted to the air is 

predominantly in particulate form. Once 

emitted, particle-bound Pb can be 

transported long or short distances 

depending on particle size, which 

influences the amount of time spent in 

the aerosol phase. In general, larger 

particles tend to deposit more quickly, 

within shorter distances from emissions 

points, while smaller particles remain in 

aerosol phase and travel longer 

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11The Pb–PM10 measurements may be used for 

NAAQS monitoring as an alternative to Pb–TSP 

measurements in certain conditions defined in 40 

CFR part 58, Appendix C, section 2.10.1.2. These 

conditions include where Pb concentrations are not 

expected to equal or exceed 0.10 mg/m3 as an 

arithmetic 3-month mean and where the source of 

Pb emissions is expected to emit a substantial 

majority of its Pb in the size fraction captured by 

PM10 monitors. 

12The Regional Administrator may waive this 

requirement for monitoring near Pb sources if the 

state or, where appropriate, local agency can 

demonstrate the Pb source will not contribute to a 

maximum 3-month average Pb concentration in 

ambient air in excess of 50 percent of the NAAQS 

level based on historical monitoring data, modeling, 

or other means (40 CFR part 58, Appendix D, 

section 4.5(a)(ii)). 

13These airports were selected based on three 

criteria: annual Pb inventory between 0.5 ton/year 

and 1.0 ton/year, ambient air within 150 meters of 

the location of maximum emissions (e.g., the end 

of the runway or run-up location), and airport 

configuration and meteorological scenario that 

leads to a greater frequency of operations from one 

runway. These criteria are expected, collectively, to 

identify airports with the highest potential to have 

ambient air Pb concentrations approaching or 

exceeding the Pb NAAQS (75 FR 81126). 

14The NCore network, that formally began in 

January 2011, is a subset of the state and local air 

monitoring stations network that is intended to 

meet multiple monitoring objectives (e.g., long-term 

trends analysis, model evaluation, health and 

ecosystem studies, as well as NAAQS compliance). 

The complete NCore network consists of 63 urban 

and 15 rural stations, with each state containing at 

least one NCore station; 46 of the states plus 

Washington, DC and Puerto Rico have at least one 

urban station. 

15http://www.census.gov/population/www/

metroareas/metroarea.html. 

distances before depositing (ISA, section 

1.2.1). Accordingly, airborne 

concentrations of Pb near sources are 

much higher (and the representation of 

larger particles generally greater) than at 

sites not directly influenced by sources 

(PA, Figure 2–11; ISA sections 2.3.1 and 

2.5.3). 

Ambient air monitoring data for Pb, in 

terms of Pb–TSP, Pb–PM10 or Pb in 

particulate matter with mean diameter 

smaller than 2.5 microns (Pb–PM2.5), are 

currently collected in several national 

networks. Monitoring conducted for 

purposes of Pb NAAQS surveillance is 

regulated to ensure accurate and 

comparable data for determining 

compliance with the NAAQS. In order 

to be used in NAAQS attainment 

designations, ambient Pb concentration 

data must be obtained using either the 

federal reference method (FRM) or a 

federal equivalent method (FEM). The 

FRMs for sample collection and analysis 

are specified in 40 CFR part 50. The 

procedures for approval of FRMs and 

FEMs are specified in 40 CFR part 53. 

In 2013, after consultation with 

CASAC’s Ambient Air Monitoring and 

Methods Subcommittee, the EPA 

adopted a new FRM for Pb–TSP, based 

on inductively coupled plasma-mass 

spectrometry (78 FR 40000, July 3, 

2013). The previous FRM was retained 

as an FEM, and existing FEMs were 

retained as well. 

The Pb monitoring network design 

requirements (40 CFR part 58, Appendix 

D, paragraph 4.5) include two types of 

monitoring sites—source-oriented 

monitoring sites and non-sourceoriented monitoring sites—as well as 

the collection of a year of Pb–TSP 

measurements at 15 specific airports. 

The indicator for the current Pb NAAQS 

is Pb–TSP, although in some 

situations,11 ambient Pb–PM10

concentrations may be used in judging 

nonattainment. Currently, 

approximately 260 Pb–TSP monitors are 

in operation; these are a mixture of 

source- and non-source-oriented 

monitors. 

Since the phase-out of Pb in on-road 

gasoline, Pb is widely recognized as a 

source-oriented air pollutant. Variability 

in air Pb concentrations is highest in 

areas including a Pb source, ‘‘with high 

concentrations downwind of the sources 

and low concentration at areas far from 

sources’’ (ISA, p. 2–92). The current 

requirements for source-oriented 

monitoring include placement of 

monitor sites near sources of air Pb 

emissions which are expected to or have 

been shown to contribute to ambient air 

Pb concentrations in excess of the 

NAAQS. At a minimum, there must be 

one source-oriented site located to 

measure the maximum Pb concentration 

in ambient air resulting from each nonairport Pb source which emits 0.50 or 

more tons of Pb per year and from each 

airport which emits 1.0 or more tons of 

Pb per year.12 The EPA Regional 

Administrators may require additional 

monitoring beyond the minimum 

requirements where the likelihood of Pb 

air quality violations is significant. Such 

locations may include those near 

additional industrial Pb sources, 

recently closed industrial sources and 

other sources of resuspended Pb dust, as 

well as airports where piston-engine 

aircraft emit Pb associated with 

combustion of leaded aviation fuel (40 

CFR part 58, Appendix D, section 

4.5(c)). A single year of monitoring was 

also required near 15 specific airports 13

in order to gather additional information 

on the likelihood of NAAQS 

exceedances due to the combustion of 

leaded aviation gasoline (75 FR 81126, 

December 27, 2010; 40 CFR part 58, 

Appendix D, 4.5(a)(iii)). These airport 

monitoring data along with other data 

gathering and analyses will inform the 

EPA’s ongoing investigation into the 

potential for Pb emissions from pistonengine aircraft to cause or contribute to 

air pollution that may reasonably be 

anticipated to endanger public health or 

welfare. This investigation is occurring 

under section 231 of the CAA, separate 

from the Pb NAAQS review. As a whole, 

the various data gathering and analyses 

are expected to improve our 

understanding of Pb concentrations in 

ambient air near airports and conditions 

influencing these concentrations. 

Monitoring agencies are also required, 

under 40 CFR part 58, Appendix D, to 

conduct non-source-oriented Pb 

monitoring at the NCore sites 14 required 

in metropolitan areas with a population 

of 500,000 or more (as defined by the 

U.S. Census Bureau).15 Either Pb–TSP 

or Pb–PM10 monitoring may be 

performed at these sites. Currently, all 

50 NCore Pb sites are operational and 

measuring Pb concentrations, with 28 

measuring Pb in TSP and 24 measuring 

Pb in PM10 (2 sites are measuring both 

Pb in TSP and Pb in PM10). In a separate 

action addressing a range of issues 

related to monitoring requirements for 

criteria pollutants, the EPA is proposing 

to remove the requirement for Pb 

monitoring at NCore sites (79 FR 54395, 

September 11, 2014). This change is 

being proposed in consideration of 

current information indicating 

concentrations at these sites to be well 

below the Pb NAAQS and of the 

presence of other monitoring networks 

that provide information on Pb 

concentrations in urban areas not 

directly impacted by Pb sources. The 

data available for these sites indicate 

maximum 3-month average 

concentrations (of Pb–PM10 or Pb–TSP) 

well below the level of the Pb NAAQS, 

with the vast majority of sites showing 

concentrations less than 0.01 mg/m3. 

Additionally, other monitoring 

networks provide data on Pb in PM10 or 

PM2.5, at non-source-oriented urban, and 

some rural, sites. These include the 

National Air Toxics Trends Stations for 

PM10 and the Chemical Speciation 

Network for PM2.5. Data on Pb in PM2.5

are also provided at the rural sites of the 

Interagency Monitoring of Protected 

Visual Environments network. 

The long-term record of Pb 

monitoring data documents the 

dramatic decline in atmospheric Pb 

concentrations that has occurred since 

the 1970s in response to reduced 

emissions (PA, Figures 2–1 and 2–7). 

Currently, the highest concentrations 

occur near some metals industries 

where some individual locations have 

concentrations that exceed the NAAQS 

(PA, Figure 2–10). Concentrations at 

non-source-oriented monitoring sites are 

much lower than those at sourceoriented sites and well below the 

standard (PA, Figure 2–11). 

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16 In addition to the review’s opening ‘‘call for 

information’’ (75 FR 8934), ‘‘literature searches 

were conducted routinely to identify studies 

published since the last review, focusing on studies 

published from 2006 (close of the previous 

scientific assessment) through September 2011,’’ 

and references ‘‘that were considered for inclusion 

or actually cited in this ISA can be found at 

http://hero.epa.gov/lead’’ (ISA, p. 1–2). 

17The at-risk population groups identified in a 

NAAQS review may include low-income or 

minority groups. Where low-income/minority 

groups are among the at-risk populations, the 

rulemaking decision will be based on providing 

protection for these and other at-risk populations 

and lifestages (e.g., children, older adults, persons 

with pre-existing heart and lung disease). To the 

extent that low-income/minority groups are not 

among the at-risk populations identified in the ISA, 

a decision based on providing protection of the atrisk lifestages and populations would be expected 

to provide protection for the low-income/minority 

groups. 

II. Rationale for Proposed Decision on 

the Primary Standard 

This section presents the rationale for 

the Administrator’s proposed decision 

to retain the existing Pb primary 

standard. As discussed more fully 

below, this rationale is based on a 

thorough review, in the ISA, of the latest 

scientific information, generally 

published through September 2011,16

on human health effects associated with 

Pb and pertaining to the presence of Pb 

in the ambient air. This proposal also 

takes into account: (1) The PA’s staff 

assessments of the most policy-relevant 

information in the ISA and staff 

analyses of air quality, human exposure 

and health risks, upon which staff 

conclusions regarding appropriate 

considerations in this review are based; 

(2) CASAC advice and 

recommendations, as reflected in 

discussions of drafts of the ISA and PA 

at public meetings, in separate written 

comments, and in CASAC’s letters to 

the Administrator; and (3) public 

comments received during the 

development of these documents, either 

in connection with CASAC meetings or 

separately. 

In presenting the rationale and its 

foundations, section II.A provides 

background on the general approach for 

review of the primary NAAQS for Pb, 

including a summary of the approach 

used in the last review (section II.A.1) 

and the general approach for the current 

review (section II.A.2). Sections II.B and 

II.C summarize the body of evidence 

supporting this rationale, focusing on 

consideration of key policy-relevant 

questions, and section II.D summarizes 

the exposure/risk information for this 

review. Section II.E presents the 

Administrator’s proposed conclusions 

on adequacy of the current standard, 

drawing on both evidence-based and 

exposure/risk-based considerations 

(sections II.E.1 and II.E.2), and advice 

from CASAC (section II.E.3). 

A. General Approach 

The past and current approaches 

described below are both based, most 

fundamentally, on using the EPA’s 

assessment of the current scientific 

evidence and associated quantitative 

analyses to inform the Administrator’s 

judgment regarding a primary standard 

for Pb that protects public health with 

an adequate margin of safety. We note 

that in drawing conclusions with regard 

to the primary standard, the final 

decision on the adequacy of the current 

standard is largely a public health 

policy judgment to be made by the 

Administrator. The Administrator’s 

final decision must draw upon scientific 

information and analyses about health 

effects, population exposure and risks, 

as well as judgments about how to 

consider the range and magnitude of 

uncertainties that are inherent in the 

scientific evidence and analyses. Our 

approach to informing these judgments, 

discussed more fully below, is based on 

the recognition that the available health 

effects evidence generally reflects a 

continuum, consisting of levels at which 

scientists generally agree that health 

effects are likely to occur, through lower 

levels at which the likelihood and 

magnitude of the response become 

increasingly uncertain. This approach is 

consistent with the requirements of the 

NAAQS provisions of the Act and with 

how the EPA and the courts have 

historically interpreted the Act. These 

provisions require the Administrator to 

establish primary standards that, in the 

judgment of the Administrator, are 

requisite to protect public health with 

an adequate margin of safety. In so 

doing, the Administrator seeks to 

establish standards that are neither more 

nor less stringent than necessary for this 

purpose. The Act does not require that 

primary standards be set at a zero-risk 

level, but rather at a level that avoids 

unacceptable risks to public health 

including the health of sensitive 

groups.17 The four basic elements of the 

NAAQS (indicator, averaging time, 

level, and form) are considered 

collectively in evaluating the health 

protection afforded by the current 

standard. 

1. Approach in the Last Review 

The last review of the NAAQS for Pb 

was completed in 2008 (73 FR 66964, 

November 12, 2008). The 2008 decision 

to substantially revise the primary 

standard was based on the extensive 

body of scientific evidence published 

over almost three decades, from the time 

the standard was originally set in 1978 

through 2005–2006. In so doing, the 

2008 decision considered the body of 

evidence as assessed in the 2006 CD 

(USEPA, 2006a), as well as the 2007 

Staff Paper assessment of the policyrelevant information contained in the 

CD and the quantitative risk/exposure 

assessment (USEPA, 2007a, 2007b), the 

advice and recommendations of CASAC 

(Henderson 2007a, 2007b, 2008a, 

2008b), and public comment. While 

recognizing that Pb has been 

demonstrated to exert ‘‘a broad array of 

deleterious effects on multiple organ 

systems,’’ the review focused on the 

effects most pertinent to ambient air 

exposures, which given ambient air Pb 

reductions over the past 30 years, are 

those associated with relatively lower 

exposures and associated blood Pb 

levels (73 FR 66975, November 12, 

2008). In so doing, the EPA recognized 

the general consensus that the 

developing nervous system in children 

is among the most sensitive health 

endpoints associated with Pb exposure, 

if not the most sensitive one. Thus, 

primary attention was given to 

consideration of nervous system effects, 

including neurocognitive and 

neurobehavioral effects, in children (73 

FR 66976, November 12, 2008). The 

body of evidence included associations 

of such effects in study populations of 

variously aged children with mean 

blood Pb levels below 10 mg/dL, 

extending from 8 down to 2 mg/dL (73 

FR 66976, November 12, 2008). The 

public health implications of effects of 

air-related Pb on cognitive function 

(e.g., IQ) in young children were given 

particular focus in the review. 

The conclusions reached by the 

Administrator in the last review were 

based primarily on the scientific 

evidence, with the risk- and exposurebased information providing support for 

various aspects of the decision. In 

reaching his conclusion on the 

adequacy of the then-current standard, 

which was set in 1978, the 

Administrator placed primary 

consideration on the large body of 

scientific evidence available in the 

review including significant new 

evidence concerning effects at blood Pb 

concentrations substantially below 

those identified when the standard was 

initially set (73 FR 66987, November 12, 

2008; 43 FR 46246, October 5, 1978). 

Given particular attention was the 

robust evidence of neurotoxic effects of 

Pb exposure in children, recognizing: (1) 

That while blood Pb levels in U.S. 

children had decreased notably since 

the late 1970s, newer epidemiological 

studies had investigated and reported 

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18The term ‘‘ultra-coarse’’ refers to particles 

collected by a TSP sampler but not by a PM10

sampler. This terminology is consistent with the 

traditional usage of ‘‘fine’’ to refer to particles 

collected by a PM2.5 sampler, and ‘‘coarse’’ to refer 

to particles collected by a PM10 sampler but not by 

a PM2.5 sampler, recognizing that there will be some 

overlap in the particle sizes in the three types of 

collected material. 

associations of effects on the 

neurodevelopment of children with 

those more recent lower blood Pb levels 

and (2) that the toxicological evidence 

included extensive experimental 

laboratory animal evidence 

substantiating well the plausibility of 

the epidemiological findings observed 

in human children and expanding our 

understanding of likely mechanisms 

underlying the neurotoxic effects (73 FR 

66987, November 12, 2008). 

Additionally, within the range of blood 

Pb levels investigated in the available 

evidence base, a threshold level for 

neurocognitive effects was not 

identified (73 FR 66984, November 12, 

2008; 2006 CD, p. 8–67). Further, the 

evidence indicated a steeper 

concentration-response (C–R) 

relationship for effects on cognitive 

function at those lower blood Pb levels 

than at higher blood Pb levels that were 

more common in the past, ‘‘indicating 

the potential for greater incremental 

impact associated with exposure at 

these lower levels’’ (73 FR 66987, 

November 12, 2008). As at the time 

when the standard was initially set in 

1978, the health effects evidence and 

exposure/risk assessment available in 

the last review supported the 

conclusion that air-related Pb exposure 

pathways contribute to blood Pb levels 

in young children by inhalation and 

ingestion (73 FR 66987, November 12, 

2008). The available information in the 

last review also indicated, however, a 

likely greater change in blood Pb per 

unit of air Pb than was estimated when 

the standard was initially set (73 FR 

66987, November 12, 2008). 

In the Administrator’s decision on the 

adequacy of the 1978 standard, the 

Administrator considered the evidence 

using a very specifically defined 

framework, referred to as an air-related 

IQ loss evidence-based framework. This 

framework integrates evidence for the 

relationship between Pb in air and Pb in 

young children’s blood with evidence 

for the relationship between Pb in 

young children’s blood and IQ loss (73 

FR 66987, November 12, 2008). This 

evidence-based approach considers airrelated effects on neurocognitive 

function (using the quantitative metric 

of IQ loss) associated with exposure in 

those areas with elevated air 

concentrations equal to potential 

alternative levels for the Pb standard. In 

simplest terms, the framework focuses 

on children exposed to air-related Pb in 

those areas with elevated air Pb 

concentrations equal to specific 

potential standard levels, providing for 

estimation of a mean air-related IQ 

decrement for young children in the 

high end of the national distribution of 

air-related exposures. Thus, the 

conceptual context for the framework is 

that it provides estimates of air-related 

IQ loss for the subset of U.S. children 

living in close proximity to air Pb 

sources that contribute to such elevated 

air Pb concentrations. In such cases, 

when a standard of a particular level is 

just met at a monitor sited to record the 

highest source-oriented concentration in 

an area, the large majority of children in 

the larger surrounding area would likely 

experience exposures to concentrations 

well below that level. 

The two primary inputs to the 

evidence-based air-related IQ loss 

framework are air-to-blood ratios and C– 

R functions for the relationship between 

blood Pb and IQ response in young 

children. Additionally taken into 

consideration in applying and drawing 

conclusions from the framework were 

the uncertainties inherent in these 

inputs. Application of the framework 

also entailed consideration of an 

appropriate level of protection from airrelated IQ loss to be used in conjunction 

with the framework. The framework 

estimates of mean air-related IQ loss are 

derived through multiplication of the 

following factors: standard level (mg/

m3), air-to-blood ratio (albeit in terms of 

mg/dL blood Pb per mg/m3 air 

concentration), and slope for the C–R 

function in terms of points IQ 

decrement per mg/dL blood Pb. 

Based on the application of the airrelated IQ loss framework to the 

evidence, the Administrator concluded 

that, for exposures projected for air Pb 

concentrations at the level of the 1978 

standard, the quantitative estimates of 

IQ loss associated with air-related Pb 

indicated risk of a magnitude that, in his 

judgment, was significant from a public 

health perspective, and that the 

evidence-based framework supported a 

conclusion that the 1978 standard did 

not protect public health with an 

adequate margin of safety (73 FR 66987, 

November 12, 2008). The Administrator 

further concluded that the evidence 

indicated the need for a substantially 

lower standard level to provide 

increased public health protection, 

especially for at-risk groups (most 

notably children), against an array of 

effects, most importantly including 

effects on the developing nervous 

system (73 FR 66987, November 12, 

2008). In addition to giving primary 

consideration to the much expanded 

evidence base since the standard was 

set, the Administrator also took into 

consideration the exposure/risk 

assessments. In so doing, he observed 

that, while taking into consideration 

their inherent uncertainties and 

limitations, the quantitative estimates of 

IQ loss associated with air-related Pb in 

air quality scenarios just meeting the 

then-current standard also indicated 

risk of a magnitude that, in his 

judgment, was significant from a public 

health perspective. Thus, the 

Administrator concluded the exposure/ 

risk estimates provided additional 

support to the evidence-based 

conclusion that the standard needed 

revision (73 FR 66987, November 12, 

2008). 

In considering appropriate revisions 

to the prior standard in the review 

completed in 2008, each of the four 

basic elements of the NAAQS (indicator, 

averaging time, form and level) was 

evaluated. The rationale for decisions 

on those elements is summarized below. 

With regard to indicator, 

consideration was given to replacing 

Pb–TSP with Pb–PM10. The EPA 

recognized, however, that Pb in all 

particle sizes contributes to Pb in blood 

and associated health effects, 

additionally noting that the difference 

in particulate Pb captured by TSP and 

PM10 monitors may be on the order of 

a factor of two in some areas (73 FR 

66991, November 12, 2008). Further, the 

Administrator recognized uncertainty 

with regard to whether a Pb–PM10-based 

standard would also effectively control 

ultra-coarse 18 Pb particles, which may 

have a greater presence in areas near 

sources where Pb concentrations are 

highest (73 FR 66991, November 12, 

2008). The Administrator decided to 

retain Pb–TSP as the indicator to 

provide sufficient public health 

protection from the range of particle 

sizes of ambient air Pb, including ultracoarse particles (73 FR 66991, 

November 12, 2008). Additionally, a 

role was provided for Pb–PM10 in the 

monitoring required for a Pb–TSP 

standard (73 FR 66991, November 12, 

2008) based on the conclusion that use 

of Pb–PM10 measurements at sites not 

influenced by sources of ultra-coarse Pb, 

and where Pb concentrations are well 

below the standard, would take 

advantage of the increased precision of 

these measurements and decreased 

spatial variation of Pb–PM10

concentrations, without raising the same 

concerns over a lack of protection 

against health risks from all particulate 

Pb emitted to the ambient air that 

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19The term ‘‘air-to-blood ratio’’ describes the 

increase in blood Pb (in mg/dL) estimated to be 

associated with each unit increase of air Pb (in mg/ 

m3). Ratios are presented in the form of 1:x, with 

the 1 representing air Pb (in mg/m3) and x 

representing blood Pb (in mg/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). 

20The geometric mean blood Pb level for U.S. 

children aged 5 years and below, reported for 

NHANES in 2003–04 (the most recent years for 

which such an estimate was available at the time 

of the 2008 decision) was 1.8 mg/dL and the 5th and 

95th percentiles were 0.7 mg/dL and 5.1 mg/dL, 

respectively (73 FR 67002). 

support retention of Pb–TSP as the 

indicator (versus revision to Pb–PM10) 

(73 FR 66991, November 12, 2008). 

Accordingly, allowance was made for 

the use of Pb–PM10 monitoring for Pb 

NAAQS attainment purposes in certain 

limited circumstances, at non-sourceoriented sites, where the Pb 

concentrations are expected to be 

substantially below the standard and 

ultra-coarse particles are not expected to 

be present (73 FR 66991, November 12, 

2008). 

With regard to averaging time and 

form for the revised standard, 

consideration was given to a monthly 

averaging time, with a form of second 

maximum, and to 3-month and calendar 

quarter averaging times, with not-to-be 

exceeded forms. While the 

Administrator recognized that there 

were some factors that might imply 

support for a period as short as a month 

for averaging time, he also noted other 

factors supporting use of a longer time. 

He additionally took note of the 

complexity inherent in this 

consideration for the primary Pb 

standard, which is greater than in the 

case of other criteria pollutants due to 

the multimedia nature of Pb and its 

multiple pathways of human exposure. 

In this situation for Pb, the 

Administrator emphasized the 

importance of considering all of the 

relevant factors, both those pertaining to 

the human physiological response to 

changes in Pb exposures and those 

pertaining to the response of air-related 

Pb exposure pathways to changes in 

airborne Pb, in an integrated manner. 

As discussed further in the PA, the 

evidence on human physiological 

response to changes in Pb exposure 

available in the last review indicated 

that children’s blood Pb levels respond 

quickly to increased Pb exposure, 

particularly during the time of leaded 

gasoline usage but likely with lessened 

immediacy since that time as children’s 

exposure pathways have changed (PA, 

section 4.1.1.2). The Administrator also 

recognized limitations and uncertainties 

in the evidence and variability with 

regard to the information regarding the 

response time of indoor dust Pb to 

ambient airborne Pb. In consideration of 

the uncertainty associated with the 

evidence, the Administrator noted that 

the two changes in form for the standard 

(to a rolling 3-month average and to 

providing equal weighting to each 

month in deriving the 3-month average) 

both afford greater weight to each 

individual month than did the calendar 

quarter form of the 1978 standard, 

tending to control both the likelihood 

that any month will exceed the level of 

the standard and the magnitude of any 

such exceedance. Thus, based on an 

integrated consideration of the range of 

relevant factors, the averaging time was 

revised to a rolling 3-month period with 

a maximum (not-to-be-exceeded) form, 

evaluated over a 3-year period. As 

compared to the previous averaging 

time and form of calendar quarter (notto-be exceeded), this revision was 

considered to be more scientifically 

appropriate and more health protective 

(73 FR 66996, November 12, 2008). The 

rolling average gives equal weight to all 

3-month periods, and the new 

calculation method gives equal weight 

to each month within each 3-month 

period (73 FR 66996, November 12, 

2008). Further, the rolling average yields 

twelve 3-month averages each year to be 

compared to the NAAQS versus four 

averages in each year for the block 

calendar quarters pertaining to the 

previous standard (73 FR 66996, 

November 12, 2008). 

Lastly, based on the body of scientific 

evidence and information available, as 

well as CASAC recommendations and 

public comment, the Administrator 

decided on a standard level that, in 

combination with the specified choice 

of indicator, averaging time, and form, 

he judged requisite to protect public 

health, including the health of sensitive 

groups, with an adequate margin of 

safety (73 FR 67006, November 12, 

2008). In reaching the decision on level 

for the revised standard, the 

Administrator considered as a useful 

guide the evidence-based framework 

developed in that review. As described 

above, that framework integrates 

evidence for the relationship between 

Pb in air and Pb in children’s blood and 

the relationship between Pb in 

children’s blood and IQ loss. 

Application of the air-related IQ loss 

evidence-based framework was 

recognized, however, to provide ‘‘no 

evidence- or risk-based bright line that 

indicates a single appropriate level’’ for 

the standard (73 FR 67006, November 

12, 2008). Rather, the framework was 

seen as a useful guide for consideration 

of health risks from exposure to ambient 

levels of Pb in the air, in the context of 

a specified averaging time and form, 

with regard to the Administrator’s 

decision on a level for a revised NAAQS 

that provides public health protection 

that is sufficient but not more than 

necessary under the Act (73 FR 67004, 

November 12, 2008). 

As noted above, use of the evidencebased air-related IQ loss framework to 

inform selection of a standard level 

involved consideration of the evidence 

with regard to two input parameters. 

The two input parameters are an air-toblood ratio and a C–R function for 

population IQ response associated with 

blood Pb level (73 FR 67004, November 

12, 2008). The evidence at the time of 

the last review indicated a broad range 

of air-to-blood ratio estimates,19 each 

with limitations and associated 

uncertainties. Based on the thenavailable evidence, the Administrator 

concluded that 1:5 to 1:10 represented 

a reasonable range to consider and 

identified 1:7 as a generally central 

value on which to focus (73 FR 67004, 

November 12, 2008). With regard to C– 

R functions, in light of the evidence of 

nonlinearity and of steeper slopes at 

lower blood Pb levels, the Administrator 

concluded it was appropriate to focus 

on C–R analyses based on blood Pb 

levels that most closely reflected the 

then-current population of children in 

the U.S.,20 recognizing the EPA’s 

identification of four such analyses and 

giving weight to the central estimate or 

median of the resultant C–R functions 

(73 FR 67003, November 12, 2008, Table 

3; 73 FR 67004, November 12, 2008). 

The median estimate for the four C–R 

slopes of ¥1.75 IQ points decrement 

per mg/dL blood Pb was selected for use 

with the framework. With the 

framework, potential alternative 

standard levels (mg/m3) are multiplied 

by estimates of air-to-blood ratio (mg/dL 

blood Pb per mg/m3 air Pb) and the 

median slope for the C–R function 

(points IQ decrement per mg/dL blood 

Pb), yielding estimates of a mean airrelated IQ decrement for a specific 

subset of young children (i.e., those 

children exposed to air-related Pb in 

areas with elevated air Pb 

concentrations equal to specified 

alternative levels). As such, the 

application of the framework yields 

estimates for the mean air-related IQ 

decrements of the subset of children 

expected to experience air-related Pb 

exposures at the high end of the 

distribution of such exposures. The 

associated mean IQ loss estimate is the 

average for this highly exposed subset 

and is not the average air-related IQ loss 

projected for the entire U.S. population 

of children. Uncertainties and 

limitations were recognized in the use 

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of the framework and in the resultant 

estimates (73 FR 67000, November 12, 

2008). 

In considering the use of the 

evidence-based air-related IQ loss 

framework to inform his judgment as to 

the appropriate degree of public health 

protection that should be afforded by 

the NAAQS to provide requisite 

protection against risk of neurocognitive 

effects in sensitive populations, such as 

IQ loss in children, the Administrator 

recognized in the 2008 review that there 

were no commonly accepted guidelines 

or criteria within the public health 

community that would provide a clear 

basis for such a judgment. During the 

2008 review, CASAC commented 

regarding the significance from a public 

health perspective of a 1–2 point IQ loss 

in the entire population of children and 

along with some commenters, 

emphasized that the NAAQS should 

prevent air-related IQ loss of a 

significant magnitude, such as on the 

order of 1–2 IQ points, in all but a small 

percentile of the population. Similarly, 

the Administrator stated that ‘‘ideally 

air-related (as well as other) exposures 

to environmental Pb would be reduced 

to the point that no IQ impact in 

children would occur’’ (73 FR 66998, 

November 12, 2008). The Administrator 

further recognized that, in the case of 

setting a NAAQS, he was required to 

make a judgment as to what degree of 

protection is requisite to protect public 

health with an adequate margin of safety 

(73 FR 66998, November 12, 2008). The 

NAAQS must be sufficient but not more 

stringent than necessary to achieve that 

result, and the Act does not require a 

zero-risk standard (73 FR 66998, 

November 12, 2008). The Administrator 

additionally recognized that the 

evidence-based air-related IQ loss 

framework did not provide estimates 

pertaining to the U.S. population of 

children as a whole. Rather, the 

framework provided estimates (with 

associated uncertainties and limitations) 

for the mean of a subset of that 

population, the subset of children 

assumed to be exposed to the level of 

the standard. As described in the final 

decision ‘‘[t]he framework in effect 

focuses on the sensitive subpopulation 

that is the group of children living near 

sources and more likely to be exposed 

at the level of the standard’’ (73 FR 

67000, November 12, 2008). As further 

noted in the final decision (73 FR 

67000, November 12, 2008): 

EPA is unable to quantify the percentile of 

the U.S. population of children that 

corresponds to the mean of this sensitive 

subpopulation. Nor is EPA confident in its 

ability to develop quantified estimates of airrelated IQ loss for higher percentiles than the 

mean of this subpopulation. EPA expects 

that the mean of this subpopulation 

represents a high, but not quantifiable, 

percentile of the U.S. population of children. 

As a result, EPA expects that a standard 

based on consideration of this framework 

would provide the same or greater protection 

from estimated air-related IQ loss for a high, 

albeit unquantifiable, percentage of the entire 

population of U.S. children. 

In reaching a judgment as to the 

appropriate degree of protection, the 

Administrator considered advice and 

recommendations from CASAC and 

public comments and recognized the 

uncertainties in the health effects 

evidence and related information as 

well as the role of, and context for, a 

selected air-related IQ loss in the 

application of the framework, as 

described above. Based on these 

considerations, the Administrator 

identified an air-related IQ loss of 2 

points for use with the framework, as a 

tool for considering the evidence with 

regard to the level for the standard (73 

FR 67005, November 12, 2008). In so 

doing, the Administrator was not 

determining that such an IQ decrement 

value was appropriate in other contexts 

(73 FR 67005, November 12, 2008). 

