[Federal Register Volume 75, Number 81 (Wednesday, April 28, 2010)]
[Proposed Rules]
[Pages 22440-22468]
[FR Doc No: 2010-9603]

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Part II

Environmental Protection Agency

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40 CFR Part 87

Advance Notice of Proposed Rulemaking on Lead Emissions From Piston-
Engine Aircraft Using Leaded Aviation Gasoline; Proposed Rule

Federal Register / Vol. 75 , No. 81 / Wednesday, April 28, 2010 /
Proposed Rules

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 87

[EPA-HQ-OAR-2007-0294; FRL-9141-7]
RIN 2060-AP79

Advance Notice of Proposed Rulemaking on Lead Emissions From
Piston-Engine Aircraft Using Leaded Aviation Gasoline

AGENCY: Environmental Protection Agency (EPA).

ACTION: Advance notice of proposed rulemaking.

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SUMMARY: EPA is issuing this Advance Notice of Proposed Rulemaking
(ANPR) to describe information currently available and information
being collected that will be used by the Administrator to issue a
subsequent proposal regarding whether, in the Administrator's judgment,
aircraft lead emissions from aircraft using leaded aviation gasoline
(avgas) cause or contribute to air pollution which may reasonably be
anticipated to endanger public health or welfare. In this ANPR we
describe and request comment on the data available for evaluating lead
emissions, ambient concentrations and potential exposure to lead from
the continued use of leaded avgas in piston-engine powered aircraft. We
also describe and request comment on additional information being
collected that will inform any future action.
    This ANPR is being issued to further respond to a petition
submitted by Friends of the Earth (FOE) in 2006. Emissions of lead from
piston-engine aircraft using leaded avgas comprise approximately half
of the national inventory of lead emitted to air. There are almost
20,000 airport facilities in the U.S. at which leaded avgas may be
used. EPA has long-standing concerns regarding exposure to lead,
particularly during childhood. The most recent review and revision of
the National Ambient Air Quality Standard (NAAQS) for lead, promulgated
in 2008, found that serious health effects occur at much lower levels
of lead in blood than previously identified and did not identify a safe
level of lead exposure.

DATES: Comments must be received on or before June 28, 2010.

ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-
OAR-2007-0294, by one of the following methods:
     http://www.regulations.gov: Follow the on-line
instructions for submitting comments.
     E-mail<EMAIL_ADDRESS>     Fax:<PHONE_NUMBER>.
     Mail: Environmental Protection Agency, Mail Code: 6102T,
1200 Pennsylvania Ave., NW., Washington, DC 20460. Please include two
copies.
     Hand Delivery: EPA Docket Center (Air Docket), U.S.
Environmental Protection Agency, EPA West Building, 1301 Constitution
Avenue, NW., Room: 3334 Mail Code: 2822T, 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-
2007-0294. EPA's policy is that all comments received will be included
in the public docket without change and may be made available online at
http://www.regulations.gov, including any personal information
provided, unless the comment includes information claimed to be
Confidential Business Information (CBI) or other information whose
disclosure is restricted by statute. Do not submit information that you
consider to be CBI or otherwise protected through http://www.regulations.gov or e-mail. The http://www.regulations.gov Web site
is an ``anonymous access'' system, which means EPA will not know your
identity or contact information unless you provide it in the body of
your comment. If you send an e-mail comment directly to EPA without
going through http://www.regulations.gov your e-mail address will be
automatically captured and included as part of the comment that is
placed in the public docket and made available on the Internet. If you
submit an electronic comment, EPA recommends that you include your name
and other contact information in the body of your comment and with any
disk or CD-ROM you submit. If EPA cannot read your comment due to
technical difficulties and cannot contact you for clarification, EPA
may not be able to consider your comment. Electronic files should avoid
the use of special characters, any form of encryption, and be free of
any defects or viruses. For additional information about EPA's public
docket visit the EPA Docket Center homepage at http://www.epa.gov/epahome/dockets.htm.
    Docket: All documents in the docket are listed in the http://www.regulations.gov index. Although listed in the index, some
information is not publicly available, e.g., CBI or other information
whose disclosure is restricted by statute. Certain other material, such
as copyrighted material, will be publicly available only in hard copy.
Publicly available docket materials are available either electronically
in http://www.regulations.gov or in hard copy at the EPA Docket Center,
EPA/DC, EPA West, Room 3334, 1301 Constitution Avenue, 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<PHONE_NUMBER>, and the telephone number for the
Air Docket is<PHONE_NUMBER>.

FOR FURTHER INFORMATION CONTACT: Marion Hoyer, Assessment and Standards
Division, Office of Transportation and Air Quality, 2000 Traverwood
Drive, Ann Arbor, MI 48105; telephone number:<PHONE_NUMBER>; fax
number:<PHONE_NUMBER>; e-mail address<EMAIL_ADDRESS>
SUPPLEMENTARY INFORMATION:

I. General Information

A. What should I consider as I prepare my comments for EPA?

    1. Submitting CBI. Do not submit this information to EPA through
http://www.regulations.gov or e-mail. Clearly mark the part or all of
the information that you claim to be CBI. For CBI information in a disk
or CD ROM that you mail to EPA, mark the outside of the disk or CD ROM
as CBI and then identify electronically within the disk or CD ROM the
specific information that is claimed as CBI. In addition to one
complete version of the comment that includes information claimed as
CBI, a copy of the comment that does not contain the information
claimed as CBI must be submitted for inclusion in the public docket.
Information so marked will not be disclosed except in accordance with
procedures set forth in 40 CFR Part 2.
    2. Tips for Preparing Your Comments. When submitting comments,
remember to:
     Identify the rulemaking by docket number and other
identifying information (subject heading, Federal Register date and
page number).
     Follow directions--The agency may ask you to respond to
specific questions or organize comments by referencing a Code of
Federal Regulations (CFR) part or section number.
     Explain why you agree or disagree, suggest alternatives,
and substitute language for your requested changes.
     Describe any assumptions and provide any technical
information and/or data that you used.
     If you estimate potential costs or burdens, explain how
you arrived at your estimate in sufficient detail to allow for it to be
reproduced.

     Provide specific examples to illustrate your concerns, and
suggest alternatives.
     Explain your views as clearly as possible, avoiding the
use of profanity or personal threats.
     Make sure to submit your comments by the comment period
deadline identified.

Table of Contents

I. Overview
    A. Background on Leaded Aviation Gasoline
    B. Background Information Regarding General Aviation and Use of
Piston-Engine Aircraft
    C. Background on the Petition and EPA's Response
    D. Statutory Authority
    1. Background
    2. Regulatory Authority for Emission Standards
    3. Regulatory Authority for Fuel Standards
    E. Federal Actions To Reduce Lead Exposure
II. Health and Welfare Effects of Lead
    A. Multimedia and Multi-Pathway Exposure Considerations
    B. Health Effects Information
    1. Blood Lead
    2. Health Effects
    3. At-Risk Populations and Life Stages
    C. Welfare Effects
    1. Terrestrial Ecosystems
    2. Aquatic Ecosystems
III. Lead Emissions from Piston-Engine Aircraft
    A. Inventory of Lead from Piston-Engine Powered Aircraft
    1. National Emissions of Lead from Piston-Engine Aircraft
    2. Airport-Specific Emissions of Lead from Piston-Engine
Aircraft
    B. Projections for Future Growth
IV. Lead Concentrations in the Vicinity of Airports
    A. Chemical and Physical Properties of Lead Emitted by Piston-
Engine Aircraft
    B. Summary of Airport Lead Monitoring and Modeling Studies
    1. Summary of Airport Lead Monitoring Studies
    2. Summary of Airport Lead Modeling Studies
V. Exposure to Lead from Piston-Engine Aircraft and Potential for
Impacts
    A. Exposure to Lead Emissions from Piston-Engine Aircraft
    1. Population Residing Near Airports
    2. Children Attending School Near Airports
    3. Agricultural Activities
    4. Pilots, Student-Trainees, Passengers
    5. Bioaccumulation of Lead in Aquatic Organisms
    B. Related Exposures of Concern
    1. Lead Contribution to Ambient Particulate Matter
    2. Ethylene Dibromide
    3. Non-Exhaust Exposure to Tetraethyl Lead
VI. Additional Information Available for the NPRM to Evaluate the
Potential for Public Health and Welfare Impacts and Considerations
Regarding Engine Emission Standards
    A. The Lead NAAQS and Lead Emissions from Piston-Engine Aircraft
    1. Monitoring Lead at Airports to Evaluate Ambient
Concentrations to Which Lead Emissions from Piston-Engine Aircraft
Contribute
    2. Evaluating the Contribution of Lead Emissions from Piston-
Engine Aircraft to Areas Approaching or Exceeding the Lead NAAQS
    B. Additional Information EPA Is Collecting to Evaluate Ambient
Lead Concentrations Attributable to Emissions from Piston-Engine
Aircraft
    C. Considerations Regarding Engine Emission Standards
VII. Statutory and Executive Order Reviews

I. Overview

    EPA is publishing this ANPR in further response to a petition
submitted by Friends of the Earth (FOE) entitled ``Petition for
Rulemaking Seeking the Regulation of Lead Emissions From General
Aviation Aircraft Under Sec.  231 of the Clean Air Act.'' \1\ In the
petition, FOE requests that the Administrator of EPA: (1) Make a
finding that lead emissions from general aviation aircraft endanger
public health and welfare and issue a proposed emission standard for
lead from general aviation aircraft under the Clean Air Act (CAA) or,
alternatively, (2) if the Administrator of EPA believes that
insufficient information exists to make such a finding, commence a
study and investigation of the health and environmental impacts of lead
emissions from general aviation aircraft, including impacts to humans,
animals and ecosystems under the CAA and issue a public report on the
findings of the study and investigation. Section I.C of this notice
discusses the background on the petition and EPA's response to date and
Section I.D discusses EPA's statutory authority under section 231(a) of
the CAA. Under the CAA, if, in the Administrator's judgment, lead
emissions from the use of leaded avgas cause or contribute to air
pollution which may reasonably be anticipated to endanger public health
or welfare, then EPA would be required under our statutory authority to
prescribe standards to control the emissions of lead from piston-engine
aircraft. In promulgating such standards, the EPA would be required to
consult with the Federal Aviation Administration (FAA), and could not
change standards if doing so would significantly increase noise and
adversely affect safety. FAA would then be required, after consultation
with EPA, to prescribe regulations to insure compliance with any
standards to control the emissions of lead from piston-engine aircraft.
Under 49 U.S.C. 44714, FAA would also be required to prescribe
standards for the composition or chemical or physical properties of
piston-engine fuel or fuel additives to control or eliminate aircraft
lead emissions.
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    \1\ See docket item EPA-HQ-OAR-2007-0294-0003.
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    In this notice, we discuss our analysis of the relevant information
and issues to date, and we seek further public input regarding FOE's
petition. For the purposes of this notice, we will refer to the
positive or negative exercise of judgment as to whether lead emissions
from aircraft engines resulting from the use of aviation gasoline
(avgas) cause or contribute to air pollution which may reasonably be
anticipated to endanger public health or welfare as the ``endangerment
finding'' and the ``cause or contribute finding.'' This short-hand use
of ``endangerment finding'' and ``cause or contribute finding'' is
strictly for purposes of simplifying the discussion, and should not be
read as implying that EPA considers the exercise of the Administrator's
judgment to require a formal ``finding'' or ``determination.''
    In 2006, EPA completed the Air Quality Criteria Document (AQCD) for
Lead, which critically assesses and integrates relevant scientific
information regarding the health effects of lead.\2\ EPA concluded that
the latest evidence indicates adverse health effects, most notably
among children, are occurring at much lower levels than previously
considered. In 2008, EPA decreased the level of the primary National
Ambient Air Quality Standard (NAAQS) for lead from 1.5 micrograms per
cubic meter ([mu]g/m\3\) to 0.15 [mu]g/m\3\ in order to provide
increased protection for children and other at-risk populations against
an array of adverse health effects, most notably neurological effects
in children, including neurocognitive and neurobehavioral effects.\3\
Neurotoxic effects in children and cardiovascular effects in adults are
among those best substantiated as occurring at blood lead
concentrations as low as 5 to 10 [mu]g/dL (or possibly lower); and
these categories are currently clearly of greatest public health
concern (AQCD for Lead, p. 8-60). The U.S. Centers for Disease Control
and Prevention (CDC) concluded in 2005 that no ``safe'' threshold for
blood lead has been identified, and emphasized the