Given the various uncertainties 

associated with the framework and the 

scientific evidence base, and the focus 

of the framework on the sensitive 

subpopulation of children that are more 

highly exposed to air-related Pb, a 

standard level selected in this way, in 

combination with the selected averaging 

time and form, was expected to 

significantly reduce and limit for a high 

percentage of U.S. children the risk of 

experiencing an air-related IQ loss of 

that magnitude (73 FR 67005, November 

12, 2008). At the standard level of 0.15 

mg/m3, with the combination of the 

generally central estimate of air-to-blood 

ratio of 1:7 and the median of the four 

C–R functions (¥1.75 IQ point 

decrement per mg/dL blood Pb), the 

framework estimates of air-related IQ 

loss were below 2 IQ points (73 FR 

67005, November 12, 2008, Table 4). 

In reaching the decision in 2008 on a 

level for the revised standard, the 

Administrator also considered the 

results of the quantitative risk 

assessment to provide a useful 

perspective on risk from air-related Pb. 

In light of important uncertainties and 

limitations for purposes of evaluating 

potential standard levels, however, the 

Administrator placed less weight on the 

risk estimates than on the evidencebased assessment. Nevertheless, in 

recognition of the general comparability 

of quantitative risk estimates for the 

case studies considered most 

conceptually similar to the scenario 

represented by the evidence-based 

framework, he judged the quantitative 

risk estimates to be ‘‘roughly consistent 

with and generally supportive’’ of the 

evidence-based framework estimates (73 

FR 67006, November 12, 2008). 

Based on consideration of the entire 

body of evidence and information 

available in the review, as well as the 

recommendations of CASAC and public 

comments, the Administrator decided 

that a level for the primary Pb standard 

of 0.15 mg/m3, in combination with the 

specified choice of indicator, averaging 

time and form, was requisite to protect 

public health, including the health of 

sensitive groups, with an adequate 

margin of safety (73 FR 67006, 

November 12, 2008). In reaching 

decisions on level as well as the other 

elements of the revised standard, the 

Administrator took note of the 

complexity associated with 

consideration of health effects caused by 

different ambient air concentrations of 

Pb and with uncertainties with regard to 

the relationships between air 

concentrations, exposures, and health 

effects. For example, selection of a 

maximum, not to be exceeded, form in 

conjunction with a rolling 3-month 

averaging time over a 3-year span was 

expected to have the effect that the atrisk population of children would be 

exposed below the standard most of the 

time (73 FR 67005, November 12, 2008). 

The Administrator additionally 

considered the provision of an adequate 

margin of safety in making decisions on 

each of the elements of the standard, 

including, for example ‘‘selection of 

TSP as the indicator and the rejection of 

the use of PM10 scaling factors; selection 

of a maximum, not to be exceeded form, 

in conjunction with a 3-month 

averaging time that employs a rolling 

average, with the requirement that each 

month in the 3-month period be 

weighted equally (rather than being 

averaged by individual data) and that a 

3-year span be used for comparison to 

the standard; and the use of a range of 

inputs for the evidence-based 

framework, that includes a focus on 

higher air-to-blood ratios than the 

lowest ratio considered to be 

supportable, and steeper rather than 

shallower C–R functions, and the 

consideration of these inputs in 

selection of 0.15 mg/m3 as the level of 

the standard’’ (73 FR 67007, November 

12, 2008). 

The Administrator additionally noted 

that a standard with this level would 

reduce the risk of a variety of health 

effects associated with exposure to Pb, 

including effects indicated in the 

epidemiological studies at lower blood 

Pb levels, particularly including 

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21Since the last Pb NAAQS review, the ISAs 

which have replaced CDs in documenting each 

review of the scientific evidence (or air quality 

criteria) employ a systematic framework for 

weighing the evidence and describing associated 

conclusions with regard to causality using 

established descriptors: ‘‘causal’’ relationship with 

relevant exposure, ‘‘likely’’ to be a causal 

relationship, evidence is ‘‘suggestive’’ of a causal 

relationship, ‘‘inadequate’’ evidence to infer a 

causal relationship, and ‘‘not likely’’ to be a causal 

relationship (ISA, Preamble). 

22 In drawing judgments regarding causality for 

the criteria air pollutants, the ISA places emphasis 

‘‘on evidence of effects at doses (e.g., blood Pb 

concentration) or exposures (e.g., air 

concentrations) that are relevant to, or somewhat 

above, those currently experienced by the 

population. The extent to which studies of higher 

concentrations are considered varies . . . but 

generally includes those with doses or exposures in 

the range of one to two orders of magnitude above 

current or ambient conditions. Studies that use 

higher doses or exposures may also be considered 

. . . [t]hus, a causality determination is based on 

weight of evidence evaluation . . ., focusing on the 

evidence from exposures or doses generally ranging 

from current levels to one or two orders of 

magnitude above current levels’’ (ISA, pp. lx–lxi). 

23 In determining a causal relationship to exist for 

Pb with specific health effects, the EPA concludes 

that ‘‘[e]vidence is sufficient to conclude that there 

is a causal relationship with relevant pollutant 

exposures (i.e., doses or exposures generally within 

one to two orders of magnitude of current levels)’’ 

(ISA, p. lxii). 

24The EPA concludes that a causal relationship 

is likely to exist between Pb exposure and cancer, 

based primarily on consistent, strong evidence from 

experimental animal studies, but inconsistent 

epidemiological evidence (ISA, section 4.10.5). 

Lead has also been classified as a probable human 

carcinogen by the International Agency for Research 

on Cancer, based mainly on sufficient animal 

evidence, and as reasonably anticipated to be a 

human carcinogen by the U.S. National Toxicology 

Program (ISA, section 4.10). 

25 In determining that there is likely to be a causal 

relationship for Pb with specific health effects, the 

EPA has concluded that ‘‘[e]vidence is sufficient to 

conclude that a causal relationship is likely to exist 

with relevant pollutant exposures, but important 

uncertainties remain’’ (ISA, p. lxii). 

neurological effects in children, and the 

potential for cardiovascular and renal 

effects in adults (73 FR 67006, 

November 12, 2008). The Administrator 

additionally considered higher and 

lower levels for the standard, 

concluding that a level of 0.15 mg/m3

provided for a standard that was neither 

more or less stringent than necessary for 

this purpose, recognizing that the Act 

does not require that primary standards 

be set at a zero-risk level, but rather at 

a level that reduces risk sufficiently so 

as to protect public health with an 

adequate margin of safety (73 FR 67007, 

November 12, 2008). For example, the 

Administrator additionally considered 

potential public health protection 

provided by standard levels above 0.15 

mg/m3, which he concluded were 

insufficient to protect public health 

with an adequate margin of safety. The 

Administrator also noted that in light of 

all of the evidence, including the 

evidence-based framework, the degree 

of public health protection likely 

afforded by standard levels below 0.15 

mg/m3 would be greater than what is 

necessary to protect public safety with 

an adequate margin of safety. 

The Administrator concluded, based 

on review of all of the evidence 

(including the evidence-based 

framework), that when taken as a whole 

the selected standard, including the 

indicator, averaging time, form, and 

level, would be ‘‘sufficient but not more 

than necessary to protect public health, 

including the health of sensitive 

subpopulations, with an adequate 

margin of safety’’ (73 FR 67007, 

November 12, 2008). 

2. Approach for the Current Review 

The approach in this review of the 

current primary standard takes into 

consideration the approach used in the 

last Pb NAAQS review, addressing key 

policy-relevant questions in light of 

currently available scientific and 

technical information. To evaluate 

whether it is appropriate to consider 

retaining the current primary Pb 

standard, or whether consideration of 

revision is appropriate, the EPA has 

adopted an approach in this review that 

builds upon the general approach used 

in the last review and reflects the 

broader body of evidence and 

information now available. As 

summarized above, the Administrator’s 

decisions in the prior review were based 

on an integration of information on 

health effects associated with exposure 

to Pb with that on relationships between 

ambient air Pb and blood Pb; expert 

judgments on the adversity and public 

health significance of key health effects; 

and policy judgments as to when the 

standard is requisite to protect public 

health with an adequate margin of 

safety. These considerations were 

informed by air quality and related 

analyses, quantitative exposure and risk 

assessments, and qualitative assessment 

of impacts that could not be quantified. 

Similarly in this review, as described 

in the PA, we draw on the current 

evidence and quantitative assessments 

of exposure pertaining to the public 

health risk of Pb in ambient air. In 

considering the scientific and technical 

information here as in the PA, we 

consider both the information available 

at the time of the last review and 

information newly available since the 

last review, including most particularly 

that which has been critically analyzed 

and characterized in the current ISA. 

We additionally consider the 

quantitative exposure/risk assessments 

from the last review that estimated Pbrelated IQ decrements associated with 

different air quality conditions in 

simulated at-risk populations in 

multiple case studies (PA, section 3.4; 

2007 REA). The evidence-based 

discussions presented below draw upon 

evidence from epidemiological studies 

and experimental animal studies 

evaluating health effects related to 

exposures to Pb, as discussed in the 

ISA. The exposure/risk-based 

discussions have drawn from the 

quantitative health risk analyses for Pb 

performed in the last Pb NAAQS review 

in light of the currently available 

evidence (PA, section 3.4; 2007 REA; 

REA Planning Document). Sections II.B 

through II.D below summarize the 

current health effects and exposure/risk 

information with a focus on the specific 

policy-relevant questions identified for 

these categories of information in the 

PA (PA, chapter 3). 

B. Health Effects Information 

1. Array of Effects 

Lead has been demonstrated to exert 

a broad array of deleterious effects on 

multiple organ systems as described in 

the assessment of the evidence available 

in this review and consistent with 

conclusions of past CDs (ISA, section 

1.6; 2006 CD, section 8.4.1). A sizeable 

number of studies on Pb health effects 

are newly available in this review and 

are critically assessed in the ISA as part 

of the full body of evidence. The newly 

available evidence reaffirms conclusions 

on the broad array of effects recognized 

for Pb in the last review (see ISA, 

section 1.10).21 Consistent with those 

conclusions, in the context of pollutant 

exposures considered relevant to the Pb 

NAAQS review,22 the ISA determines 

that causal relationships 23 exist for Pb 

with effects on the nervous system in 

children (cognitive function decrements 

and the group of externalizing behaviors 

comprising attention, impulsivity and 

hyperactivity), the hematological system 

(altered heme synthesis and decreased 

red blood cell survival and function), 

and the cardiovascular system 

(hypertension and coronary heart 

disease), and on reproduction and 

development (postnatal development 

and male reproductive function) (ISA, 

Table 1–2). Additionally, the ISA 

describes relationships between Pb and 

effects on the nervous system in adults, 

on immune system function and with 

cancer 24 as likely to be causal 25 (ISA, 

Table 1–2, sections 1.6.4 and 1.6.7). 

In some categories of health effects, 

there is newly available evidence 

regarding some aspects of the effects 

described in the last review or that 

strengthens our conclusions regarding 

aspects of Pb toxicity on a particular 

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26Several of these studies involve NHANES III 

cohorts for which early childhood exposures were 

generally much higher than those common in the 

U.S. today (ISA, section 4.8.5). 

27Studies from the late 1960s and 1970s suggest 

that adult blood Pb levels during that period ranged 

from roughly 13 to 16 mg/dL and from 15 to 30 mg/ 

dL in children aged 6 and younger (ISA, section 

4.4.1). 

physiological system. Among the 

nervous system effects of Pb, the newly 

available evidence is consistent with 

conclusions in the previous review 

which recognized that ‘‘[t]he neurotoxic 

effects of Pb exposure are among those 

most studied and most extensively 

documented among human population 

groups’’ (2006 CD, p. 8–25) and took 

note of the diversity of studies in which 

such effects of Pb exposure early in 

development (from fetal to postnatal 

childhood periods) have been observed 

(2006 CD, p. E–9). Nervous system 

effects that receive prominence in the 

current review, as in previous reviews, 

include those affecting cognitive 

function and behavior in children (ISA, 

section 4.3), with conclusions that are 

consistent with findings of the last 

review. 

Across the broad array of Pb effects 

for systems and processes other than the 

nervous system, the evidence base has 

been augmented with additional 

epidemiological investigations in a 

number of areas, including 

developmental outcomes, such as 

puberty onset, and adult outcomes 

related to cardiovascular function, for 

which several large cohorts have been 

analyzed (ISA, Table 1–8 and sections 

4.4 and 4.8). Conclusions on these other 

systems and processes are generally 

consistent with conclusions reached in 

the last review, while also extending our 

conclusions on some aspects of these 

effects (ISA, section 4.4 and Table 1–8). 

Based on the extensive assessment of 

the full body of evidence available in 

this review, the major conclusions 

drawn by the ISA regarding health 

effects of Pb in children include the 

following (ISA, p. lxxxvii). 

Multiple epidemiologic studies conducted 

in diverse populations of children 

consistently demonstrate the harmful effects 

of Pb exposure on cognitive function (as 

measured by IQ decrements, decreased 

academic performance and poorer 

performance on tests of executive 

function). . . . Evidence suggests that some 

Pb-related cognitive effects may be 

irreversible and that the neurodevelopmental 

effects of Pb exposure may persist into 

adulthood (Section 1.9.4). Epidemiologic 

studies also demonstrate that Pb exposure is 

associated with decreased attention, and 

increased impulsivity and hyperactivity in 

children (externalizing behaviors). This is 

supported by findings in animal studies 

demonstrating both analogous effects and 

biological plausibility at relevant exposure 

levels. Pb exposure can also exert harmful 

effects on blood cells and blood producing 

organs, and is likely to cause an increased 

risk of symptoms of depression and anxiety 

and withdrawn behavior (internalizing 

behaviors),decreases in auditory and motor 

function, asthma and allergy, as well as 

conduct disorders in children and young 

adults. There is some uncertainty about the 

Pb exposures contributing to the effects and 

blood Pb levels observed in epidemiologic 

studies; however, these uncertainties are 

greater in studies of older children and 

adults than in studies of young children 

(Section 1.9.5). 

Based on the extensive assessment of 

the full body of evidence available in 

this review, the major conclusions 

drawn by the ISA regarding health 

effects of Pb in adults include the 

following (ISA, p. lxxxviii). 

A large body of evidence from both 

epidemiologic studies of adults and 

experimental studies in animals 

demonstrates the effect of long-term Pb 

exposure on increased blood pressure (BP) 

and hypertension (Section 1.6.2). In addition 

to its effect on BP, Pb exposure can also lead 

to coronary heart disease and death from 

cardiovascular causes and is associated with 

cognitive function decrements, symptoms of 

depression and anxiety, and immune effects 

in adult humans. The extent to which the 

effects of Pb on the cardiovascular system are 

reversible is not well-characterized. 

Additionally, the frequency, timing, level, 

and duration of Pb exposure causing the 

effects observed in adults has not been 

pinpointed, and higher past exposures may 

contribute to the development of health 

effects measured later in life. 

As in prior reviews of the Pb NAAQS, 

this review is focused on those effects 

most pertinent to ambient air Pb 

exposures. Given the reductions in 

ambient air Pb concentrations over the 

past decades, these effects are generally 

those associated with the lowest levels 

of Pb exposure that have been 

evaluated. Additionally, we recognize 

the limitations on our ability to draw 

conclusions regarding the exposure 

conditions contributing to the findings 

from epidemiological analyses of blood 

Pb levels in populations of older 

children and adults, particularly in light 

of their history of higher Pb exposures. 

Evidence available in future reviews 

may better inform this issue. In the last 

review, while recognizing the range of 

health effects in variously aged 

populations related to Pb exposure, we 

focused on the health effects for which 

the evidence was strongest with regard 

to relationships with the lowest 

exposure levels, neurocognitive effects 

in young children. 

As is the case for studies of nervous 

system effects in children (discussed in 

more detail in section II.B.3 below), 

newly available studies of other effects 

in child and adult cohorts include 

cohorts with similar or somewhat lower 

mean blood Pb levels than in previously 

available studies. Categories of effects 

for which a causal relationship has been 

concluded in the ISA and for which 

there are a few newly available 

epidemiological studies indicating 

blood Pb associations with effects in 

study groups with somewhat lower 

blood Pb levels than previously 

available for these effects include effects 

on development (delayed puberty onset) 

and reproduction (male reproductive 

function) and on the cardiovascular 

system (hypertension) (ISA, sections 4.4 

and 4.8; 2006 CD, sections 6.5 and 6.6). 

With regard to the former category, 

study groups in the newly available 

studies include groups composed of 

older children ranging up to age 18 

years, for which there is increased 

uncertainty regarding historical 

exposures and their role in the observed 

effects.26 An additional factor that 

handicaps our consideration of 

exposure levels associated with these 

findings is the appreciable uncertainty 

associated with our understanding of Pb 

biokinetics during this lifestage (ISA, 

sections 3.2, 3.3, and 4.8.6). The 

evidence newly available for Pb 

relationships with cardiovascular effects 

in adults include some studies with 

somewhat lower blood Pb levels than in 

the last review. The long exposure 

histories of these cohorts, as well as the 

generally higher Pb exposures of the 

past, complicate conclusions regarding 

exposure levels that may be eliciting 

observed effects (ISA, sections 4.4.2.4 

and 4.4.7).27 Accordingly, as discussed 

further below, we focus in this review, 

as in the last, on neurocognitive effects 

in young children. 

2. Critical Periods of Exposure 

As in the last review, we base our 

current understanding of health effects 

associated with different Pb exposure 

circumstances at various stages of life or 

in different populations on the full body 

of available evidence and primarily on 

epidemiological studies of health effects 

associated with population Pb 

biomarker levels (discussed further in 

section II.B.3 below). The 

epidemiological evidence is 

overwhelmingly composed of studies 

that rely on blood Pb for the exposure 

metric, with the remainder largely 

including a focus on bone Pb. Because 

these metrics reflect Pb in the body (e.g., 

as compared to Pb exposure 

concentrations) and, in the case of blood 

Pb, reflect Pb available for distribution 

to target sites, they strengthen the 

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28The declines in Pb exposure concentrations 

occurring from the 1970s through the early 1990s 

(and experienced by middle aged and older adults 

of today), as indicated by NHANES blood Pb 

information, were particularly dramatic (ISA, 

section 3.4.1). 

29The evidence from experimental animal studies 

can be informative with regard to key aspects of 

exposure circumstances in eliciting specific effects, 

thus informing our interpretation of 

epidemiological evidence. For example, the animal 

evidence base with regard to Pb effects on blood 

pressure demonstrates the etiologically-relevant 

role of long-term exposure (ISA, section 4.4.1). This 

finding then informs consideration of 

epidemiological studies of adult populations for 

whom historical exposures were likely more 

substantial than concurrent ones, suggesting that 

the observed effects may be related to the past 

exposure (ISA, section 4.4.1). For other health 

effects, the animal evidence base may or may not 

be informative in this manner. 

30 In the collective body of evidence of nervous 

system effects in children, it is difficult to 

distinguish exposure in later lifestages (e.g., school 

age) and its associated risk from risks resulting from 

exposure in prenatal and early childhood (ISA, 

section 4.3.11). While early childhood is recognized 

as a time of increased susceptibility, a difficulty in 

identifying a discrete period of susceptibility from 

epidemiological studies has been that the period of 

peak exposure, reflected in peak blood Pb levels, is 

around 18–27 months when hand-to-mouth activity 

is at its maximum (ISA, section 3.4.1 and 5.2.1.1; 

2006 CD, p. 6–60). The task is additionally 

complicated by the role of maternal exposure 

history in contributing Pb to the developing fetus 

(ISA, section 3.2.2.4.). 

evidence base for purposes of drawing 

causal conclusions with regard to Pb 

generally. The complexity of Pb 

exposure pathways and internal 

dosimetry, however, tends to limit the 

extent to which these types of studies 

inform our more specific understanding 

of the Pb exposure circumstances (e.g., 

timing within lifetime, duration, 

frequency and magnitude) eliciting the 

various effects. 

As at the time of the last review (and 

discussed more fully in section II.B.3 

below), assessment of the full evidence 

base, including evidence newly 

available in this review, demonstrates 

that Pb exposure prenatally and also in 

early childhood can contribute to 

neurocognitive impacts in childhood, 

with evidence also indicating the 

potential for effects persisting into 

adulthood (ISA, sections 1.9.4, 1.9.5, 

and 1.10). In addition to the observed 

associations of prenatal and childhood 

blood Pb with effects at various ages in 

childhood, there is also evidence of Pbrelated cognitive function effects in nonoccupationally exposed adults (ISA, 

section 4.3.11). This includes evidence 

of associations of such effects in 

adulthood with childhood blood Pb 

levels and in other cohorts, with 

concurrent (adult) blood Pb levels (ISA, 

sections 4.3.2.1, 4.3.2.7 and 4.3.11). As 

the studies finding associations of adult 

effects with childhood blood Pb levels 

did not examine adult blood Pb levels, 

the relative influence of adult Pb 

exposure cannot be ascertained, and a 

corresponding lack of early life 

exposure or biomarker measurements 

for the latter studies limits our ability to 

draw conclusions regarding specific Pb 

exposure circumstances eliciting the 

observed effects (4.3.11). Findings of 

stronger associations for adult 

neurocognitive effects with bone Pb, 

however, indicate the role of historical 

or cumulative exposures for those 

effects (ISA, section 4.3). 

A critical aspect of much of the 

epidemiological evidence, particularly 

studies focused on adults (and older 

children) in the U.S. today, is the 

backdrop of generally declining 

environmental Pb exposure (from higher 

exposures during their younger years) 

that is common across many study 

populations (ISA, p. 4–2).28 An 

additional factor complicating the 

interpretation of health effect 

associations with blood Pb 

measurements in older children and 

younger adults is the common behaviors 

of younger children (e.g., hand-to-mouth 

contact) that generally contribute to 

relatively greater exposures earlier in 

life (ISA, sections 3.1.1, 4.2.1). Such 

exposure histories for adults and older 

children complicate our ability to draw 

conclusions regarding critical time 

periods and lifestages for Pb exposures 

eliciting the effects for which 

associations with Pb biomarkers have 

been observed in these populations (e.g., 

ISA, section 1.9.6).29 Thus, our 

confidence is greatest in the role of early 

childhood exposure in contributing to 

Pb-related neurocognitive effects that 

have been associated with blood Pb 

levels in young children. This is due, in 

part, to the relatively short exposure 

histories of young children (ISA, 

sections 1.9.4, 1.9.6 and 4.3.11). 

Epidemiological analyses evaluating 

risk of neurocognitive impacts (e.g., 

reduced IQ) associated with different 

blood Pb metrics in cohorts with 

differing exposure patterns (including 

those for which blood Pb levels at 

different ages were not highly 

correlated) also indicate associations 

with blood Pb measurements concurrent 

with full scale IQ (FSIQ) tests at ages of 

approximately 6–7 years. The analyses 

did not, however, conclusively 

demonstrate stronger findings for early 

(e.g., age 2 years) or concurrent blood Pb 

(ISA, section 4.3.11).30 The 

experimental animal evidence 

additionally indicates early life 

susceptibility (ISA, section 4.3.15 and p. 

5–21). Thus, while uncertainties remain 

with regard to the role of Pb exposures 

during a particular age of life in eliciting 

nervous system effects, such as 

cognitive function decrements, the full 

evidence base continues to indicate 

prenatal and early childhood lifestages 

as periods of increased Pb-related risk 

(ISA, sections 4.3.11 and 4.3.15). We 

recognize increasing uncertainty, 

however, in our understanding of the 

relative impact on neurocognitive 

function of additional Pb exposure of 

children by school age or later that is 

associated with limitations of the 

currently available evidence, including 

epidemiological cohorts with generally 

similar temporal patterns of exposure. 

As in the last review, there is also 

substantial evidence of other 

neurobehavioral effects in children, 

including effects on externalizing 

behaviors (reduced attention span, 

increased impulsivity, hyperactivity, 

and conduct disorders) and on 

internalizing behaviors. The evidence 

for many of these endpoints, as with 

neurocognitive effects, also includes 

associations of effects at various ages in 

childhood and for some effects, into 

adulthood, with blood Pb levels 

reflective of several different lifestages 

(e.g., prenatal and several different ages 

in childhood) (ISA, sections 4.3.3 and 

4.3.4). There is similar or relatively less 

extensive evidence to inform our 

understanding of such effects associated 

with specific time periods of exposure 

at specific lifestages than is the case for 

effects on cognitive function. 

Across the range of Pb effects on 

physiological systems and processes 

other than the nervous system, the 

evidence base for blood pressure and 

hypertension is somewhat more 

informative with regard to the 

circumstances of Pb exposure eliciting 

the observed effects than are the 

evidence bases for many other effects. In 

the case of Pb-induced increases in 

blood pressure, the evidence indicates 

an importance of long-term exposure 

(ISA, sections 1.6.2 and 4.4.7.1). The 

greater uncertainties regarding the time, 

duration and magnitude of exposure 

contributing to these observed health 

effects complicate identification of 

sensitive lifestages and associated 

exposure patterns that might be 

compared with our understanding of the 

sensitivity of young children to 

neurocognitive impacts of Pb. Thus, 

while augmenting the evidence base on 

these additional endpoints, the newly 

available evidence does not lead us to 

identify a health endpoint expected to 

be more sensitive to Pb exposure than 

neurocognitive endpoints in children, 

leading us to continue to conclude that 

the appropriate primary focus for our 

review is on neurocognitive endpoints 

in children. 

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31The value of 2 mg/dL refers to the regression 

analysis of blood Pb and end-of-grade test scores, 

in which blood Pb was represented by categories for 

integer values of blood Pb from 1 mg/dL to 9 and 

>10 mg/dL from large statewide database. A 

significant effect estimate was reported for test 

scores with all blood Pb categories in comparison 

to the reference category (1 mg/dL), which included 

results at and below the limit of detection. Mean 

levels are not provided for any of the categories 

(Miranda et al., 2009). 

32The 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), 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. These tests, however, are not appropriate for 

children under age 3. For such children, studies 

generally use the age-appropriate Bayley Scales of 

Infant Development as a measure of cognitive 

development. 

33Limitations of this study included a lack of 

consideration of potential confounding by parental 

caregiving quality or IQ (ISA, Table 4–3). 

In summary, as in the last review, we 

continue to recognize a number of 

uncertainties regarding the 

circumstances of Pb exposure, including 

timing or lifestages, eliciting specific 

health effects. Consideration of the 

evidence newly available in this review 

has not appreciably changed our 

understanding on this topic. The 

relationship of long-term exposure to Pb 

with hypertension and increased blood 

pressure in adults is substantiated 

despite some uncertainty regarding the 

exposures circumstances (e.g., 

magnitude and timing) contributing to 

blood Pb levels measured in 

epidemiological studies. Across the full 

evidence base, the effects for which our 

understanding of relevant exposure 

circumstances is greatest are 

neurocognitive effects in young 

children. Moreover, available evidence 

does not suggest a more sensitive 

endpoint. Thus, we continue to 

recognize and give particular attention 

to the role of Pb exposures relatively 

early in childhood in contributing to 

neurocognitive effects, some of which 

may persist into adulthood. 

3. Nervous System Effects in Children 

In considering the question of levels 

of Pb exposure at which health effects 

occur, we recognize, as discussed in 

sections II.B.1 and II.B.2 above, that the 

epidemiological evidence base for our 

consideration in this review, as in the 

past, includes substantial focus on 

internal biomarkers of exposure, such as 

blood Pb, with relatively less 

information specific to exposure levels, 

including those derived from air-related 

pathways. Given that blood and bone Pb 

are integrated markers of aggregate 

exposure across all sources and 

exposure pathways, our interpretation 

of studies relying on them is informed 

by what is known regarding the 

historical context and exposure 

circumstances of the study populations. 

For example, a critical aspect of much 

of the epidemiological evidence is the 

backdrop of generally declining Pb 

exposure over the past several decades 

(e.g., ISA, sections 2.5 and 3.4.1; 2006 

CD, section 3.4). Thus, as a generality, 

recent epidemiological studies of 

populations with similar characteristics 

as those studied in the past tend to 

involve lower overall Pb exposures and 

accordingly lower blood Pb levels. This 

has been of particular note in the 

evidence of blood Pb associations with 

nervous system effects, particularly 

impacts on cognitive function in 

children, for which we have seen 

associations with progressively lower 

childhood blood Pb levels across past 

reviews (ISA, section 4.3.12; 1986 CD; 

USEPA, 1990a; 2006 CD; 73 FR 66976, 

November 12, 2008). 

The evidence currently available with 

regard to the magnitude of blood Pb 

levels associated with neurocognitive 

effects in children is generally 

consistent with that available in the 

review completed in 2008. Nervous 

system effects in children, specifically 

effects on cognitive function, continue 

to be the effects that are best 

substantiated as occurring at the lowest 

blood Pb concentrations (ISA, pp. 

lxxxvii–lxxxviii). Associations of blood 

Pb with effects on cognitive function 

measures in children have been 

reported in many studies across a range 

of childhood blood Pb levels, including 

study group (mean/median) levels 

ranging down to 2 mg/dL (e.g., ISA, p. 

lxxxvii and section 4.3.2).31

Among the analyses of lowest study 

group blood Pb levels at the youngest 

ages are analyses available in the last 

review of Pb associations with 

neurocognitive function decrement in 

study groups with mean levels on the 

order of 3–4 mg/dL in children aged 24 

months or ranging from 5 to 7 years (73 

FR 66978–66979, November 12, 2008; 

ISA, sections 4.3.2.1 and 4.3.2.2; 

Bellinger and Needleman, 2003; 

Canfield et al., 2003; Lanphear et al., 

2005; Tellez-Rojo et al., 2006; Bellinger, 

2008; Canfield, 2008; Tellez-Rojo, 2008; 

Kirrane and Patel, 2014).32 Newly 

available in this review are two studies 

reporting association of blood Pb levels 

prior to 3 years of age with academic 

performance on standardized tests in 

primary school; mean blood Pb levels in 

these studies were 4.2 and 4.8 mg/dL 

(ISA, section 4.3.2.5; Chandramouli et 

al., 2009; Miranda et al., 2009). One of 

these two studies, which represented 

integer blood Pb levels as categorical 

variables, indicated a small effect on 

end-of-grade reading score of blood Pb 

levels as low as 2 mg/dL, after 

adjustment for age of measurement, 

race, sex, enrollment in free or reduced 

lunch program, parental education, and 

school type (Miranda et al., 2009). 

In a newly available study of blood Pb 

levels at primary school age, a 

significant association of blood Pb in 

children aged 8–11 years and 

concurrently measured FSIQ was 

reported for a cross-sectional cohort in 

Korea with a mean blood Pb level of 1.7 

mg/dL and range of 0.43–4.91 mg/dL 

(Kim et al., 2009).33 In considering the 

blood Pb levels in this study, we note 

that blood Pb levels in children aged 8– 

11 are generally lower than those in preschool children, for reasons related to 

behavioral and other factors (ISA, 

sections 3.3.5, 3.4.1 and 5.2.1.1). It is 

likely that the blood Pb levels of this 

study group at earlier ages, e.g., prior to 

school entry, were higher and the 

available information does not provide 

a basis to judge whether the blood Pb 

levels in this study represent lower 

exposure levels than those experienced 

by the younger study groups. In still 

older children, a large cross-sectional 

investigation of blood Pb association 

with effects on memory and learning 

that was available in the last review was 

focused on children aged 6–16 years, 

born during 1972–1988, with a mean 

blood Pb of 1.9 mg/dL (Lanphear et al., 

2000). A study newly available in this 

review, focused on a subset of the 

earlier study cohort (ages 12–16, born 

during 1975–1982), also reports a 

significant negative association of blood 

Pb with learning and memory test 

results with mean blood Pb levels of 

approximately 2 mg/dL (ISA, section 

4.3.2.3; Lanphear et al., 2000; Krieg et 

al., 2010). In considering these study 

findings with regard to the question of 

exposure levels eliciting effects, we 

recognize, however, that blood Pb levels 

are, in general, lower among teenagers 

than young children and also that, for 

these subjects specifically, the 

magnitude of blood Pb levels during the 

earlier childhood (e.g., pre-school ages) 

was much higher. For example, the 

mean blood Pb levels for the 1–5 year 

old age group in the NHANES 1976–80 

sample was 15 mg/dL, declining to 3.6 

mg/dL in the NHANES 1988–1991 

sample (Pirkle et al., 1994; ISA, section 

3.4.1). In summary, the available 

information is for population groups of 

ages for which the NHANES samples 

indicate exposure levels were higher 

earlier in childhood. Thus, in light of 

the NHANES information, although the 

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34 In focusing on effects associated with blood Pb 

levels in early childhood, however, we additionally 

recognize the evidence across categories of effects 

that relate to blood Pb levels in older child study 

groups (for which early childhood exposure may 

have had an influence) which provides additional 

support to an emphasis on nervous system effects 

(ISA, sections 4.3, 4.4, 4.5, 4.6, 4.7, 4.8). 

35The Bayley Scales of Infant Development, 

Mental Development Index is a well-standardized 

and widely used assessment measure of infant 

cognitive development. Scores earlier than 24 

months are not necessarily strongly correlated with 

later FSIQ scores in children with normal 

development (ISA, section 4.3.15.1). 

blood Pb levels in the studies of 

cognitive effects in older child 

population groups are lower (at the time 

of the study) than the younger child 

study levels, the studies of older 

children do not provide a basis for 

concluding a role for lower Pb exposure 

levels than those experienced by the 

younger study groups. 

With regard to other nervous system 

effects in children, the evidence base at 

lower blood Pb levels is somewhat 

extended since the last review with 

regard to the evidence on Pb and effects 

on externalizing behaviors, such as 

attention, impulsivity, hyperactivity and 

conduct disorders (ISA, section 4.3.3 

and Table 4–17). Several newly 

available studies investigating the role 

of blood Pb levels in older children 

(primary school age and older) have 

reported significant associations for 

these effects with concurrent blood Pb 

levels, with mean levels generally on 

the order of 5 mg/dL or higher (ISA, 

section 4.3.3). One exception is the 

newly available cross-sectional, 

categorical analysis of the NHANES 

2001–2004 sample of children aged 

8–15 years, which found higher 

prevalence of conduct disorder in the 

subgroup with concurrent blood Pb 

levels of 0.8–1.0 mg/dL as compared to 

the <0.8 mg/dL group (ISA, section 4.3.4 

and Table 4–12). As noted above, we 

recognize that many of these children, 

born between 1986 and 1996, are likely 

to have had much higher Pb exposures 

(and associated blood Pb levels) in their 

earlier years than those commonly 

experienced by young children today, 

thus making this study relatively 

uninformative with regard to evidence 

of effects associated with lower 

exposure levels than provided by 

evidence previously available. 

In summary, our conclusions 

regarding exposure levels at which Pb 

health effects occur, particularly with 

regard to such levels that might be 

common in the U.S. today, are 

complicated now, as in the last review, 

by several factors. These factors include 

the scarcity of information in 

epidemiological studies on cohort 

exposure histories, as well as by the 

backdrop of higher past exposure levels 

which frame the history of most, if not 

all, older study cohorts. Recognizing the 

complexity, as well as the potential role 

of higher exposure levels in the past, we 

continue to focus our consideration of 

this question on the evidence of effects 

in young children for which our 

understanding of exposure history is 

less uncertain.34 Within this evidence 

base, we recognize the lowest study 

group blood Pb levels to be associated 

with effects on cognitive function 

measures, indicating that to be the most 

sensitive endpoint. As described above, 

the evidence available in this review is 

generally consistent with that available 

in the last review with regard to blood 

Pb levels at which such effects had been 

reported (ISA, section 4.3.2; 2006 CD, 

section 8.4.2.1; 73 FR 66976–66979, 

November 12, 2008). As blood Pb levels 

are a reflection of exposure history, 

particularly in early childhood (ISA, 

section 3.3.2), we conclude, by 

extension, that the currently available 

evidence does not indicate Pb effects at 

exposure levels appreciably lower than 

recognized in the last review. 

We additionally note that, as in the 

last review, a threshold blood Pb level 

with which nervous system effects, and 

specifically cognitive effects, occur in 

young children cannot be discerned 

from the currently available studies 

(ISA, sections 1.9.3 and 4.3.12). 

Epidemiological analyses have reported 

blood Pb associations with cognitive 

effects (FSIQ or BSID MDI 35) for young 

child population subgroups (age 5 years 

or younger) with individual blood Pb 

measurements as low as approximately 

1 mg/dL and mean concentrations as low 

as 2.9 to 3.8 mg/dL (ISA, section 4.3.12; 

Bellinger and Needleman, 2003; 

Bellinger, 2008; Canfield et al., 2003; 

Canfield, 2008; Tellez-Rojo et al., 2006; 

Tellez-Rojo, 2008). As concluded in the 

ISA, however, ‘‘the current evidence 

does not preclude the possibility of a 

threshold for neurodevelopmental 

effects in children existing with lower 

blood levels than those currently 

examined’’ (ISA, section 4.3.13). 

Important uncertainties associated 

with the evidence of effects at low 

exposure levels are similar to those 

recognized in the last review, including 

the shape of the concentration-response 

relationship for effects on 

neurocognitive function at low blood Pb 

levels in today’s young children. Also of 

note is our interpretation of associations 

between blood Pb levels and effects in 

epidemiological studies, with which we 

recognize uncertainty with regard to the 

specific exposure circumstances 

(timing, duration, magnitude and 

frequency) that have elicited the 

observed effects, as well as uncertainties 

in relating ambient air concentrations 

(and associated air-related exposures) to 

blood Pb levels in early childhood, as 

discussed in section II.B.2 above. We 

additionally recognize uncertainties 

associated with conclusions drawn with 

regard to the nature of the 

epidemiological associations with blood 

Pb (e.g., ISA, section 4.3.13), but note 

that, based on consideration of the full 

body of evidence for neurocognitive 

effects, the EPA has determined a causal 

relationship to exist between relevant 

blood Pb levels and neurocognitive 

impacts in children (ISA, section 

4.3.15.1). 

Based primarily on studies of FSIQ, 

the assessment of the currently available 

studies, as was the case in the last 

review, continues to recognize a 

nonlinear relationship between blood 

Pb and effects on cognitive function, 

with a greater incremental effect (greater 

slope) at lower relative to higher blood 

Pb levels within the range thus far 

studied, extending from well above 10 

mg/dL to below 5 mg/dL (ISA, section 

4.3.12). This was supported by the 

evidence available in the last review, 

including the analysis of the large 

pooled international dataset comprised 

of blood Pb measurements and IQ test 

results from seven prospective cohorts 

(Lanphear et al., 2005; Rothenberg and 

Rothenberg, 2005; ISA, section 4.3.12). 

The blood Pb measurements in this 

pooled dataset that were concurrent 

with the IQ tests ranged from 2.5 mg/dL 

to 33.2 mg/dL. The study by Lanphear et 

al. (2005) additionally presented 

analyses that stratified the dataset based 

on peak blood Pb levels (e.g., with 

cutpoints of 7.5 mg/dL and 10 mg/dL 

peak blood Pb) and found that the 

coefficients from linear models of the 

association for IQ with concurrent blood 

Pb were higher in the lower peak blood 

Pb level subsets than the higher groups 

(ISA, section 4.3.12; Lanphear et al., 

2005). 

We note that since the completion of 

the ISA, two errors have been identified 

with the pooled dataset analyzed by 

Lanphear et al. (2005) (Kirrane and 

Patel, 2014). A recent publication and 

the EPA have separately recalculated 

the statistics and mathematical model 

parameters of Lanphear et al. (2005) 

using the corrected pooled dataset (see 

Kirrane and Patel, 2014). While the 

magnitude of the loglinear and linear 

regression coefficients are modified 

slightly based on the corrections, the 

conclusions drawn from these 

coefficients, including the finding of a 

steeper slope at lower (as compared to 

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36One of these four is from the analysis of the 

lowest blood Pb subset of the pooled international 

study by Lanphear et al. (2005). The nonlinear 

model developed from the full pooled dataset is the 

basis of the C–R functions used in the 2007 REA, 

in which risk was estimated over a large range of 

blood Pb levels (PA, section 3.4.3.3). Given the 

narrower focus of the evidence-based framework on 

IQ response at the end of studied blood Pb levels 

(closer to U.S. mean level), the C–R functions in 

Table 1 are from linear analyses (each from separate 

publications) for the study group subsets with blood 

Pb levels closest to mean for children in the U.S. 

today. 

37 In the context of ‘‘at-risk populations,’’ the term 

‘‘population’’ refers to persons having one or more 

qualities or characteristics including, for example, 

a specific pre-existing illness or a specific age or 

lifestage, with lifestage referring to a distinguishable 

time frame in an individual’s life characterized by 

unique and relatively stable behavioral and/or 

physiological characteristics that are associated 

with development and growth. 

higher) blood Pb concentrations, are not 

affected (Kirrane and Patel, 2014). 

In other publications, stratified 

analyses of several individual cohorts 

also observed higher coefficients for 

blood Pb relationships with measures of 

neurocognitive function in lower as 

compared to higher blood Pb subgroups 

(ISA, section 4.3.12; Canfield et al., 

2003; Bellinger and Needleman, 2003; 

Kordas et al., 2006; Tellez-Rojo et al., 

2006). Of these subgroup analyses, those 

involving the lowest mean blood Pb 

levels and closest to the current mean 

for U.S. preschool children are listed in 

Table 1 (drawn from Table 3 of the 2008 

final rulemaking notice [73 FR 67003, 

November 12, 2008], and Kirrane and 

Patel, 2014).36 These analyses were 

important inputs for the evidence-based, 

air-related IQ loss framework which 

informed decisions on a revised 

standard in the last review (73 FR 

67005, November 12, 2008), discussed 

in section II.A.1 above. As the 

framework focused on the median of the 

four slopes in Table 1, the change to the 

one from Lanphear et al. (2005) based 

on the recent recalculation described 

above has no impact on conclusions 

drawn from the framework. 

TABLE 1—SUMMARY OF QUANTITATIVE RELATIONSHIPS OF IQ AND BLOOD PB FOR ANALYSES WITH BLOOD PB LEVELS

CLOSEST TO THOSE OF YOUNG CHILDREN IN THE U.S. TODAY

Blood Pb levels 

(μg/dL) 

Study/analysis 

Average linear 

slope A

(IQ B points 

Geometric mean per μg/dL) Range 

(min–max) 

2.9 ................................................................................. 0.8–4.9 Tellez-Rojo et al. (2006)B, subgroup w. concurrent 

blood Pb <5 μg/dL.

¥1.71 

3.3 ................................................................................. 0.9–7.4 Lanphear et al. (2005)C, subgroup w. peak blood Pb 

<7.5 μg/dL.

¥2.53 

3.32 ............................................................................... 0.5–8.4 Canfield et al. (2003) C D, subgroup w. peak blood Pb 

<10 μg/dL.

¥1.79 

3.8 ................................................................................. 1–9.3 Bellinger and Needleman (2003) C E, subgroup w. 

peak blood Pb <10 μg/dL.

¥1.56 

Median value ......................................................... ........................ ....................................................................................... ¥1.75 

A—Average linear slope estimates here are generally for relationship with IQ assessed concurrently with blood Pb measurement. As exceptions, Bellinger & Needleman (2003) slope is relationship for 10 year old IQ with blood Pb levels at 24 months, and the data for Boston cohort included in Lanphear et al. (2005) slope are relationship for 10 year old IQ with blood Pb levels at 5 years. 

B—The slope for Tellez-Rojo et al. (2006) is for BSID (MDI), a measure of cognitive development appropriate to study population age (24- 

mos). The blood Pb levels for this subgroup are from Tellez-Rojo (2008). 

C—The Lanphear et al. (2005) pooled international study also 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). Thus, the ages 

at the blood Pb measurements used in derivation of the linear slope for the Lanphear et al. (2005) subgroup shown here are 5 to 7 years. The 

blood Pb levels and coefficient presented here for Lanphear et al. (2005) study group reflect the recalculation using the corrected pooled dataset 

(Kirrane and Patel, 2014). 

D—Blood Pb levels for this subgroup are from Canfield (2008). 

E—Blood Pb levels for this subgroup are from Bellinger (2008). 

Several studies newly available in the 

current review have, in all but one 

instance, also found a nonlinear blood 

Pb-cognitive function relationship in 

nonparametric regression analyses of 

the cohort blood Pb levels analyzed 

(ISA, section 4.3.12). These studies, 

however, used statistical approaches 

that did not produce quantitative results 

for each blood Pb group (ISA, section 

4.3.12). Thus, newly available studies 

have not extended the range of 

observation for quantitative estimates of 

this relationship to lower blood Pb 

levels than those of the previous review. 

The ISA further notes that the potential 

for nonlinearity has not been examined 

in detail within a lower, narrower range 

of blood Pb levels than those of the full 

cohorts thus far studied in the currently 

available evidence base (ISA, section 

4.3.12). Such an observation in the last 

review supported the consideration of 

linear slopes with regard to blood Pb 

levels at and below those represented in 

Table 1. In summary, the newly 

available evidence does not 

substantively alter our understanding of 

the C–R relationship (including 

quantitative aspects) for neurocognitive 

impact, such as IQ with blood Pb in 

young children. 

4. At-Risk Populations 

In this section, we use the term ‘‘atrisk populations’’ 37 to recognize 

populations that have a greater 

likelihood of experiencing Pb-related 

health effects, i.e., groups with 

characteristics that contribute to an 

increased risk of Pb-related health 

effects. These populations are also 

sometimes referred to as sensitive 

groups (as in section I.A above). In 

identifying factors that increase risk of 

Pb-related health effects, the EPA has 

considered evidence regarding factors 

contributing to increased susceptibility, 

generally including physiological or 

intrinsic factors contributing to a greater 

response for the same exposure, and 

those contributing to increased 

exposure, including that resulting from 

behavior leading to increased contact 

with contaminated media (ISA, Chapter 

5). Physiological risk factors include 

both conditions contributing to a 

group’s increased risk of effects at a 

given blood Pb level, and those that 

contribute to blood Pb levels higher 

than those otherwise associated with a 

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38As noted in the ISA, ‘‘in most instances, 

‘susceptibility’ refers to biological or intrinsic 

factors (e.g., age and sex) while ‘vulnerability’ refers 

to nonbiological or extrinsic factors (e.g., 

socioeconomic status [SES])’’ and the terms ‘‘atrisk’’ and ‘‘sensitive’’ populations have in various 

instances been used to encompass these concepts 

more generally (ISA, p. 5–1). In providing detail 

regarding factors contributing to an ‘‘at-risk’’ status 

in this section, we have used the other terms in 

particular instances, with our usage consistent with 

these common definitions. 

39The ISA concludes that studies of race/

ethnicity provide adequate evidence that race/

ethnicity is an at-risk factor based on the higher 

exposure observed among non-white populations 

and some modification observed in studies of 

associations between Pb levels and some health 

effects, such as hypertension (ISA, section 6.4). 

40The evidence for SES continues to indicate 

increased blood Pb levels in lower income children, 

although its role with regard to an increased health 

risk for the same blood Pb level is unclear and its 

role generally with regard to Pb-related risk is 

somewhat complicated. SES often serves as a 

marker term for one or a combination of unspecified 

or unknown environmental or behavioral variables. 

Further, it is independently associated with an 

adverse impact on neurocognitive development, 

and a few studies have examined SES as a potential 

modifier of the association of childhood Pb 

exposure with cognitive function with inconsistent 

findings regarding low SES as a potential risk 

factor. The ISA concludes the evidence for SES as 

a Pb risk factor is suggestive, based on the greater 

exposures or blood Pb levels in some low SES 

groups (ISA, section 5.4). 

41The ISA identifies older adulthood as a 

lifestage of potentially greater risk of Pb-related 

health effects based primarily on the evidence of 

increases in blood Pb levels during this lifestage 

(ISA, sections 5.2.1.2, 5.3.1.2, and 5.4), as well as 

observed associations of some cardiovascular and 

nervous system effects with bone and blood Pb in 

older populations, with biological plausibility for 

the role of Pb provided by experimental animal 

studies (ISA, sections 4.3.5, 4.3.7 and 4.4). Exposure 

histories of older adult study populations, which 

included younger years during the time of leaded 

gasoline usage and other sources of Pb exposures 

which were more prevalent in the past than today, 

are likely contributors to their blood Pb levels (ISA, 

pp. lx–lxi; Figure 2–1 and sections 2.5.2, 3.3.5 and 

5.2.1.2). 

given Pb exposure (e.g., ISA, sections 

5.3 and 5.1, respectively). 

The information newly available in 

this review has not substantially altered 

our previous understanding of at-risk 

populations for Pb in ambient air. As in 

the last review, the factor most 

prominently recognized to contribute to 

increased risk of Pb effects is childhood 

(ISA, section 1.9.6). As noted in section 

II.B.2 above, although the specific ages 

or lifestages of greatest susceptibility 38

or risk have not been established (e.g., 

ISA, section 4.3.11), the at-risk status of 

young children to the 

neurodevelopmental effects of Pb is well 

recognized (e.g., ISA, sections 1.9.6, 4.3, 

5.2.1, 5.3.1, and 5.4). The evidence 

indicates that prenatal blood Pb levels 

are associated with nervous system 

effects, including mental development 

in very young children and can also be 

associated with cognitive decrements in 

older children (ISA, section 4.3). 

Additionally, the coincidence during 

early childhood of behaviors that 

increase exposure, such as hand-tomouth contact by which children 

transfer Pb in settled particles to their 

mouths, and the development of the 

nervous system also contributes 

increased risk during this time (ISA, 

sections 3.7.1, 4.3.2.6, 5.2.1.1, 5.3.1.1 

and 5.4). Collectively, however, the 

evidence indicates both the 

susceptibility of the developing fetus 

and early postnatal years, as well as the 

potential for continued susceptibility 

through childhood as the human central 

nervous system continues to mature and 

be vulnerable to neurotoxicants (ISA, 

sections 1.9.5 and 4.3.15; 2006 CD, 

section 6.2.12). As discussed in section 

II.B.2 above, while uncertainties remain 

with regard to the role of Pb exposures 

during a particular age of life in eliciting 

nervous system effects, such as 

cognitive function decrements, the full 

evidence base continues to indicate 

prenatal and early childhood lifestages 

as periods of increased Pb-related risk 

(ISA, sections 4.3.11 and 4.3.15). 

Several physiological factors increase 

the risk of Pb-related health effects by 

contributing to increased blood Pb 

levels over those otherwise associated 

with a given Pb exposure (ISA, sections 

3.2, 3.3 and 5.1). These include 

nutritional status, which plays a role in 

Pb absorption from the gastrointestinal 

tract (ISA, sections 3.2.1.2, 5.1, 5.3.10 

and 5.4). For example, diets deficient in 

iron, calcium or zinc can contribute to 

increased Pb absorption and associated 

higher blood Pb levels (ISA, sections 

3.2.1.2, and 5.1). Evidence is suggestive 

of some genetic characteristics as 

potential risk factors, such as presence 

of the d-aminolevulinic acid 

dehydratase-2 (ALAD–2) allele which 

has been indicated to increase blood Pb 

levels or Pb-related risk of health effects 

in some studies (ISA, sections 3.3.2 and 

5.1). 

Risk factors based on increased 

exposure include spending time in 

proximity to sources of Pb to ambient 

air or other environmental media (e.g., 

large active metals industries or 

locations of historical Pb contamination) 

(ISA, sections 1.9.6, 3.7.1, 5.2.5 and 5.4). 

Residential factors associated with other 

sources of Pb exposure (e.g., leaded 

paint or plumbing with Pb pipes or 

solder) are another exposure-related risk 

factor (ISA, sections 3.7.1, 5.2.6 and 

5.4). Additionally, some races or 

ethnicities have been associated with 

higher blood Pb levels, with differential 

exposure indicated in some cases as the 

cause (ISA, sections 5.2.3 and 5.4). 

Lower socioeconomic status (SES) has 

been associated with higher Pb exposure 

and higher blood Pb concentration, 

leading the ISA to conclude the 

evidence is suggestive for low SES as a 

risk factor (ISA, sections 5.3.16, 5.2.4 

and 5.4). Although the differences in 

blood Pb levels between children of 

lower and higher income levels (as well 

as among some races or ethnicities) have 

lessened, blood Pb levels continue to be 

higher among lower-income children 

indicating higher exposure and/or 

greater influence of factors independent 

of exposure, such as nutritional factors 

(ISA, sections 1.9.6, 5.2.1.1 and 5.4). 

In considering risk factors associated 

with increased Pb exposure or increased 

blood Pb levels, we note that the 

currently available evidence continues 

to support a nonlinear relationship 

between neurocognitive effects and 

blood Pb that indicates incrementally 

greater impacts at lower as compared to 

higher blood Pb levels (ISA, section 

4.3.12), as described in section II.B.3 

above. An important implication of this 

finding is that while children with 

higher blood Pb levels are at greater risk 

of Pb-related effects than children with 

lower blood Pb levels, on an 

incremental basis (e.g., per mg/dL), the 

risk is greater for children at lower 

blood Pb levels. This was given 

particular attention in the last review of 

the Pb NAAQS, in which the standard 

was revised with consideration of the 

incremental impact of air-related Pb on 

young children in the U.S. and the 

recognition of greater impact for those 

children with lower absolute blood Pb 

levels (73 FR 67002, November 12, 

2008). Such consideration included a 

focus on those C–R studies involving 

the lowest blood Pb levels, as described 

in section II.A.1 above. 

In summary, the information newly 

available in this review has not 

appreciably altered our understanding 

of human populations that are 

particularly sensitive to Pb exposures. 

In the current review, as at the time of 

the last review of the Pb NAAQS, we 

recognize young children as an 

important at-risk population, with 

sensitivity extending to prenatal 

exposures and into childhood 

development. Additional risk factors for 

increased blood Pb levels include 

deficiencies in dietary minerals (iron, 

calcium and zinc), some racial or ethnic 

backgrounds,39 and spending time in 

proximity to environmental sources of 

Pb or residing in older houses with Pb 

exposure related to paint or plumbing.40

The currently available evidence 

continues to additionally suggest a 

potential for increased risk associated 

with several other factors, including 

older adulthood,41 pre-existing disease 

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42The ISA states that the ‘‘persistence of effects 

appears to depend on the duration and window of 

exposure as well as other factors that may affect an 

individual’s ability to recover from an insult,’’ with 

some evidence of greater recovery in children 

reared in households with more optimal caregiving 

characteristics and low concurrent blood Pb levels 

(ISA, p. 1–77; Bellinger et al., 1990). 

43Such uncertainties include those with regard to 

specific source characteristics and meteorology, not 

explicitly considered in the analysis. In light of 

such uncertainties, the PA interprets the emissionsbased analysis to provide a bounding estimate 

below which the true value is expected to fall (PA, 

p. 3–37). 

(e.g., hypertension), variants for certain 

genes and increased stress (ISA, section 

5.3.4). As discussed above, we recognize 

the sensitivity of the prenatal period 

and several lifestages of childhood to an 

array of neurocognitive and behavioral 

effects, and we particularly recognize 

young children as an important at-risk 

population in light of current 

environmental exposure levels. Age or 

lifestage was used to distinguish 

potential groups on which to focus in 

the last review in recognition of its role 

in exposure and susceptibility, and 

young children were the focus of the 

REA in consideration of the health 

effects evidence regarding endpoints of 

greatest public health concern and in 

recognition of effects on the developing 

nervous system as a sentinel endpoint 

for public health impacts of Pb. This 

identification continues to be supported 

by the evidence available in the current 

review. 

5. Potential Impacts on Public Health 

There are several potential public 

health impacts associated with Pb 

exposure in the current U.S. population. 

In recognition of effects causally related 

to blood Pb levels somewhat near those 

most recently reported for today’s 

population and for which the weight of 

the evidence is greatest, the potential 

public health impacts most prominently 

recognized in the ISA are population IQ 

impacts associated with childhood Pb 

exposure and prevalence of 

cardiovascular effects in adults (ISA, 

section 1.9.1). With regard to the latter 

category, as discussed above, the full 

body of evidence indicates a role of 

long-term cumulative exposure, with 

uncertainty regarding the specific 

exposure circumstances contributing to 

the effects in the epidemiological 

studies of adult populations, for whom 

historical Pb exposures were likely 

much higher than exposures that 

commonly occur today (ISA, section 

4.4). There is less uncertainty regarding 

the exposure patterns contributing to 

the blood Pb levels reported in studies 

of younger populations (ISA, sections 

1.9.4 and 1.10). Accordingly, the 

discussion of public health implications 

relevant to this review is focused 

predominantly on nervous system 

effects, including IQ decrements, in 

children. 

The magnitude of a public health 

impact is dependent upon the type or 

severity of the effect, as well as the size 

of populations affected. Intelligence 

quotient is a well-established, widely 

recognized and rigorously standardized 

measure of neurocognitive function, as 

well as a global measure reflecting the 

integration of numerous processes (ISA, 

section 4.3.2; 2006 CD, sections 6.2.2 

and 8.4.2). Examples of other measures 

of cognitive function negatively 

associated with Pb exposure include 

other measures of intelligence and 

cognitive development and measures of 

other cognitive abilities, such as 

learning, memory, and executive 

functions, as well as academic 

performance and achievement (ISA, 

section 4.3.2). Although some 

neurocognitive effects of Pb in children 

may be transient, some may persist into 

adulthood (ISA, section 1.9.5).42 We 

also note that deficits in 

neurodevelopment early in life may 

have lifetime consequences as 

‘‘[n]eurodevelopmental deficits 

measured in childhood may set affected 

children on trajectories more prone 

toward lower educational attainment 

and financial well-being’’ (ISA, section 

4.3.14). Thus, population groups for 

which neurodevelopment is affected by 

Pb exposure in early childhood are at 

risk of related impacts on their success 

later in life. Further, in considering 

population risk, the ISA notes that 

‘‘[s]mall shifts in the population mean 

IQ can be highly significant from a 

public health perspective’’ (ISA, p. 

xciii). For example, if Pb-related 

decrements are manifested uniformly 

across the range of IQ scores in a 

population, ‘‘a small shift in the 

population mean IQ may be significant 

from a public health perspective 

because such a shift could yield a larger 

proportion of individuals functioning in 

the low range of the IQ distribution, 

which is associated with increased risk 

of educational, vocational, and social 

failure’’ as well as a decrease in the 

proportion with high IQ scores (ISA, 

section 1.9.1). 

As summarized above, young children 

are the at-risk population that may be 

most at risk of health effects associated 

with exposure to Pb and children at 

greatest risk from air-related Pb are 

those children with highest air-related 

Pb exposure which we consider to be 

those living in areas of higher ambient 

air Pb concentrations. To inform our 

understanding of the extent of this 

population potentially at risk from airrelated Pb, the PA includes two 

analyses. The first analysis is based on 

consideration of the available air Pb 

monitoring information. As the air 

quality data set available for the first 

analysis may not be inclusive of all of 

the newly sited monitors (as discussed 

in section 2.2.1 of the PA) and there 

may be other areas with elevated Pb 

concentrations, a second analysis was 

performed in consideration of emissions 

estimates from the National Emissions 

Inventory (NEI), although with 

recognition of uncertainties associated 

with inferences drawn from such 

estimates with regard to ambient air Pb 

concentrations and exposures (PA, pp. 

3–36 to 3–38).43

The first PA analysis indicates that 

approximately one hundredth of one 

percent of the full population of 

children aged 5 or under in the U.S. 

reside within 0.5 km of monitors 

exceeding or within 10 percent of the 

level of the current standard (PA, 

section 2.2.2.2, pp. 3–36 to 3–37, 4–25 

and Table 3–4). In the second analysis, 

the size of young child populations 

residing in areas near large Pb sources 

was approximately four hundredths of 

one percent of the full U.S. population 

of children aged 5 years or younger (PA, 

pp. 3–37 to 3–38, 4–25). The PA 

recognized uncertainties and potential 

limitations associated with the use of 

the emissions estimates in the second 

analysis to make inferences regarding 

ambient air Pb exposures, uncertainties 

both with regard to the accuracy of such 

estimates and also with regard to the 

role of specific source characteristics 

and meteorology, not explicitly 

considered here, in influencing ambient 

air Pb concentrations and contributing 

to substantial variation in air Pb 

concentrations at source locations (e.g., 

PA, Figure 2–11). Accordingly, while 

the second analysis is considered 

informative with regard to the potential 

prevalence of airborne Pb emissions and 

potential exposure of human 

populations, it is limited with regard to 

its ability to identify populations living 

in areas of elevated ambient air Pb 

concentrations. The PA interprets the 

two analyses together to indicate that 

well below one tenth of one percent of 

the full population of children aged 5 

years or younger in the U.S. today live 

in areas with air Pb concentrations near 

or above the current standard, with the 

current monitoring data indicating the 

size of this population to be 

approximately one hundredth of a 

percent of the full population of 

children aged 5 or younger (PA, pp. 

3–36 to 3–38, 4–25, 4–32). 

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44The quantitative relationship between ambient 

air Pb and blood Pb, often termed a slope or ratio, 

describes the increase in blood Pb (in mg/dL) 

estimated to be associated with each unit increase 

of air Pb (in mg/m3). Ratios are presented in the form 

of 1:x, with the 1 representing air Pb (in mg/m3) and 

x representing blood Pb (in mg/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. 

45The 2006 CD did not include an assessment of 

then-current evidence on air-to-blood ratios. 

C. Blood Lead as a Biomarker of 

Exposure and Relationships With Air 

Lead 

Blood Pb is well established as a 

biomarker of Pb exposure and of 

internal dose, with relationships 

between air Pb concentrations and 

blood Pb concentrations informing 

consideration of the NAAQS for Pb 

since its initial establishment in 1978. 

Lead associated with inhaled particles 

may, depending on particle size and Pb 

solubility, be absorbed into the systemic 

circulation or transported with particles 

to the gastrointestinal tract (ISA, section 

3.2.1.1), where its absorption is 

influenced by a range of factors (ISA, 

section 3.2.1.2). Lead in the blood 

stream is quickly distributed throughout 

the body (e.g., within days), available 

for exchange with the soft and skeletal 

tissues, the latter of which serves as the 

largest storage compartment (ISA, 

section 3.2.2.2). Given the association 

with exposure and the relative ease of 

collection, blood Pb levels are 

extensively used as an index or 

biomarker of exposure by national and 

international health agencies, as well as 

in epidemiological and toxicological 

studies of Pb health effects and doseresponse relationships (ISA, sections 

3.3.2, 3.4.1, 4.3, 4.4, 4.5, 4.6, 4.7, and 

4.8). While bone Pb measurements are 

also used in epidemiological studies as 

an indicator of cumulative Pb exposure, 

blood Pb measurements remain the 

predominant, well-established and wellcharacterized exposure approach. 

Since 1976, the CDC has been 

monitoring blood Pb levels nationally 

through the NHANES. This survey has 

documented the dramatic decline in 

mean blood Pb levels in all ages of the 

U.S. population that has occurred since 

the 1970s (PA, Figure 3–1), and that 

coincides with actions on leaded fuels, 

leaded paint, Pb in food packaging, and 

Pb-containing plumbing materials that 

have reduced Pb exposure in the U.S. 

(ISA, section 3.4.1; Pirkle et al., 1994; 

Schwemberger et al., 2005). This decline 

has continued over the more recent past. 