importance of preventative measures.4 5 To provide increased
protection against lead-related welfare effects, in 2008 EPA revised
the secondary standard to be identical in all respects to the revised
primary standard. Section II of this ANPR provides more detail
regarding health and welfare effects of lead.
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    \2\ U.S. Environmental Protection Agency (2006) Air Quality
Criteria for Lead. Washington, DC, EPA/600/R-5/144aF. Available
online at: http://www.epa.gov/ncea/.
    \3\ National Ambient Air Quality Standards for Lead 73 FR 66965
(Nov. 12, 2008).
    \4\ Centers for Disease Control and Prevention (2005) Preventing
lead poisoning in young children: a statement by the Centers for
Disease Control and Prevention. Atlanta, GA: U.S. Department of
Health and Human Services, Public Health Service. August.
    \5\ Advisory Committee on Childhood Lead Poisoning Prevention
(ACCLPP) (2007) Interpreting and managing blood lead levels <10 ug/
dL in children and reducing childhood exposures to lead:
Recommendations of CDC's Advisory Committee on Childhood Lead
Poisoning Prevention. Morbidity and Mortality Weekly Report. 56(RR-
8). November 2, 2007.
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    Given the recent findings of the science summarized by EPA in the
AQCD for Lead as well as the findings of the CDC, the Agency is
concerned about the potential for health and welfare effects from
exposure to lead emissions from aircraft engines using leaded avgas. On
a national basis, emissions of lead from aircraft engines using leaded
avgas are the largest single source category for emissions of lead to
air, comprising approximately half of the national inventory.\6\ There
are almost 20,000 airport facilities in the U.S. at which leaded avgas
may be used, and in some areas of the country there are densely
populated residential developments immediately adjacent to these
airport facilities. As described in Section V, we estimate that up to
16 million people reside and three million children attend school in
close proximity to airport facilities servicing piston-engine aircraft
that are operating on leaded avgas.
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    \6\ U.S. Environmental Protection Agency Electronic Report on
the Environment. Available at: http://cfpub.epa.gov/eroe. Updated in
December 2009 using the 2005 National Emissions Inventory.
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    Exposure to lead occurs through multiple routes (e.g., inhalation,
ingestion and dermal adsorption), and lead emitted to the atmosphere
can contribute to lead levels in multiple media (e.g., air, soil and
water). The lead monitoring studies conducted at or near airports,
described in Section IV of this ANPR, indicate that lead levels in
ambient air on and near airports servicing piston-engine aircraft are
higher than lead levels in areas not directly influenced by a lead
source. In addition, the emissions of lead from these engines are also
expected to distribute widely through the environment. This is in part
due to the emission of lead at various altitudes during aircraft
operations as well as the fine particle size of lead emitted by piston
engines. Continued use of leaded avgas provides an ongoing source of
new lead that is deposited in various environmental media and
participates in long term cycling mechanisms in the environment, thus
adding to the pool of lead available for uptake by humans and biota. We
expect the lead from avgas to be bioavailable in the same way as the
lead emitted by motor vehicles in the past, which was well documented
to contribute to blood levels through both ingestion and inhalation.
    As noted in Section II of this ANPR, once deposited to surfaces,
lead can subsequently be resuspended into the ambient air and, because
of the persistence of lead, emissions of this metal contribute to
environmental media concentrations for many years into the future. Lead
that is a soil or dust contaminant today may have been airborne
yesterday or many years ago. Therefore lead emissions from piston-
engine aircraft could contribute to increased lead exposure and risk
currently or at some time in the future.
    Section VI of this ANPR provides an overview of additional
information that will be available for the NPRM to evaluate the
potential for public health and welfare impacts from lead emitted by
piston-engine aircraft. These additional data will come from lead
monitoring being planned to satisfy requirements of the Lead NAAQS, air
quality modeling planned at EPA and any information submitted to EPA
during the comment period for this ANPR.
    The remainder of this section provides background on leaded avgas,
FOE's petition and EPA's response to the petition to date, and
statutory authority over emissions, fuel for aircraft and Federal
actions to reduce lead exposure. Section II provides a discussion of
the health and welfare effects of lead. Sections III, IV and V describe
the emissions of lead from avgas, ambient lead concentration in the
vicinity of airports and potential exposure to lead from leaded avgas,
respectively. In Section VI, we describe the additional information EPA
is collecting and considerations regarding engine emission standards.
Section VII contains information on statutory and executive order
reviews covering this action.

A. Background on Leaded Aviation Gasoline

    In 1996, EPA promulgated regulations that banned the use of leaded
gasoline in highway vehicles.\7\ The addition of lead to fuel used in
piston-engine powered aircraft was not banned in this action, and the
use of leaded avgas is the largest remaining source category of lead
emissions. Lead is not added to jet fuel that is used in commercial
aircraft, most military aircraft, or other turbine-engine powered
aircraft. Most piston-engine aircraft fall into the categories of
either general aviation (GA) or air taxi (AT). GA and AT aircraft
include a diverse set of aircraft types and engine models and are used
in a wide variety of applications.\8\
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    \7\ See ``Prohibition on Gasoline Containing Lead or Lead
Additives for Highway Use'' 61 FR 3832 (Feb. 2, 1996).
    \8\ Commercial aircraft include those used for scheduled service
transporting passengers, freight, or both. Air taxis fly scheduled
and for-hire service carrying passengers, freight or both, but they
usually are smaller aircraft than those operated by commercial air
carriers. General aviation includes most other aircraft (fixed and
rotary wing) used for recreational flying, business, and personal
transportation.
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    Lead is added to fuel for piston-engine aircraft in the form of
tetraethyl lead (TEL). This lead additive helps boost fuel octane,
prevents knock, and prevents valve seat recession and subsequent loss
of compression for engines without hardened valves. There are two main
types of leaded avgas: 100 Octane, which can contain up to 4.24 grams
of lead per gallon; and 100 Octane Low Lead (100 LL), which can contain
up to 2.12 grams of lead per gallon. Currently, 100LL is the most
commonly available and most commonly used type of avgas.9 10
TEL was first used in piston-engine aircraft in 1927.\11\ Into the
1950s commercial and military aircraft in the U.S. operated on 100
Octane leaded avgas, but in subsequent years, the commercial and
military aircraft fleet largely converted to jet turbine-engine
propelled aircraft. However, the use of avgas containing 4 grams of
lead per gallon continued in piston-engine aircraft until the early
1970s when 100LL became the dominant leaded fuel in use. Currently,
very little 100 Octane is supplied in the U.S. and we use the lead
content of 100LL (2.12 grams per gallon) to characterize the lead
available from avgas.
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    \9\ ChevronTexaco (2006) Aviation Fuels Technical Review. FTR-3.
Available online at: http://www.chevronglobalaviation.com/docs/aviation_tech_review.pdf.
    \10\ ASTM International (2007) Standard Specification for
Aviation Gasolines D910-06.
    \11\ Ogston, A.R. (1981) A Short History of Aviation Gasoline
Development, 1903-1980. Society of Automotive Engineers. Paper
number 810848.
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    Since lead is a persistent pollutant, it is important to
characterize the historical use of this fuel.

Approximately 14.6 billion gallons of leaded avgas have been consumed
in the U.S. between 1970 and 2007. If this fuel was all 100LL, it would
account for approximately 34,000 tons \12\ of lead emitted to the
air.\13\ In terms of the potential impacts from long-term use of leaded
avgas at and near airports, older facilities would be expected to have
a legacy of lead, particularly those that supported military and
commercial aircraft operating on 100 Octane. Over 3,000 of the 20,000
airport facilities in the U.S. are at least 50 years old and some
airports have been in operation since the early 1900s.
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    \12\ In this ANPR and in EPA's National Emissions Inventory, the
use of the unit tons refers to short tons.
    \13\ Oak Ridge National Laboratory (2009) Transportation Energy
Data Book: Edition 28. Available at: http://cta.ornl.gov/data. Table
A.7.
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    The Department of Energy's (DOE's) Energy Information
Administration (EIA) provides information on the volume of leaded avgas
supplied in the U.S.\14\ The Department of Transportation's (DOT's) FAA
provides information on the volume of leaded avgas consumed in the
U.S.\15\ EPA has historically used the DOE EIA avgas fuel volumes
supplied to calculate national lead inventories from the consumption of
leaded avgas. We are currently evaluating methods used by DOE and DOT
to calculate annual avgas supply and consumption volumes. In this
document, we provide avgas fuel volume data supplied by DOE and DOT and
we note the source of the data for clarity. Over the past ten years,
DOE estimates of the volume of leaded avgas supplied has ranged from
326 million gallons in 1999 to 235 million gallons in 2008 (Figure 1).
Applying the concentration of lead in 100LL (2.12 grams of lead per
gallon), the total quantity of lead supplied in avgas in the nation has
ranged from 762 tons in 1999 to 550 tons in 2008 (a 28% decrease over
that time period). The decrease in fuel consumption is attributed to
the decrease in piston-engine aircraft activity over that time period
and not due to a shift to unleaded fuel. There are currently over
200,000 piston-engine aircraft in the U.S. that continue to consume
leaded avgas and approximately 2,000 new piston-engine aircraft
requiring leaded avgas are manufactured annually.\16\ As described in
Section III.B of this ANPR, there is a slight growth in the activity of
general aviation aircraft projected to 2025.
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    \14\ Department of Energy Information Administration. Fuel
production volume data obtained from http://tonto.eia.doe.gov/dnav/pet/hist/mgaupus1A.htm accessed June 2009.
    \15\ U.S. Department of Transportation Federal Aviation
Administration Aviation Policy and Plans. FAA Aerospace Forecast
Fiscal Years 2009-2025. p.81. Available at: http://www.faa.gov/data_research/aviation/aerospace_forecasts/2009-2025/media/2009%20Forecast%20Doc.pdf. This document provides historical data
for 2000-2008 as well as forecast data.
    \16\ General Aviation Manufacturers Association (2008) General
Aviation Statistical Databook & Industry Outlook. Available online
at: http://www.gama.aero/files/2008_general_aviation_statistical_databook__indust_499b0dc37b.pdf.
[GRAPHIC] [TIFF OMITTED] TP28AP10.014

B. Background Information Regarding General Aviation and Use of Piston-
Engine Aircraft

    In the U.S., general aviation aircraft fly over 27 million hours
and carry 166 million passengers annually.\17\ Approximately 66 percent
of hours flown by general aviation are conducted by piston-engine
aircraft.\18\ Aircraft in the general aviation fleet are used for
personal transportation (36 percent), instructional flying (19
percent), corporate uses (11 percent), business (11 percent), air taxi
and air tours (8 percent) and the remainder include hours spent in
other applications such as aerial observation and aerial
application.\19\ According to the 2008 General Aviation Statistical
Databook & Industry Outlook report by the General Aviation
Manufacturers Association (GAMA) there were 578,541 pilots in the
United States in 2008.\20\ According to GAMA, in 2008, the number of
active single-engine piston-powered aircraft was 144,220 and the number
of active twin-engine piston-powered aircraft was 18,385. In 2008,
1,791 new piston-engine aircraft were manufactured in the U.S.
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    \17\ General Aviation Manufacturers Association (2008) General
Aviation Statistical Databook and Industry Outlook, p.30. Retrieved
on August 17, 2009 from: http://www.gama.aero/files/2008_general_aviation_statistical_databook__indust_499b0dc37b.pdf.
    \18\ General Aviation Manufacturers Association (2008) General
Aviation Statistical Databook and Industry Outlook, p.30. Retrieved
on August 17, 2009 from: http://www.gama.aero/files/2008_general_aviation_statistical_databook__indust_499b0dc37b.pdf.
    \19\ General Accounting Office Report to Congressional
Requesters (2001) General Aviation Status of the Industry, Related
Infrastructure, and Safety Issues. GAO-01-916.
    \20\ General Aviation Manufacturers Association (2008) General
Aviation Statistical Databook and Industry Outlook, pp.51-55.
Retrieved on August 17, 2009 from: http://www.gama.aero/files/2008_general_aviation_statistical_databook__indust_499b0dc37b.pdf.
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    FAA's Office of Air Traffic provides a complete listing of
operational airport facilities in the National Airspace System
Resources (NASR) database.\21\ In 2008, there were 19,896 airport
facilities in the U.S., the vast majority of which are expected to have
activity by piston-engine aircraft that operate on leaded avgas. FAA's
National Plan of Integrated Airport Systems identifies approximately
3,400 airports that are significant to national air transportation.
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    \21\ An electronic report can be generated from the NASR
database and is available for download from the Internet at the
following Web site. http://www.faa.gov/airports_airtraffic/airports/airport_safety/airportdata_5010/. This database is
updated every 56 days.
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C. Background on the Petition and EPA's Response

    In a 2003 letter to the EPA, FOE initially raised the issue of the
potential for endangerment caused or contributed to by lead emissions
from the use of leaded avgas.\22\ In 2006, FOE filed a petition with
EPA requesting that the Administrator find endangerment or, if there
was insufficient information to find endangerment, commence a study of
lead emissions from piston-engine aircraft. In 2007, the EPA issued a
Federal Register notice on the petition requesting comments and
information related to a wide range of issues regarding the use of
leaded avgas and potential public health and welfare exposure
issues.\23\ We sought comments regarding exposure to lead from avgas
combustion, emissions of lead, fuel options, and piston-engine
technology. The comments received to date are publicly available in the
docket (EPA-HQ-OAR-2007-0294). The majority of comments received
concerned the nature of the industry and fuel supply issues. The
commenters did not supply information regarding health or exposure
issues. In 2008, the EPA initiated a lead study which will improve the
manner in which EPA models emissions from piston-engine aircraft. This
study is described in further detail in Section VI of this document. At
the time we received FOE's petition, the EPA was in the process of a
full re-evaluation of the science supporting the lead NAAQS.
Information from that re-evaluation and the relationship between the
new lead standard and the emissions of lead from piston-engine aircraft
are discussed in this ANPR.
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    \22\ FOE letter dated December 12, 2003 submitted to EPA Docket
EPA-HQ-OAR-2002-0030.
    \23\ See ``Petition Requesting Rulemaking To Limit Lead
Emissions from General Aviation Aircraft; Request for Comments'' 72
FR 64570 (Nov. 16, 2007).
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D. Statutory Authority