For example, the 2009–2010 geometric 

mean blood Pb level in U.S. children 

aged 1–5 years is 1.17 mg/dL, as 

compared to 1.51 mg/dL in 2007–2008 

(ISA, section 3.4.1) and 1.8 mg/dL in 

2003–2004, the most recent data 

available at the time of the last review 

(73 FR 67002, November 12, 2008). 

Somewhat less dramatic declines have 

been reported in the upper tails of the 

distribution and in different groups with 

higher blood Pb levels than the general 

child population (ISA, Figures 3–17 and 

3–19). 

The blood Pb concentration in 

childhood (particularly early childhood) 

can more quickly (than in adulthood) 

reflect changes in total body burden 

(associated with the shorter exposure 

history) and can also reflect changes in 

recent exposures (ISA, section 3.3.5). 

The relationship of children’s blood Pb 

to recent exposure may reflect their 

labile bone pool, with their rapid bone 

turnover in response to rapid childhood 

growth rates (ISA, section 3.3.5). The 

relatively smaller skeletal compartment 

of Pb in children (particularly very 

young children) compared to adults is 

subject to more rapid turnover. The 

distribution of Pb in the body is 

dynamic throughout life, with Pb in the 

body being exchanged between blood 

and bone and between blood and soft 

tissues (ISA, sections 3.3.5 and 3.2.2; 

2006 CD, section 4.3.2). The rates of 

these exchanges vary with age, exposure 

and various physiological variables. For 

example, resorption of bone, which 

results in the mobilization of Pb from 

bone into the blood, is a somewhat 

rapid and ongoing process during 

childhood and a more gradual process 

in later adulthood (ISA, sections 3.2.2.2, 

3.3.5 and 3.7.2; PA, pp. 3–2 to 3–3). 

Lead in ambient air contributes to Pb 

in blood by multiple exposure pathways 

by both inhalation and ingestion 

exposure routes (ISA, section 3.1.1). 

Multiple studies have demonstrated 

young children’s blood Pb levels to 

reflect Pb exposures, including 

exposures to Pb in surface dust (e.g., 

Lanphear and Roghmann, 1997; 

Lanphear et al., 1998). These and 

studies of child populations near 

sources of air Pb emissions, such as 

metal smelters, have further 

demonstrated the effect of airborne Pb 

on interior dust and on blood Pb (ISA, 

sections 3.4.1, 3.5.1 and 3.5.3; Hilts, 

2003; Gulson et al., 2004). 

As blood Pb is an integrated marker 

of aggregate Pb exposure across all 

pathways, the blood Pb C–R 

relationships described in 

epidemiological studies of Pb-exposed 

populations do not distinguish among 

different sources of Pb or pathways of 

Pb exposure (e.g., inhalation, ingestion 

of indoor dust, ingestion of dust 

containing leaded paint). Thus, our 

interpretation of the health effects 

evidence for purposes of this review 

necessitates characterization of the 

relationships between Pb from those 

sources and pathways of interest in this 

review (i.e., those related to Pb emitted 

into the air) and blood Pb. 

The evidence for air-to-blood 

relationships derives from analyses of 

datasets for populations residing in 

areas with differing air Pb 

concentrations, including datasets for 

circumstances in which blood Pb levels 

have changed in response to changes in 

air Pb. The control for variables other 

than air Pb that can affect blood Pb 

varies across these analyses. At the 

conclusion of the last review in 2008, 

the EPA interpreted the evidence as 

providing support for use (in informing 

the Administrator’s decision on 

standard level) of a range of air-to-blood 

ratios 44 ‘‘inclusive at the upper end of 

estimates on the order of 1:10 and at the 

lower end on the order of 1:5’’ (73 FR 

67002, November 12, 2008). This 

conclusion reflected consideration of 

the air-to-blood ratios presented in the 

1986 CD 45 and associated observations 

regarding factors contributing to 

variation in such ratios, ratios reported 

subsequently and ratios estimated based 

on modeling performed in the REA, as 

well as advice from CASAC (73 FR 

66973–66975, 67001–67002, November 

12, 2008). The information available in 

this review, which is assessed in the 

ISA and largely, although not 

completely, comprises studies that were 

available in the last review, does not 

alter the primary scientific conclusions 

drawn in the last review regarding the 

relationships between Pb in ambient air 

and Pb in children’s blood. The ratios 

summarized in the ISA in this review 

span a range generally consistent with 

the range concluded in 2008 (ISA, 

section 3.5.1). 

The evidence pertaining to the 

quantitative relationship between air Pb 

and children’s blood Pb 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 a variety of Pb 

exposure circumstances. Accordingly, 

there is significant variability in air-toblood ratios among the different study 

populations exposed to Pb through 

different air-related exposure pathways 

and at different exposure levels. This 

variability in air-to-blood estimates can 

relate to the representation of air-related 

pathways and study populations, 

including, for example, relatively 

narrow age ranges for the population in 

order to reduce age-related variability in 

blood Pb, or including populations with 

narrowly specified dietary sources. It 

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46Sources of uncertainty include the role of 

factors other than ambient air Pb reduction in 

influencing decreases in blood Pb (ISA, section 

3.5.1). The author cited remedial programs (e.g., 

community and home-based dust control and 

education) as potentially responsible for some of 

the blood Pb reduction seen during the study period 

(1997 to 2001), although the author notes that these 

programs were in place in 1992, suggesting they are 

unlikely to have contributed to the sudden drop in 

blood Pb levels occurring after 1997 (Hilts, 2003). 

Other aspects with potential implications for ratios 

include the potential for children with lower blood 

Pb levels not to return for subsequent testing, and 

the age range of 6 to 36 months in the 2001 blood 

screening compared to ages up to 60 months in 

earlier years of the study (Hilts, 2003). 

47This study considered changes in ambient air 

Pb levels and associated blood Pb levels over a 5- 

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, the 

EPA calculated an alternate air-to-blood Pb ratio 

based on ambient air Pb and blood Pb reductions 

in the first time period, after opening of the new 

facility in 1997 (ISA, section 3.5.1). 

48 In the dataset reviewed by Brunekreef (1984), 

air-to-blood ratios from the subset of those studies 

that used quality control protocols and presented 

adjusted slopes include values of 3.6, (Zielhuis et 

al., 1979), 5.2 (Billick et al., 1979, 1980); 2.9 

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

The studies cited here adjusted for parental 

education (Zielhuis et al., 1979), age and race 

(Billick et al., 1979, 1980) and air Pb monitor height 

(Billick, 1983); Brunekreef (1984) used multiple 

regression to control for several confounders (73 FR 

66974). 

can relate to the study population 

exposure and blood Pb levels (ISA, 

section 3.7.4). It can also relate to the 

precision of air and blood 

measurements and of the study 

circumstances, such as with regard to 

spatial and temporal aspects. 

Additionally, in situations where 

exposure to nonair sources covaries 

with air-related exposures that are not 

accounted for in deriving ratio 

estimates, uncertainties may relate to 

the potential for confounding by nonair 

exposure covariance (ISA, section 3.5). 

Most of the studies assessed in the ISA 

and PA have reported ratios for which 

the relationship is linear, while a subset 

are derived from nonlinear models (PA, 

Table 3–1; ISA, section 3.7.4). 

As was noted in the last review, age 

is an important influence on the 

magnitude of air-to-blood ratio estimates 

derived. Ratios for children are 

generally higher than those for adults, 

and higher for young children than 

older children, perhaps due to 

behavioral differences between the age 

groups, as well as their shorter exposure 

history. Similarly, given the common 

pattern of higher blood Pb levels in preschool-aged children than during the 

rest of childhood, related to behaviors 

that increase environmental exposures 

(e.g., hand-to-mouth activity), ratios 

would be expected to be highest in 

earlier childhood. Additionally, 

estimates of air-to-blood ratios that 

include 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 (1986 CD, 

p. 11–106). Thus, the extent to which 

studies account for the full set of airrelated inhalation and ingestion 

exposure pathways affects the 

magnitude of the resultant air-to-blood 

estimates, such that including fewer 

pathways as ‘‘air-related’’ yields lower 

ratios. Estimates of air-to-blood ratios 

can also be influenced by population 

characteristics that may influence blood 

Pb; accordingly, some analyses include 

adjustments. 

Given the recognition of young 

children as a key at-risk population in 

this review, as in the last (as discussed 

in section II.B.3 above), as well as the 

influence of age on blood Pb levels, we 

have considered the available studies in 

groups based on the extent of their 

inclusion of children younger than or 

barely school age (less than or equal to 

5 years of age). Among the first group 

of studies, focused exclusively on young 

children, only one study dates from the 

end of or after the phase-out of leaded 

gasoline usage (Hilts, 2003). This study 

reports 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 5). 

Given the timing of this study, after the 

leaded gasoline phase-out, and its 

setting near a smelter, the ambient air 

Pb in this study may be somewhat more 

comparable to that near sources in the 

U.S. today than other studies discussed 

herein. The study authors report an airto-blood ratio of 1:6.46 An EPA analysis 

of the air and blood data reported for 

1996, 1999 and 2001 results in a ratio 

of 1:6.5, and an analysis focused only on 

the 1996 and 1999 data (pre- and postthe new technology) yields a ratio of 1:7 

(ISA, section 3.5.1; Hilts, 2003).47 The 

two other studies that focused on 

children of age 5 or younger analyzed 

variations in air Pb as a result of 

variations in leaded gasoline usage in 

Chicago, Illinois and reported somewhat 

higher ratios of 1:8 and 1:8.6 (Hayes et 

al., 1994; Schwartz and Pitcher, 1989). 

We note, however, the blood Pb 

concentrations in the two leaded 

gasoline studies are appreciably higher 

(a factor of two or more) than those in 

the study near the smelter (Hilts, 2003), 

and also than those commonly reported 

in the U.S. today. 

The second group of studies includes 

but is not limited to children less than 

or equal to 5 years of age. This group 

includes a complex statistical analysis 

and associated dataset for a cohort of 

children born in Mexico City from 1987 

through 1992 (Schnaas et al., 2004). 

Although this study, which was not 

assessed in the last review, encompasses 

the period of leaded gasoline usage, it 

further informs our understanding of 

factors influencing the quantitative 

relationship between air Pb and 

children’s blood Pb. Air-to-blood ratios 

developed from this study are 

influenced by a number of factors and 

appear to range from roughly 1:2 to 1:6, 

in addition to an estimate of 1:9 (ISA, 

section 3.5.1), although the latter is 

derived from a data set restricted to the 

latter years of the study when little 

change in air Pb concentration occurred, 

such that the role of air Pb may be more 

uncertain. Estimates associated with the 

developmental period of highest 

exposure (e.g., age 2 years) range up to 

approximately 1:6, illustrating the 

influence of age on the ratio (ISA, 

section 3.5.1). Also in the second group 

of studies are two much older studies of 

populations with age ranges extending 

well beyond 6 years. The first is the 

review and meta-analysis by Brunekreef 

(1984) using datasets available at the 

time for variously aged children as old 

as 18 years with identified air 

monitoring methods and reliable blood 

Pb data for 18 locations in the U.S. and 

internationally.48 Two air-to-blood ratio 

estimates derived from this study based 

on log-log models both round to 1:5 (for 

air concentrations corresponding to the 

geometric means of the two sets of data 

pairs [1.5 and 0.54 mg/m3]). A ratio on 

the order of 1:9 was derived based on 

the study by Schwartz and Pitcher 

(1989) of the relationship between U.S. 

NHANES II blood Pb levels for white 

subjects, aged ≤74 years, and national 

usage of leaded gasoline, adjusted for 

age and other covariates (Henderson, 

2007a, pp. D–2 to D–3; ISA, Table 3–12). 

The last two studies are focused on 

older children, ages 6–11 in India and 

Germany (Tripathi et al., 2001; Ranft et 

al., 2008) and employed methods to 

characterize media Pb concentrations 

that differed from the other studies 

assessed (PA, p. 3–11). The locationspecific geometric mean blood Pb levels 

in the Indian study (8.6–14.4 mg/dL) 

indicate blood Pb distributions in this 

age group much higher than those 

pertinent to similarly aged children in 

the U.S. today and the air-to-blood ratio 

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49Blood Pb measurements were available on a 

total of 843 children across five time periods, in the 

first of which the average child age was 9 years 

while it was approximately 6 years in each of the 

latter years: 1983 (n=356), 1991 (n=147), 1994 

(n=122), 1997 (n=56), and 2000 (n=162) (Ranft et 

al., 2008). 

50The 1983 air Pb concentrations were based on 

two monitoring stations, while a combination of 

dispersion modeling and monitoring data was used 

in the later years. Surface soil Pb measurements 

were from 2000–2001, but geo-matched to blood Pb 

measurements across full study period (Ranft et al., 

2008). 

estimate reported was 1:3.6 (Tripathi et 

al., 2001). The more recent German 

study by Ranft et al. (2008) analyzed 

data from a nearly 20-year period 

associated with the leaded gasoline 

phase-out, during which average blood 

Pb levels declined from 9 mg/dL in 1983 

(345 children, average age of 9 years) to 

3 mg/dL in 2000 (162 children, average 

of 6 years).49 Average air Pb 

concentration declined from 0.45 mg/m3

to 0.06 mg/m3 over the same period, 

with the largest reduction occurring 

between the first study year (derived 

from two monitoring sites for full study 

area) and the second study year, 1991, 

for which air concentrations were 

derived from a combination of 

dispersion modeling and the two 

monitoring sites.50 For a mean air Pb 

concentration of 0.1 mg/m3, the study’s 

multivariate loglinear regression model 

predicted air-to-blood ratios of 3.2 and 

6.4 for ‘‘background’’ blood Pb 

concentrations of 1.5 and 3 mg/dL, 

respectively. In this study, background 

referred to Pb in blood from other 

sources; the blood Pb distribution over 

the study period, including levels when 

air Pb concentrations are lowest, 

indicates 3 mg/dL may be the better 

estimate of background for this study 

population. Inclusion of soil Pb as a 

variable in the model may have 

contributed to an underestimation of the 

blood Pb-air Pb ratios for this study 

because some of the Pb in soil likely 

originated in air and the blood Pb-air Pb 

slope does not include the portion of the 

soil/dust Pb ingestion pathway that 

derives from air Pb. Using univariate 

linear, log-log and loglinear models on 

the median air and blood Pb 

concentrations reported for the 5 years 

included in this study, the ISA also 

derived air-to-blood ratio estimates for 

data from this study ranging from 9 to 

17 (ISA, p. 3–126; Ranft et al., 2008, 

Table 2). Uncertainties related to this 

study’s estimates include those related 

to the bulk of air concentration 

reduction occurring between the first 

two time points (1983 and 1991) and the 

difference among the year’s air datasets 

(e.g., two data sources [air monitors] in 

1983 and multiple geographical points 

from a combination of the monitors and 

modeling in subsequent years). 

In this review, as in the 2008 Pb 

NAAQS review, in addition to 

considering the evidence presented in 

the published literature and that 

reviewed in the 1986 CD, we also 

consider air-to-blood ratios derived from 

the exposure assessment (PA, p. 3–14; 

73 FR 66974, November 12, 2008; 2007 

REA, section 5.2.5.2). In the exposure 

assessment (summarized in section II.D 

below), current modeling tools and 

information on children’s activity 

patterns, behavior and physiology were 

used to estimate blood Pb levels 

associated with multimedia and 

multipathway Pb exposure. The results 

from the various case studies assessed, 

with consideration of the context in 

which they were derived (e.g., the 

extent to which the range of air-related 

pathways was simulated, and the 

limitations associated with those 

simulations), and the multiple sources 

of uncertainty are also informative to 

our understanding of air-to-blood ratios. 

Estimates of air-to-blood ratios for the 

two REA case studies that represent 

localized population exposures 

exhibited an increasing trend across air 

quality scenarios representing 

decreasing air concentrations. For 

example, across the alternative standard 

levels assessed, which ranged from a 

calendar quarter average of 1.5 mg/m3

down to a monthly average of 0.02 mg/ 

m3, the ratios ranged from 1:2 to 1:9 for 

the generalized (local) urban case study, 

with a similar trend, although of 

generally higher ratio, for the primary 

smelter case study subarea. This pattern 

of model-derived ratios is generally 

consistent with the range of ratios 

obtained from the literature, briefly 

discussed above. We continue to 

recognize a number of sources of 

uncertainty associated with these 

model-derived ratios which may 

contribute to high or low biases (as 

discussed further in section 3.1 of the 

PA). 

The evidence on the quantitative 

relationship between air Pb and airrelated Pb in blood is now, as in the 

past, limited by the circumstances (such 

as those related to Pb exposure) in 

which the data were collected. Previous 

reviews have recognized the significant 

variability in air-to-blood ratios for 

different populations exposed to Pb 

through different air-related exposure 

pathways and at different air and blood 

levels, with the 1986 CD noting that 

ratios derived from studies involving 

the higher blood and air Pb levels 

pertaining to occupationally exposed 

workers are generally smaller than ratios 

from studies involving lower blood and 

air Pb levels (ISA, p. 3–132; 1986 CD, 

p. 11–99). Consistent with this 

observation, slopes in the range of 3 to 

5 were estimated for child population 

datasets assessed in the 1986 CD (ISA, 

p. 3–132; 1986 CD p. 11–100; 

Brunekreef, 1984). Additional studies 

considered in the last review and those 

assessed in the ISA provide evidence of 

ratios above this older range (ISA, p. 3– 

133). For example, a ratio of 1:6.5–1:7 is 

indicated by the study by Hilts (2003), 

one of the few studies that evaluate the 

air Pb-blood Pb relationship in 

conditions that are closer to the current 

state in the U.S. (ISA, p. 3–132). We 

additionally note the variety of factors 

identified in the ISA that may 

potentially affect estimates of various 

ratios (including potentially coincident 

reductions in nonair Pb sources during 

the course of the studies), and for which 

a lack of complete information may 

preclude any adjustment of estimates to 

account for their role (ISA, section 3.5). 

In summary, as at the time of the last 

review of the NAAQS for Pb, the 

currently available evidence includes 

estimates of air-to-blood ratios, both 

empirical and model-derived, with 

associated limitations and related 

uncertainties. These limitations and 

uncertainties, which are summarized 

here and also noted in the ISA, usually 

include uncertainty associated with 

reductions in other Pb sources during 

the study period. The limited amount of 

new information available in this review 

has not appreciably altered the scientific 

conclusions reached in the last review 

regarding relationships between Pb in 

ambient air and Pb in children’s blood 

or with regard to the range of ratios. The 

currently available evidence continues 

to indicate ratios relevant to the 

population of young children in the U.S. 

today, reflecting multiple air-related 

pathways in addition to inhalation, to 

be generally consistent with the 

approximate range of 1:5 to 1:10 given 

particular attention in the 2008 NAAQS 

decision, including the ‘‘generally 

central estimate’’ of 1:7 (73 FR 67002, 

67004, November 12, 2008; ISA, pp. 

3–132 to 3–133). 

D. Summary of Risk and Exposure 

Assessment Information 

The risk information available for this 

review and summarized here is based 

primarily on the exposure and risk 

assessment developed in the last review 

of the Pb NAAQS, described in the 2007 

REA, the 2007 Staff Paper and the 2008 

notice of final decision (USEPA, 2007a; 

USEPA, 2007b; 73 FR 66964, November 

12, 2008), as considered in the context 

of the evidence newly available in this 

review (PA, section 3.4). As described in 

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51 In their review of the draft PA, the CASAC Pb 

Review Panel reinforced their concurrence with the 

EPA’s decision not to develop a new REA (Frey, 

2013). 

52The pathways represented in this modeling 

included childhood inhalation and ingestion 

pathways, as well as maternal contributions to 

newborn body burden (2007 REA, Appendix H, 

Exhibit H–6). 

the REA Planning Document, careful 

consideration of the information newly 

available in this review, with regard to 

designing and implementing a full REA 

for this review, led to the conclusion 

that performance of a new REA for this 

review was not warranted. We did not 

find the information newly available in 

this review to provide the means by 

which to develop an updated or 

enhanced risk model that would 

substantially improve the utility of risk 

estimates in informing the current Pb 

NAAQS review (REA Planning 

Document, section 2.3). Based on their 

consideration of the REA Planning 

Document analysis, the CASAC Pb 

Review Panel generally concurred with 

the conclusion that a new REA was not 

warranted in this review (Frey, 

2011b).51 Accordingly, the risk/

exposure information considered in this 

review is drawn primarily from the 2007 

REA, augmented by a limited new 

computation for one case study focused 

on risk associated with the current 

standard, as described below (PA, 

section 3.4 and Appendix 3A). 

1. Overview 

The focus for the risk assessment and 

associated estimates is on Pb derived 

from sources emitting Pb to ambient air. 

As discussed in section I.D above, the 

multimedia and persistent nature of Pb, 

the role of multiple exposure pathways, 

and the contributions of nonair sources 

of Pb to human exposure media all 

present challenges and contribute 

significant additional complexity to the 

health risk assessment that goes far 

beyond the situation for similar 

assessments typically performed for 

other NAAQS pollutants (e.g., that focus 

only on the inhalation pathway). The 

conceptual model that informed 

planning for the 2007 REA identified 

sources, pathways, routes, exposed 

populations, and health endpoints, 

focusing on those aspects of Pb 

exposure most relevant to the review, 

while also recognizing the role of Pb 

exposure pathways unrelated to Pb in 

ambient air (2007 REA, section 2.1). 

Limitations in the available data and 

models affected our characterization of 

the various complexities associated with 

exposure to ambient air Pb. As a result, 

the assessment included a number of 

simplifying assumptions in a number of 

areas and the estimates of air-related Pb 

risk produced are approximate and are 

characterized by upper and lower 

bounds. 

As recognized in I.D above, sources of 

human Pb exposure include current and 

historical air emissions sources, as well 

as miscellaneous nonair sources, which 

can contribute to multiple exposure 

media and associated pathways (e.g., 

inhalation of ambient air, ingestion of 

indoor dust, outdoor soil/dust and diet 

or drinking water). In addition to 

airborne emissions (recent or those in 

the past), sources of Pb to these 

pathways also include old leaded paint, 

including Pb mobilized indoors during 

renovation/repair activities, and 

contaminated soils. Lead in diet and 

drinking water may have air pathwayrelated contributions as well as 

contributions from nonair sources (e.g., 

Pb solder on water distribution pipes 

and Pb in materials used in food 

processing). Limitations in our data and 

modeling tools handicapped our ability 

to fully separate the nonair 

contributions to Pb exposure from 

estimates of air-related Pb exposure and 

risk. As a result, we have developed 

bounds within which we estimate airrelated Pb risk to fall. The lower bound 

is based on a combination of pathwayspecific estimates that do not 

completely represent all air-related 

pathways, while the upper bound is 

based on a combination of pathwayspecific estimates that includes 

pathways that are not air-related but the 

separating out of which is precluded by 

modeling and data limitations. 

Inclusion of exposure populations, 

exposure/dose metric, health effects 

endpoint and risk metric in the 2007 

REA were based on consideration of the 

then-currently available evidence as 

assessed in detail in the 2006 CD. As 

discussed in the REA Planning 

Document (USEPA, 2011b), these 

selections continue to be supported by 

the evidence now available in this 

review as described in the ISA. The REA 

focused on risk to the central nervous 

system in childhood as the most 

sensitive effect that could be 

quantitatively assessed, with decrement 

in IQ used as the risk metric. Exposure 

and biokinetic modeling was used to 

estimate blood Pb concentrations in 

children exposed to Pb up to age 7 

years.52 This focus reflected the 

evidence for young children with regard 

to air-related exposure pathways and 

susceptibility to Pb health impacts (e.g., 

ISA, sections 3.1.1, 4.3, 5.2.1.1, 5.3.1.1, 

and 5.4). For example, the hand-tomouth activity of young children 

contributes to their Pb exposure (i.e., 

incidental soil and indoor dust 

ingestion) and ambient air-related Pb 

has been shown to contribute to Pb in 

outdoor soil and indoor house dust 

(ISA, sections 3.1.1 and 3.4.1; 2006 CD, 

section 3.2.3). 

The 2007 REA relied on a case study 

approach to provide estimates that 

inform our understanding of air-related 

exposure and risk in different types of 

air Pb exposure situations. Lead 

exposure and associated risk were 

estimated for multiple case studies that 

generally represent two types of 

residential population exposures to airrelated Pb: (1) Location-specific urban 

populations of children with a broad 

range of air-related exposures, reflecting 

existence of urban concentration 

gradients; and (2) children residing in 

localized areas with air-related 

exposures representing air 

concentrations specifically reflecting the 

standard level being evaluated (see PA, 

Table 3–6). Thus, the two types of case 

studies differed with regard to the 

extent to which they represented 

population variability in air-related Pb 

exposure. 

In drawing on the 2007 REA for our 

purposes in this review, we focused on 

two case studies, one from each of these 

two categories: (1) The location-specific 

urban case study for Chicago and (2) the 

generalized (local) urban case study 

(PA, Table 3–6). Accordingly, our 

summary of analysis details below 

focuses on details particular to these 

two case studies. The generalized (local) 

urban case study (also referred to as 

general urban case study) was not based 

on a specific geographic location and 

reflected several simplifying 

assumptions 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. Based on 

the nature of the population exposures 

represented by the two categories of 

case study, the generalized (local) urban 

case study includes populations that are 

relatively more highly exposed by way 

of air pathways to air Pb concentrations 

near the standard level evaluated, 

compared with the populations in the 

location-specific urban case. The 

location-specific urban case studies 

provided representations of urban 

populations with a broad range of airrelated 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) were found in 

very small parts of the study areas, 

while a large majority of the case study 

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53Additional detail on estimation of ambient 

(outdoor) and indoor air concentrations is presented 

in section 5.2.2 and Appendices A through D of the 

2007 REA. 

54The alternatives lower than the NAAQS at the 

time of the last review for which air quality 

scenarios were assessed were a maximum calendar 

quarter average of 0.2 mg/m3 and maximum monthly 

averages of 0.5, 0.2, 0.05 and 0.02 mg/m3 (PA, Table 

3–8). 

55Characterization of Pb concentrations in 

outdoor surface soil/dust for the generalized (local) 

and location-specific urban cases studies was based 

on the use of nationally representative residential 

soil measurements obtained from the literature 

(2007 REA, sections 3.1.3 and 5.2.2.2 and Appendix 

F). Diet and drinking water intake and 

concentrations, as well as other model inputs, were 

based on the most current information (2007 REA, 

Appendix H). 

56As in the last review, we give primary 

emphasis to estimates based on the concurrent 

blood Pb metric, consistent with CASAC advice in 

the last review (Henderson, 2007b). 

57The 5th percentile for the concurrent blood Pb 

measurements in that dataset is 2.5 mg/dL, and the 

median is 9.7 mg/dL (Lanphear et al., 2005). 

58As noted in section II.B.3 above, since the 

completion of the ISA in the current review, two 

errors have been identified with the pooled dataset 

analyzed by Lanphear et al., (2005) (Kirrane and 

Patel, 2014). The EPA and a recent publication have 

separately recalculated the statistics and 

mathematical models of Lanphear et al., (2005) 

using the corrected pooled dataset (Kirrane and 

Patel, 2014). While the conclusions drawn from 

these coefficients, including the finding of a steeper 

slope at lower (as compared to higher) blood Pb 

concentrations, are unaffected, the magnitude of the 

loglinear and linear regression coefficients are 

somewhat lower based on the corrections. For 

example, the loglinear model coefficient used for 

the C–R function, on which the EPA focused in the 

last review and also focuses on here, changed only 

negligibly from ¥2.7 to ¥2.65 when recalculated 

using the corrected pooled dataset (Kirrane and 

Patel, 2014). As a result, the risk estimates for this 

function would be expected to be very similar 

although slightly lower if derived using the 

recalculated loglinear model coefficient for the 

corrected dataset. Since the loglinear model 

coefficient calculated from the corrected dataset is 

unchanged at two significant figures from that 

original reported, any change to the risk estimates 

would be very small and, particularly in light of 

other uncertainties in the analysis, does not 

materially affect staff’s consideration of the results. 

populations resided in areas with much 

lower air concentrations. 

2. Summary of Design Aspects 

The approach to assessing exposure 

and risk for the two categories of case 

studies was comprised of four main 

analytical steps: (1) Estimation of 

ambient air Pb concentrations, (2) 

estimation of Pb concentrations in other 

key exposure media, including outdoor 

soil and indoor dust, (3) use of exposure 

media Pb concentrations, with other 

pathway Pb intake rates (e.g., diet), to 

estimate blood Pb levels in children 

using biokinetic modeling, and (4) use 

of C–R functions derived from 

epidemiological studies to estimate IQ 

loss associated with the blood Pb levels. 

Concentrations of Pb were estimated 

in ambient media and indoor dust using 

a combination of empirical data and 

modeling projections. The use of 

empirical data brings with it uncertainty 

related to the potential inclusion of 

nonair source signals in these 

measurements (e.g., house paint 

contributions to indoor dust and 

outdoor soil Pb). Conversely, the use of 

modeling tools introduces other 

uncertainties (e.g., model and parameter 

uncertainties). 

Characterization of Pb in ambient air 

relied on (1) the use of ambient monitor 

data for the location-specific urban case 

studies and (2) an assumption of 

uniform ambient air Pb levels (matching 

the standard level being considered) for 

the generalized (local) urban case study. 

For the location-specific urban case 

studies, we used Pb monitors within 

each study area to characterize spatial 

gradients. By contrast, the generalized 

(local) urban case study is designed to 

assess exposure and risk for a smaller 

group of residents (e.g., neighborhood) 

exposed at the level of the standard and, 

therefore, did not rely on monitor data; 

rather, ambient air Pb concentration was 

fixed at the standard being assessed. For 

the generalized (local) urban case study, 

which has a single exposure zone in 

which air Pb concentrations do not vary 

spatially, we derived a single air Pb 

concentration estimate to meet the 

standard assessed. Concentrations in the 

location-specific urban study areas, 

which relied on empirical (monitorbased) data to define ambient air Pb 

concentrations, reflected contributions 

from all sources affecting the 

concentrations in those locations, be 

they currently active stationary or 

mobile sources, resuspension of 

previously deposited Pb or other.53

The air quality scenarios assessed in 

the 2007 REA included conditions just 

meeting the NAAQS that was current at 

the time of the last review (1.5 mg/m3, 

as a calendar quarter average), 

conditions meeting several alternative, 

lower standards,54 and current 

conditions in the three location-specific 

urban case studies (PA, section 3.4.3.2). 

The full impact of changes in air Pb 

conditions associated with attainment of 

lower standards was not simulated, 

however, due to limitations in the 

available data and modeling tools that 

precluded simulation of linkages 

between some media and air Pb. 

Specifically, while Pb concentrations in 

indoor dust were simulated to change 

with the different air quality scenarios 

for which there were differing ambient 

air Pb concentrations (outdoors and 

indoors), dietary and drinking water Pb 

concentrations, as well as soil Pb 

concentrations, were not varied across 

the air quality scenarios in any case 

study (see PA, Table 3–7).55

In estimating blood Pb levels using 

the IEUBK model, Pb concentrations in 

exposure media (e.g., ambient air, diet, 

water, indoor dust) were held constant 

throughout the 7-year simulation 

period, while behavioral and 

physiological variables were changed 

with age of child (2007 REA, sections 

3.2.1.1 and 5.2.4). Detail on methods 

used to characterize media Pb 

concentrations and all IEUBK inputs for 

each case study are in the 2007 REA, 

sections 3.1, 3.2, 5.2.3 and 5.2.4, and 

appendices C through H. Population 

variability in Pb intake and uptake was 

simulated through use of the IEUBK 

model to first generate a centraltendency estimate of the blood Pb levels 

for the group of children within a given 

exposure zone of a study area, coupled 

with use of a geometric standard 

deviation (GSD) and for the locationspecific case studies, Monte Carlo-based 

population sampling (PA, section 3.4; 

2007 REA, Appendix H). The risk 

characterization step employed in the 

2007 REA generated a distribution of IQ 

loss estimates for the set of children 

simulated in the assessment. 

Specifically, blood Pb estimates for 

the concurrent blood Pb metric 56 were 

combined with four C–R functions for 

blood Pb concentration with IQ loss 

based on the analysis by Lanphear et al. 

(2005) of a pooled international dataset 

of blood Pb and IQ (see the 2007 REA, 

section 5.3.1.1). We used the four 

different C–R functions to provide 

different characterizations of behavior at 

low exposures in recognition of 

uncertainty related to modeling this 

endpoint, particularly at lower blood Pb 

levels for which there is limited 

representation in the Lanphear et al. 

(2005) pooled dataset.57 In considering 

the risk estimates here (as in the last 

review), we focus on estimates for one 

of the four functions (referred to as the 

loglinear with low-exposure 

linearization C–R function [PA, section 

3.4.3.3]). The range of risk estimates 

reflecting all four C–R functions provide 

perspective on the impact of uncertainty 

in this key modeling step. Additional 

detail on the C–R functions is provided 

in the PA and the 2007 Pb Staff Paper 

(PA, section 3.4.3.3; USEPA, 2007b, 

section 4.2.1).58 We focus on the median 

IQ loss estimates, as in the last review, 

due to increased confidence in these 

estimates relative to the higher 

percentile estimates, for which we 

recognize significant uncertainty (PA, 

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59The 2008 decision on the level for the revised 

NAAQS was based primarily on consideration of 

the evidence-based air-related IQ loss framework; 

risk estimates available for scenarios simulated in 

the 2007 REA were concluded to be roughly 

consistent with and generally supportive of the 

evidence-based air-related IQ loss estimates (see 

section II.A.1 above). 60 In the Chicago urban case study, the maximum 

monthly average concentration was 0.31 mg/m3, and 

the maximum calendar quarter average 

concentration was 0.14 mg/m3 (2003–2005 data; 

2007 REA, Appendix O). 

61We did not interpolate risk estimates for the 

current standard for the other case studies (i.e., the 

primary Pb smelter and location-specific urban case 

studies) because those case studies utilized a more 

complex, spatially-differentiated and populationbased approach (see 2007 REA) which precludes 

application of the simple linear interpolation 

approach described, without introduction of 

substantial added uncertainty (relative to the other 

estimates for the same case study). The simplicity 

of the generalized (local) urban study area, 

however, with its single exposure zone, is amenable 

to the linear interpolation of risk described here. 

sections 3.4.5, 3.4.6 and 3.4.7; 2007 Staff 

Paper, p. 4–20). 

As the 2007 REA did not include an 

air quality scenario simulated to just 

meet the standard selected by the 2008 

decision,59 we employed two different 

approaches to estimate risk pertaining to 

conditions just meeting the current Pb 

standard (set in 2008) for our purposes 

in this review. First, given the similarity 

to the current standard of the thencurrent conditions scenario for the 

Chicago case study (among all the 2007 

REA scenarios), we consider the risk 

estimates for that scenario as 

informative with regard to risk 

associated with the current standard.60

To augment the risk information 

available in this current review and in 

recognition of the variation among 

specific locations and urban areas with 

regard to air quality patterns and 

exposed population, we have also newly 

developed estimates for an air quality 

scenario just meeting the current Pb 

NAAQS in the context of the 

generalized (local) urban case study. 

These estimates were derived based on 

interpolation from the risk estimates 

available for scenarios previously 

assessed for the generalized (local) 

urban case study. Such interpolated 

estimates were only developed for the 

generalized urban case study due to its 

use of a single exposure zone which 

greatly simplified the method 

employed.61

The general approach we followed to 

newly develop estimates for the current 

standard in the generalized (local) urban 

case study was to identify the two 

alternative standard scenarios simulated 

in the 2007 REA which represented air 

quality conditions bracketing those for 

the current standard and then linearly 

interpolate an estimate of risk for the 

current standard based on the slope 

created from the two bracketing 

estimates (PA, section 3.4.3.3.2 and 

Appendix 3A). By this method, the air 

quality scenario for the current standard 

(0.15 mg/m3, as a not-to-be-exceeded 3- 

month average) was found to be 

bracketed by the scenarios for 

alternative standards of 0.20 mg/m3

(maximum calendar quarter average) 

and 0.20 mg/m3 (maximum monthly 

average). Using interpolation between 

the risk estimates for these two 

scenarios, we developed median risk 

estimates for the current standard (PA, 

Appendix 3A). 

3. Key Limitations and Uncertainties 

In characterizing risk associated with 

Pb from air-related exposure pathways, 

we faced a variety of challenges and 

employed a number of methods. The 

challenges related to significant data 

and modeling limitations which affected 

our ability to parse out the portion of 

total (all-pathway) blood Pb and IQ loss 

attributable to air-related pathways, as 

well as our representation of key 

sources of variability and 

characterization of uncertainty. 

Although we separated total estimates 

into risk estimates for diet/drinking 

water and two air-related categories 

(‘‘recent air’’ and ‘‘past air’’), significant 

limitations in our modeling tools and 

data resulted in an inability to parse risk 

estimates specific to the air-related 

pathways. For example, we recognize 

that Pb in diet and drinking water 

sources may include some Pb derived 

from Pb in the ambient air, as well as 

Pb from nonair sources, but limitations 

precluded explicit modeling of the 

contribution from air pathways to these 

exposure pathways, such that the airrelated component of these exposures 

was not estimated. Rather, we focused 

on estimates from the two air-related 

categories, which we considered to 

under- and over-estimate air-related 

risk, respectively, to create bounds 

within which we consider air-related 

risk to fall. 

The first air-related category 

(‘‘recent’’) included 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). Importantly, 

media concentrations associated with 

the pathways in this category were 

simulated to change in response to air 

concentrations (as noted in section 

II.D.2 above and described in section 

3.4.3.1 of the PA). The air-related Pb 

exposure pathways in the second airrelated category (‘‘past air’’), all of 

which are associated with atmospheric 

deposition, included 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. While 

there is the potential for these other airrelated exposures to be affected (over 

some time frame) by changes in air Pb 

concentrations (associated with an 

adjustment to the Pb standard), 

limitations in our data and tools 

precluded simulation of that 

relationship. Consequently, risk 

estimated for this category reflects 

media measurements available for the 

2007 REA and is identical for all air 

quality scenarios. Further, although 

paint is not an air-related source of Pb 

exposure, it may be reflected somewhat 

in estimates developed for the ‘‘past air’’ 

category, due to modeling constraints 

(2007 Staff Paper, section 4.2.4). Thus, 

as exposures included in the first airrelated category (‘‘recent’’) do not 

completely capture all air-related 

pathways, we consider risk for this 

category an underestimate of air-related 

risk. Yet, as exposures included in the 

second air-related category include 

pathways that are not air-related, we 

consider the summed risk across both 

categories to include a slight overestimate of air-related risk. 

In summary, because of limitations in 

the assessment design, data and 

modeling tools, we consider our 

estimates of risk attributable to airrelated exposure pathways to be 

approximate and 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. With 

regard to the latter, we are additionally 

cognizant of the modeling and data 

limitations which reduce the extent to 

which the upper end of these bounds 

reflects impacts of alternative air quality 

conditions simulated. We note that this 

limitation will tend to contribute to 

estimates for the ‘‘past air’’ category 

representing relatively greater 

overestimates with relatively lower air 

Pb air quality scenarios. 

We recognize several important 

sources of variability in air-related Pb 

exposures and associated risk, for which 

the approaches by which they were 

addressed in the 2007 REA are 

summarized here (PA, section 3.4.6). 

• Variation in distributions of 

potential urban residential exposure and 

risk across U.S. urban residential areas 

is addressed by the inclusion of 

location-specific urban study areas that 

reflect a diverse set of urban areas in the 

U.S. 

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• Representation of a more highly 

exposed subset of urban residents 

potentially exposed at the level of the 

standard is addressed by the inclusion 

of the generalized (local) urban study 

area. 

• Variation in residential exposure to 

ambient air Pb within an urban area of 

the location-specific case studies is 

addressed through the partitioning of 

these study areas into exposure zones to 

provide some representation of spatial 

gradients in ambient air Pb and their 

interaction with population distribution 

and demographics. 

• Inter-individual variability in blood 

Pb levels is addressed through the use 

of empirically derived GSDs to develop 

blood Pb distribution for the child 

population in each exposure zone, with 

GSDs selected particular to each case 

study population. 

• Inter-individual variability in IQ 

response to blood Pb is addressed 

through the use of C–R functions for IQ 

loss based on a pooled analysis 

reflecting studies of diverse 

populations. 

With regard to uncertainties, we 

recognize one overarching area 

concerning the precision of our 

estimation of the neurocognitive risk (as 

represented by IQ loss) associated with 

ambient air Pb. For reasons related to 

the evidence of nonlinear responses of 

blood Pb to Pb exposure and of Pbassociated IQ response to blood Pb, the 

2007 REA first estimated blood Pb levels 

and associated risk for total Pb exposure 

(i.e., including Pb from air-related and 

nonair exposure pathways) and then 

separated out estimates for pathways of 

interest (PA, section 3.4.4). However, as 

described above, significant limitations 

in our modeling tools affected our 

ability to develop precise estimates for 

air-related exposure pathways. We 

believe these limitations led to a slight 

overestimation of the risks for the ‘‘past 

air’’ category and to an underrepresentation of air-related pathways 

for the ‘‘recent air’’ category. Thus, we 

characterized the risk attributable to airrelated exposure pathways to be 

bounded by the estimates developed for 

the ‘‘past air’’ category and the sum of 

estimates for the ‘‘recent air’’ and ‘‘past 

air’’ categories. For air quality scenarios 

other than those for the previous 

NAAQS, this upper bound is recognized 

as having a potential upward bias with 

regard to its reflection of the simulated 

air quality conditions because modeling 

and data limitations precluded 

simulation of the influence of lower air 

Pb concentrations on the outdoor dust 

and soil exposure pathways (PA, section 

3.4.4). 

We recognize a range of additional 

uncertainties, limitations, and 

assumptions that are reflected in various 

ways in the 2007 REA and associated 

results (PA, section 3.4.7), which 

include the following. 

• Temporal Aspects: During the 

7-year exposure period, media 

concentrations remain fixed and the 

simulated child resides at the same 

residence (although exposure factors, 

including behavioral and physiological 

parameters, are adjusted to match the 

aging of the child). These aspects 

introduce uncertainty into the risk 

estimates, although the existence of a 

directional bias is unclear. 

• Generalized (local) Urban Case 

Study: The design for this case study 

employs assumptions regarding 

uniformity that are reasonable in the 

context of a general description 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. An additional area 

of uncertainty concerns the 

representation of variability in air 

quality. Given the relatively greater 

variability common in areas of high Pb 

concentrations, the approach used to 

reflect variability may bias the estimates 

high. 

• Location-specific Urban Case 

Studies: Limitations in the spatial 

density of ambient air monitors in the 

simulated areas limit our 

characterization of spatial gradients of 

ambient air Pb levels in these case 

studies. This factor introduces 

uncertainty into the risk estimates for 

this category of case study; the existence 

of a directional bias is unclear. 

• Air Quality Simulation: Focus on 

only then-current conditions (2003– 

2005) scenario for the Chicago urban 

case study in this review precludes 

uncertainty associated with simulations 

of alternative air quality scenarios in the 

2007 REA. 

• Outdoor Soil/Dust Pb 

Concentrations: Limitations in datasets 

on Pb levels in surface soil/dust Pb in 

urban areas and in our ability to 

simulate the impact of reduced air Pb 

levels related to lowering the NAAQS in 

the 2007 REA contribute uncertainty to 

air-related risk estimates for the current 

standard in the generalized (local) urban 

case study. The likely impact is a high 

bias on these risk estimates (related to 

low bias on estimating risk reduction for 

lower standard levels in the 2007 REA) 

given lack of simulated changes in soil 

Pb related to changes in ambient air Pb. 

• 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 airrelated risk estimates. Although the 

indoor dust modeling does link changes 

in ambient air Pb to changes in indoor 

dust Pb, it does not include a link 

between ambient air Pb, outdoor soil Pb 

and subsequent changes in the level of 

Pb carried (or ‘‘tracked’’) into the house. 

This could introduce low bias into the 

total estimates of air-related Pb exposure 

and risk. 

• Interindividual Variability in Blood 

Pb Levels: Uncertainty related to 

population variability in blood Pb levels 

related to interindividual variability in 

factors other than media concentration 

and limitations in modeling of this 

introduces significant uncertainty into 

blood Pb and IQ loss estimates for the 

95th percentile of the population. The 

extent of any systematic bias from this 

source of uncertainty is unknown. 

• Pathway Apportionment for Higher 

Percentile Blood Pb and Risks: 

Limitations, primarily in data, 

prevented us from characterizing the 

degree of correlation among high-end Pb 

exposures for the various pathways (e.g., 

the degree to which an individual 

experiencing high drinking water Pb 

exposure would also experience high Pb 

paint exposure and high ambient airrelated Pb exposure). Our inability to 

characterize potential correlations 

between exposure pathways 

(particularly at the higher percentile 

exposure levels) limited our ability to 

(1) effectively model high-end Pb risk 

and (2) apportion that risk between 

different exposure pathways, including 

ambient air-related pathways. 

• IQ Loss C–R Functions: 

Specification of the quantitative 

relationship between blood Pb level and 

IQ loss is subject to greater uncertainty 

at lower blood Pb levels. The use of four 

C–R functions models (which each treat 

the response at low blood Pb levels in 

a different manner) is considered to 

provide a reasonable characterization of 

this source of uncertainty and its impact 

on risk estimates. Comparison of risk 

estimates from the four models indicates 

this source of uncertainty to have a 

potentially significant impact on risk. 

4. Summary of Risk Estimates and Key 

Observations 

In this summary of risk estimates, 

drawn from the PA, we focus on the 

estimates of air-related IQ loss derived 

using the C–R function in which we 

have greatest confidence (see PA, 

sections 3.4.3.3.1 and 3.4.7) for the 

median child in a given case study 

(exposure modeled through age 7 years), 

given the substantially greater 

uncertainty associated with air-related 

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62There is uncertainty associated with judging 

differences between the current standard and these 

potential alternative standards due to the difference 

in air quality datasets used to estimate air 

concentration variability of the 2007 REA estimates 

versus the interpolated risk estimate. 

risk estimates for extremes of the risk 

distribution, such as the 95th percentile 

(PA, section 3.4). Estimates for other 

risk metrics and the full range of case 

studies and air quality scenarios are 

described elsewhere in detail (e.g., 2007 

REA, sections 4.2 and 5.3.2 and 

appendices; 2007 Staff Paper, chapter 4; 

73 FR 66964, November 12, 2008). 

Based on results from the 2007 REA for 

a location-specific urban study area 

(Chicago case study) and on those newly 

derived in this review based on 

interpolation from the 2007 REA results 

(for the generalized [local] urban case 

study), median air-related IQ loss for the 

current standard is estimated, with 

rounding, to generally fall near or 

somewhat above a rough lower bound of 

1 point IQ loss and below a rough upper 

bound of 3 points IQ loss. As would be 

expected by the use of interpolation, the 

newly derived estimates are consistent 

with the estimates for similar air quality 

scenarios that were available in the last 

review (PA, section 3.4.5). For example, 

the generalized (local) urban case study 

current standard scenario estimates for 

median air-related IQ loss are identical 

to those for the scenario of just meeting 

a potential alternative of 0.2 mg/m3

maximum calendar quarter average for 

that case study (PA, Table 3–11). 

Further, the upper bound below which 

the median IQ loss is estimated to fall 

is also approximately 3 IQ points in the 

generalized (local) urban case study 

scenarios for just meeting potential 

alternatives of 0.2 mg/m3, 0.05 and 0.02 

mg/m3 maximum monthly average, 

providing an indication of the 

limitations associated with estimating 

air-related Pb exposures and risk for 

lower air Pb scenarios (PA, sections 

3.4.4 and 3.4.5). 

As summarized in section II.D.3 

above, a range of limitations and areas 

of uncertainty were associated with the 

information available in the last review 

(PA, sections 3.4.4, 3.4.6 and 3.4.7). In 

this review, the REA Planning 

Document concluded that none of the 

primary sources of uncertainty 

identified to have the greatest impact on 

risk estimates would be substantially 

reduced through the use of newly 

available information (USEPA, 2011b). 

Thus, the key observations regarding 

air-related Pb risk modeled for the set of 

standard levels assessed in the 2007 

REA, as well as the risk estimates 

interpolated for the current standard, 

are not significantly affected by the new 

information. Further, our overall 

characterization of uncertainty and 

variability associated with those 

estimates (as summarized above and in 

sections 3.4.6 and 3.4.7 of the PA) is not 

appreciably affected by new 

information. As recognized at the time 

of the last review, exposure and risk 

modeling conducted for this analysis 

was complex and subject to significant 

uncertainties due to limitations in the 

data and models, among other aspects. 

Of particular note, limitations in the 

assessment design, data and modeling 

tools handicapped us from sharply 

separating Pb linked to ambient air from 

Pb that is not air related. 

In summary, the estimates of risk 

attributable to air-related exposures, 

with which we recognize a variety of 

sources of uncertainty, are considered to 

be approximate, falling within upper 

and lower bounds. These bounds for 

scenarios just meeting the current 

standard are roughly estimated, with 

rounding, as 3 and 1 IQ points, which 

over- and underestimate risk, 

respectively. In characterizing the 

magnitude of air-related risk associated 

with the current standard, we focus on 

median estimates, for which we have 

appreciably greater confidence than 

estimates for outer ends of the risk 

distribution (see PA, section 3.4.7) and 

on risks derived using the C–R function 

in which we have greatest confidence 

(see PA, sections 3.4.3.3.1 and 3.4.7). 

These risk results for the current 

standard, both those estimated in the 

last review for one of the locationspecific urban study area populations 

and those newly derived in this review 

using interpolation of the estimates from 

the last review for the generalized 

(local) urban case study, which is 

recognized to reflect a generalized high 

end of air-related exposure for localized 

populations, provide approximate 

bounds for air-related risk, with 

attendant uncertainties described above. 

Focusing on the results for the 

generalized (local) urban case study, the 

interpolated estimates for the scenario 

representing the current standard are 

very similar to estimates for the two 0.2 

mg/m3 scenarios (maximum monthly 

and calendar quarter averages) 

simulated in the 2007 REA 62 and are 

appreciably lower than those associated 

with the previous standard. For this 

case study, across the two 0.2 mg/m3

scenarios, the current standard scenario 

and the more restrictive air quality 

scenarios, the upper bound below 

which air-related risk is estimated to fall 

rounds to the same value, reflecting the 

significant limitations associated with 

developing precise estimates of airrelated risk, particularly for the lower 

air Pb scenarios (PA, sections 3.4.4, 

3.4.5, and 3.4.7). 

E. Conclusions on Adequacy of the 

Current Primary Standard 

In evaluating whether, in view of the 

advances in scientific knowledge and 

additional information now available, it 

is appropriate to retain or revise the 

current standard, the Administrator 

builds upon the last review and reflects 

upon the body of evidence and 

information now available. 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. Evidence-based 

considerations draw upon the EPA’s 

assessment and integrated synthesis of 

the scientific evidence from 

epidemiological studies and 

experimental animal studies evaluating 

health effects related to exposures to Pb, 

with a focus on policy-relevant 

considerations as discussed in the PA. 

The exposure/risk-based considerations 

draw from the results of the quantitative 

analyses presented in the 2007 REA, 

augmented as described in the PA, and 

summarized in section II.D above, and 

consideration of those results in the PA. 

More specifically, estimates of the 

magnitude of ambient Pb-related 

exposures for young children and 

associated impacts on IQ associated 

with just meeting the current primary 

Pb NAAQS have been considered. 

Together the evidence-based and riskbased considerations have informed the 

Administrator’s proposed conclusions 

related to the adequacy of the current Pb 

standard in light of the currently 

available scientific evidence. 

As described in section II.A.2 above, 

consideration of the evidence and the 

exposure/risk information in the PA and 

by the Administrator is framed by 

consideration of a series of key policyrelevant questions. The following 

sections describe the consideration of 

these questions in the PA, the advice 

received from CASAC, as well as the 

comments received from various parties, 

and then present the Administrator’s 

proposed conclusions regarding the 

adequacy of the current primary 

standard. 

1. Evidence-Based Considerations in the 

Policy Assessment 

In considering the evidence with 

regard to the issue of adequacy of the 

current standard, the PA addresses 

several questions that build on the 

information summarized in sections II.B 

and II.C above (and sections 3.1 through 

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63The older study by Hayes et al. (1994) during 

time of leaded gasoline indicated a generally similar 

ratio of 1:8, although the blood Pb levels in that 

study were much higher than those in the study by 

Hilts (2003). Among the studies focused on this age 

group, the latter study includes blood Pb levels 

closest to those in U.S. today. 

64Concentrations near air sources are higher than 

those at more distant sites (as described in PA, 

section 2.2.2); it is near-source locations where 

there is the potential for concentrations at or near 

the current standard. 

3.3 of the PA) to more broadly address 

the extent to which the current evidence 

base supports the adequacy of the 

public health protection afforded by the 

current primary standard. The first 

question addresses the integrated 

consideration of the health effects 

evidence, in light of aspects described 

in sections II.A.1 and II.A.2 above. The 

second question focuses on 

consideration of associated areas of 

uncertainty. The third question then 

integrates consideration of the prior two 

questions with a focus on the standard, 

including each of the four elements. The 

PA considerations and conclusions with 

regard to these questions are 

summarized below. 

In considering the extent to which 

information newly available in this 

review may have altered scientific 

support for the occurrence of health 

effects associated with Pb in ambient 

air, the PA concludes that the current 

evidence continues to support the EPA’s 

conclusions from the previous review 

regarding key aspects of the health 

effects evidence for Pb and the health 

effects of multimedia exposure 

associated with levels of Pb occurring in 

ambient air in the U.S. (PA, section 

4.2.1). The conclusions in this regard 

are based on consideration of the 

assessment of the currently available 

evidence in the ISA, particularly with 

regard to key aspects summarized in 

Chapter 3 of the PA, in light of the 

assessment of the evidence in the last 

review as described in the 2006 CD and 

summarized in the notice of final 

rulemaking (73 FR 66964, November 12, 

2008). Key aspects of these conclusions 

are summarized below. 

As at the time of the last review, 

blood Pb continues to be the 

predominant biomarker employed to 

assess exposure and health risk of Pb 

(ISA, Chapters 3 and 4), as discussed in 

section II.C above. This widely accepted 

role of blood Pb in assessing exposure 

and risk is illustrated by its established 

use in programs to prevent both 

occupational Pb poisoning and 

childhood Pb poisoning, with the latter 

program, implemented by the CDC, 

recently issuing updated guidance on 

blood Pb measurement interpretation 

(CDC, 2012). As in the past, the current 

evidence continues to indicate the close 

linkage of blood Pb levels in young 

children to their body burden; this 

linkage is associated with the ongoing 

bone remodeling during that lifestage 

(ISA, section 3.3.5). This tight linkage 

plays a role in the somewhat rapid 

response of children’s blood Pb to 

changes in exposure (particularly to 

exposure increases), which contributes 

to its usefulness as an exposure 

biomarker (ISA, sections 3.2.2, 3.3.5, 

and 3.3.5.1). Additionally, the weight of 

evidence documenting relationships 

between children’s blood Pb and health 

effects, most particularly those on the 

nervous and hematological systems 

(e.g., ISA, sections 4.3 and 4.7), speaks 

to its usefulness in assessing health risk. 

As in the last review, the evidence on 

air-to-blood relationships available 

today continues to be composed of 

studies based on an array of 

circumstances and population groups 

(of different age ranges), analyzed by a 

variety of techniques, which together 

contribute to appreciable variability in 

the associated quantitative estimates 

and uncertainty with regard to the 

relationships existing in the U.S. today. 

Accordingly, interpretation of this 

evidence base, as discussed in section 

II.C above, also includes consideration 

of factors that may be influencing 

various study estimates. We consider 

the study estimates in light of such 

factors both with regard to the extent to 

which the factors affect the usefulness 

of specific study estimates for the 

general purpose here of quantitatively 

characterizing relationships between Pb 

in ambient air and air-related Pb in 

children’s blood and also with regard to 

the pertinence of such factors more 

specifically to conditions and 

populations in the U.S. today. As noted 

in the PA, the current evidence, while 

including two additional studies not 

available at the time of the last review, 

is not appreciably changed from that 

available in the last review (PA, section 

3.1). The range of estimates that can be 

derived from the full dataset is broad 

and not changed by the inclusion of the 

newly available estimates. Further, the 

PA recognizes significant uncertainties 

regarding the air Pb to air-related blood 

Pb relationship for the current 

conditions where concentrations of Pb 

in both ambient air and children’s blood 

are substantially lower than they have 

been in the past. In considering the 

strengths, limitations and uncertainties 

associated with the full dataset, the 

currently available evidence appears to 

continue to support a range of estimates 

for the purpose at hand that is generally 

consistent with the range given weight 

in the last review, 1:5 to 1:10 (ISA, 

section 3.7.4 and Table 3–12; 73 FR 

67001–2, 67004, November 12, 2008). 

The PA additionally notes that the 

generally central estimate of 1:7 

identified for this range in the last 

review is consistent with the study 

involving blood Pb for pre-school 

children and air Pb conditions near a 

large source of Pb to ambient air with 

concentrations near (and/or previously 

above) the level of the current Pb 

standard (ISA, section 3.5.1; Hilts, 

2003).63 In so noting, the PA also 

recognizes the general overlap of such 

circumstances with those represented 

by the evidence-based, air-related IQ 

loss framework,64 for which air-to-blood 

ratio is a key input. In characterizing the 

range of air-to-blood ratio estimates, we 

recognize uncertainty inherent in such 

estimates as well as the variation in 

currently available estimates resulting 

from a variety of factors, including 

differences in the populations 

examined, as well as in the Pb sources 

or exposure pathways addressed in 

those study analyses (ISA, section 

3.7.4). 

The scientific evidence continues to 

recognize a broad array of health effects 

on multiple organ systems or biological 

processes related to blood Pb, including 

Pb in blood prenatally (ISA, section 1.6). 

The currently available evidence 

continues to support identification of 

neurocognitive effects in young children 

as the most sensitive endpoint 

associated with blood Pb concentrations 

(ISA, section 1.6.1), which as an 

integrated index of exposure reflects the 

aggregate exposure to all sources of Pb 

through multiple pathways (inhalation 

and ingestion). Evidence continues to 

indicate that some neurocognitive 

effects in young children may not be 

reversible and may have effects that 

persist into adulthood (ISA, section 

1.9.5). Thus, as discussed in section II.B. 

above, the evidence of Pb effects at the 

low end of the studied blood Pb levels 

(closest to those common in the U.S. 

today) continues to be strongest and of 

greatest concern for effects on the 

nervous system, most particularly those 

on cognitive function in children. 

As in the last review, evidence on risk 

factors continues to support the 

identification of young children as an 

important at-risk population for Pb 

health effects (ISA, section 5.4). The 

current evidence also continues to 

indicate important roles as factors that 

increase risk of Pb-related health effects 

for the following: Nutritional factors, 

such as iron and calcium intake; 

elevated blood Pb levels; and proximity 

to sources of Pb exposure, such as 

industrial releases or buildings with old, 

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deteriorating, leaded paint. Further, 

some races or ethnic groups continue to 

demonstrate increased blood Pb levels 

relative to others, which may be related 

to these and other factors (ISA, sections 

5.1, 5.2 and 5.4). 

With regard to our understanding of 

the relationship between exposure or 

blood Pb levels in young children and 

neurocognitive effects, the PA notes that 

the evidence in this review, as in the 

last, does not establish a threshold 

blood Pb level for neurocognitive effects 

in young children (ISA, sections 1.9.4 

and 4.3.12). The lowest blood Pb levels 

at which associations with 

neurocognitive impacts have been 

observed in pre-school and school age 

children continue to range down below 

5 mg/dL, with the lowest group levels 

that have been associated with such 

effects ranging down to 2 mg/dL (ISA, 

sections 1.6.1 and 4.3.15.1). 

Additionally, as in the last review, there 

is evidence that the relationship of 

young children’s blood Pb with 

neurocognitive impacts, such as IQ, is 

nonlinear across a wide range of blood 

Pb, with greater incremental impacts at 

lower versus higher blood Pb levels 

(ISA, sections 1.9.4 and 4.3.12). 

Accordingly, as in the last review, the 

PA focuses on C–R relationships from 

study groups with blood Pb levels 

closest to those in children in the U.S. 

today, which are generally lower than 

epidemiological study groups. The 

currently available evidence does not 

identify additional C–R slopes for study 

groups of young children (e.g., ≤7 years) 

with mean blood Pb levels below that of 

groups identified in the last review, 2.9 

¥ 3.8 mg/dL, as discussed in section 

II.B.3 above (ISA, section 4.3.12). Thus, 

the blood Pb concentration—IQ 

response functions or slopes identified 

in this review for epidemiological study 

groups of young children with mean 

blood Pb levels closest to that of 

children in the U.S. today include the 

same set recognized at the time of the 

last review (see Table 1 above), the 

median of which is 1.75 IQ points 

decrement per mg/dL blood Pb (73 FR 

67003, November 12, 2008). 

In considering the evidence with 

regard to the extent to which important 

uncertainties identified in the last 

review have been reduced or to which 

new uncertainties have emerged, as 

summarized in discussing the previous 

question and in section II.B above, the 

PA concludes that no new uncertainties 

were identified as emerging since the 

last review. However, the PA recognizes 

important uncertainties identified in the 

last review that remain today. 

Importantly, given our focus in this 

review, as in the last review, on 

neurocognitive impacts associated with 

Pb exposure in early childhood, the PA 

recognizes remaining uncertainties in 

our understanding of the C–R 

relationship of neurocognitive impacts, 

such as IQ decrements, with blood Pb 

level in young children, particularly 

across the range of blood Pb levels 

common in the U.S. today. With regard 

to C–R relationships for IQ, the evidence 

available in this review does not include 

studies that appreciably extend the 

range of blood Pb levels studied beyond 

those available in the last review. As in 

the last review, the early childhood 

(e.g., 2 to 7 years of age) blood Pb levels 

for which associations with IQ response 

have been reported continue to extend 

at the low end of the range to study 

group mean blood Pb levels of 2.9 to 3.8 

mg/dL (e.g., 73 FR 67003, November 12, 

2008, Table 3). The studies examining 

C–R relationships down to these blood 

Pb levels, as summarized in section 

II.B.3 above, continue to indicate higher 

C–R slopes in those groups with lower 

blood Pb levels than in study groups 

with higher blood Pb levels (ISA, 

section 4.3.12). The lack of studies 

considering C–R relationships for Pb 

effects on IQ at still lower blood Pb 

levels contributes to uncertainty 

regarding the quantitative relationship 

between blood Pb and IQ response in 

populations with mean blood Pb levels 

closer to the most recently available 

mean for children aged 1 to 5 years of 

age (e.g., 1.17 mg/dL in 2009–2010 [ISA, 

p. 3–85]). 