1. Background
    Section 231 of the CAA sets forth EPA's authority to regulate
aircraft emissions of air pollution. As described further in Section
I.D.2 of this ANPR, Section 231(a)(2)(A) requires EPA to, from time to
time, issue proposed emission standards applicable to the emission of
any air pollutant from any class or classes of aircraft engines which,
in the Administrator's judgment, cause or contribute to air pollution
which may reasonably be anticipated to endanger public health or
welfare. EPA has broad authority in exercising its judgment regarding
whether emissions from certain sources cause or contribute to air
pollution which may reasonably be anticipated to endanger public health
or welfare.\24\ EPA has discussed its ``endangerment finding''
authority at length in recent notices for greenhouse gases published in
the Federal Register, and we refer readers to those notices for
detailed discussions of the analytical and legal framework.\25\
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    \24\ See, e.g., Ethyl Corp. v. EPA, 541 F.2d 1, 6 (DC Cir.),
cert. denied 426 U.S. 941 (1976); see also Massachusetts v. EPA, 549
U.S. 497, 506, n.7 (2007).
    \25\ See, ``Endangerment and Cause or Contribute Findings for
Greenhouse Gases under Section 202(a) of the Clean Air Act; Final
Rule,'' 74 FR 66496, 66505 (Dec. 15, 2009); see also, ``Proposed
Endangerment and Cause or Contribute Findings for Greenhouse Gases
Under Section 202(a) of the Clean Air Act,'' 74 FR 18886, 18890-94
(April 24, 2009); see also ``Regulating Greenhouse Gas Emissions
Under the Clean Air Act; Advance Notice of Proposed Rulemaking,'' 73
FR 44354, 44421-23 (July 30, 2008).
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    In 1976, EPA listed lead under CAA section 108, making it what is
called a ``criteria pollutant.'' As part of the listing decision, EPA
determined that lead was an air pollutant which, in the Administrator's
judgment, has an adverse effect on public health or welfare under then
section 108(a). Once lead was listed, EPA issued primary and secondary
NAAQS that the Administrator determined were requisite to protect
public health with an adequate margin of safety and to protect public
welfare from any known or anticipated adverse effects. Section
109(b)(1) and (2). As discussed elsewhere in this notice, EPA issued
the first NAAQS for lead in 1978, and recently revised the lead NAAQS
by reducing the level of the standard from 1.5 [mu]g/m\3\ to 0.15
[mu]g/m\3\, measured over a 3-month averaging period. These actions are
part of the context for the issues before EPA under section 231(a).
    The first part of the endangerment test concerns identification of
air pollution which may reasonably be anticipated to endanger public
health or welfare. The CAA defines both ``air pollutant'' and
``welfare.'' Air pollutant is defined in CAA section 302(g) as: ``Any
air pollution agent or combination of such agents, including any
physical, chemical, biological, radioactive (including source material,
special nuclear material, and byproduct material) substance or matter
which is emitted into or otherwise enters the ambient air. Such term
includes any precursors to the formation of any air pollutant, to the
extent the Administrator has identified such precursor or precursors
for the particular purpose for which the term `air pollutant' is
used.'' Lead fits within

this capacious definition, and has long been regulated as an air
pollutant by EPA under the CAA (see Section I.E. of this ANPR).
    There is no definition of public health in the CAA. The U.S.
Supreme Court has discussed the concept in the context of whether costs
can be considered when setting NAAQS. Whitman v. American Trucking
Ass'n, 531 U.S. 457 (2001). In Whitman, the Court imbued the term with
its most natural meaning: ``the health of the public.'' Id., at 466.
When considering public health, EPA has looked at morbidity, including
acute and chronic health effects, as well as mortality. EPA has long
regulated emissions of lead air pollution due to their adverse impacts
on public health (see section I.E. of this ANPR). Exposure to lead
causes ``a broad array of deleterious effects on multiple organ
systems,'' among children and adults (AQCD for Lead, p.8-24 and Section
8.4.1). Of particular concern are the neurotoxic effects of lead in
young children.\26\ See Section II of this ANPR for a more complete
overview of the public health effects of lead.
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    \26\ See ``National Ambient Air Quality Standards for Lead'' 73
FR 66970-67007 (Nov. 12, 2008).
---------------------------------------------------------------------------

    Regarding ``welfare,'' CAA section 302(h) states that ``[a]ll
language referring to effects on welfare includes, but is not limited
to, effects on soils, water, crops, vegetation, man-made materials,
animals, wildlife, weather, visibility, and climate, damage to and
deterioration of property, and hazards to transportation, as well as
effects on economic values and on personal comfort and well-being,
whether caused by transformation, conversion, or combination with other
air pollutants.'' This definition is quite broad, and may include
effects other than those listed here as effects on welfare. Welfare
effects caused by lead have been evaluated by EPA and were the basis
for establishing the secondary lead standard.\27\
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    \27\ See ``National Ambient Air Quality Standards for Lead'' 73
FR 67007-67012 (Nov. 12, 2008).
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    By instructing the Administrator to consider whether emissions of
an air pollutant cause or contribute to air pollution, the statute is
clear that she need not find that emissions from any one sector or
group of sources are the sole or even the major part of an air
pollution problem. Moreover, section 231(a) does not contain a modifier
on its use of the term contribute. Unlike some other CAA provisions, it
does not require ``significant'' contribution.\28\ Congress made it
clear that the Administrator is to exercise her judgment in determining
contribution, and authorized regulatory controls to address air
pollution even if the air pollution problem results from a wide variety
of sources. The cause or contribute test is designed to authorize EPA
to identify and then address what may well be many different sectors or
groups of sources that are each part of an air pollution problem.
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    \28\ See, e.g., CAA sections 111(b); 213(a)(2), (4).
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    Section 231(a)(2) refers to contribution and does not specify that
the contribution must be significant before an affirmative finding can
be made. Any finding of a ``contribution'' requires some threshold to
be met; a truly trivial or de minimis ``contribution'' might not count
as such. In the past, the Administrator has evaluated the emissions of
the source or sources in different ways, based on the particular
circumstances involved. In some mobile source rulemakings, the
Administrator has used the percent of emissions from the regulated
mobile source category compared to the total mobile source inventory
for that air pollutant as the best way to evaluate contribution.\29\ In
other instances the Administrator has looked at the percent of
emissions compared to the total nonattainment area inventory of the air
pollution at issue.\30\ EPA has found that air pollutant emissions that
amount to 1.2 percent of the total inventory met the statutory test for
contribution, triggering EPA's regulatory authority.\31\
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    \29\ See, e.g., 66 FR 5001 (January 18, 2001) (heavy duty engine
and diesel sulfur rule).
    \30\ See, e.g., 67 FR 68242 (November 8, 2002) (snowmobile
rule).
    \31\ Bluewater Network v. EPA, 370 F.3d 1, 15 (DC Cir. 2004)
(For Fairbanks, this contribution was equivalent to 1.2 percent of
the total daily CO inventory for 2001).
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2. Regulatory Authority for Emission Standards
    Section 231 of the CAA sets forth EPA's authority to regulate
aircraft emissions of air pollution. Section 231(a)(2)(A) requires EPA
to, from time to time, issue proposed emission standards applicable to
the emission of any air pollutant from any class or classes of aircraft
engines which, in the Administrator's judgment, cause or contribute to
air pollution which may reasonably be anticipated to endanger public
health or welfare. Section 231(a)(2)(B)(i) directs EPA to consult with
FAA on aircraft engine emission standards, and section 231(a)(2)(B)(ii)
provides that EPA shall not change the aircraft engine emission
standards if such change would significantly increase noise and
adversely affect safety. Section 231(a)(3) directs EPA to issue final
regulations with such modifications as the Administrator ``deems
appropriate.''
    In setting or revising standards, section 231(b) provides that EPA
shall have them take effect after such period as EPA finds necessary
(after consultation with the Secretary of Transportation) to permit the
development and application of the requisite technology, giving
appropriate consideration to the cost of compliance within such period.
Section 231(c) then states that EPA's regulations regarding aircraft
shall not apply if disapproved by the President, after notice and
opportunity for public hearing, on the basis of a finding by DOT that
such regulations would create a hazard to aircraft safety. Section 232
directs DOT to issue and implement regulations to insure compliance
with EPA's standards, while section 233 pre-empts States and local
governments from adopting or enforcing any aircraft emission standards
that are not identical to EPA's standards.
    In recently reviewing this statutory scheme, the U.S. Court of
Appeals for the District of Columbia Circuit ruled that it constitutes
a ``both explicit and extraordinarily broad'' delegation of ``expansive
authority to EPA to enact appropriate regulations applicable to the
emissions of air pollutants from aircraft engines.'' \32\
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    \32\ NACAA v. EPA, 489 F.3d 1221, 1229-30 (DC Cir. 2007).
---------------------------------------------------------------------------

3. Regulatory Authority for Fuel Standards
    Section 211(c) of the CAA allows EPA to regulate fuels used in
motor vehicles and nonroad vehicles or engines where emission products
of the fuel either: (1) Cause or contribute to air pollution that
reasonably may be anticipated to endanger public health or welfare, or
(2) will impair to a significant degree the performance of any emission
control device or system which is in general use, or which the
Administrator finds has been developed to a point where in a reasonable
time it will be in general use were such a regulation to be
promulgated. This section of the CAA was used to eliminate lead from
fuel used in motor vehicles. EPA's authority to regulate fuels is
limited to those fuels used in motor vehicles, motor vehicle engines,
or nonroad engines or vehicles, under CAA section 211(c)(1). The CAA
defines ``motor vehicle,'' ``nonroad engine,'' and ``nonroad vehicle''
in section 216 for purposes of part A of title II of the CAA. Part A is
also where the authority to regulate fuels under section 211 resides.
However, EPA's authority to regulate aircraft resides in

part B of title II, and therefore the definitions of section 216 do not
apply to aircraft. This means that aircraft are not ``nonroad
vehicles,'' and aircraft engines are not ``nonroad engines.''
Consequently, EPA's authority to regulate fuels under section 211 does
not extend to fuels used exclusively in aircraft, such as leaded avgas,
that are not also used in motor vehicles or nonroad vehicles or engines
(excluding fuel used in vehicles exclusively).
    Instead, fuels used exclusively in aircraft engines are to be
regulated by the FAA. Title 49 (49 U.S.C. 44714) requires that ``the
Administrator of the Federal Aviation Administration shall prescribe
(1) standards for the composition or chemical or physical properties of
an aircraft fuel or fuel additive to control or eliminate aircraft
emissions the Administrator of the Environmental Protection Agency
decides under section 231 of the Clean Air Act (42 U.S.C. 7571)
endanger the public health or welfare; and (2) regulations providing
for carrying out and enforcing those standards.''

E. Federal Actions To Reduce Lead Exposure

    The U.S. has made tremendous progress in reducing lead
concentrations in the outdoor air. Nationwide, average concentrations
of lead in the air have dropped 91 percent between 1980 and 2008.\33\
Much of this dramatic improvement occurred as a result of the permanent
phase-out of lead in motor vehicle gasoline discussed in this section
of the ANPR. However, lead continues to be emitted into the air from
many different types of stationary sources and piston-engine aircraft
as well as certain high performance engines such as race cars.
---------------------------------------------------------------------------

    \33\ See http://www.epa.gov/airtrends/lead.html.
---------------------------------------------------------------------------

    Federal programs provide for nationwide reductions in emissions of
lead and other air pollutants through several provisions in the CAA. In
the early 1970s, EPA issued regulations regarding lead in gasoline in
order to accomplish two purposes.\34\ First, EPA issued regulations
designed to ensure the availability of unleaded gasoline for use in
motor vehicles equipped with emission control systems such as catalytic
converters. EPA had determined that lead additives would impair to a
significant degree the performance of emission control systems. Second,
EPA issued regulations designed to gradually reduce the content of lead
in leaded gasoline, because EPA found that lead emissions from motor
vehicles presented a significant risk of harm to the health of urban
population groups, especially children. Children are at a sensitive
life stage with regard to the adverse health effects of lead. In 1985,
EPA, noting the significant reduction in adverse health effects, mainly
among pre-school age children, that would result from reductions in
lead content in gasoline, promulgated additional regulations to
decrease the allowable concentration of lead in gasoline for motor
vehicles to 0.10 grams per gallon.\35\ In 1990 Congress added section
211(n) to the CAA which provides that after December 31, 1995, it shall
be unlawful to sell any gasoline for use in any motor vehicle which
contains lead or lead additives. In 1996, EPA incorporated the CAA
statutory ban on gasoline containing lead or lead additives for highway
use into the Agency's existing regulations on the lead content of
gasoline.\36\ In this regulation, it was noted that the petroleum
industry may continue to make and market gasoline produced with lead
additives for all remaining uses, including use as fuel in aircraft,
racing cars, and nonroad engines such as farm equipment engines and
marine engines, to the extent otherwise allowed by law.\37\
---------------------------------------------------------------------------