Further, the PA recognizes important 

uncertainties in our understanding of 

the relationship between ambient air Pb 

concentrations and air-related Pb in 

children’s blood. The evidence newly 

available in this review has not reduced 

such key uncertainties. As in the last 

review, air-to-blood ratios based on the 

available evidence continue to vary, 

with our conclusions based on the 

current evidence generally consistent 

with the range of 1:5 to 1:10 given 

emphasis in the last review (73 FR 

67002, November 12, 2008; ISA, section 

3.7.4). There continues to be uncertainty 

regarding the extent to which this range 

represents the relationship between 

ambient air Pb and Pb in children’s 

blood (derived from the full set of airrelated exposure pathways) and with 

regard to its reflection of exposures 

associated with ambient air Pb levels 

common in the U.S. today and to 

circumstances reflecting just meeting 

the current Pb standard (ISA, section 

3.7.4). The PA additionally notes the 

significant uncertainty remaining with 

regard to the temporal relationships of 

ambient Pb levels and associated 

exposure with occurrence of a health 

effect (73 FR 67005, November 12, 

2008). 

In integrating consideration of the 

prior two questions with a focus on the 

standard, the PA then addresses the 

question regarding the extent to which 

newly available information supports or 

calls into question any of the basic 

elements of the current Pb standard. The 

PA addresses this question for each of 

the elements of the standard in light of 

the health effects evidence and other 

relevant information available in this 

review (and summarized in sections II.B 

and II.C above). As an initial matter, the 

PA recognizes the weight of the 

scientific evidence available in this 

review that continues to support our 

focus on effects on the nervous system 

of young children, specifically 

neurocognitive decrements, as the most 

sensitive endpoint. Consistent with the 

evidence available in the last review, 

the currently available evidence 

continues to indicate that a standard 

that provides requisite public health 

protection against the occurrence of 

such effects in at-risk populations 

would also provide the requisite public 

health protection against the full array 

of health effects of Pb. Accordingly, the 

discussion of the elements below is 

framed by that background. 

Indicator 

The indicator for the current Pb 

standard is Pb-TSP. Key considerations 

in retaining this indicator in the last 

review are summarized in section II.A.1. 

Exposure to Pb in all sizes of particles 

passing through ambient air can 

contribute to Pb in blood and associated 

health effects by a wide array of 

exposure pathways (ISA, section 3.1). 

These pathways include the ingestion 

route, as well as inhalation (ISA, section 

3.1), and a wide array of particle sizes 

play a role in these pathways (ISA, 

section 3.1.1.1). As at the time of the last 

review, the PA recognizes the variability 

of the Pb-TSP FRM in its capture of 

airborne Pb particles (as discussed in 

section 2.2.1.3.1 of the PA). As in the 

last review, the PA also notes that an 

alternative approach for collection of a 

conceptually comparable range of 

particle sizes, including ultra-coarse 

particles, is not yet available. 

Additionally, the limited available 

information regarding relationships 

between Pb-TSP and Pb in other size 

fractions indicates appreciable variation 

in this relationship, particularly near 

sources of Pb emissions where 

concentrations and potential exposures 

are greatest. Thus, the PA concludes 

that the information available in this 

review does not address previously 

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65As discussed further below, the Administrator 

also considered the exposure/risk-based 

information, which he found to be roughly 

consistent and generally supportive of the 

framework estimates (73 FR 67004). 

identified limitations and uncertainties 

for the current indicator. Nor does the 

newly available information identify 

additional limitations or uncertainties. 

The PA notes that the evidence 

available in this review continues to 

indicate the role of a range of air Pb 

particle sizes in contributing to Pb 

exposure (e.g., ISA, section 3.1.1.1) that 

contributes to Pb in blood and 

associated health effects. For example, 

the evidence indicates larger particle 

sizes for Pb that occurs in soil and 

house dust and may be ingested as 

compared to Pb particles commonly 

occurring in the atmosphere and the 

size fraction of the latter that may be 

inhaled (ISA, section 3.1.1.1). Taken 

together, the PA concludes that the 

evidence currently available reinforces 

the appropriateness of an indicator for 

the Pb standard that reflects a wide 

range of airborne Pb particles. 

Averaging Time and Form 

The averaging time and form of the 

standard were revised in the last Pb 

NAAQS review, based on 

considerations summarized in section 

II.A.1 above. The current standard is a 

not-to-be-exceeded rolling 3-month 

average (40 CFR 50.16), derived from 

three monthly averages calculated in 

accordance with the current data 

handling procedures (40 CFR part 50, 

Appendix R). The form is a maximum, 

evaluated within a 3-year period (40 

CFR 50.16). As at the time of the last 

review, the PA notes that evidence 

continues to support the importance of 

periods on the order of 3 months and 

the prominent role of deposition-related 

exposure pathways, with uncertainty 

associated with characterization of 

precise time periods associating ambient 

air Pb with air-related health effects. 

The PA concludes that relevant factors 

continue to be those pertaining to the 

human physiological response to 

changes in Pb exposures and those 

pertaining to the response of air-related 

Pb exposure pathways to changes in 

airborne Pb. The PA concludes that the 

newly available evidence in this review 

does not appreciably improve our 

understanding of the period of time in 

which air Pb concentrations would lead 

to the health effects most at issue in this 

review (PA, section 4.2.1). Newly 

available evidence accordingly also does 

not appreciably improve our 

understanding of the period of time for 

which control of air Pb concentrations 

would protect against exposures most 

pertinent to the health effects most at 

issue in this review. Thus, while there 

continue to be limitations in the 

evidence to inform our consideration of 

these elements of the standard and 

associated uncertainty, the available 

evidence continues to provide support 

for the decisions made in the last review 

regarding these elements of the current 

Pb standard. 

Level 

The level of the current standard is 

0.15 mg/m3 (40 CFR 50.16). As described 

in section II.A.1 above, this level was 

selected in 2008 with consideration of, 

among other factors, an evidence-based 

air-related IQ loss framework, for which 

there are two primary inputs: Air-toblood ratios and C–R functions for blood 

Pb–IQ response in young children. 

Additionally taken into consideration 

were the uncertainties inherent in these 

inputs.65 Application of the framework 

also entailed consideration of a 

magnitude of air-related IQ loss, which 

as further described in section II.A.1 

above, is used in conjunction with this 

specific framework in light of the 

framework context, limitations and 

uncertainties. Additionally, selection of 

a level for the standard in 2008 was 

made in conjunction with decisions on 

indicator, averaging time and form. 

As an initial matter, the PA considers 

the extent to which the evidence-based, 

air-related IQ loss framework which 

informed the Administrator’s decision 

in the last review is supported by the 

currently available evidence and 

information. In so doing, the PA 

recognizes the support provided by the 

currently available evidence for the key 

conclusions drawn in the last review 

with regard to health effects of greatest 

concern, at-risk populations, the 

influence of Pb in ambient air on Pb in 

children’s blood and the association 

between children’s blood Pb and 

decrements in neurocognitive function 

(e.g., IQ). The PA additionally notes the 

complexity associated with interpreting 

the scientific evidence with regard to 

specific levels of Pb in ambient air, 

given the focus of the evidence on blood 

Pb as the key biomarker of children’s 

aggregate exposure. The need to make 

such interpretations in the face of the 

associated complexity supported use of 

the evidence-based framework in the 

last review. In considering the currently 

available evidence for the same 

purposes in this review, the PA 

concludes that the evidence-based 

framework continues to provide a useful 

tool for consideration of the evidence 

with regard to the level of the standard. 

The PA next turned to consideration 

of the primary inputs to the framework: 

Air-to-blood ratios and C–R functions 

for blood Pb–IQ response in young 

children. With regard to the former, the 

PA concludes the limited newly 

available information assessed in the 

ISA, and discussed in section II.C above, 

to be generally consistent with the 

information in this area that was 

available at the time of the last review. 

The PA additionally recognizes the 

variability and uncertainty associated 

with quantitative air-to-blood ratios 

based on this information, as also 

existed in the last review. As in the last 

review, factors contributing to the 

variability and uncertainty of these 

estimates are varied and include aspects 

of the study populations (e.g., age and 

Pb exposure pathways) and the study 

circumstances (e.g., length of study 

period and variations in sources of Pb 

exposure during the study period). The 

PA notes that the full range of estimates 

associated with the available evidence is 

wide and considers it appropriate to 

give emphasis to estimates pertaining to 

circumstances closest to those in the 

U.S. today with regard to ambient air Pb 

and children’s blood Pb concentrations, 

while recognizing the limitations 

associated with the available 

information. With that in mind, the PA 

considers the currently available 

evidence to continue to support the 

range of estimates for air-to-blood ratios 

concluded in the last review to be most 

appropriate for the current population 

of young children in the U.S., in light 

of the multiple air-related exposure 

pathways by which children are 

exposed and of the levels of air and 

blood Pb common today. Identification 

of this range also included 

consideration of the limitations 

associated with the available 

information and inherent uncertainties. 

This range of air-to-blood ratios 

included 1:10 at the upper end and 1:5 

at the lower end. The PA further 

recognizes that the limited evidence for 

air Pb and children’s blood Pb 

concentrations closest to those in U.S. 

today continues to provide support for 

the Administrator’s emphasis in the 

2008 decision on the relatively central 

estimate of 1:7. 

With regard to the second input to the 

evidence-based framework, C–R 

functions for the relationship of young 

children’s blood Pb with neurocognitive 

impacts (e.g., IQ decrements), the PA 

considers several aspects of the 

evidence. First, as discussed in section 

II.B.3 above, the currently available 

information continues to provide 

evidence that this C–R relationship is 

nonlinear across the range of blood Pb 

levels from the higher concentrations 

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66We note that the value of the upper bound is 

influenced by risk associated with exposure 

pathways that were not varied with alternative 

standard levels, a modeling limitation with the 

potential to contribute to overestimation of the 

upper bound with air quality scenarios involving 

air Pb levels below current conditions for the study 

area (see sections 3.4.4 and 3.4.7 above). 

more prevalent in the past to lower 

concentrations more common today. 

Thus, the PA continues to consider it 

particularly appropriate to focus on the 

evidence from studies with blood Pb 

levels closest to those of today’s 

population which, as in the last review, 

includes studies with study group mean 

blood Pb levels ranging roughly from 3 

to 4 mg/dL in children aged 24 months 

to 7 years (PA, Table 3–3). As discussed 

in section II.B.3 above, this is also 

consistent with the evidence currently 

available for this age group of young 

children, which does not include 

additional C–R slopes for incremental 

neurocognitive decrement with blood 

Pb levels at or below this range. In 

considering whether this set of 

functions continues to be well 

supported by the evidence, as assessed 

in the ISA (ISA, section 4.3.2), the PA 

notes the somewhat wide range in 

slopes encompassed by these study 

groups, while also noting the stability of 

the median. For example, omission of 

any of the four slopes considered in the 

last review does not appreciably change 

the median (e.g., the median would 

change from ¥1.75 IQ points per mg/dL 

blood Pb to ¥1.71 or ¥1.79). Thus, 

while differing judgments might be 

made with regard to inclusion of each 

of the four study groups, these estimates 

are generally supported by the current 

review of the evidence in the ISA. 

Further, the stability of the median to 

modifications to this limited dataset 

lead the PA to conclude that the 

currently available evidence continues 

to support consideration of ¥1.75 IQ 

points per mg/dL blood Pb as a wellfounded and stable estimate for 

purposes of describing the 

neurocognitive impact quantitatively on 

this age group of U.S. children. 

In summary, in considering the 

evidence and information available in 

this review pertaining to the level of the 

current Pb standard, the PA notes that 

the evidence available in this review, as 

summarized in the ISA, continues to 

support the air-related IQ loss evidencebased framework, with the inputs that 

were used in the last review. These 

include estimates of air-to-blood ratios 

ranging from 1:5 to 1:10, with a 

generally central estimate of 1:7. 

Additionally, the C–R functions most 

relevant to blood Pb levels in U.S. 

children today continue to be provided 

by the set of four analyses considered in 

the last review for which the median 

estimate is ¥1.75 IQ points per mg/dL 

Pb in young children’s blood. Thus, the 

PA observed that the evidence available 

in this review has changed little if at all 

with regard to the aspects given weight 

in the conclusion on level for the new 

standard in the last review and would 

not appear to call into question any of 

the basic elements of the standard. In so 

doing, the PA additionally recognizes 

that the overall decision on adequacy of 

the current standard is a public health 

policy judgment by the Administrator. 

2. Exposure/Risk-Based Considerations 

in the Policy Assessment 

In consideration of the issue of 

adequacy of public health protection 

provided by the current standard, the 

PA also considered the quantitative 

exposure/risk assessment completed in 

the last review, augmented as described 

in section II.C above. The PA recognizes 

substantial uncertainty inherent in the 

REA estimates of air-related risk 

associated with localized conditions just 

meeting the current standard, which we 

have characterized as approximate and 

falling within rough bounds.66 This 

approximate estimate of risk for 

children living in such areas is generally 

overlapping with and consistent with 

the evidence-based air-related IQ loss 

estimates described in section II.A.1 

above. The PA discussion with regard to 

interpretation of the exposure/risk 

information for air quality conditions 

associated with just meeting the current 

standard is organized around two 

questions, as summarized here (PA, 

section 4.2.2). 

In considering the level of confidence 

associated with estimates of air-related 

risk generated for simulations just 

meeting the current Pb standard, the PA 

recognizes, as an initial matter, the 

significant limitations and complexity 

associated with the risk and exposure 

assessments for Pb that are far beyond 

those associated with similar 

assessments typically performed for 

other criteria pollutants. In completing 

the assessment, we were constrained by 

significant limitations with regard to 

data and tools particular to the problem 

at hand. Further, the multimedia and 

persistent nature of Pb and the role of 

multiple exposure pathways contribute 

significant additional complexity to the 

assessment as compared to other 

assessments that focus only on the 

inhalation pathway. As a result, the 

estimates of air-related exposure and 

risk are approximate, presented as 

upper and lower bounds within which 

we consider air-related risk likely to fall. 

The description of overall confidence in 

this characterization of air-related risk is 

based on consideration of the overall 

design of the analysis (summarized in 

section II.D), the degree to which key 

sources of variability are reflected in the 

design of the analysis (summarized in 

section II.D.3), and our characterization 

of key sources of uncertainty 

(summarized in section II.D.3). 

With regard to key sources of 

uncertainty, the PA notes particularly 

those affecting the precision of the airrelated risk estimates. Associated 

sources of uncertainty include the 

inability to simulate changes in airrelated Pb as a function of changes in 

ambient air Pb in exposure pathways 

other than those involving inhalation of 

ambient air and ingestion of indoor 

dust. This contributes to the positive 

bias of the upper bound for the airrelated risk estimates. The PA 

additionally recognizes the significant 

uncertainty associated with estimating 

upper percentiles of the distribution of 

air-related blood Pb concentration 

estimates (and associated IQ loss 

estimates) due to limitations in available 

information. Lastly, the PA recognizes 

the uncertainty associated with 

application of the C–R function at the 

lower blood Pb levels in the 

distribution; this relates to the limited 

representation of blood Pb levels of this 

magnitude in the dataset from which the 

C–R function is derived (PA, section 

4.2.2). 

In the quantitative risk information 

available in this review, we have airrelated risk estimates for simulations 

just meeting the current standard from 

one of the location-specific urban case 

studies (Chicago) and from the 

generalized (local) urban case study. 

With regard to the latter, the PA notes 

its simplified design that does not 

include multiple exposure zones; thus 

reducing the dimensions simulated. The 

PA concludes a reasonable degree of 

confidence in aspects of the generalized 

(local) urban case study for the specific 

situation we consider it to represent 

(i.e., a temporal pattern of air Pb 

concentrations that just meets the level 

of the standard), and when the 

associated estimates are characterized as 

approximate, within upper and lower 

bounds (as described above), while also 

recognizing considerable associated 

uncertainty. 

In considering the extent to which the 

estimated air-related risks remaining 

upon just meeting the current Pb 

standard are important from a public 

health perspective, the PA considers the 

nature and magnitude of such estimated 

risks (and attendant uncertainties), 

including such impacts on the affected 

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67The areas included in this estimate where the 

standard is currently exceeded are treated, for 

present purposes, as areas with air Pb 

concentrations just meeting the current standard 

and are included for purposes of this analysis (PA, 

pp. 3–36 to 3–38). This is in light of the 

requirement for areas not in attainment with the 

standard to attain the standard as expeditiously as 

practicable, but no later than 5 years after 

designation. 

68A second PA analysis, performed in recognition 

of the potential for the first analysis to underrepresent sites with elevated Pb concentrations, but 

with its own attendant uncertainties, indicates the 

potential for the population group in such areas to 

be only slightly larger, in terms of hundredths of 

a percent of the full population of children in this 

age group (PA, pp. 3–36 to 3–38, 4–25, 4–32). 

69As noted in section II.E.3 above, written 

comments submitted to the agency, as well as 

transcripts and minutes of the public meetings held 

in conjunction with CASAC’s reviews of documents 

for the review will be available in the docket for 

this rulemaking. 

population, and additionally considers 

the size of the affected population. In 

considering the quantitative risk 

estimates for decrements in IQ, we 

recognize that although some 

neurocognitive effects may be transient, 

some effects may persist into adulthood, 

affecting success later in life (ISA, 

sections 1.9.5 and 4.3.14). The PA 

additionally recognizes the potential 

population impacts of small changes in 

population mean values of metrics such 

as IQ, presuming a uniform 

manifestation of Pb-related decrement 

across the range of population IQ (ISA, 

section 1.9.1; PA, section 3.3). 

As summarized in sections II.D above, 

limitations in modeling tools and data 

affected our ability to develop precise 

risk estimates for air-related Pb 

exposure pathways and contributed 

uncertainties to the risk estimates. The 

results are approximate estimates which 

we describe through the use of rough 

upper and lower bounds within which 

we estimate air-related risk to fall. We 

have recognized a number of 

uncertainties in the underlying risk 

estimates from the 2007 REA and in the 

interpolation approach employed in the 

new analyses for this review. We have 

characterized the magnitude of airrelated risk associated with the current 

standard with a focus on median 

estimates, for which we have 

appreciably greater confidence than 

estimates for outer ends of risk 

distribution (see section 3.4.7 of the PA) 

and on risks derived using the C–R 

function in which we have greatest 

confidence (see sections 3.4.3.3.1 and 

3.4.7 of the PA). These risk estimates 

include estimates from the last review 

for one of the location-specific urban 

study area populations as well as 

estimates newly derived in this review 

based on interpolation from 2007 REA 

results for the generalized (local) urban 

case study, which is recognized to 

reflect a generalized high end of airrelated exposure for localized 

populations. Taken together, these 

results for just meeting the current 

standard include a high-end localized 

risk estimate for air-related Pb of a 

magnitude falling within general rough 

bounds of 1 and 3 points IQ loss, with 

attendant uncertainties, and with 

appreciably lower risks with increasing 

distance from the highest exposure 

locations. 

In considering the importance of such 

risk from a public health perspective, 

the PA also considers the size of at-risk 

populations represented by the REA 

case studies. As summarized in section 

II.D.1 above (and described more fully 

in the PA, section 3.4), the generalized 

(local) urban case study is considered to 

represent a localized urban population 

exposed near the level of the standard, 

such as a very small, compact 

neighborhood near a source contributing 

to air Pb concentrations just meeting the 

standard. This case study provides 

representation in the risk assessment for 

such small populations at the upper end 

of the gradient in ambient air 

concentrations expected to occur near 

sources; thus estimates for this case 

study reflect exposures nearest the 

standard being evaluated. While we do 

not have precise estimates of the 

number of young children living in such 

areas of the U.S. today, we have 

information that informs our 

understanding of their magnitude. For 

example, as summarized in section 

II.B.5 above, the PA estimates some 

2,700 children, aged 5 years and 

younger, to be living in localized areas 

with elevated air Pb concentrations that 

are above or near the current standard. 

Based on the 2010 census estimates of 

approximately 24.3 million children in 

the U.S. aged 5 years or younger, this 

indicates the size of the population of 

young children of this age living in 

areas in close proximity to areas where 

air Pb concentrations may be above or 

near the current standard to be generally 

on the order of a hundredth of a percent 

of the full population of 

correspondingly aged children.67 68

While these estimates pertain to the age 

group of children aged 5 years and 

younger, the PA additionally notes that 

a focus on an alternative age range (e.g., 

through age 7), while increasing the 

number for children living in such 

locations, would not be expected to 

appreciably change the percentage of 

the full U.S. age group that the subset 

represents. 

3. CASAC Advice 

In the current review of the primary 

standard for Pb, the CASAC has 

provided advice and recommendations 

in their review of drafts of the ISA, of 

the REA Planning Document, and of the 

draft PA. We have additionally received 

comments from the public on drafts of 

these documents.69

In their comments on the draft PA, the 

CASAC concurred with staff’s overall 

preliminary conclusions that it is 

appropriate to consider retaining the 

current primary standard without 

revision, stating that ‘‘the current 

scientific literature does not support a 

revision to the Primary Lead (Pb) 

National Ambient Air Quality Standard 

(NAAQS)’’ (Frey, 2013b). They further 

noted that ‘‘[a]lthough the current 

review incorporates a substantial body 

of new scientific literature, the new 

literature does not justify a revision to 

the standards because it does not 

significantly reduce substantial data 

gaps and uncertainties (e.g., air-blood Pb 

relationship at low levels; sources 

contributing to current population blood 

Pb levels, especially in children; the 

relationship between Pb and childhood 

neurocognitive function at current 

population exposure levels; the 

relationship between ambient air Pb and 

outdoor dust and surface soil Pb 

concentrations).’’ In recognition of these 

limitations in the available information, 

the CASAC provided recommendations 

on research to address these data gaps 

and uncertainties so as to inform future 

Pb NAAQS reviews (Frey, 2013b). 

The CASAC comments indicated 

agreements with key aspects of staff’s 

consideration of the exposure/risk 

information and currently available 

evidence in this review (Frey, 2013b, 

Consensus Response to Charge 

Questions, p. 7). 

The use of exposure/risk information from 

the previous Pb NAAQS review appears 

appropriate given the absence of significant 

new information that could fundamentally 

change the interpretation of the exposure/

risk information. This interpretation is 

reasonable given that information supporting 

the current standard is largely unchanged 

since the current standard was issued. 

The CASAC agrees that the adverse impact 

of low levels of Pb exposure on 

neurocognitive function and development in 

children remains the most sensitive health 

endpoint, and that a primary Pb NAAQS 

designed to protect against that effect will 

offer satisfactory protection against the many 

other health impacts associated with Pb 

exposure. 

The CASAC concurs with the draft PA that 

the scientific findings pertaining to air-toblood Pb ratios and the C–R relationships 

between blood Pb and childhood IQ 

decrements that formed the basis of the 

current Pb NAAQS remain valid and are 

consistent with current data. 

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The CASAC concurred with the 

appropriateness of the application of the 

evidence-based framework from the last 

Pb NAAQS review. With regard to the 

key inputs to that framework, CASAC 

concluded that ‘‘[t]he new literature 

published since the previous review 

provides further support for the health 

effect conclusions presented in that 

review’’ and that the studies newly 

available in this review ‘‘do not 

fundamentally alter the uncertainties for 

air-to-blood ratios or C–R functions for 

IQ decrements in young children’’ (Frey, 

2013b, Consensus Response to Charge 

Questions, p. 6). 

The comments from CASAC also took 

note of the uncertainties that remain in 

this review, which contribute to the 

uncertainties associated with drawing 

conclusions regarding air-related 

exposures and associated health risk at 

or below the level of the current 

standard, stating their agreement with 

‘‘the EPA conclusion that ‘there is 

appreciable uncertainty associated with 

drawing conclusions regarding whether 

there would be reductions in blood Pb 

levels from alternative lower levels as 

compared to the level of the current 

standard’ ’’ (Frey, 2013b, Consensus 

Response to Charge Questions, p. 6). 

Of the limited public comments 

received on this review to date that have 

addressed adequacy of the current 

primary Pb standard, all but one state 

support for retaining the current 

standard without revision, citing 

uncertainties in the available evidence 

and risk information. The other 

commenter expressed the view that the 

standard should be revised to be more 

restrictive given the evidence of Pb 

effects in populations with mean blood 

Pb levels below 10 mg/dL. 

4. Administrator’s Proposed 

Conclusions on the Adequacy of the 

Current Primary Standard 

Based on the large body of evidence 

concerning the health effects and 

potential public health impacts of 

exposure to Pb emitted into ambient air, 

and taking into consideration the 

attendant uncertainties and limitations 

of the evidence, the Administrator 

proposes to conclude that the current 

primary standard provides the requisite 

protection of public health, with an 

adequate margin of safety and should be 

retained. 

In considering the adequacy of the 

current standard, the Administrator has 

carefully considered the assessment of 

the available evidence and conclusions 

contained in the ISA; the technical 

information, including exposure/risk 

information, staff conclusions, and 

associated rationale, presented in the 

PA; the advice and recommendations 

from CASAC; and public comments to 

date in this review. In the discussion 

below, the Administrator gives weight 

to the PA conclusions, with which 

CASAC has concurred, and takes note of 

key aspects of the rationale presented 

for those conclusions which contribute 

to her proposed decision. 

As an initial matter, the Administrator 

takes note of the PA discussion with 

regard to the complexity involved in 

considering the adequacy of protection 

in the case of the primary Pb standard, 

which differs substantially from that 

involved in consideration of the primary 

NAAQS for other pollutants, for which 

the limited focus on the inhalation 

pathway is a relatively simpler context. 

Additionally, while an important 

component of the evidence base for 

most other NAAQS pollutants is the 

availability of studies that have 

investigated an association between 

current concentrations of the pollutant 

in ambient air and the occurrence of 

health effects plausibly related to 

ambient air exposure to that pollutant, 

the evidence base that supports 

conclusions in this review of the Pb 

NAAQS includes most prominently 

epidemiological studies focused on 

associations of blood Pb levels in U.S. 

populations with health effects 

plausibly related to Pb exposures. 

Support for conclusions regarding the 

plausibility for ambient air Pb to play a 

role in such findings derives, in part, 

from studies linking Pb in ambient air 

with the occurrence of health effects. 

However, such studies (dating from the 

past or from other countries) involve 

ambient air Pb concentrations many 

times greater than those that would 

meet the current standard. Thus, in 

considering the adequacy of the current 

Pb standard, rather than considering 

studies that have directly investigated 

current concentrations of Pb in ambient 

air (including in locations where the 

current standard is met) and the 

occurrence of health effects, we 

primarily consider the evidence for, and 

risk estimated from, models, based upon 

key relationships, such as those among 

ambient air Pb, Pb exposure, blood Pb 

and health effects. This evidence, with 

its associated limitations and 

uncertainties, contributes to the EPA’s 

conclusions regarding a relationship 

between ambient air Pb conditions 

under the current standard and health 

effects. 

With regard to the current evidence, 

the Administrator first takes note of the 

well-established body of evidence on 

the health effects of Pb, augmented in 

some aspects since the last review, 

which continues to support 

identification of neurocognitive effects 

in young children as the most sensitive 

endpoint associated with Pb exposure. 

The evidence, as summarized in the PA 

and discussed in detail in the ISA, 

continues to indicate that a standard 

that provides protection from 

neurocognitive effects in young children 

additionally provides protection for 

other health effects of Pb, such as those 

reported in adult populations. The 

Administrator takes note of the PA 

finding that application of the evidencebased, air-related IQ loss framework, 

developed in the last review, continues 

to provide a useful approach for 

considering and integrating the 

evidence on relationships between Pb in 

ambient air and Pb in children’s blood 

and risks of neurocognitive effects (for 

which IQ loss is used as an indicator). 

She additionally takes note of the PA 

finding (described in section II.E.1 

above) that the currently available 

evidence base, while somewhat 

expanded since the last review, is not 

appreciably expanded or supportive of 

appreciably different conclusions with 

regard to air-to-blood ratios or C–R 

functions for neurocognitive decrements 

in young children. She concurs with the 

PA findings, summarized in section 

II.E.1 above, that application of this 

framework, in light of the current 

evidence and exposure/risk information, 

continues to support a standard as 

protective as the current standard. 

In considering the nature and 

magnitude of the array of uncertainties 

that are inherent in the scientific 

evidence and analyses, the 

Administrator recognizes that our 

understanding of the relationships 

between the presence of a pollutant in 

ambient air and associated health effects 

is based on a broad body of information 

encompassing not only more established 

aspects of the evidence, but also aspects 

in which there may be substantial 

uncertainty. In the case of the Pb 

NAAQS review, she takes note of the 

recognition in the PA of increased 

uncertainty in characterizing the 

relationship of effects on IQ with blood 

Pb levels below those represented in the 

evidence base and in projecting the 

magnitude of blood Pb response to 

ambient air Pb concentrations at and 

below the level of the current standard. 

The PA recognizes this increased 

uncertainty, particularly in light of the 

multiple factors that play a role in such 

a projection (e.g., meteorology, 

atmospheric dispersion and deposition, 

human physiology and behavior), each 

of which carry attendant uncertainties. 

The Administrator recognizes that 

collectively, these aspects of the 

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evidence and associated uncertainties 

contribute to a recognition that for Pb, 

as for other pollutants, the available 

health effects evidence generally reflects 

a continuum, consisting of levels at 

which scientists generally agree that 

health effects are likely to occur, 

through lower levels at which the 

likelihood and magnitude of the 

response become increasingly uncertain. 

In making a judgment on the point at 

which health effects associated with Pb 

become important from a public health 

perspective, the Administrator has 

considered the public health 

significance of a decrement of a very 

small number of IQ points in the at-risk 

population of young children, in light of 

associated uncertainties. She notes that 

her judgment on this matter relates to 

her consideration of the IQ loss 

estimates yielded by the air-related IQ 

loss evidence-based framework for 

specific combinations of standard level, 

air-to-blood ratio and C–R function. In 

considering the public health 

significance of IQ loss estimates in 

young children, the Administrator gives 

weight to the comments of CASAC and 

some public commenters in the last 

review which recognized a population 

mean IQ loss of 1 to 2 points to be of 

public health significance and 

recommended that a very high 

percentage of the population be 

protected from such a magnitude of IQ 

loss (73 FR 67000, November 12, 2008). 

In so doing, the Administrator 

additionally notes that the EPA is aware 

of no new information or new 

commonly accepted guidelines or 

criteria within the public health 

community for interpreting public 

health significance of neurocognitive 

effects in the context of a decision on 

adequacy of the current Pb standard 

(PA, pp. 4–33 to 4–34). 

With the objective identified by 

CASAC in the 2008 review in mind, the 

Administrator considers the role of the 

air-related IQ loss evidence-based 

framework in informing consideration 

of standards that might be concluded to 

provide such a level of protection. In so 

doing, she first recognizes, like the 

Administrator at the time of the last 

review, that the IQ loss estimates 

produced with the evidence-based 

framework do not correspond to a 

specific quantitative public health 

policy goal for air-related IQ loss that 

would be acceptable or unacceptable for 

the entire population of children in the 

U.S. Rather, the conceptual context for 

the evidence-based framework is that it 

provides estimates for the mean airrelated IQ loss of a subset of the 

population of U.S. children (i.e., the 

subset living in close proximity to air Pb 

sources that contributed to elevated air 

Pb concentrations that equal the current 

level of the standard). This is the subset 

expected to experience air-related Pb 

exposures at the high end of the 

national distribution of such exposures. 

The associated mean IQ loss estimate is 

the average for this highly exposed 

subset and is not the average air-related 

IQ loss projected for the entire U.S. 

population of children. Further, the 

Administrator recognizes uncertainties 

associated with those estimates, and 

notes the PA conclusion that the 

uncertainties increase with estimates 

associated with successively lower 

standard levels. The Administrator 

additionally takes note of the PA 

estimates for the size of such a 

population, drawn from information on 

numbers of young children (aged 5 years 

or younger) living near monitors 

registering ambient Pb concentrations 

above or within 10 percent of the 

NAAQS, which indicate it to be on the 

order of one hundredth of one percent 

of the U.S. population of children of this 

age, with an upper bound of 

approximately four hundredths of one 

percent, drawn from similar 

demographic information based on 

proximity to large Pb sources, as 

identified using the NEI (PA, pp. 3–36 

to 3–38). In summary, the current 

evidence, as considered within the 

conceptual and quantitative context of 

the evidence-based framework, and 

current air monitoring information 

indicates that the current standard 

would be expected to satisfy the public 

health policy goal recommended by 

CASAC in the last Pb NAAQS review, 

and CASAC did not provide a different 

goal in the present review. Thus, the 

evidence indicates that the current 

standard provides protection for young 

children from neurocognitive impacts, 

including IQ loss, consistent with 

advice from CASAC regarding IQ loss of 

public health significance. 