    \34\ ``Regulation of Fuels and Fuel Additives'' 38 FR 1254 (Dec.
4, 1973).
    \35\ ``Regulation of Fuels and Fuel Additives; Gasoline Lead
Content'' 50 FR 9386 (March 7, 1985).
    \36\ ``Prohibition on Gasoline Containing Lead or Lead Additives
for Highway Use'' 61 FR 3832 (Feb. 2, 1996).
    \37\ ``Prohibition on Gasoline Containing Lead or Lead Additives
for Highway Use'' 61 FR 3834 (Feb. 2, 1996).
---------------------------------------------------------------------------

    In fact, there have been no regulatory limits placed on the
production and consumption of leaded avgas, and, as noted in Section
I.A of this ANPR, emissions of lead from piston-engine aircraft account
for an increasing fraction of the lead emissions to air (e.g.,
accounting for approximately half the national inventory of lead
emission in 2005). This is in spite of the decrease in the supply of
leaded avgas nationally from 374 million gallons (875 tons of lead) in
1990 to 235 million gallons (550 tons of lead) in 2008.\38\ The
decrease in fuel consumption is attributed to the decrease in piston-
engine aircraft activity over that time period and not due to a shift
to unleaded fuel. There are over 200,000 piston-engine aircraft in the
U.S. that continue to consume leaded avgas and approximately 2,000 new
piston-engine aircraft requiring leaded avgas are manufactured
annually. Projected growth for this industry is discussed in Section
III.B.
---------------------------------------------------------------------------

    \38\ These fuel volume estimates are from the Department of
Energy Information Administration. http://tonto.eia.doe.gov/dnav/pet/hist/mgaupus1A.htm.
---------------------------------------------------------------------------

    Significant reductions in emission of lead from stationary sources
have been achieved between 1985 and 2002, totaling almost 2,000 tons of
lead.\39\ Regulations promulgated in 1995, 1997 and 1999 controlled
emissions of lead from primary and secondary lead smelters,
contributing to these reductions.40 41 42 Currently, metal
industry emissions of lead comprise 23% of the national inventory (298
tons). Additional reductions in the emission of lead have been
accomplished through controls on waste incineration and other
stationary sources.43 44 45 These standards have been set at
``maximum achievable control technology'' (MACT) levels, and under CAA
sections 112 and 129 EPA must revisit these standards in the future to
determine whether they are sufficiently stringent to provide an ample
margin of safety to protect public health and prevent an adverse
environmental effect.
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    \39\ U.S. Environmental Protection Agency (2008) EPA's Report on
the Environment EPA/600/R-07/045F. Available at: http://www.epa.gov/roe/.
    \40\ ``National Emission Standards for Hazardous Air Pollutants
From Secondary Lead Smelting'' 60 FR 32587 (June 23, 1995).
    \41\ ``National Emission Standards for Hazardous Air Pollutants
From Secondary Lead Smelting'' 62 FR 32209 (June 13, 1997).
    \42\ ``National Emission Standards for Hazardous Air Pollutants
for Primary Lead Smelting'' 64 FR 30194 (June 4, 1999).
    \43\ ``Standards of Performance for New Stationary Sources and
Emission Guidelines for Existing Sources: Municipal Waste
Combustors'' 60 FR 65387 (Dec. 19, 1995).
    \44\ ``Emission Guidelines for Existing Sources and Standards of
Performance for New Stationary Sources'' 62 FR 45124 (Aug. 25,
1997).
    \45\ ``Standards of Performance for New Stationary Sources and
Emission Guidelines for Existing Sources: Large Municipal Waste
Combustors'' 71 FR 27324-27348 (May 10, 2006).
---------------------------------------------------------------------------

    As lead is a multimedia pollutant, a broad range of Federal
programs beyond those that focus on air pollution control provide for
nationwide reductions in environmental releases and human exposures. In
addition, the U.S. Centers for Disease Control and Prevention (CDC)
programs provide for the tracking of children's blood lead levels
nationally and provide guidance on levels at which medical and
environmental case management activities should be
implemented.46 47 In

1991, the Secretary of the U.S. Department of Health and Human Services
(HHS) characterized lead poisoning as the ``number one environmental
threat to the health of children in the United States.'' \48\ In 1997,
President Clinton created, by Executive Order 13045, the President's
Task Force on Environmental Health Risks and Safety Risks to Children
in response to increased awareness that children face disproportionate
risks from environmental health and safety hazards (62 FR 19885).\49\
By Executive Orders issued in October 2001 and April 2003, President
Bush extended the work for the Task Force for an additional three and a
half years beyond its original charter (66 FR 52013 and 68 FR 19931).
The Task Force set a Federal goal of eliminating childhood lead
poisoning by the year 2010, and reducing lead poisoning in children was
identified as the Task Force's top priority.
---------------------------------------------------------------------------

    \46\ Centers for Disease Control and Prevention (2005)
Preventing lead poisoning in young children: a statement by the
Centers for Disease Control and Prevention. Atlanta, GA: U.S.
Department of Health and Human Services, Public Health Service.
August.
    \47\ Advisory Committee on Childhood Lead Poisoning Prevention
(2007) Interpreting and managing blood lead levels <10 [micro]g/dL
in children and reducing childhood exposures to lead:
Recommendations of CDC's Advisory Committee on Childhood Lead
Poisoning Prevention. Morbidity and Mortality Weekly Report. 56(RR-
8). November 2, 2007.
    \48\ Alliance to End Childhood Lead Poisoning (1991) The First
Comprehensive National Conference; Final Report. October 6, 7, 8,
1991.
    \49\ Co-chaired by the Secretary of the HHS and the
Administrator of the EPA, the Task Force consisted of
representatives from 16 Federal departments and agencies.
---------------------------------------------------------------------------

    Federal abatement programs provide for the reduction in human
exposures and environmental releases from in-place materials containing
lead (e.g., lead-based paint, urban soil and dust, and contaminated
waste sites). Federal regulations on disposal of lead-based paint waste
help facilitate the removal of lead-based paint from residences (68 FR
36487). Further, in 1991, EPA lowered the maximum levels of lead
permitted in public water systems from 50 parts per billion (ppb) to 15
ppb measured at the consumer's tap (56 FR 26460).
    Federal programs to reduce exposure to lead in paint, dust, and
soil are specified under the comprehensive Federal regulatory framework
developed under the Residential Lead-Based Paint Hazard Reduction Act
(Title X). Under Title X and Title IV of the Toxic Substances Control
Act (TSCA), EPA has established regulations and associated programs
with the goal of reducing exposure to lead via lead-based paint. For
example, under Title IV of TSCA, EPA established standards identifying
hazardous levels of lead in residential paint, dust, and soil in 2001.
On March 31, 2008, the Agency issued a new rule (73 FR 21692) to
further protect children from lead-based paint hazards resulting from
renovation and repair work occurring in housing in which they live.
    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 lead and other pollutants. For example, EPA
determines and implements protective levels for lead 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.\50\
Federal regulations concerning batteries in municipal solid waste
control the collection and recycling or proper disposal of batteries
containing lead.\51\ Similarly, Federal programs provide for the
reduction in environmental releases of hazardous substances such as
lead in the management of wastewater.\52\
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    \50\ See, e.g., 66 FR 58258.
    \51\ See, e.g., ``Implementation of the Mercury-Containing and
Rechargeable Battery Management Act'' http://www.epa.gov/epaoswer/hazwaste/recycle/battery.pdf and ``Municipal Solid Waste Generation,
Recycling, and Disposal in the United States: Facts and Figures for
2005'' http://www.epa.gov/epaoswer/osw/conserve/resources/msw-2005.pdf.
    \52\ http://www.epa.gov/owm/.
---------------------------------------------------------------------------

    A variety of Federal nonregulatory programs also provide for
reduced environmental release of lead-containing materials through
voluntary measures and more general encouragement of pollution
prevention, promotion of reuse and recycling, reduction of priority and
toxic chemicals in products and waste, and conservation of energy and
materials. These include the voluntary partnership between EPA and the
National Association for Stock Car Auto Racing (NASCAR) which has
achieved the goal of removing alkyl lead (organic forms of lead) from
racing fuels used in the Nextel Cup, Busch and Craftsman Truck
Series.\53\ Other programs include the Resource Conservation
Challenge,\54\ the National Waste Minimization Program,\55\ ``Plug in
to eCycling'' (a partnership between EPA and consumer electronics
manufacturers and retailers),\56\ and activities to reduce the practice
of backyard trash burning.\57\
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    \53\ U.S. Environmental Protection Agency Persistent,
Bioaccumulative, and Toxic Pollutants (PBT) Program (2002) PBT
national action plan for alkyl-Pb. Washington, DC. Available online
at: http://www.epa.gov/pbt/pubs/Alkyl_lead_action_plan_final.pdf.
    \54\ http://www.epa.gov/epawaste/rcc/index.htm.
    \55\ http://www.epa.gov/epawaste/hazard/wastemin/.
    \56\ http://www.epa.gov/epawaste/partnerships/plugin/index.htm.
    \57\ http://www.epa.gov/epawaste/nonhaz/municipal/backyard/index.htm.
---------------------------------------------------------------------------

    In addition to the lead control programs summarized above, EPA's
research program, with other Federal agencies, identifies, encourages
and conducts research needed to locate and assess serious risks and to
develop methods and tools to characterize and help reduce risks. For
example, EPA's Integrated Exposure Uptake Biokinetic Model for Lead in
Children (IEUBK model) and the Adult Lead Methodology are widely used
and accepted as tools that provide guidance in evaluating site specific
data. More recently, in recognition of the need for a single model that
predicts lead concentrations in tissue for children and adults, EPA is
developing the All Ages Lead Model (AALM) to provide researchers and
risk assessors with a pharmacokinetic model capable of estimating
blood, tissue, and bone concentrations of lead based on estimates of
exposure over the lifetime of the individual. EPA research activities
on substances including lead focus on better characterizing aspects of
health and environmental effects, exposure, and control or management
of environmental releases.\58\
---------------------------------------------------------------------------

    \58\ http://www.epa.gov/ord/.
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II. Health and Welfare Effects of Lead

A. Multimedia and Multi-Pathway Exposure Considerations

    This section briefly summarizes the information presented in the
2008 NAAQS for Lead,\59\ the 2007 Lead Staff Paper \60\ and the 2006
Air Quality Criteria Document for Lead (AQCD for Lead).\61\ Lead is an
unusual pollutant in that the distribution of lead to different
environmental media (e.g., air, soil, water) is important for
evaluating public health and welfare effects. Lead emitted to the air
can result in exposure via multiple pathways (e.g., inhalation,
ingestion, dermal absorption). Some key multimedia and multi-pathway
considerations for lead include the following:
---------------------------------------------------------------------------

    \59\ National Ambient Air Quality Standards for Lead 73 FR
66970-67007 (Nov. 12, 2008) Section II.A.
    \60\ U.S. Environmental Protection Agency Review of the National
Ambient Air Quality Standards for Lead: Policy Assessment of
Scientific and Technical Information OAQPS Staff Paper (2007)
Chapter 2. EPA-452/R-07-013 November.
    \61\ U.S. Environmental Protection Agency Air Quality Criteria
for Lead (2006) Volume I: Chapters 2 & 3. EPA/600/R-5/144aF.
October.
---------------------------------------------------------------------------

    (1) Lead is emitted into the air from many sources encompassing a
wide

variety of stationary and mobile source types. Lead emitted to the air
is predominantly in particulate form, with the particles occurring in
various sizes. Once emitted, the particles can be transported long or
short distances depending on their size, which influences the amount of
time spent in the aerosol phase. In general, larger particles tend to
deposit more quickly, within shorter distances from emissions points
(e.g., kilometers), while smaller particles will remain in the aerosol
phase and travel longer distances before depositing (e.g., hundreds to
thousands of kilometers).\62\ As summarized in the AQCD for Lead,
airborne concentrations of lead at sites near sources are much higher
than at sites not known to be directly influenced by sources.
---------------------------------------------------------------------------

    \62\ U.S. Environmental Protection Agency (2004) Air quality
criteria for particulate matter. Research Triangle Park, NC: Office
of Research and Development, National Center for Environmental
Assessment; EPA report no. EPA-600/P-99/0028aF.
---------------------------------------------------------------------------

    (2) Once deposited to surfaces, lead can subsequently be
resuspended into the ambient air and, because of the persistence of
lead, emissions of this metal contribute to environmental media
concentrations for many years into the future as it is cycled within
and between environmental media such as soil, air and water. Lead that
is a soil or dust contaminant today may have been airborne yesterday or
many years ago.\63\
---------------------------------------------------------------------------

    \63\ National Ambient Air Quality Standards for Lead 73 FR 66971
(Nov. 12, 2008), AQC for Lead, Section 2.5.
---------------------------------------------------------------------------