In drawing conclusions from 

application of the evidence-based 

framework with regard to adequacy of 

the current standard, the Administrator 

further recognizes the degree to which 

IQ loss estimates drawn from the airrelated IQ loss evidence-based 

framework reflect mean blood Pb levels 

that are below those represented in the 

currently available evidence for young 

children. For example, in the case of the 

current standard level of 0.15 mg/m3, 

multiplication by the air-to-blood ratio 

of 1:7, the value that was the focus of 

the last review and which the evidence 

continues to support in this review, 

yields a mean air-related blood Pb level 

of 1.05 mg/dL. This blood Pb level is half 

the level of the lowest blood Pb 

subgroup of pre-school children in 

which neurocognitive effects have been 

observed (PA, Table 3–2; Miranda et al., 

2009) and well below the means of 

subgroups for which continuous C–R 

functions have been estimated (Table 1 

above). The Administrator views such 

an extension below the lowest studied 

levels to be reasonable given the lack of 

identified blood Pb level threshold in 

the current evidence base for 

neurocognitive effects and the need for 

the NAAQS to provide a margin of 

safety. She takes note, however, of the 

PA finding that the framework IQ loss 

estimates for standard levels lower than 

the current standard level represent still 

greater extrapolations from the current 

evidence base with corresponding 

increased uncertainty (PA, section 3.2, 

pp. 4–32 to 4–33). 

In considering application of the 

evidence-based framework in this 

review with regard to the extent there is 

support within the evidence for a 

standard with greater protection, the 

Administrator additionally takes note of 

the uncertainties that remain in our 

understanding of important aspects of 

ambient air Pb exposure and associated 

health effects, as discussed in the PA 

(PA, Chapter 3) and summarized in 

sections II.B and II.C above. With regard 

to the air-to-blood ratios that reflect the 

relationship between concentrations of 

Pb in ambient air and air-related Pb in 

children’s blood, she particularly notes 

the limitations and uncertainties 

identified in the ISA and PA with regard 

to the available studies and the gaps and 

uncertainties in the evidence base. 

These include gaps and uncertainties 

with regard to studies that have 

investigated such quantitative 

relationships under conditions 

pertaining to the current standard (e.g., 

in localized areas near air Pb sources 

where the standard is just met in the 

U.S. today), as well as with regard to 

evidence to inform our understanding of 

the quantitative aspects of relationships 

between ambient air Pb and outdoor 

soil/dust Pb and indoor dust Pb. These 

critical exposure pathways are also 

represented in the evidence-based airrelated IQ loss framework within the 

estimates of air-to-blood ratios. In light 

of these uncertainties and limitations in 

the evidence base, the Administrator 

gives weight to the PA conclusion of 

greater uncertainty with regard to 

relationships between concentrations of 

Pb in ambient air and air-related Pb in 

children’s blood, and with regard to 

estimates of the slope of the C–R 

function of neurocognitive impacts (IQ 

loss) for application of the framework to 

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70 In addition to the review’s opening ‘‘call for 

information’’ (75 FR 8934), ‘‘literature searches 

were conducted routinely to identify studies 

published since the last review, focusing on studies 

published from 2006 (close of the previous 

scientific assessment) through September 2011’’ 

and references ‘‘that were considered for inclusion 

or actually cited in this ISA can be found at http:// 

hero.epa.gov/lead’’ (ISA, p. 1–2). 

levels below the current standard, given 

the weaker linkage with existing 

evidence as discussed in the PA (PA, 

sections 3.1, 3.2 and 4.2.1). 

With respect to exposure/risk-based 

considerations, as in the last review, the 

Administrator notes the complexity of 

the REA modeling analyses and the 

associated limitations and uncertainties. 

Based on consideration of the riskrelated information for conditions just 

meeting the current standard, the 

Administrator takes note of the 

attendant uncertainties, discussed in 

detail in the PA (PA, sections 3.4 and 

4.2.2), while finding that the 

quantitative risk estimates, with a focus 

on those for the generalized (local) 

urban case study, are ‘‘roughly 

consistent with and generally 

supportive’’ of estimates from the 

evidence-based air-related IQ loss 

framework. She further takes note of the 

PA finding of increasing uncertainty for 

air quality scenarios involving air Pb 

concentrations increasingly below the 

current conditions for each case study, 

due in part to modeling limitations that 

derive from uncertainty regarding 

relationships between ambient air Pb 

and outdoor soil/dust Pb and indoor 

dust Pb (PA, sections 3.4.3.1 and 3.4.7). 

Based on the above considerations 

and with consideration of advice from 

CASAC, the Administrator reaches the 

conclusion that the current body of 

evidence, in combination with the 

exposure/risk information, supports a 

primary standard as protective as the 

current standard. Based on 

consideration of the evidence and 

exposure/risk information available in 

this review with its attendant 

uncertainties and limitations and 

information that might inform public 

health policy judgments, as well as 

advice from CASAC, including their 

concurrence with the PA conclusions 

that revision of the primary Pb standard 

is not warranted at this time, the 

Administrator further concludes that it 

is appropriate to consider retaining the 

current standard without revision. 

The Administrator bases these 

proposed conclusions on consideration 

of the health effects evidence, including 

consideration of this evidence in the 

context of the evidence-based, airrelated IQ loss framework, and with 

support from the exposure/risk 

information, recognizing the 

uncertainties attendant with both. In so 

doing, she takes note of the PA 

description of the complexities and 

limitations in the evidence base 

associated with reaching conclusions 

regarding the magnitude of risk 

associated with the current standard, as 

well as the increasing uncertainty of risk 

estimates for lower air Pb 

concentrations. Inherent in the 

Administrator’s conclusions are public 

health policy judgments on the public 

health implications of the blood Pb 

levels and risk estimated for air-related 

Pb under the current standard, 

including the public health significance 

of the Pb effects being considered, as 

well as aspects of the use of the 

evidence-based framework that may be 

considered to contribute to the margin 

of safety. These public health policy 

judgments include judgments related to 

the appropriate degree of public health 

protection that should be afforded to 

protect against risk of neurocognitive 

effects in at-risk populations, such as IQ 

loss in young children, as well as with 

regard to the appropriate weight to be 

given to differing aspects of the 

evidence and exposure/risk information, 

and how to consider their associated 

uncertainties. Based on these 

considerations and the judgments 

identified here, the Administrator 

concludes that the current standard 

provides the requisite protection of 

public health with an adequate margin 

of safety, including protection of at-risk 

populations, such as young children 

living near Pb emissions sources where 

ambient concentrations just meet the 

standard. 

In reaching this conclusion with 

regard to the adequacy of public health 

protection afforded by the existing 

primary standard, the Administrator 

recognizes that in establishing primary 

standards under the Act that are 

requisite to protect public health with 

an adequate margin of safety, she is 

seeking to establish standards that are 

neither more nor less stringent than 

necessary for this purpose. The Act does 

not require that primary standards be set 

at a zero-risk level, but rather at a level 

that avoids unacceptable risks to public 

health, even if the risk is not precisely 

identified as to nature or degree. The 

CAA requirement that primary 

standards provide an adequate margin 

of safety was intended to address 

uncertainties associated with 

inconclusive scientific and technical 

information available at the time of 

standard setting, as described in section 

I.A above. This requirement was also 

intended to provide a reasonable degree 

of protection from hazards that research 

has not yet identified. 

In this context, the Administrator’s 

proposed conclusion that the current 

standard provides the requisite 

protection and that a more restrictive 

standard would not be requisite 

additionally recognizes that the 

uncertainties and limitations associated 

with the many aspects of the estimated 

relationships between air Pb 

concentrations and blood Pb levels and 

associated health effects are amplified 

with consideration of increasingly lower 

air concentrations. In so doing, she takes 

note of the PA conclusion, with which 

CASAC has agreed, that based on the 

current evidence, there is appreciable 

uncertainty associated with drawing 

conclusions regarding whether there 

would be reductions in blood Pb levels 

and risk to public health from 

alternative lower levels of the standard 

as compared to the level of the current 

standard (PA, pp. 4–35 to 4–36; Frey, 

2013b, p. 6). The Administrator judges 

this uncertainty to be too great for the 

current evidence and exposure/risk 

information to provide a basis for 

revising the current standard. Thus, 

based on the public health policy 

judgments described above, including 

the weight given to uncertainties in the 

evidence, the Administrator proposes to 

conclude that the current standard 

should be retained, without revision. 

The Administrator solicits comment on 

this conclusion. 

III. Rationale for Proposed Decision on 

the Secondary Standard 

This section presents information 

relevant to the rationale for the 

Administrator’s proposed decision to 

retain the existing secondary Pb 

standard, which as discussed more fully 

below, is based on a thorough review in 

the ISA of the latest scientific 

information, generally published 

through September 2011,70 on 

ecological or welfare effects associated 

with Pb and pertaining to the presence 

of Pb in the ambient air. This proposal 

also takes into account: (1) The PA’s 

staff assessments of the most policyrelevant information in the ISA and staff 

analyses of potential ecological 

exposures and risk, upon which staff 

conclusions regarding appropriate 

considerations in this review are based; 

(2) CASAC advice and 

recommendations, as reflected in 

discussions of drafts of the ISA and PA 

at public meetings, in separate written 

comments, and in CASAC’s letters to 

the Administrator; and (3) public 

comments received during the 

development of these documents, either 

in connection with CASAC meetings or 

separately. 

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Section III.A provides background on 

the general approach for review of the 

secondary NAAQS for Pb, including a 

summary of the approach used in the 

last review (section III.A.1) and the 

general approach for the current review 

(section III.A.2). Section III.B 

summarizes the body of evidence on 

ecological or welfare effects associated 

with Pb exposures, focusing on 

consideration of key policy-relevant 

questions, and section III.C summarizes 

the exposure/risk information in this 

review. Section III.D presents the 

Administrator’s proposed conclusions 

on adequacy of the current standard, 

drawing on both evidence-based and 

exposure/risk-based considerations 

(sections III.D.1), and advice from 

CASAC (section III.D.2). 

A. General Approach 

The past and current approaches 

described below are all based most 

fundamentally on using the EPA’s 

assessment of the current scientific 

evidence and previous quantitative 

analyses to inform the Administrator’s 

judgment with regard to the secondary 

standard for Pb. In drawing conclusions 

for the Administrator’s consideration 

with regard to the secondary standard, 

we note that the final decision on the 

adequacy of the current secondary Pb 

standard is largely a public welfare 

policy judgment to be made by the 

Administrator. The Administrator’s 

final decision must draw upon scientific 

information and analyses about welfare 

effects, exposure and risks, as well as 

judgments about the appropriate 

response to the range of uncertainties 

that are inherent in the scientific 

evidence and analyses. This approach is 

consistent with the requirements of the 

NAAQS provisions of the Act. These 

provisions require the Administrator to 

establish a secondary standard that, in 

the judgment of the Administrator, 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.’’ In so 

doing, the Administrator seeks to 

establish standards that are neither more 

nor less stringent than necessary for this 

purpose. 

1. Approach in the Last Review 

In the last review, completed in 2008, 

the current secondary standard for Pb 

was set equal to the primary standard 

(73 FR 66964, November 12, 2008). As 

summarized in sections I.C and II.A.1 

above, the primary standard was 

substantially revised in the last review. 

The 2008 decision considered the body 

of evidence as assessed in the 2006 CD 

(USEPA, 2006a) as well as the 2007 Staff 

Paper assessment of the policy-relevant 

information contained in the 2006 CD 

and the screening-level ecological risk 

assessment (2006 REA; USEPA, 2007b), 

the advice and recommendations of 

CASAC (Henderson 2007a, 2007b, 

2008a, 2008b), and public comment. 

In the previous review, the Staff Paper 

concluded, based on laboratory studies 

and current media concentrations in a 

wide range of locations, that it seemed 

likely that adverse effects were 

occurring from ambient air-related Pb, 

particularly near point sources, under 

the then-current standard (73 FR 67010, 

November 12, 2008). Given the limited 

data on Pb effects in ecosystems, and 

associated uncertainties, such as those 

with regard to factors such as the 

presence of multiple metals and historic 

environmental burdens, it was at the 

time, as it is now, necessary to look at 

evidence of Pb effects on organisms and 

extrapolate to ecosystem effects. Taking 

into account the available evidence and 

current media concentrations in a wide 

range of locations, the Administrator 

concluded that there was potential for 

adverse effects occurring under the 

then-current standard; however there 

were insufficient data to provide a 

quantitative basis for setting a secondary 

standard different from the primary (73 

FR 67011, November 12, 2008). 

Therefore, citing a general lack of data 

that would indicate the appropriate 

level of Pb in environmental media that 

may be associated with adverse effects, 

as well as the comments of the CASAC 

Pb panel that a significant change to 

current air concentrations (e.g., via a 

significant change to the standard) was 

likely to have significant beneficial 

effects on the magnitude of Pb 

exposures in the environment, the 

secondary standard was revised to be 

consistent with the revised primary 

standard (73 FR 67011, November 12, 

2008). 

2. Approach for the Current Review 

Our approach for reviewing the 

current secondary standard takes into 

consideration the approaches used in 

the last Pb NAAQS review and involves 

addressing key policy-relevant 

questions in light of currently available 

scientific and technical information. In 

evaluating whether it is appropriate to 

consider retaining the current secondary 

Pb standard, or whether consideration 

of revision is appropriate, we have 

adopted an approach in this review that 

builds on the general approach from the 

last review and reflects the body of 

evidence and information now 

available. As summarized above, the 

Administrator’s decisions in the 

previous review were based on the 

conclusion that there was the potential 

for adverse ecological effects under the 

previous standard. 

In our approach here, we focus on 

consideration of the extent to which a 

broader body of scientific evidence is 

now available that would inform 

decisions on either the potential for 

adverse effects to ecosystems under the 

current standard or the ability to set a 

more ecologically relevant secondary 

standard than was feasible in the 

previous review. In considering the 

scientific and technical information in 

sections II.B and II.C below, as in the 

PA, we draw on the ecological effects 

evidence presented in detail in the ISA 

and aspects summarized in the PA, 

along with the information associated 

with the screening-level risk assessment 

also in the PA. In section III.D below, 

we have taken into account both 

evidence-based and risk-based 

considerations framed by a series of 

policy-relevant questions presented in 

the PA. These questions generally 

discuss the extent to which we are able 

to better characterize effects and the 

likelihood of adverse effects in the 

environment under the current 

standard. Our approach to considering 

these issues recognizes that the 

available welfare effects evidence 

generally reflects laboratory-based 

evidence of toxicological effects on 

specific organisms exposed to 

concentrations of Pb. It is widely 

recognized, however, that 

environmental exposures from 

atmospherically derived Pb are likely to 

be lower than those commonly assessed 

in laboratory studies and that studies of 

exposures similar to those in the 

environment are often accompanied by 

significant confounding and modifying 

factors (e.g., other metals, acidification), 

increasing our uncertainty about the 

likelihood and magnitude of organism 

and ecosystem responses. 

B. Welfare Effects Information 

Welfare effects addressed by the 

secondary NAAQS include, but are not 

limited to, effects on soils, water, crops, 

vegetation, manmade materials, 

animals, wildlife, weather, visibility and 

climate, damage to and deterioration of 

property, and hazards to transportation, 

as well as effects on economic values 

and on personal comfort and wellbeing. 

This discussion presents key aspects of 

the current evidence of Pb-related 

welfare effects that are assessed in the 

ISA and the 2006 CD, drawing from the 

summary of policy-relevant aspects in 

the PA (PA, section 5.1). 

Lead has been demonstrated to have 

harmful effects on reproduction and 

development, growth, and survival in 

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71Since the last Pb NAAQS review, the ISAs, 

which have replaced CDs in documenting each 

review of the scientific evidence (or air quality 

criteria), employ a systematic framework for 

weighing the evidence and describing associated 

conclusions with regard to causality, using 

established descriptors: ‘‘causal’’ relationship with 

relevant exposure, ‘‘likely’’ to be a causal 

relationship, evidence is ‘‘suggestive’’ of a causal 

relationship, ‘‘inadequate’’ evidence to infer a 

causal relationship, and ‘‘not likely’’ to be a causal 

relationship (ISA, Preamble). 

72 In determining that a causal relationship exists 

for Pb with specific ecological or welfare effects, the 

EPA has concluded that ‘‘[e]vidence is sufficient to 

conclude that there is a causal relationship with 

relevant pollutant exposures (i.e., doses or 

exposures generally within one to two orders of 

magnitude of current levels)’’ (ISA, p. lxii). 

73 In determining a likely causal relationship 

exists for Pb with specific ecological or welfare 

effects, the EPA has concluded that ‘‘[e]vidence is 

sufficient to conclude that there is a likely causal 

association with relevant pollutant exposures . . . 

but uncertainties remain’’ (ISA, p. lxii). 

many species as described in the 

assessment of the evidence available in 

this review and consistent with the 

conclusions drawn in the last review 

(ISA, section 1.7; 2006 CD, sections 

7.1.5 and 7.2.5). A number of studies on 

ecological effects of Pb are newly 

available in this review and are 

critically assessed in the ISA as part of 

the full body of evidence. The full body 

of currently available evidence reaffirms 

conclusions on the array of effects 

recognized for Pb in the last review 

(ISA, section 1.7). In so doing, in the 

context of pollutant exposures 

considered relevant the ISA 

determines 71 that causal 72 or likely 

causal 73 relationships exist in both 

freshwater and terrestrial ecosystems for 

Pb with effects on reproduction and 

development in vertebrates and 

invertebrates; growth in plants and 

invertebrates; and survival in 

vertebrates and invertebrates (ISA, Table 

1–3). In drawing judgments regarding 

causality for the criteria air pollutants, 

the ISA places emphasis on ‘‘evidence 

of effects at doses (e.g., blood Pb 

concentration) or exposures (e.g., air 

concentrations) that are relevant to, or 

somewhat above, those currently 

experienced by the population.’’ The 

ISA notes that the ‘‘extent to which 

studies of higher concentrations are 

considered varies . . . but generally 

includes those with doses or exposures 

in the range of one to two orders of 

magnitude above current or ambient 

conditions.’’ Studies ‘‘that use higher 

doses or exposures may also be 

considered . . . [t]hus, a causality 

determination is based on weight of 

evidence evaluation for health, 

ecological or welfare effects, focusing on 

the evidence from exposures or doses 

generally ranging from current levels to 

one or two orders of magnitude above 

current levels’’ (ISA, pp. lx to lxi). 

Although considerable uncertainties 

are recognized in generalizing effects 

observed under particular, small-scale 

conditions, up to the ecosystem level of 

biological organization, the ISA 

determines that the cumulative 

evidence reported for Pb effects at such 

higher levels of biological organization 

and for endpoints in single species with 

direct relevance to population and 

ecosystem level effects (i.e., 

development and reproduction, growth, 

survival) is sufficient to conclude that a 

causal relationship is likely to exist 

between Pb exposures and community 

and ecosystem-level effects in 

freshwater and terrestrial systems (ISA, 

section 1.7.3.7). 

The ISA also presents evidence for 

saltwater ecosystems, concluding that 

current evidence is inadequate to make 

causality determinations for most 

population-level responses, as well as 

community and ecosystem effects, while 

finding the evidence to be suggestive 

linking Pb and effects on reproduction 

and development in marine 

invertebrates (ISA, Table 1–3, sections 

6.3.12 and 6.4.21). 

As in prior reviews of the Pb NAAQS, 

this review is focused on those effects 

most pertinent to ambient air Pb 

exposures. Given the reductions in 

ambient air Pb concentrations over the 

past decades, these effects are generally 

those associated with the lowest levels 

of Pb exposure that have been 

evaluated. Additionally, we recognize 

the limitations on our ability to draw 

conclusions about environmental 

exposures from ecological studies of 

organism-level effects, as most studies 

were conducted in laboratory settings 

which may not accurately represent 

field conditions or the multiple 

variables that govern exposure. 

The relationship between ambient air 

Pb and ecosystem response is important 

in making the connection between 

current emissions of Pb and the 

potential for adverse ecological effects. 

The limitations in the data available on 

this subject for the last review were 

significant. There is no new evidence 

since the last review that substantially 

improves our understanding of the 

relationship between ambient air Pb and 

measurable ecological effects. As stated 

in the last review, the role of ambient air 

Pb in contributing to ecosystem Pb has 

been declining over the past several 

decades. It remains difficult to 

apportion exposure between air and 

other sources to inform our 

understanding of the potential for 

ecosystem effects that might be 

associated with air emissions. As noted 

in the ISA, ‘‘[t]he amount of Pb in 

ecosystems is a result of a number of 

inputs and it is not currently possible to 

determine the contribution of 

atmospherically-derived Pb from total 

Pb in terrestrial, freshwater or saltwater 

systems’’ (ISA, section 6.5). Further, 

considerable uncertainties also remain 

in drawing conclusions from effects 

evidence observed under laboratory 

conditions with regard to effects 

expected at the ecosystem level in the 

environment. In many cases it is 

difficult to characterize the nature and 

magnitude of effects and to quantify 

relationships between ambient 

concentrations of Pb and ecosystem 

response due to the existence of 

multiple stressors, variability in field 

conditions, and differences in Pb 

bioavailability at that level of 

organization (ISA, section 6.5). In 

summary, the ISA concludes that 

‘‘[r]ecent information available since the 

2006 Pb AQCD, includes additional 

field studies in both terrestrial and 

aquatic ecosystems, but the connection 

between air concentration and 

ecosystem exposure continues to be 

poorly characterized for Pb and the 

contribution of atmospheric Pb to 

specific sites is not clear’’ (ISA, section 

6.5). 

It is also important to consider the 

fate and transport of both current Pb and 

Pb emitted in the past. It is this past 

legacy of Pb that was cited as a 

significant source of uncertainty in the 

last review. The extensive history of Pb 

uses in developed countries coupled 

with atmospheric transport processes 

has left a legacy of Pb in ecosystems 

globally (e.g., 2006 CD, sections 2.3.1 

and 7.1; 1977 CD, section 6.3.1). 

Records of U.S. atmospheric emissions 

of Pb in the twentieth and late 

nineteenth centuries have been 

documented in sediment cores (PA, 

section 2.3; ISA, section 2.6.2; Landers 

et al., 2010). Once deposited, Pb can be 

transported by stormwater runoff or 

resuspension to catchments and nearby 

water bodies or stored in soil layers in 

forested areas, its further movement 

influenced by soil or sediment 

composition and chemistry and 

physical processes. Some new studies 

are available that provide additional 

information, briefly summarized below, 

on Pb cycling, flux and retention within 

terrestrial and aquatic systems. This 

new information does not 

fundamentally change our 

understanding from the last review of 

Pb movement through or accumulation 

in ecosystems over time but rather 

improves our understanding of some of 

the underlying processes and 

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mechanisms in soil, water and 

sediment. There is little new 

information, however, on fate and 

transport in ecosystems specifically 

related to air-derived Pb (ISA, section 

2.3). There is limited newly available 

information with regard to the timing of 

ecosystem recovery from historic 

atmospheric deposition of Pb (ISA, 

sections 2.3.2.4 and 2.3.3.3). 

Overall, recent studies in terrestrial 

ecosystems provide deposition data 

consistent with deposition fluxes 

reported in the 2006 CD and 

demonstrate consistently that 

atmospheric deposition of Pb has 

decreased since the phase-out of leaded 

on-road gasoline (PA, section 2.3.2.2; 

ISA, section 2.3.3). Follow-up studies in 

several locations at high elevation sites 

indicate little change in soil Pb 

concentrations since the phase-out of 

leaded onroad gasoline in surface soils, 

consistent with the high retention 

reportedly associated with reduced 

microbial activity at lower temperatures 

associated with high elevation sites. 

However, amounts of Pb in the surface 

soils at some lower altitude sites were 

reduced over the same time period in 

the same study (ISA, section 2.3.3). New 

studies in the ISA also enhance our 

understanding of Pb sequestration in 

forest soils by providing additional 

information on the role of leaf litter as 

a Pb reservoir in some situations and the 

effect of litter decomposition on Pb 

distribution (ISA, section 2.3.3). 

Recent research on Pb transport in 

aquatic systems has provided a large 

body of observations confirming that 

such transport is dominated by colloids 

rich in iron and organic material (ISA, 

section 2.3.2). Recent research on Pb 

flux in sediments provides greater detail 

on resuspension processes than was 

available in the 2006 CD, including 

research on resuspended Pb largely 

associated with organic material or iron 

and manganese particles and research 

on the important role played by anoxic 

or depleted oxygen environments in Pb 

cycling in aquatic systems. This newer 

research is consistent with prior 

evidence in indicating that appreciable 

resuspension and release from 

sediments largely occurs during discrete 

events related to storms. It has also 

confirmed that resuspension is an 

important process that strongly 

influences the lifetime of Pb in bodies 

of water. Finally, there have been 

advances in understanding and 

modeling of Pb partitioning between 

organic material and sediment in 

aquatic environments (ISA, section 

2.7.2). 

The bioavailability of Pb is also an 

important component of understanding 

the effects Pb is likely to have on 

organisms and ecosystems (ISA, section 

6.3.3). It is the amount of Pb that can 

interact within the organism that leads 

to toxicity, and there are many factors 

which govern this interaction (ISA, 

sections 6.2.1 and 6.3.3). The 

bioavailability of metals varies widely 

depending on the physical, chemical, 

and biological conditions under which 

an organism is exposed (ISA, section 

6.3.3). Studies newly available since the 

last Pb NAAQS review provide 

additional insight into factors that 

influence the bioavailability of Pb to 

specific organisms (ISA, section 6.3.3). 

In general, this evidence is supportive of 

previous conclusions and does not 

identify significant new variables from 

those identified previously. Section 

6.3.3 of the ISA provides a detailed 

discussion of bioavailability in 

terrestrial systems. With regard to 

aquatic systems, a detailed discussion of 

bioavailability in freshwater systems is 

provided in sections 6.4.3 and 6.4.4 of 

the ISA, and section 6.4.14 of the ISA 

discusses bioavailability in saltwater 

systems. 

In terrestrial systems, the amount of 

bioavailable Pb present determines the 

impact of soil Pb to a much greater 

extent than does the total amount 

present (ISA, section 6.3.11). In such 

ecosystems, Pb is deposited either 

directly onto plant surfaces or onto soil 

where it can bind with organic matter or 

dissolve in pore water. The Pb dissolved 

in pore water is particularly bioavailable 

to organisms in the soil and, therefore, 

the impact of this Pb on the ecosystem 

is potentially greater than soil Pb that is 

not in pore water (ISA, section 6.3.11). 

In aquatic systems as in terrestrial 

systems, the amount of Pb bioavailable 

to organisms is a better predictor of 

effect on organisms than the overall 

amount of Pb in the system. Once 

atmospherically derived Pb enters 

surface water bodies through deposition 

or runoff, its fate and bioavailability are 

influenced by many water quality 

characteristics, such as pH, suspended 

solids levels and organic content (ISA, 

section 6.4.2). In sediments, 

bioavailability of Pb to sedimentdwelling organisms may be influenced 

by the presence of other metals, 

sulfides, iron oxides and manganese 

oxides and also by physical disturbance 

(ISA, section 2.6.2). For many aquatic 

organisms, Pb dissolved in the water 

column can be the primary exposure 

route, while for others sediment 

ingestion is significant (ISA, section 

2.6.2). As recognized in the 2006 CD 

and further supported in the ISA, there 

is a body of evidence showing that 

uptake and elimination of Pb vary 

widely among aquatic species. 

There is a substantial amount of new 

evidence in this review regarding the 

ecological effects of Pb on individual 

terrestrial and aquatic species with less 

new information available on marine 

species and ecosystems. On the whole, 

this evidence supports previous 

conclusions that Pb has effects on 

growth, reproduction and survival, and 

that under some conditions these effects 

can be adverse to organisms and 

ecosystems. The ISA provides evidence 

of effects in additional species and in a 

few cases at lower exposures than 

reported in the previous review, but 

does not substantially alter our 

understanding of the ecological 

endpoints affected by Pb from the 

previous review. Looking beyond 

organism-level evidence, the evidence 

of adversity in natural systems remains 

sparse due to the difficulty in 

determining the effects of confounding 

factors such as co-occurring metals or 

system characteristics that influence 

bioavailability of Pb in field studies. 

The following paragraphs summarize 

the information presented in this review 

for terrestrial, aquatic and marine 

systems. 

With regard to terrestrial ecosystems, 

recent studies cited in this review 

support previous conclusions about the 

effects of Pb, namely that increasing soil 

Pb concentrations in areas of Pb 

contamination (e.g., mining sites and 

industrial sites) can cause decreases in 

microorganism abundance, diversity, 

and function. Previous reviews have 

also reported on effects on bird and 

plant communities (2006 CD, section 

AX7.1.3). The shifts in bacterial species 

and fungal diversity have been observed 

near long-established sources of Pb 

contamination (ISA, section 6.3.12.7). 

Most recent evidence for Pb toxicity to 

terrestrial plants, invertebrates and 

vertebrates is from single-species assays 

in laboratory studies which do not 

capture the complexity of bioavailability 

and other modifiers of effect in natural 

systems (ISA, section 6.3.12.7). Further, 

models that might account for modifiers 

of bioavailability have proven difficult 

to develop (ISA, p. 6–16). 

Evidence presented in the ISA and 

prior CDs demonstrates the toxicity of 

Pb in aquatic ecosystems and the role of 

many factors, including Pb speciation 

and various water chemistry properties, 

in modifying toxicity (ISA, section 

1.7.2). Since the 2006 CD, additional 

evidence for community and ecosystem 

level effects of Pb is available, primarily 

in microcosm studies or field studies 

with other metals present (ISA, section 

6.4.11). Such evidence described in 

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previous CDs includes alteration of 

predator-prey dynamics, species 

richness, species composition, and 

biodiversity. New studies available in 

this review provide evidence in 

additional habitats for these community 

and ecological-scale effects, specifically 

in aquatic plant communities and 

sediment-associated communities at 

both acute and chronic exposures 

involving concentrations similar to 

those previously reported (ISA, section 

6.4.7). In many cases, it is difficult to 

characterize the nature and magnitude 

of effects and to quantify relationships 

between ambient concentrations of Pb 

and ecosystem response due to 

existence of multiple ecosystem-level 

stressors, variability in field conditions, 

and differences in Pb bioavailability 

(ISA, sections 1.7.3.7 and 6.4.7). 

Additionally, the degree to which air 

concentrations have contributed to such 

effects in freshwater ecosystems is 

largely unknown. 

With regard to evidence in marine 

ecosystems, recently available evidence 

on the toxicity of Pb to marine algae 

augments the 2006 CD findings of 

variation in sensitivity across marine 

species. Recent studies on Pb exposure 

include reports of growth inhibition and 

oxidative stress in a few additional 

species of marine algae (ISA, section 

6.4.15). Recent literature provides little 

new evidence of endpoints or effects in 

marine invertebrates beyond those 

reported in the 2006 CD. For example, 

some recent studies strengthen the 

evidence presented in the 2006 CD 

regarding negative effects of Pb 

exposure on marine invertebrates (ISA, 

section 6.4.15.2). Recent studies also 

identify several species exhibiting 

particularly low sensitivity to high acute 

exposures (ISA, section 6.4.15.2). Little 

new evidence is available of Pb effects 

on marine fish and mammals for 

reproductive, growth and survival 

endpoints that are particularly relevant 

to the population level of biological 

organization and higher (ISA, section 

6.4.15). New studies on organism-level 

effects from Pb in saltwater ecosystems 

(ISA, section 6.4.15) provide little 

evidence to inform our understanding of 

linkages among atmospheric 

concentrations, ambient exposures in 

saltwater systems and such effects or to 

inform our conclusions regarding the 

likelihood of adverse effects under 

conditions associated with the current 

NAAQS for Pb. Nor does the currently 

available evidence indicate significantly 

different exposure levels from the 

previous review at which ecological 

systems or receptors are expected to 

experience effects. 

During the last review, the 2006 CD 

assessed the available information on 

critical loads for Pb (2006 CD, section 

7.3). This information included 

publications on methods and example 

applications, primarily in Europe, 

specific to the bedrock geology, soil 

types, vegetation, and historical 

deposition trends in each European 

country (2006 CD, p. E–24), with no 

analyses available for U.S. locations 

(2006 CD, sections 7.3.4–7.3.6). As a 

result, the 2006 CD concluded that 

‘‘[c]onsiderable research is necessary 

before critical load estimates can be 

formulated for ecosystems extant in the 

United States’’ (2006 CD, p. E–24). 

For this current review, newly 

available evidence pertaining to critical 

loads analysis includes limited recent 

research on consideration of 

bioavailability in characterizing Pb 

effect concentrations or indices and on 

modeling approaches to incorporate 

chemistry effects on Pb speciation and 

bioavailability (ISA, sections 6.3.7 and 

6.4.8). With consideration of this 

information and the four critical load 

analysis studies newly available in this 

review (none of which are for U.S. 

ecosystems), the ISA does not modify 

the conclusions noted above from the 

2006 CD (ISA, sections 6.1.3, 6.3.7 and 

6.4.8). In summary, the new information 

in this review does not appreciably 

change our evidence base or further 

inform our understanding of critical 

loads of Pb, including critical loads in 

sensitive U.S. ecosystems. 

There is no new evidence since the 

last review that substantially improves 

our understanding of the relationship 

between ambient air Pb and measurable 

ecological effects. As stated in the last 

review, the role of ambient air Pb in 

contributing to ecosystem Pb has been 

declining over the past several decades. 

It remains difficult to apportion 

exposure between air and other sources 

to better inform our understanding of 

the potential for ecosystem effects that 

might be associated with air emissions. 

As noted in the ISA, ‘‘[t]he amount of 

Pb in ecosystems is a result of a number 

of inputs and it is not currently possible 

to determine the contribution of 

atmospherically-derived Pb from total 

Pb in terrestrial, freshwater or saltwater 

systems’’ (ISA, section 6.5). Further, 

considerable uncertainties also remain 

in drawing conclusions from evidence 

of effects observed under laboratory 

conditions with regard to effects 

expected at the ecosystem level in the 

environment. In many cases it is 

difficult to characterize the nature and 

magnitude of effects and to quantify 

relationships between ambient 

concentrations of Pb and ecosystem 

response due to the existence of 

multiple stressors, variability in field 

conditions, and differences in Pb 

bioavailability at that level of 

organization (ISA, section 6.5). In 

summary, the ISA concludes that 

‘‘[r]ecent information available since the 

2006 Pb AQCD, includes additional 

field studies in both terrestrial and 

aquatic ecosystems, but the connection 

between air concentration and 

ecosystem exposure continues to be 

poorly characterized for Pb and the 

contribution of atmospheric Pb to 

specific sites is not clear’’ (ISA, section 

6.5). 

C. Summary of Risk Assessment 

Information 

The risk assessment information 

available in this review and summarized 

here is based on the screening-level risk 

assessment performed for the last 

review, described in the 2006 REA, 2007 

Staff Paper and 2008 notice of final 

decision (73 FR 66964, November 12, 

2008), as considered in the context of 

the evidence newly available in this 

review (PA, section 5.2). As described in 

the REA Planning Document, careful 

consideration of the information newly 

available in this review, with regard to 

designing and implementing a full REA 

for this review, led us to conclude that 

performance of a new REA for this 

review was not warranted (REA 

Planning Document, section 3.3). Based 

on their consideration of the REA 

Planning Document analysis, the 

CASAC Pb Review Panel generally 

concurred with the conclusion that a 

new REA was not warranted in this 

review (Frey, 2011b). Accordingly, the 

risk/exposure information considered in 

this review is drawn primarily from the 

2006 REA as summarized below (PA, 

section 5.2 and Appendix 5A; REA 

Planning Document, section 3.1). 

The 2006 screening-level assessment 

focused on estimating the potential for 

ecological risks associated with 

ecosystem exposures to Pb emitted into 

ambient air (PA, section 5.2; 2006 REA, 

section 7). A national-scale screen was 

used to evaluate surface water and 

sediment monitoring locations across 

the U.S. for the potential for ecological 

impacts that might be associated with 

atmospheric deposition of Pb (2006 

REA, section 7.1.2). In addition to the 

national-scale screen (2006 REA, section 

3.6), the assessment involved a case 

study approach, with case studies for 

areas surrounding a primary Pb smelter 

(2006 REA, section 3.1) and a secondary 

Pb smelter (2006 REA, section 3.2), as 

well as a location near a non-urban 

roadway (2006 REA, section 3.4). An 

additional case study, focused on 

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consideration of atmospherically 

derived Pb effects on an ecologically 

vulnerable ecosystem (Hubbard Brook 

Experimental Forest), was identified 

(2006 REA, section 3.5). The Hubbard 

Brook Experimental Forest (HBEF), in 

the White Mountain National Forest, 

near North Woodstock, New Hampshire, 

was selected as a fourth case study 

because of its location and its long 

record of available data on 

concentration trends of Pb in three 

media (air or deposition from air, soil, 

and surface water). The HBEF case 

study was a qualitative analysis 

focusing on a summary review of the 

literature, without new quantitative 

analyses (2006 REA, Appendix E). For 

the other three case studies, exposure 

concentrations of Pb in soil, surface 

water, and/or sediment concentrations 

were estimated from available 

monitoring data or modeling analysis 

and then compared to ecological 

screening benchmarks (2006 REA, 

section 7.1). 

In interpreting the results from the 

2006 REA, the PA considers newly 

available evidence that may inform 

interpretation of risk under the now 

current standard (PA, section 5.2). 

Factors that could alter our 

interpretation of risk would include 

new evidence of harm at lower 

concentrations of Pb, new linkages that 

enable us to draw more explicit 

conclusions as to the air contribution of 

environmental exposures, and new 

methods of interpreting confounding 

factors that were largely uncontrolled in 

the previous risk assessment. In general, 

however, the key uncertainties 

identified in the last review remain 

today. 

The results for the ecological 

screening assessment for the three case 

studies and the national-scale screen for 

surface water and for sediment in the 

last review indicated a potential for 

adverse effects from ambient Pb to 

multiple ecological receptor groups in 

terrestrial and aquatic locations. 

Detailed descriptions of the locationspecific case studies and the national 

screening assessment, key findings of 

the risk assessment for each, and an 

interpretation of the results with regard 

to past air conditions can be found in 

the 2006 REA. In considering the 

potential for adverse welfare effects to 

result from levels of air-related Pb that 

would meet the current standard, the 

findings of the 2006 REA, as 

summarized in the PA, are discussed 

below. 

While the contribution to Pb 

concentrations from air as compared to 

nonair sources is not quantified, air 

emissions from the primary Pb smelter 

case study facility were substantial 

(2006 REA, Appendix B). In addition, 

this facility, which closed in 2013, had 

been emitting Pb for many decades, 

including some seven decades prior to 

establishment of any Pb NAAQS, such 

that it is likely air concentrations 

associated with the facility were 

substantial relative to the 1978 NAAQS, 

which it exceeded at the time of the last 

review. At the time of the last review 

and also since the adoption of the 

current standard, concentrations 

monitored near this facility have 

exceeded the level of the applicable 

NAAQS (2007 Staff Paper, Appendix 

2B–1; PA, Appendices 2D and 5A). 

Accordingly, this case study is not 

informative for considering the 

likelihood of adverse welfare effects 

related to Pb from air sources under air 

quality conditions associated with 

meeting the current Pb standard. 

The secondary Pb smelter case study 

location continues to emit Pb, and the 

county where this facility is located 

does not meet the current Pb standard 

(PA, Appendices 2D and 5A). Given the 

exceedances of the current standard, 

which likely extend back over 4 to 5 

decades, this case study also is not 

informative for considering the 

likelihood of adverse welfare effects 

related to Pb from air sources under air 

quality conditions associated with 

meeting the current Pb standard. 

The locations for the near-roadway 

non-urban case study are highly 

impacted by past deposition of gasoline 

Pb. It is unknown whether current 

conditions at these sites exceed the 

current Pb standard, but, given evidence 

from the past of Pb concentrations near 

highways that ranged above the 

previous (1978) Pb standard (1986 CD, 

section 7.2.1), conditions at these 

locations during the time of leaded 

gasoline very likely exceeded the 

current standard. Similarly, those 

conditions likely resulted in Pb 

deposition associated with leaded 

gasoline that exceeds that being 

deposited under air quality conditions 

that would meet the current Pb 

standard. Given this legacy, 

consideration of the potential for 

environmental risks from levels of airrelated Pb associated with meeting the 

current Pb standard in these locations is 

highly uncertain. 

The extent to which past air 

emissions of Pb have contributed to 

surface water or sediment Pb 

concentrations at the locations 

identified in the national scale surface 

water and sediment screen is unclear. 

For some of the surface water locations, 

nonair sources likely contributed 

significantly to the surface water Pb 

concentrations. For other locations, a 

lack of nearby nonair sources indicated 

a potential role for air sources to 

contribute to observed surface water Pb 

concentrations. Additionally, these 

concentrations may have been 

influenced by Pb in resuspended 

sediments and may reflect contribution 

of Pb from erosion of soils with Pb 

derived from historic as well as current 

air emissions. 

The most useful case study to the 

current review is that of the Vulnerable 

Ecosystem Case Study located in the 

HBEF. This case study was focused on 

consideration of information which 

included a long record (from 1976 

through 2000) of available data on 

concentration trends of Pb in three 

media (air or deposition from air, soil, 

and surface water). While no 

quantitative analyses were performed, a 

summary review of literature published 

on HBEF was developed. This review 

indicated: (1) Atmospheric Pb inputs do 

not directly affect stream Pb levels at 

HBEF because deposited Pb is almost 

entirely retained in the soil profile; and 

(2) soil horizon analysis results showed 

Pb to have become more concentrated at 

lower soil depths over time, with the 

soil serving as a Pb sink, appreciably 

reducing Pb in pore water as it moves 

through the soil layers to streams 

(dissolved Pb concentrations were 

reduced from 5 mg/L to about 5 ng/L 

from surface soil to streams). As a result, 

the HBEF studies concluded that the 

contribution of dissolved Pb from soils 

to streams was insignificant (2006 REA, 

Appendix E). Further, atmospheric 

input of Pb, based on bulk precipitation 

data, was estimated to decline 

substantially from the mid-1970s to 

1989; forest floor soil Pb concentrations 

between 1976 and 2000 were also 

estimated to decline appreciably (2006 

REA, sections E.1 and E.2). In 

considering HBEF and other terrestrial 

sites with Pb burdens derived primarily 

from long-range atmospheric transport, 

the 2006 CD found that ‘‘[d]espite years 

of elevated atmospheric Pb inputs and 

elevated concentrations in soils, there is 

little evidence that sites affected 

primarily by long-range Pb transport 

have experienced significant effects on 

ecosystem structure or function’’ (2006 

CD, p. AX7–98). The explanation 

suggested by the 2006 CD for this 

finding is ‘‘[l]ow concentrations of Pb in 

soil solutions, the result of strong 

complexation of Pb by soil organic 

matter’’ (2006 CD, p. AZX7–98). While 

more recent soil or stream data on Pb 

concentrations are not available, we find 

it unlikely, given the general evidence 

for air Pb emissions and concentration 

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declines over the past several decades 

(e.g., PA, Figures 2–1, 2–7 and 2–8), that 

conditions would have worsened from 

those on which these conclusions were 

drawn (e.g., soil data through 2000). 

Therefore, this information suggests that 

the now-lower ambient air 

concentrations associated with meeting 

the current standard would not be 

expected to directly impact stream Pb 

levels. 

With regard to new evidence of Pb 

effects at lower concentrations, it is 

necessary to consider that the evidence 

of adversity due specifically to Pb in 

natural systems is limited, in no small 

part because of the difficulty in 

determining the effects of confounding 

factors such as multiple metals and 

modifying factors influencing 

bioavailability in field studies. 

Modeling of Pb-related exposure and 

risk to ecological receptors is subject to 

a wide array of sources of both 

variability and uncertainty. Variability 

is associated with geographic location, 

habitat types, physical and chemical 

characteristics of soils and water that 

influence Pb bioavailability and 

terrestrial and aquatic community 

composition. Lead uptake rates by 

invertebrates, fish, and plants may vary 

by species and season. For wildlife, 

variability also is associated with food 

ingestion rates by species and season, 

prey selection, and locations of home 

ranges for foraging relative to the Pb 

contamination levels (USEPA, 2005b). 

There are significant difficulties in 

quantifying the role of air emissions 

under the current standard, which is 

significantly lower than the previous 

standard. As recognized in the PA, Pb 

deposited before the standard was 

enacted remains in soils and sediments, 

complicating interpretations regarding 

the impact of the current standard; 

historic Pb emitted from leaded gasoline 

usage continues to move slowly through 

systems along with more recently 

deposited Pb and Pb derived from 

nonair sources (PA, section 1.3.2). The 

results from the location-specific case 

studies and the surface and sediment 

screen performed in the last review are 

difficult to interpret in light of the 

current standard and are largely not 

useful in informing judgments of the 

potential for adverse effects at levels of 

deposition meeting the current 

standard. 

D. Conclusions on Adequacy of the 

Current Secondary Standard 

1. Evidence- and Risk-Based 

Considerations in the Policy Assessment 

The current evidence, as discussed 

more fully in the PA, continues to 

support the conclusions from the 

previous review regarding key aspects of 

the ecological effects evidence for Pb 

and the effects of exposure associated 

with levels of Pb occurring in ecological 

media in the U.S. The EPA’s 

conclusions in this regard are based on 

consideration of the assessment of the 

currently available evidence in the ISA, 

particularly with regard to key aspects 

summarized in the PA. 

In considering the welfare effects 

evidence with respect to the adequacy 

of the current standard, the PA 

considers the array of evidence newly 

assessed in the ISA with regard to the 

degree to which this evidence supports 

conclusions about the effects of Pb in 

the environment that were drawn in the 

last review and the extent to which it 

reduces previously recognized areas of 

uncertainty. Further, the PA considers 

the current evidence and associated 

conclusions about the potential for 

effects to occur as a result of the much 

lower ambient Pb concentrations 

allowed by the current secondary 

standard (set in 2008) than those 

allowed by the prior standard, which 

was the focus of the last review. These 

considerations, as discussed below, 

inform the Administrator’s conclusions 

regarding the extent to which the 

evidence supports or calls into question 

the adequacy of protection afforded by 

the current standard. 

The range of effects that Pb can exert 

on terrestrial and aquatic organisms 

indicated by information available in 

the current review is summarized in the 

ISA (ISA, sections 1.7, 6.3 and 6.4) and 

largely mirrors the findings of the 

previous review (PA, section 5.1). The 

integrated synthesis contained in the 

ISA conveys how effects of Pb can vary 

with species and life stage, duration of 

exposure, form of Pb, and media 

characteristics such as soil and water 

chemistry. A wide range of organism 

effects are recognized, including effects 

on growth, development (particularly of 

the nervous system) and reproductive 

success (ISA, sections 6.3 and 6.4). Lead 

is recognized to distribute from the air 

into multiple environmental media, as 

summarized in section I.D above, 

contributing to multiple exposure 

pathways for ecological receptors. As 

discussed in section 5.1 of the PA, many 

factors affect the bioavailability of Pb to 

receptors in terrestrial and aquatic 

ecosystems, contributing to differences 

between laboratory-assessed toxicity 

and Pb toxicity in these ecosystems, and 

challenging our consideration of 

environmental impacts of Pb emitted to 

ambient air. 

In studies in a variety of ecosystems, 

adverse ecosystem-level effects 

(including decreases in species 

diversity, loss of vegetation, changes to 

community composition, primarily in 

soil microbes and plants, decreased 

growth of vegetation, and increased 

number of invasive species) have been 

demonstrated near smelters, mines and 

other industries that have released 

substantial amounts of Pb, among other 

materials, to the environment (ISA, 

sections 6.3.12 and 6.4.12). As noted in 

the PA, however, our ability to 

characterize the role of air emissions of 

Pb in contributing to these effects is 

complicated because of coincident 

releases to other media and of other 

pollutants. Co-released pollutants 

include a variety of other heavy metals, 

in addition to sulfur dioxide, which 

may cause toxic effects in themselves 

and may interact with Pb in the 

environment, contributing uncertainty 

to characterization of the role of Pb from 

ambient air with regard to the reported 

effects (PA, section 5.1). These 

uncertainties limit our ability to draw 

conclusions regarding the extent to 

which Pb-related effects may be 

associated with ambient air conditions 

that would meet the current standard. 

The role of historically emitted Pb 

poses additional complications in 

addressing this question, as discussed in 

the PA (PA, section 1.3.2). The vast 

majority of Pb in the U.S. environment 

today, particularly in terrestrial 

ecosystems, was deposited in the past 

during the use of Pb additives in 

gasoline (2006 CD, pp. 2–82, AX7–36 to 

AX7–38, AX7–98; Johnson et al., 2004), 

although contributions from industrial 

activities, including metals industries, 

have also been documented (ISA, 

section 2.2.2.3, Jackson et al., 2004). The 

gasoline-derived Pb was emitted in very 

large quantities (2006 CD, p. AX7–98 

and ISA, Figure 2–8) and predominantly 

in small sized particles which were 

widely dispersed and transported across 

large distances, within and beyond the 

U.S. (ISA, section 2.2). As recognized in 

the PA, historical records provided by 

sediment cores in various environments 

document the substantially reduced Pb 

deposition (associated with reduced Pb 

emissions) in many locations (PA, 

sections 2.3.1 and 2.3.3.2; ISA, section 

2.2.1). As Pb is persistent in the 

environment, these substantial past 

environmental releases are expected to 

generally dominate current nonair 

media concentrations. 

There is very limited evidence to 

relate specific ecosystem effects with 

current ambient air concentrations of Pb 

through deposition to terrestrial and 

aquatic ecosystems and subsequent 

movement of deposited Pb through the 

environment (e.g., soil, sediment, water, 

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74All written comments submitted to the agency 

will be available in the docket for this rulemaking, 

as will be transcripts and minutes of the public 

meetings held in conjunction with CASAC’s review 

of drafts of the PA, the REA Planning Document 

and the ISA. 

organisms). The potential for ecosystem 

effects of Pb from atmospheric sources 

under conditions meeting the current 

standard is difficult to assess due to 

limitations on the availability of 

information to fully characterize the 

distribution of Pb from the atmosphere 

into ecosystems over the long term, as 

well as limitations on information on 

the bioavailability of atmospherically 

deposited Pb (as affected by the specific 

characteristics of the receiving 

ecosystem). Therefore, while 

information available since the 2006 CD 

includes additional terrestrial and 

aquatic field studies, ‘‘the connection 

between air concentration and 

ecosystem exposure and associated 

potential for welfare effects continues to 

be poorly characterized for Pb’’ (ISA, 

section 6.5). Such a connection is even 

harder to characterize with respect to 

the current standard than it was in the 

last review with respect to the previous, 

much higher, standard. 

The current evidence also continues 

to support conclusions from the last 

review with regard to interpreting the 

risk and exposure results. These 

conclusions are based on consideration 

of the screening-level ecological risk 

assessment results from the last review 

as described in the 2006 REA and 

summarized in the notice of final 

rulemaking (73 FR 67009, November 12, 

2008) and in light of the currently 

available evidence in the ISA (PA, 

section 5.2). As noted in section III.C 

above, the results from three of the four 

case studies and from the national 

screens are largely not useful in 

informing judgments of the potential for 

adverse effects at levels of deposition 

associated with conditions that meet the 

current standard. The Vulnerable 

Ecosystem Case Study at the HBEF is 

more illustrative with regard to the 

current review and, accordingly, is 

given primary consideration. The EPA 

concluded that atmospheric Pb inputs of 

the past did not directly affect stream Pb 

levels at HBEF because deposited Pb is 

almost entirely retained in the soil 

profile and that there was ‘‘little 

evidence that sites affected primarily by 

long-range Pb transport [such as this 

one] have experienced significant effects 

on ecosystem structure or function’’ 

(2006 CD, p. AX–98). We further note 

here that, as conditions are unlikely to 

have worsened since those on which 

those conclusions were based, we find 

it likely that current ambient air 

concentrations do not directly impact 

stream Pb levels under air quality 

conditions associated with meeting the 

now-current standard. 

The available risk and exposure 

information continues to be sufficient to 

conclude that the 1978 standard was not 

providing adequate protection to 

ecosystems and, when considered with 

regard to air-related ecosystem 

exposures likely to occur with air Pb 

levels that just meet the now-current 

standard, additionally does not provide 

evidence of adverse effects under the 

current standard. 

2. CASAC Advice 

In the current review of the secondary 

standard for Pb, the CASAC has 

provided advice and recommendations 

in their review of drafts of the ISA, of 

the REA Planning Document, and of the 

draft PA. We have additionally received 

comments from the public on drafts of 

these documents.74

In their advice and comments 

conveyed in the context of their review 

of the draft PA, the CASAC agreed with 

staff’s preliminary conclusions that the 

available information since the last 

review is not sufficient to warrant 

revision to the secondary standard 

(Frey, 2013b). On this subject, the 

CASAC letter said that ‘‘[o]verall, the 

CASAC concurs with the EPA that the 

current scientific literature does not 

support a revision to the Primary Lead 

(Pb) National Ambient Air quality 

Standard (NAAQS) nor the Secondary 

Pb NAAQS’’ (Frey, 2013b, p. 1). The 

CASAC also recognized the many 

uncertainties and data gaps in the new 

scientific literature and recommended 

that research be performed in the future 

to address these limitations (Frey, 

2013b, p. 2). 

Given the existing scientific data, the 

CASAC concurs with retaining the current 

secondary standard without revision. 

However, the CASAC also notes that 

important research gaps remain. For example 

questions remain regarding the relevance of 

the primary standard’s indicator, level, 

averaging time, and form for the secondary 

standard. Other areas for additional research 

to address data gaps and uncertainty include 

developing a critical loads approach for U.S. 

conditions and a multi-media approach to 

account for legacy Pb and contributions from 

different sources. Addressing these gaps may 

require reconsideration of the secondary 

standard in future assessments. 

The very few public comments 

received on this review to date that have 

addressed adequacy of the current 

secondary Pb standard indicate support 

for retaining the current standard 

without revision, generally grouping the 

secondary standard with their similar 

view on the primary standard. 

3. Administrator’s Proposed 

Conclusions on the Adequacy of the 

Current Standard 

Based on the evidence and risk 

assessment information that is available 

in this review concerning the ecological 

effects and potential public welfare 

impacts of Pb emitted into ambient air, 

the Administrator proposes to conclude 

that the current secondary standard 

provides the requisite protection of 

public welfare from adverse effects and 

should be retained. 

In considering the adequacy of the 

current standard, the Administrator has 

considered the assessment of the 

available evidence and conclusions 

contained in the ISA; the staff 

assessment of and conclusions regarding 

the policy-relevant technical 

information, including screening-level 

risk information, presented in the PA; 

the advice and recommendations from 

CASAC; and public comments to date in 

this review. In the discussion below, the 

Administrator gives weight to the PA 

conclusions, with which CASAC has 

concurred, and takes note of key aspects 

of the rationale presented for those 

conclusions which contribute to her 

proposed decision. 

The Administrator notes the 

conclusion in the PA that the body of 

evidence on the ecological effects of Pb, 

expanded in some aspects since the last 

review, continues to support 

identification of ecological effects in 

organisms relating to growth, 

reproduction, and survival as the most 

relevant endpoints associated with Pb 

exposure. In consideration of the 

appreciable influence of site-specific 

environmental characteristics on the 

bioavailability and toxicity of 

environmental Pb in our assessment 

here, the PA noted the lack of studies 

conducted under conditions closely 

reflecting the natural environment. The 

currently available evidence, while 

somewhat expanded since the last 

review, does not include evidence of 

significant effects at lower 

concentrations or evidence of higher 

level ecosystem effects beyond those 

reported in the last review. There 

continue to be significant difficulties in 

interpreting effects evidence from 

laboratory studies to the natural 

environment and linking those effects to 

ambient air Pb concentrations. Further, 

the PA notes that the EPA is aware of 

no new critical loads information that 

would inform our interpretation of the 

public welfare significance of the effects 

of Pb in various U.S. ecosystems (PA, 

section 5.1). In summary, while new 

research has added to the understanding 

of Pb biogeochemistry and expanded the 

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list of organisms for which Pb effects 

have been described, the PA notes there 

remains a significant lack of knowledge 

about the potential for adverse effects on 

public welfare from ambient air Pb in 

the environment and the exposures that 

occur from such air-derived Pb, 

particularly under conditions meeting 

the current standard (PA, section 6.2.1). 

Thus, the scientific evidence presented 

in detail in the ISA, inclusive of that 

newly available in this review, is not 

substantively changed, most particularly 

with regard to the adequacy of the now 

current standard, from the information 

that was available in and supported the 

decision for revision in the last review 

(PA, section 6.2.1). 

With respect to exposure/risk-based 

considerations, the PA recognizes the 

complexity of interpreting the previous 

risk assessment with regard to the 

ecological risk of ambient air Pb 

associated with conditions meeting the 

current standard and the associated 

limitations and uncertainties of such 

assessments. For example, the locationspecific case studies as well as the 

national screen conducted in the last 

review reflect both current air Pb 

deposition as well as past air and nonair 

source contributions (PA, section 6.3). 

The Administrator takes note of the PA 

conclusion that the previous assessment 

is consistent with and generally 

supportive of the evidence-based 

conclusions about Pb in the 

environment, yet the limitations on our 

ability to apportion Pb between past and 

present air contributions and between 

air and nonair sources remain 

significant. 

In the Administrator’s consideration 

of the information available in this 

review of the Pb secondary standard, 

she gives weight to the PA conclusion 

that the currently available evidence 

and exposure/risk information do not 

call into question the adequacy of the 

current standard to provide the requisite 

protection for public welfare (PA, 

section 6.3). In so doing, she also notes 

the advice from CASAC in this review, 

including that ‘‘[g]iven the existing 

scientific data, the CASAC concurs with 

retaining the current secondary standard 

without revision.’’ In light of these and 

the above considerations, the 

Administrator finds that the currently 

available information does not call into 

question the adequacy of the current 

standard to provide the requisite 

protection for public welfare and, 

accordingly, reaches the conclusion that 

it is appropriate to retain the current 

secondary standard without revision. 

The Administrator solicits comment on 

this conclusion. 

IV. Statutory and Executive Order 

Reviews 

Additional information about these 

statutes and Executive Orders can be 

found at http://www2.epa.gov/lawsregulations/laws-and-executive-orders. 

A. Executive Order 12866: Regulatory 

Planning and Review and Executive 

Order 13563: Improving Regulation and 

Regulatory Review 

This action is not a significant 

regulatory action and was, therefore, not 

submitted to the Office of Management 

and Budget for review. 

B. Paperwork Reduction Act 

This action does not impose an 

information collection burden under the 

Paperwork Reduction Act. There are no 

information collection requirements 

directly associated with revisions to a 

NAAQS under section 109 of the CAA 

and this action does not propose any 

revisions to the NAAQS. 

C. Regulatory Flexibility Act 

I certify that this action will not have 

a significant economic impact on a 

substantial number of small entities 

under the Regulatory Flexibility Act. 

This action will not impose any 

requirements on small entities. Rather, 

this action proposes to retain, without 

revision, existing national standards for 

allowable concentrations of lead in 

ambient air as required by section 109 

of the CAA. See also American Trucking 

Associations v. EPA. 175 F.3d at 1044– 

45 (NAAQS do not have significant 

impacts upon small entities because 

NAAQS themselves impose no 

regulations upon small entities). 

D. Unfunded Mandates Reform Act 

This action does not contain any 

unfunded mandate as described in the 

Unfunded Mandates Reform Act, 2 

U.S.C. 1531–1538 and does not 

significantly or uniquely affect small 

governments. This action imposes no 

enforceable duty on any state, local or 

tribal governments or the private sector. 

E. Executive Order 13132: Federalism 

This action does not have federalism 

implications. It will not have substantial 

direct effects on the states, on the 

relationship between the national 

government and the states, or on the 

distribution of power and 

responsibilities among the various 

levels of government. 

F. Executive Order 13175: Consultation 

and Coordination With Indian Tribal 

Governments 

This action does not have tribal 

implications, as specified in Executive 

Order 13175. This action does not 

change existing regulations. It does not 

have a substantial direct effect on one or 

more Indian Tribes, since Tribes are not 

obligated to adopt or implement any 

NAAQS. The Tribal Authority Rule 

gives Tribes the opportunity to develop 

and implement CAA programs such as 

the Pb NAAQS, but it leaves to the 

discretion of the Tribe whether to 

develop these programs and which 

programs, or appropriate elements of a 

program, they will adopt. Thus, 

Executive Order 13175 does not apply 

to this action. 

G. Executive Order 13045: Protection of 

Children From Environmental Health 

and Safety Risks 

This action is not subject to Executive 

Order 13045 because it is not 

economically significant as defined in 

Executive Order 12866. The health 

effects evidence and risk assessment 

information for this action, which 

focuses on children in addressing the atrisk population, is summarized in 

sections II.B, II.C and II.D, and 

described in the ISA and PA, copies of 

which are in the public docket for this 

action. 

H. Executive Order 13211: Actions That 

Significantly Affect Energy Supply, 

Distribution or Use 

This action is not subject to Executive 

Order 13211, because it is not a 

significant regulatory action under 

Executive Order 12866. 

I. National Technology Transfer and 

Advancement Act 

This rulemaking does not involve 

technical standards. 

J. Executive Order 12898: Federal 

Actions To Address Environmental 

Justice in Minority Populations and 

Low-Income Populations 

The EPA believes that this action will 

not have disproportionately high and 

adverse human health or environmental 

effects on minority, low-income or 

indigenous populations. The action 

proposed in this notice is to retain 

without revision the existing NAAQS 

for Pb based on the Administrator’s 

conclusion that the existing standards 

protect public health, including the 

health of sensitive groups, with an 

adequate margin of safety. As discussed 

earlier in this preamble (see section II), 

the EPA expressly considered the 

available information regarding health 

effects among at-risk populations in 

reaching the proposed decision that the 

existing standards are requisite. 

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322 Federal Register / Vol. 80, No. 2 / Monday, January 5, 2015 / Proposed Rules 

K. Determination Under Section 307(d) 

Section 307(d)(1)(V) of the CAA 

provides that the provisions of section 

307(d) apply to ‘‘such other actions as 

the Administrator may determine.’’ 

Pursuant to section 307(d)(1)(V), the 

Administrator determines that this 

action is subject to the provisions of 

section 307(d). 

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List of Subjects in 40 CFR Part 50 

Environmental protection, Air 

pollution control, Carbon monoxide, 

Lead, Nitrogen dioxide, Ozone, 

Particulate matter, Sulfur oxides. 

Dated: December 19, 2014. 

Gina McCarthy, 

Administrator. 

[FR Doc. 2014–30681 Filed 1–2–15; 8:45 am] 

BILLING CODE 6560–50–P 

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