    (3) Exposure to lead emitted into the ambient air can occur
directly by inhalation, or indirectly by ingestion of lead-contaminated
food, water or other materials including dust and soil. This occurs due
to the environmental cycling of this persistent metal which, once
emitted into the ambient air is distributed to other environmental
media and can contribute to human exposures via indoor and outdoor
dusts, outdoor soil, food and drinking water, as well as inhalation of
air. Atmospheric deposition is estimated to comprise a significant
proportion of lead in food (AQCD for Lead, p. 3-48). For example,
livestock may be exposed to lead in vegetation (e.g., grasses and
silage) and in surface soils via incidental ingestion of soil while
grazing (USEPA 1986, Section <IP_ADDRESS>.2).\64\ And dietary intake may be
a predominant source of lead exposure among adults, greater than
consumption of water and beverages or inhalation (73 FR 66971). These
exposure pathways are described more fully in Section 8.2.2 of the AQCD
for Lead.
---------------------------------------------------------------------------

    \64\ U.S. Environmental Protection Agency (1986) Air quality
criteria for lead. Research Triangle Park, NC: Office of Health and
Environmental Assessment, Environmental Criteria and Assessment
Office; EPA report no. EPA-600/8-83/028aF-dF. 4v. Available from:
NTIS, Springfield, VA; PB87-142378.
---------------------------------------------------------------------------

    (4) Air-related exposure pathways are affected by changes to air
quality, including changes in concentrations of lead in air and changes
in atmospheric deposition of lead. Further, because of its persistence
in the environment, lead deposited from the air may contribute to human
and ecological exposures for years into the future as described above.
    Additionally, human exposures to lead include pathways that are not
related to ambient air concentrations. The pathways of human exposure
to lead that are not air-related include ingestion of indoor lead
paint,\65\ lead in diet as a result of inadvertent additions during
food processing, and lead in drinking water attributable to lead in
distribution systems, as well as other generally less prevalent
pathways, as described in the AQCD for Lead (pp. 3-50 to 3-51).
---------------------------------------------------------------------------

    \65\ Weathering of outdoor lead paint may also contribute to
soil lead levels adjacent to the house.
---------------------------------------------------------------------------

B. Health Effects Information

    In 2008, EPA decreased the level of the primary (health-based)
NAAQS for Lead from 1.5 [mu]g/m\3\ to 0.15 [mu]g/m\3\ in order to
provide increased protection for children and other at-risk populations
against an array of adverse health effects, most notably neurological
effects in children, including neurocognitive and neurobehavioral
effects.\66\ This section summarizes information provided in the
numerous recent documents summarizing health and welfare effects from
exposure to lead, including the AQCD for Lead, CDC documents, the EPA
Staff Paper \67\ and the proposed and final NAAQS for Lead. First, the
use of blood lead as a measure of exposure to lead is described
followed by a brief summary of the broad array of lead-induced health
effects. Particular focus is given here to the effects of lead on the
developing nervous system in children since this is among the most
sensitive endpoints identified for this toxic metal. The section ends
with a description of at-risk populations and life stages.
---------------------------------------------------------------------------

    \66\ National Ambient Air Quality Standards for Lead 73 FR 66965
(Nov. 12, 2008).
    \67\ U.S. Environmental Protection Agency (2007) Review of the
National Ambient Air Quality Standards for Lead: Policy Assessment
of Scientific and Technical Information, OAQPS Staff Paper. EPA-452/
R-07-013. Office of Air Quality Planning and Standards, Research
Triangle Park.
---------------------------------------------------------------------------

1. Blood Lead
    Lead enters the body most commonly via the respiratory system and/
or gastrointestinal tract, from which it is quickly absorbed into the
blood stream and distributed throughout the body.\68\ Less commonly,
lead, particularly organic forms of lead such as alkyl lead, can be
absorbed through the skin (AQCD for Lead, page 4-12). Blood lead levels
are extensively used as an index or biomarker of exposure by national
and international health agencies, as well as in epidemiological (AQCD
for Lead, Sections <IP_ADDRESS> and 8.3.2) and toxicological studies of lead
health effects and dose-response relationships (AQCD for Lead, Chapter
5). The U.S. CDC, and its predecessor agencies, has for many years used
blood lead level as a metric for identifying children at risk of
adverse health effects and for specifying particular public health
recommendations.\69\ Most recently, in 2005, with consideration of a
review of the evidence by their advisory committee, CDC revised their
statement on Preventing Lead Poisoning in Young Children.\70\ CDC
specifically recognized the evidence of adverse health effects in
children with blood lead levels below 10 [mu]g/dL,\71\ the data
demonstrating that no ``safe'' threshold for blood lead had been
identified, and emphasized the importance of preventative measures.\72\
---------------------------------------------------------------------------

    \68\ Additionally, lead freely crosses the placenta resulting in
continued fetal exposure throughout pregnancy, with that exposure
increasing during the latter half of pregnancy (AQC for Lead,
Section 6.6.2).
    \69\ Centers for Disease Control (1991) Preventing lead
poisoning in young children: a statement by the Centers for Disease
Control. Atlanta, GA: U.S. Department of Health and Human Services,
Public Health Service; October 1. Available online at: http://wonder.cdc.gov/wonder/prevguid/p0000029/p0000029.asp.
    \70\ Centers for Disease Control and Prevention (2005)
Preventing lead poisoning in young children: a statement by the
Centers for Disease Control and Prevention. Atlanta, GA: U.S.
Department of Health and Human Services, Public Health Service.
August.
    \71\ As described by the Advisory Committee on Childhood Lead
Poisoning Prevention, ``In 1991, CDC defined the blood lead level
(BLL) that should prompt public health actions as 10 [mu]g/dL.
Concurrently, CDC also recognized that a BLL of 10 [mu]g/dL did not
define a threshold for the harmful effects of lead. Research
conducted since 1991 has strengthened the evidence that children's
physical and mental development can be affected at BLLS <10 [mu]g/
dL'' (ACCLPP, 2007).
    \72\ Advisory Committee on Childhood Lead Poisoning Prevention
(2007) Interpreting and managing blood lead levels <10 [mu]g/dL in
children and reducing childhood exposures to lead: Recommendations
of CDC's Advisory Committee on Childhood Lead Poisoning Prevention.
Morbidity and Mortality Weekly Report. 56(RR-8). November 2, 2007.
---------------------------------------------------------------------------

    Since 1976, the CDC has been monitoring blood lead levels in
multiple age groups nationally through the National Health and
Nutrition Examination Survey (NHANES).\73\ The

NHANES information has documented the dramatic decline in mean blood
lead levels in the U.S. population that has occurred since the 1970s
and that coincides with regulations regarding leaded motor vehicle
fuels, leaded paint, and lead-containing plumbing materials that have
reduced lead exposure among the general population (AQCD for Lead,
Sections <IP_ADDRESS> and 8.3.3).
---------------------------------------------------------------------------

    \73\ This information documents a variation in mean blood lead
levels across the various age groups monitored. For example, mean
blood lead levels in 2001-2002 for ages 1-5, 6-11, 12-19 and greater
than or equal to 20 years of age, are 1.70, 1.25, 0.94, and 1.56
[mu]g/dL, respectively (AQC for Lead, p. 4-22).
---------------------------------------------------------------------------

    While blood lead levels in the U.S. general population, including
geometric mean levels in children aged 1-5 have declined significantly,
levels have been found to vary among children of different
socioeconomic status (SES) and other demographic characteristics (AQCD
for Lead, p. 4-21), as well as by age.\74\ Racial/ethnic and income
disparities in blood lead levels in children persist. For example,
blood lead levels for lower income and African American children are
higher than those for the general population.
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    \74\ Axelrad, D., U.S. EPA (November 4, 2009) E-mail message to
Marion Hoyer, U.S. EPA. Available in docket number EPA-HQ-OAR-2007-
0294.
---------------------------------------------------------------------------

    The spectrum of health effects discussed in the following section
is relevant for all forms of lead that enter the blood stream. Once in
the blood stream, lead bioaccumulates in the body, with the bone
serving as a large, long-term storage compartment. Soft tissues (e.g.,
kidney, liver, brain, etc.) serve as smaller compartments, in which
lead may be more mobile (AQCD for Lead, Sections <IP_ADDRESS> and 8.3.1).
During childhood development, bone represents approximately 70% of a
child's body burden of lead, and this accumulation continues through
adulthood, when more than 90% of the total lead body burden is stored
in the bone (AQCD for Lead, Section 4.2.2). Lead in bone can be
mobilized during critical periods including pregnancy and lactation
(AQCD for Lead, Section 5.8.6).
2. Health Effects
    Lead, as with mercury and arsenic, has no known biological
function.\75\ Lead has been demonstrated to exert ``a broad array of
deleterious effects on multiple organ systems via widely diverse
mechanisms of action'' (AQCD for Lead, p. 8-24 and Section 8.4.1). This
array of health effects includes effects on heme biosynthesis and
related functions; neurological development and function; reproduction
and physical development; kidney function; cardiovascular function; and
immune function. The weight of evidence varies across this array of
effects and is comprehensively described in the AQCD for Lead. There is
also some evidence of lead carcinogenicity, primarily from animal
studies, together with limited human evidence of suggestive
associations (AQCD for Lead, Sections 5.6.2, 6.7, and 8.4.10). The U.S.
EPA has listed lead under current EPA guidelines as a probable human
carcinogen based on the available animal data (AQCD for Lead, p. 6-
195).\76\ Inorganic lead has been classified as a probable human
carcinogen by the International Agency for Research on Cancer
(inorganic lead compounds), based mainly on sufficient animal
evidence,\77\ and classified as reasonably anticipated to be a human
carcinogen by the U.S. National Toxicology Program (lead and lead
compounds) (AQCD for Lead, Section 6.7.2).78 79
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    \75\ U.S. Environmental Protection Agency (2007) Framework for
Metals Risk Assessment. Office of the Science Advisor. EPA 120/R-07/
001.
    \76\ U.S. Environmental Protection Agency, Integrated Risk
Information System (IRIS) (1993) IRIS Summary for Lead and compounds
(CASRN 7439-92-1), Available online at: http://www.epa.gov/ncea/iris/subst/0277.htm.
    \77\ International Agency for Research on Cancer (IARC) (2006)
Inorganic and organic lead compounds. Lyon, France: International
Agency for Research on Cancer. IARC monographs on the evaluation of
the carcinogenic risk of chemicals to humans: volume 87. Available
online at: http://monographs.iarc.fr/ENG/Monographs/vol87/index.php.
    \78\ National Toxicology Program (2003) Report on carcinogens
background document for lead and lead compounds. Research Triangle
Park, NC: U.S. Department of Health and Human Services. Available
online at: http://ntp.niehs.nih.gov/ntp/newhomeroc/roc11/Lead-Public.pdf.
    \79\ National Toxicology Program. (2004) Lead (CAS no. 7439-92-
1) and lead compounds. In: Report on carcinogens, eleventh edition.
Research Triangle Park, NC: U.S. Department of Health and Human
Services. Available online at: http://ntp.niehs.nih.gov/ntp/roc/eleventh/profiles/s101lead.pdf.
---------------------------------------------------------------------------

    As described in the AQCD for Lead, the key effects associated with
individual blood lead levels in children and adults in the range of 10
[mu]g/dL and lower include neurological, hematological and immune \80\
effects for children, and hematological, cardiovascular and renal
effects for adults (AQCD for Lead, Tables 8-5 and 8-6, pp. 8-60 to 8-
62). As evident from the discussions in Chapters 5, 6 and 8 of the AQCD
for Lead, ``neurotoxic effects in children and cardiovascular effects
in adults are among those best substantiated as occurring at blood lead
concentrations as low as 5 to 10 [mu]g/dL (or possibly lower); and
these categories are currently clearly of greatest public health
concern'' (AQCD for Lead, p. 8-60).81 82 The AQCD for Lead
states, ``There is no level of lead exposure that can yet be
identified, with confidence, as clearly not being associated with some
risk of deleterious health effects'' (AQCD for Lead, p. 8-63).
---------------------------------------------------------------------------

    \80\ At mean blood lead levels, in children, on the order of 10
[mu]g/dL, and somewhat lower, associations have been found with
effects to the immune system, including altered macrophage
activation, increased IgE levels and associated increased risk for
autoimmunity and asthma (AQC for Lead, Sections 5.9, 6.8, and
8.4.6).
    \81\ With regard to blood lead levels in individual children
associated with particular neurological effects, the AQC for Lead
states ``Collectively, the prospective cohort and cross-sectional
studies offer evidence that exposure to lead affects the
intellectual attainment of preschool and school age children at
blood lead levels <10 [mu]g/dL (most clearly in the 5 to 10 [mu]g/dL
range, but, less definitively, possibly lower).'' (p. 6-269)
    \82\ Epidemiological studies have consistently demonstrated
associations between lead exposure and enhanced risk of deleterious
cardiovascular outcomes, including increased blood pressure and
incidence of hypertension. A meta-analysis of numerous studies
estimates that a doubling of blood-lead level (e.g., from 5 to 10
[mu]g/dL) is associated with ~1.0 mm Hg increase in systolic blood
pressure and ~0.6 mm Hg increase in diastolic pressure (AQC for
Lead, p. E-10).
---------------------------------------------------------------------------

    While adults are susceptible to lead effects at lower blood lead
levels than previously understood (e.g., AQCD for Lead, p. 8-25), among
the wide variety of health endpoints associated with lead exposures,
there is general consensus that the developing nervous system in
children is among the, if not the, most sensitive. Blood lead levels in
U.S. children have decreased notably since the late 1970s. Studies
evaluating current blood lead levels in children have reported
associations with neurodevelopment effects (AQCD for Lead, Chapter 6).
Functional manifestations of lead neurotoxicity during childhood
include sensory, motor, cognitive and behavioral impacts. Numerous
epidemiological studies have reported neurocognitive, neurobehavioral,
sensory, and motor function effects in children with blood lead levels
below 10 [mu]g/dL (AQCD Lead, Sections 6.2 and 8.4).
    Cognitive effects associated with lead exposures that have been
observed in epidemiological studies have included decrements in
intelligence test results, such as the widely used IQ score, and in
academic achievement as assessed by various standardized tests as well
as by class ranking and graduation rates (AQCD for Lead, Section 6.2.16
and pp 8-29 to 8-30). As noted in the AQCD for Lead with regard to the
latter, ``Associations between lead exposure and academic achievement
observed in the above-noted studies were significant even after
adjusting for IQ, suggesting that lead-sensitive neuropsychological
processing and learning factors not

reflected by global intelligence indices might contribute to reduced
performance on academic tasks'' (AQCD for Lead, pp 8-29 to 8-30).
    With regard to potential implications of lead effects on IQ, the
AQCD for Lead recognizes the ``critical'' distinction between
population and individual risk, identifying issues regarding declines
in IQ for an individual and for the population. The AQCD for Lead
further states that a ``point estimate indicating a modest mean change
on a health index at the individual level can have substantial
implications at the population level'' (AQCD for Lead, p. 8-77).\83\ A
downward shift in the mean IQ value is associated with both substantial
decreases in percentages achieving very high scores and substantial
increases in the percentage of individuals achieving very low scores
(AQCD for Lead, p. 8-81).\84\ For an individual functioning in the low
IQ range due to the influence of developmental risk factors other than
lead, a lead-associated IQ decline of several points might be
sufficient to drop that individual into the range associated with
increased risk of educational, vocational, and social failure (AQCD for
Lead, p. 8-77).
---------------------------------------------------------------------------

    \83\ As an example, the AQC for Lead states ``although an
increase of a few mmHg in blood pressure might not be of concern for
an individual's well-being, the same increase in the population mean
might be associated with substantial increases in the percentages of
individuals with values that are sufficiently extreme that they
exceed the criteria used to diagnose hypertension'' (AQC for Lead,
p. 8-77).
    \84\ For example, for a population mean IQ of 100 (and standard
deviation of 15), 2.3% of the population would score above 130, but
a shift of the population to a mean of 95 results in only 0.99% of
the population scoring above 130 (AQC for Lead, pp. 8-81 to 8-82).
---------------------------------------------------------------------------

    Other cognitive effects observed in studies of children have
included decrements in attention, executive functions, language,
memory, learning and visuospatial processing (AQCD for Lead, Sections
5.3.5, 6.2.5 and <IP_ADDRESS>), with attention and executive function
effects associated with lead exposures indexed by blood lead levels
below 10 [mu]g/dL (AQCD for Lead, Section 6.2.5 and pp. 8-30 to 8-31).
The evidence for the role of lead in this suite of effects includes
experimental animal findings (discussed in the AQCD for Lead, Section
<IP_ADDRESS>; p. 8-31), which provide strong biological plausibility of lead
effects on learning ability, memory and attention (AQCD for Lead,
Section 5.3.5), as well as associated mechanistic findings.
    The persistence of such lead-induced effects is described in the
AQCD for Lead (e.g., AQCD for Lead Sections 5.3.5, 6.2.11, and 8.5.2).
The persistence or irreversibility of such effects can be the result of
damage occurring without adequate repair offsets or of the persistence
of lead in the body (AQCD for Lead, Section 8.5.2). It is additionally
important to note that there may be long-term consequences of such
deficits over a lifetime. Poor academic skills and achievement can have
``enduring and important effects on objective parameters of success in
real life,'' as well as increased risk of antisocial and delinquent
behavior (AQCD for Lead, Section 6.2.16).
    The current evidence reviewed in the AQCD for Lead with regard to
the quantitative relationship between neurocognitive decrement, such as
IQ, and blood lead levels indicates that the slope for lead effects on
IQ is nonlinear and is steeper at lower blood lead levels, such that
each [mu]g/dL increase in blood lead may have a greater effect on IQ at
lower blood lead levels (e.g., below 10 [mu]g/dL) than at higher levels
(AQCD for Lead, Section 6.2.13; pp. 8-63 to 8-64; Figure 8-7). As noted
in the AQCD for Lead, a number of examples of non- or supralinear dose-
response relationships exist in toxicology (AQCD for Lead, pp. 6-76 and
8-38 to 8-39). With regard to the effects of lead on neurodevelopmental
outcomes such as IQ, the AQCD for Lead suggests that initial
neurodevelopmental effects at lower lead levels may be disrupting very
different biological mechanisms (e.g., early developmental processes in
the central nervous system) than more severe effects of high exposures
that result in symptomatic lead poisoning and frank mental retardation
(AQCD for Lead, p. 6-76). The AQCD for Lead describes this issue in
detail with regard to lead (summarized in AQCD for Lead at p. 8-39).
Various findings within the toxicological evidence, presented in the
AQCD for Lead, provide biologic plausibility for a steeper IQ loss at
low blood lead levels, with a potential explanation being that the
predominant mechanism at very low blood lead levels is rapidly
saturated and that a different, less-rapidly-saturated process becomes
predominant at blood lead levels greater than 10 [mu]g/dL.
3. At-Risk Populations and Life Stages
    Individuals potentially at risk from exposure to environmental
pollutants include those with increased susceptibility and
vulnerability. The terms ``susceptibility'' and ``vulnerability'' have
been used to characterize those with a greater likelihood of an adverse
outcome given a specific exposure in comparison with the general
population. This increased likelihood of response to a pollutant can
result from a multitude of factors, including genetic or developmental
factors, life stages (i.e., childhood or old age), gender differences,
or preexisting disease states. In addition, new attention has been paid
to the concept of some population groups having increased responses to
pollution-related effects due to factors including socioeconomic status
(SES) (e.g., reduced access to health care, poor nutritional status) or
particularly elevated exposure levels.
    EPA uses the term ``life stage'' to refer 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. To recognize the rapid changes
that occur during childhood related to physiology, metabolism, anatomy
and behavior that can impact exposure and risk to environmental
hazards, EPA now views childhood as a sequence of life stages, from
conception through fetal development, infancy, and adolescence. EPA
published several exposure and risk assessment guidance documents
beginning in 2005,85 86 87 in which we emphasized the
importance of considering the potential for increased sensitivity of
different life stages or age groups in addition to that of groups that
form a fixed portion of the population based on characteristics such as
pre-existing disease, gender, socioeconomic status, geographical
location, culture/ethnicity, or genetic make-up.
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    \85\ U.S. EPA (2005) Guidance on Selecting Age Groups for
Monitoring and Assessing Childhood Exposure to Environmental
Contaminants. EPA/630/P-03/003F.
    \86\ U.S. EPA (2006) A Framework for Assessing Health Risks of
Environmental Exposures to Children. EPA/600/R-05/093A.
    \87\ U.S. EPA (2008) Child-Specific Exposure Factors Handbook.
EPA/600/R-06/096F.
---------------------------------------------------------------------------

    Physiological, behavioral and demographic factors contribute to
increased risk of lead-related health effects. Children are at
increased risk of lead-related health effects due to various factors
that enhance their exposures (e.g., via the hand-to-mouth activity that
is prevalent in very young children, AQCD for Lead, Section 4.4.3) and
susceptibility. While children are considered to be at a period of
maximum exposure around 18-27 months, the current evidence has found
even stronger associations between blood lead levels at school age and
IQ at school age. The evidence ``supports the idea that lead exposure
continues to be toxic to children as they reach school age, and [does]
not lend support to the interpretation that all the damage is done by
the time the child reaches 2 to

3 years of age'' (AQCD for Lead, Section 6.2.12). Physiological factors
that can affect risk of lead-related effects in children include
genetic polymorphisms and nutritional status. Children with particular
genetic polymorphisms (e.g., presence of the [delta]-aminolevulinic
acid dehydratase-2 [ALAD-2] allele) have increased sensitivity to lead
toxicity, which may be due to increased susceptibility to the same
internal dose and/or to increased internal dose associated with the
same exposure (AQCD for Lead, p. 8-71, Sections 6.3.5, <IP_ADDRESS> and
6.3.6). Some children may have blood lead levels higher than those
otherwise associated with a given lead exposure (AQCD for Lead, Section
8.5.3) as a result of nutritional status (e.g., iron deficiency,
calcium intake), as well as genetic and other factors (AQCD for Lead,
Chapter 4 and Sections 3.4, 5.3.7 and 8.5.3).
    Demographic factors that can affect risk of lead-related effects in
children include residential location, poverty, and race. As noted in
previous EPA actions on lead, situations of elevated exposure, such as
residing near sources of ambient lead, as well as socioeconomic
factors, such as reduced access to health care or low socioeconomic
status can also contribute to increased blood lead levels and increased
risk of associated health effects from air-related lead.\88\
Additionally, as described in the NAAQS for Lead, children in poverty
and black, non-Hispanic children have notably higher blood lead levels
than do economically well-off children and white children, in
general.\89\
---------------------------------------------------------------------------

    \88\ U.S. Environmental Protection Agency (2007) Review of the
National Ambient Air Quality Standards for Lead: Policy Assessment
of Scientific and Technical Information, OAQPS Staff Paper. EPA-452/
R-07-013. Office of Air Quality Planning and Standards, Research
Triangle Park.
    \89\ See 73 FR 66973 (November 12, 2008).
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C. Welfare Effects

    Lead is persistent in the environment and accumulates in soils,
aquatic systems (including sediments), and some biological tissues of
plants, animals and other organisms, thereby providing long-term,
multi-pathway exposures to organisms and ecosystems. In 2008, EPA
established a secondary lead standard of 0.15 ug/m\3\. This standard is
intended to protect the public welfare from known or anticipated
adverse effects associated with the presence of lead in the ambient
air. This section provides a summary of information regarding welfare
effects of lead, focusing on terrestrial and aquatic ecosystems. This
information is largely drawn from the 2006 AQCD for Lead, Chapter 6 of
the Office of Air Quality Planning and Standards Staff Paper on Lead
(SP) \90\ and the Lead NAAQS.
---------------------------------------------------------------------------

    \90\ U.S. Environmental Protection Agency (2007) Review of the
National Ambient Air Quality Standards for Lead: Policy Assessment
of Scientific and Technical Information, OAQPS Staff Paper. EPA-452/
R-07-013. Office of Air Quality Planning and Standards, Research
Triangle Park.
---------------------------------------------------------------------------

1. Terrestrial Ecosystems
    Lead is removed from the atmosphere and deposited on soil and other
surfaces via wet or dry deposition. In soils, most lead is retained via
the formation of stable solid phase compounds, precipitates, or
complexes with organic matter. Thus, terrestrial ecosystems remain
primarily sinks for lead but amounts retained in various soil layers
vary based on forest type, climate, and litter cycling (AQCD for Lead,
Section 7.1). Once in the soil, the migration and distribution of lead
is controlled by a multitude of factors including pH, precipitation,
litter composition and other factors, which in turn, govern the rate at
which lead is bound to organic materials in the soil (AQCD for Lead,
Section 2.3.5, and Section AX <IP_ADDRESS>).
    Lead exists in the environment in different forms which vary widely
in their ability to cause adverse effects on ecosystems and organisms.
Many forms of lead in the ambient air are quite insoluble and thus not
easily leached to underground water once deposited to surfaces.
However, leaching may occur under acidic conditions, where lead
concentrations are extremely high, or in the presence of substances
(e.g., soluble organic matter, high concentrations of chlorides or
sulfates) that form relatively soluble complexes with lead (AQCD for
Lead, Section 2.3.5).
    Plants take up lead via their foliage and through their root
systems. The rate of plant uptake from soil varies by plant species,
soil conditions, and lead species. Most lead in plants is stored in
roots, and very little is stored in fruits. Metals that are applied to
soil as salts (usually as sulfate, chloride, or nitrate salt) are
accumulated more readily than the same quantity of metal added via
sewage sludge, flue dust, or fly ash (AQCD for Lead, Section 2.3.7).
    Surface deposition of lead onto plants may represent a significant
contribution to the total lead in and on the plant, as has been
observed for plants near smelters and along roadsides (AQCD for Lead,
page E-19). Atmospheric deposition of lead also contributes to lead in
vegetation as a result of contact with above-ground portions of the
plant (AQCD for Lead, pp. 7-9 and AXZ7-39; USEPA, 1986, Sections 6.5.3
and <IP_ADDRESS>.1). Wildlife may subsequently be exposed to lead in
vegetation (e.g., grasses and silage) and in surface soils via
incidental ingestion of soil while grazing (USEPA 1986, Section
<IP_ADDRESS>.2).\91\
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    \91\ U.S. Environmental Protection Agency (1986) Air quality
Criteria for Lead. Research Triangle Park, NC: Office of Health and
Environmental Assessment, Environmental Criteria and Assessment
Office; EPA report no. EPA-600/8-83/028aF-dF. 4v. Available from:
NTIS, Springfield, VA; PB87-142378.
---------------------------------------------------------------------------

    By far, the majority of air-related lead found in natural
terrestrial ecosystems was deposited in the past during the use of lead
additives in motor vehicle gasoline. Many sites receiving lead
predominantly through long-range transport of gasoline-derived small
particles have accumulated large amounts of lead in soils (AQCD for
Lead, p. AX7-98). There is little evidence that terrestrial sites
exposed as a result of this long range transport of lead have
experienced significant effects on ecosystem structure or function
(AQCD for Lead, Section AX<IP_ADDRESS> and p. AX7-98). Strong complexation
of lead by organic matter in soil may explain why few ecological
effects have been observed (AQCD for Lead, p. AX7-98). Studies have
shown decreasing levels of lead in vegetation, which appears to
correlate with decreases in atmospheric deposition of lead resulting
from the removal of lead additives to motor vehicle gasoline (AQCD for
Lead, Section AX <IP_ADDRESS>).
    The deposition of gasoline-derived lead into forest soils has
produced a legacy of slow moving lead that remains bound to organic
materials despite dramatic reductions in the use of leaded additives to
motor vehicle fuels. Current levels of lead in soil vary widely
depending on the source of lead but in all ecosystems lead
concentrations exceed natural background levels. For areas influenced
by point sources of air lead, concentrations of lead in soil may exceed
by many orders of magnitude the concentrations which are considered
harmful to laboratory organisms. Adverse effects in terrestrial
organisms associated with lead include neurological, physiological and
behavioral effects which may influence ecosystem structure and
functioning (73 FR 67008).
2. Aquatic Ecosystems
    Atmospheric lead enters aquatic ecosystems primarily through
deposition (wet and dry) and the erosion and runoff of soils containing
lead. While overall deposition rates of atmospheric lead have decreased
dramatically since the removal of lead additives from motor vehicle
gasoline,

lead continues to accumulate and may be re-exposed in sediments and
water bodies throughout the United States (AQCD for Lead, Section
2.3.6).
    Several physical and chemical factors govern the fate and
bioavailability of lead in aquatic systems. A significant portion of
lead remains bound to suspended particulate matter in the water column
and eventually settles into the substrate. Species, pH, salinity,
temperature, turbulence and other factors govern the bioavailability of
lead in surface waters (AQCD for Lead, Section 7.2.2). Lead can
bioaccumulate in the tissues of aquatic organisms through ingestion of
food and water, and adsorption from water, and can subsequently lead to
adverse effects if tissue levels are sufficiently high.\92\ The
accumulation of lead is influenced by pH and decreasing pH favors
bioavailability and bioaccumulation. Organisms that bioaccumulate lead
with little excretion must partition the metal such that it has limited
bioavailability, otherwise toxicity will occur if a sufficiently high
concentration is reached.\93\ The general symptoms of lead toxicity in
fish include production of excess mucus, lordosis, anemia, darkening of
the dorsal tail region, degeneration of the caudal fin, destruction of
spinal neurons, aminolevulinic acid dehydratase (ALAD) inhibition,
growth inhibition, renal pathology, reproductive effects, growth
inhibition, and mortality.\94\ Toxicity in fish has been closely
correlated with duration of lead exposure and uptake.\95\
---------------------------------------------------------------------------

    \92\ AQC for Lead I. 7-24: (Vink, 2002; Rainbow, 1996).
    \93\ AQC for Lead AX<IP_ADDRESS>.
    \94\ AQC for Lead page 232, Annex 7.
    \95\ AQC for Lead page 232, Annex 7.
---------------------------------------------------------------------------

    Lead exists in the aquatic environment in various forms and under
various chemical and physical parameters which determine the ability of
lead to cause adverse effects either from dissolved lead in the water
column or lead in sediment. Current levels of lead in water and
sediment vary widely depending on the source of lead. Conditions exist
in which adverse effects to organisms and thereby ecosystems may be
anticipated given experimental results. It is unlikely that dissolved
lead in surface water constitutes a threat to ecosystems that are not
directly influenced by point sources. For lead in sediment, the
evidence regarding the effects is less clear. It is likely that some
areas with long-term historical deposition of lead to sediment from a
variety of sources as well as areas influenced by point sources have
the potential for adverse effects to aquatic communities. The long
residence time of lead in sediment and its ability to be resuspended by
turbulence make lead likely to be a factor for consideration regarding
potential risk to aquatic systems for the foreseeable future (73 FR
67008).

III. Lead Emissions From Piston-Engine Aircraft

    Currently, lead emitted by piston-engine aircraft operating on
leaded avgas is the largest source of lead to the air, contributing
about 50% of the National Emission Inventory in 2005. This section
describes the draft 2008 avgas lead inventory which is currently
undergoing review by State, local and Tribal air agencies. We describe
and request comment on input data used to derive airport-specific lead
inventories. This section ends with a summary of data forecasting the
potential growth of the industry using leaded avgas.

A. Inventory of Lead From Piston-Engine Powered Aircraft

    Every three years, the EPA prepares a National Emissions Inventory
(NEI) of air emissions of criteria pollutants and hazardous air
pollutants with input from numerous State, local, and Tribal air
agencies and from industry.\96\ For the purposes of this ANPR, EPA is
describing piston-engine aircraft lead information provided in the
draft 2008 NEI as well as information from the final 2005 NEI. We have
chosen to describe the draft 2008 NEI for the following reasons: (1)
This is the first version of the NEI that will include airport-specific
lead inventories that use our most recently developed methods for
estimating lead (described below); (2) this inventory is the first NEI
to include approximately 20,000 airport facilities in the U.S.; and (3)
to increase awareness of the opportunity for State, local, and Tribal
governments and industry to review this draft NEI and provide
information that could improve airport lead inventories. Comments and
data can be supplied to EPA for the 2008 NEI until mid-2010. While we
are describing the draft 2008 NEI for piston-engine aircraft emissions
of lead, we do not have draft inventory estimates for 2008 for all
sources of lead. The 2008 NEI will be final in 2010.
---------------------------------------------------------------------------

    \96\ http://www.epa.gov/air/data/neidb.html.
---------------------------------------------------------------------------

1. National Emissions of Lead From Piston-Engine Aircraft
    To calculate the national avgas lead inventory, the volume of
leaded avgas produced in a given year is multiplied by the
concentration of lead in the avgas and by the fraction of lead emitted
from a combustion system operating on leaded fuel (to account for the
lead that is retained in the engine, engine oil and/or exhaust system).
For example, the volume of avgas produced in the U.S. in 2008 according
to DOE was 235,326,000 gallons.\97\ The concentration of lead in avgas
([Pb] in the equation below) can be one of four levels (ranging from
0.14 to 1.12 grams of lead per liter or 0.53 to 4.24 grams of lead per
gallon) as specified by the American Society for Testing and Materials
(ASTM). By far the most common avgas supplied is ``100 Low Lead'' or
100LL which has a maximum lead concentration specified by ASTM of 0.56
grams per liter or 2.12 grams per gallon.98 99 A fraction of
lead is retained in the engine, engine oil and/or exhaust system which
we currently estimate at 5%.\100\
---------------------------------------------------------------------------

    \97\ DOE Energy Information Administration. Fuel production
volume data obtained from http://tonto.eia.doe.gov/dnav/pet/hist/mgaupus1A.htm accessed November 2006.
    \98\ ChevronTexaco (2006) Aviation Fuels Technical Review. FTR-
3. Available online at: http://www.chevronglobalaviation.com/docs/aviation_tech_review.pdf.
    \99\ ASTM International (2007) Standard Specification for
Aviation Gasolines D910-06.
    \100\ U.S. Environmental Protection Agency (2008) Lead Emissions
from the Use of Leaded Aviation Gasoline in the United States,
Technical Support Document. EPA420-R-08-020. Available online at:
http://www.epa.gov/otaq/aviation.htm.
---------------------------------------------------------------------------

    For 2008, using DOE fuel volume estimates, the national estimate of
lead emissions from the consumption of avgas is 522 tons as calculated
according to the following equation:
[GRAPHIC] [TIFF OMITTED] TP28AP10.015

    As described in the Overview section of this ANPR, DOT's FAA also
provides estimates of annual avgas fuel consumption. For 2008, DOT
estimates 351,000,000 gallons of avgas were consumed. Consumption of
this volume of avgas equates to a national lead emissions estimate for
this source of 779 short tons. DOT fuel volume data are derived from
FAA estimates of piston-engine activity annually.\101\ We are working
to identify the source(s) of the information used to derive DOE fuel
volume estimates. In the draft 2008 NEI, we are using DOT fuel volume
estimates.
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    \101\ U.S. Department of Transportation Federal Aviation
Administration Aviation Policy and Plans. FAA Aerospace Forecast
Fiscal Years 2009-2025. p.81. Available at: http://www.faa.gov/data_research/aviation/aerospace_forecasts/2009-2025/media/2009%20Forecast%20Doc.pdf. This document provides historical data
for 2000-2008 as well as forecast data.
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    We currently cannot estimate the fraction of total lead emissions
these estimates comprise since the inventories for all other sources of
lead to air are not yet in the draft 2008 NEI. In 2005, lead from avgas
comprised about 50% of the national lead inventory for emissions to
air. As point source emissions of lead have decreased, lead emissions
from piston-engine aircraft have become the largest single source of
lead to air (Figure 2). These lead emissions estimates do not include
evaporative losses of lead and minimal military aircraft data. Few
military aircraft are piston-engine powered and consume leaded
avgas.\102\ Military aircraft data are supplied by States, and data
provided to EPA during the 2008 NEI review will be included in the
final 2008 inventory.
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    \102\ ChevronTexaco (2006) Aviation Fuels Technical Review p.
44. Available online at: http://www.chevronglobalaviation.com/docs/aviation_tech_review.pdf.
[GRAPHIC] [TIFF OMITTED] TP28AP10.016

2. Airport-Specific Emissions of Lead From Piston-Engine Aircraft
    Aircraft gaseous and particulate matter (PM) emissions are
calculated through the FAA's Emissions and Dispersion Modeling System
(EDMS).\103\ This modeling system was designed to develop emission
inventories for the purpose of assessing potential air quality impacts
of airport operations and proposed airport development projects. Lead
emissions from piston-engine aircraft are not included in EDMS. To
estimate airport-specific lead inventories we use engine data and other
attributes of general aviation (GA) and air taxi (AT) that are used in
EDMS for GA and AT and we use methods similar to those in EDMS that are
described in an EPA Technical Support Document (TSD) and briefly

summarized here.\104\ The data required to estimate airport-specific
lead inventories includes the landing and take-off (LTO) activity of
piston-engine aircraft at a facility; fuel consumption rates by these
aircraft during the various modes of the landing and take-off cycle;
the time spent in each mode of the LTO (taxi/idle-out, takeoff, climb-
out, approach, and taxi/idle-in); the concentration of lead in the
fuel; and the retention of lead in the engine and oil. The equation
used to calculate airport-specific lead emissions during the LTO cycle
is below, followed by a description of each of the input parameters.
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    \103\ EDMS is available online at: http://www.faa.gov/about/office_org/headquarters_offices/aep/models/edms_model/.
    \104\ U.S. Environmental Protection Agency (2008) Lead Emissions
from the Use of Leaded Aviation Gasoline in the United States,
Technical Support Document. EPA420-R-08-020. Available online at:
http://www.epa.gov/otaq/aviation.htm.
[GRAPHIC] [TIFF OMITTED] TP28AP10.017

    Piston-engine LTO: Most piston-engine aircraft fall into the
categories of either GA or AT. Some GA and AT activity is conducted by
turboprop and turbojet aircraft which do not use leaded avgas. There
are no national databases that provide airport-specific LTO activity
data for piston-engine aircraft separately from turbojet and turboprop
aircraft. The fraction of GA and AT aircraft that use piston engines
will vary by airport. However, in the absence of airport-specific data,
EPA calculated a national default estimate using FAA's GA and AT
Activity (GAATA) Survey.\105\ The 2005 GAATA Survey reports that
approximately 72% of all GA and AT LTOs are from piston-engine aircraft
which use avgas, and about 28% are turboprop and turbojet powered which
use jet fuel, such as Jet A.\106\ Lead is not added to jet fuel.
Therefore, to calculate piston-engine aircraft LTO as input for this
equation, the total GA plus AT LTOs are multiplied by 0.72.
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    \105\ The FAA GAATA is a database collected from surveys of
pilots flying aircraft used for general aviation and air taxi
activity. For more information on the GAATA, see Appendix A, online
at: http://www.faa.gov/data_statistics/aviation_data_statistics/general_aviation/.
    \106\ There are about 194,000 piston-engine aircraft in the U.S.
general aviation and air taxi fleet (175,000 single-engine and
19,000 twin-engine aircraft) according to FAA's 2005 GAATA Survey.
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    Avgas use (gal/LTO): Piston-engine aircraft can have either one or
two engines. EDMS version 5.0.2 contains information on the amount of
avgas used per LTO for some single and twin-engine aircraft. The
proportion of piston-engine LTOs conducted by single- versus twin-
engine aircraft was taken from the FAA's GAATA Survey for 2005 (90% of
LTOs are conducted by aircraft having one engine and 10% of LTOs by
aircraft having two engines). Since twin-engine aircraft have higher
fuel consumption rates than those with single engines, a weighted
average LTO fuel usage rate was established to apply to the population
of piston-engine aircraft as a whole. For the single-engine aircraft,
the average amount of fuel consumed per LTO was determined from the six
types of single piston-engine aircraft within EDMS.\107\ This was
accomplished by averaging the single-engine EDMS outputs for fuel
consumed per LTO using the EDMS scenario property of ICAO/USEPA
Default--Times in Mode (TIM), with a 16 minute taxi-in/taxi-out time
according to EPA's Procedures for Emission Inventory Preparation,
Volume IV: Mobile Sources, 1992.\108\ This gives a value of 16.96
pounds of fuel per LTO (lbs/LTO). Next, the average single-engine
consumption rate was divided by the average density of 100LL avgas, 6
pounds per gallon (lbs/gal), producing an average fuel usage for
single-engine piston aircraft of 2.83 gallons per LTO (gal/LTO). This
same calculation was performed for the two twin-engine piston aircraft
within EDMS, producing an average LTO fuel usage rate for twin-engine
piston aircraft of 9.12 gal/LTO.
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    \107\ EPA understands that EDMS 5.0.2 has a limited list of
piston engines, but these are currently the best data available.
    \108\ U.S. Environmental Protection Agency (1992) Procedures for
Emission Inventory Preparation, Volume IV: Mobile Sources, EPA-450/
4-81-026d (Revised).
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    Using these single- and twin-engine piston aircraft fuel
consumption rates, a weighted average fuel usage rate per LTO was
computed by multiplying the average fuel usage rate for single-engine
aircraft (2.83 gal/LTO) by the fleet percentage of single-engine
aircraft LTOs (90%). Next, the twin-engine piston aircraft average fuel
usage rate (9.12 gal/LTO) was multiplied by the fleet percentage of
twin-engine aircraft LTOs (10%). By summing the results of the single-
and twin-engine aircraft usage rates, the overall weighted average fuel
usage rate per LTO of 3.46 gal/LTO is obtained.
    Concentration of lead in fuel, [Pb]: The maximum lead concentration
specified by ASTM for 100LL is 0.56 grams per liter or 2.12 grams per
gallon. This amount of lead is normally added to assure that the
required lean and rich mixture knock values are achieved. As noted
above, 100 Octane (containing 1.12 grams of lead per liter or 4.24
grams of lead per gallon) is used by a small number of piston-engine
aircraft. We currently do not include estimates of lead emissions using
100 Octane and we are requesting comment on the airport facilities
where 100 Octane is used and the LTO activity associated with the use
of this fuel.
    Retention of lead in engine and oil (1-Pb Retention): Recent data
collected from aircraft piston engines operating on leaded avgas
suggests that about 5% of the lead from the fuel is retained in the
engine and engine oil.\109\ Thus the emitted fraction is 0.95.
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    \109\ The information used to develop this estimate is from the
following references: (a) Todd L. Petersen, Petersen Aviation, Inc,
Aviation Oil Lead Content Analysis, Report Number EPA 1-2008,
January 2, 2008, available at William J. Hughes Technical Center
Technical Reference and Research Library at http://actlibrary.tc.faa.gov/ and (b) E-mail from Theo Rindlisbacher of
Switzerland Federal Office of Civil Aviation to Bryan Manning of
U.S. EPA, regarding lead retained in engine, September 28, 2007.
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    Multiplying the lead concentration in 100LL avgas by the weighted
average fuel usage rate produces an overall average value of 7.34 grams
of lead per LTO (g Pb/LTO) for piston engines: 3.46 gal/LTO x 2.12 g
Pb/gal = 7.34 g Pb/LTO. The denominator is a unit conversion factor
used to express the lead inventory in units of short tons.
    Applying these parameters in the equation above yields the
following equation:

[GRAPHIC] [TIFF OMITTED] TP28AP10.018

which simplifies to: Pb = (piston-engine LTO) (7.7 x 10-6
short tons) or 7 grams of lead per LTO where piston-engine LTO = (GA
LTO + AT LTO)(0.72). EPA used similar methods to estimate lead
emissions from piston-engine powered helicopters which are described
separately.\110\ We currently estimate there are 6 grams of lead
emitted by piston-engine helicopters per LTO.
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    \110\ U.S. EPA (March 2010) Memorandum from Meredith Pedde to
docket EPA-HQ-OAR-2007-0294, titled, ``Calculating Aviation Gasoline
Lead Emissions in the 2008 NEI.'' pp.8-9.
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    Lead emitted during the LTO cycle is assigned to the airport
facility where the aircraft operations occur.\111\ FAA's Office of Air
Traffic provides a complete listing of operational airport facilities
in the National Airspace System Resources (NASR) database.\112\ In
2008, there were 19,896 airport facilities in the U.S., the vast
majority of which are expected to have activity by piston-engine
aircraft that operate on leaded avgas. There are seven types of airport
facilities: airports, balloonports, seaplane bases, gliderports,
heliports, stolports,\113\ and ultralight facilities. Among these,
balloonports are the only facilities not expected to have piston-engine
aircraft activity.
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    \111\ An aircraft operation is defined as any landing or take-
off event, therefore, to calculate LTOs, operations are divided by
two. Most data sources from FAA report aircraft activity in numbers
of operations which, for the purposes of calculating lead emissions
using the method described in the TSD, need to be converted to LTO
events.
    \112\ An electronic report can be generated from the NASR
database and is available for download from the Internet at the
following Web site. http://www.faa.gov/airports_airtraffic/airports/airport_safety/airportdata_5010/. This database is
updated every 56 days.
    \113\ Stolport is an airport designed with STOL (Short Take-Off
and Landing) operations in mind, normally having a short single
runway.
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    Preparing airport-specific lead inventories requires information
regarding LTO activity.
    These activity data are reported to the FAA for only a small subset
of the approximately 20,000 facilities in the U.S. EPA obtains LTO
information for approximately 3,400 facilities from FAA's Terminal Area
Forecast (TAF) database that is prepared by FAA's Office of Aviation
Policy and Plans.\114\ The TAF database currently includes information
for airports in FAA's National Plan of Integrated Airport Systems
(NPIAS), which identifies airports that are significant to national air
transportation. For airports not listed in the TAF, operations data are
obtained from the NASR database, where available. Operations data
provided by the NASR database may be self-reported by airport operators
through data collection accomplished by airport inspectors who work for
the State Aviation Agency, or operations data can be obtained through
other means.\115\
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    \114\ http://aspm.faa.gov/main/taf.asp.
    \115\ In the absence of updated information from States, local
authorities or Tribes, we are using the LTO data provided in the FAA
database.
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    We are using the January 15, 2009 version of the NASR database to
evaluate airport lead emissions inventories for 2008. Using the TAF
database as the primary source of LTO information and the NASR as a
secondary source, we have LTO activity data for approximately 5,600
airport facilities. There are approximately 14,000 facilities in the
NASR database for which there are no LTO activity data.\116\ We
developed methods based on previous work conducted by the FAA to
estimate LTO activity at the remaining airport and heliport facilities.
We are requesting comment on these methods which are described here
briefly. The details regarding the method described here are available
in the docket.\117\
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    \116\ No Commuter, GA Itinerant, GA Local, or Air Taxi
operations data.
    \117\ U.S. EPA (March 2010) Memorandum from Meredith Pedde to
docket EPA-HQ-OAR-2007-0294, titled, ``Calculating Aviation Gasoline
Lead Emissions in the 2008 NEI.''
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    The FAA has used regression models to estimate operations at
facilities where operations data are not available.118 119
In this work and other work, FAA identified characteristics of small
towered airports for which there were statistically significant
relationships with operations at these airports.\120\ Regression models
based on the airport characteristics were then used to estimate general
aviation operations for a set of non-towered airports. The airport
characteristics identified by the FAA and used to estimate general
aviation operations at small airports include: the number and type of
aircraft based at the facility (i.e., ``based aircraft''), population
in the vicinity of the airport, airport regional prominence, per capita
income, region of the country, and the presence of certificated flight
schools. We were able to obtain data from the NASR and the U.S. Census
Bureau to evaluate relationships between several airport
characteristics and LTO activity. LTO estimates were derived using
different models depending on data availability.
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    \118\ Federal Aviation Administration, Office of Aviation Policy
and Plans, Statistics and Forecast Branch. (July 2001) Model for
Estimating General Aviation Operations at Non-Towered Airports Using
Towered and Non-towered Airport Data. Prepared by GRA, Inc.
    \119\ Hoekstra, M. (April 2000) Model for Estimating General
Aviation Operations at Non-Towered Airports. Prepared for FAA Office
of Aviation Policy and Plans.
    \120\ GRA, Inc. ``Review of TAF Methods,'' Final Report,
prepared for FAA Office of Aviation Policy and Plans under Work
Order 45, Contract No. DTFA01-93-C-00066, February 25, 1998.
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    The number of based aircraft and county population in which the
airport is located were the most highly significant and positive
regressors to LTO activity that our analysis provided.\121\ The
regression equation for based aircraft and county population is: LTOs =
1248 + 203.04*Aircraft + 0.0019*County Population with an R\2\ = 0.64.
For approximately 7,800 facilities that do not report LTO activity to
FAA, we used based aircraft and county population to estimate activity.
We request comment on the method we are using to estimate LTO activity
at these airport facilities.
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    \121\ U.S. EPA (March 2010) Memorandum from Meredith Pedde to
docket EPA-HQ-OAR-2007-0294, titled, ``Calculating Aviation Gasoline
Lead Emissions in the 2008 NEI.''
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    To estimate LTO activity at the airport facilities that do not
report based aircraft, we used a regression equation based on county
population and region of the country. The regression equation using
county population and regression of the country is: LTOs = 6200.2 +
0.0087*county population--175.07*West State - 5567.3*Alaska +
854.83*Northeast with an R\2\ = 0.15. This equation has a low
correlation coefficient and we are exploring additional options for
estimating LTO activity at these facilities for which very little
information is reported to the FAA. We request comment on applying the
regression equation above and alternative methods to estimate LTO
activity at these facilities.
    For heliports, which comprise approximately 5,500 facilities in the
NASR database, we had insufficient information on which to develop a
regression equation and are currently using the median of activity (141
LTOs/year) at heliports for which we have LTO activity data.
Nationally, 25% of helicopters are piston-engine powered and therefore
use leaded avgas. The FAA and EPA have limited information

regarding the specific heliports that have activity by piston-engine
helicopters. We are requesting information regarding heliport
facilities at which piston-engine powered aircraft operate and the
activity of these aircraft.
    The draft 2008 NEI is the first inventory for which we are
implementing the use of LTO-based lead estimates at almost 20,000
airport facilities and we are expecting State, local and Tribal air
agency review of these data to improve our current estimates. The
specific information on which we are requesting data include: (1) The
fraction of GA and AT LTO activity reported to FAA that is conducted by
piston-engine versus jet-engine powered aircraft, (2) airport-specific
LTO activity for single- versus twin-engine piston-powered aircraft,
(3) fuel consumption rates for the piston-engine aircraft operating at
each airport, (4) the time spent in each mode of operation including
run-up checks conducted by piston-engine aircraft prior to take-off,
and (5) the concentration of lead in fuel delivered to individual
airports. Methods for providing information to EPA as part of the
review process involved in finalizing the 2008 NEI are available.\122\
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    \122\ All documentation for use in preparing 2008 emission
inventories can be found on the NEI/EIS Implementation Web site:
http://www.epa.gov/ttn/chief/net/neip/index.html.
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    The discussion above pertains only to lead emissions during the LTO
cycle. Lead emitted outside the LTO cycle occurs during aircraft cruise
mode and portions of the climb-out and approach modes. This part of an
aircraft operation emits lead at various altitudes as well as close to
and away from airports. We are developing methods to estimate lead
emissions outside the LTO cycle which we anticipate will be available
in 2010.

B. Projections for Future Growth

    The FAA publishes an annual forecast of the number of piston-engine
powered aircraft, hours flown, the consumption of avgas, the numbers of
pilots and student pilots.\123\ The most recent forecast is for the
years 2009 through 2025. The General Aviation Manufacturers Association
(GAMA) reproduces the FAA forecast in their annual statistical
databook.\124\ According to the GAMA summary, the number of active
single-engine piston-powered aircraft is projected to increase annually
at a 0.5% growth rate, with the aircraft population increasing from
144,220 in 2008 to 157,400 in 2025. The number of active twin-engine
piston-powered aircraft is projected to decrease 0.9% annually, with
aircraft population decreasing from 18,385 in 2008 to 15,650 in 2025.
The piston-powered helicopter population is expected to grow 4.7%
annually from a population of 3,970 in 2008 to 8,295 in 2025.
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    \123\ FAA Aerospace Forecast Fiscal Years 2009-2025. Available
online at: http://www.faa.gov/data_research/aviation.
    \124\ General Aviation Manufacturers Association (2008) General
Aviation Statistical Databook and Industry Outlook, pp.51-55.
Available online at: http://www.gama.aero/files/2008_general_aviation_statistical_databook__indust_499b0dc37b.pdf.
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    The FAA forecast predicts the number of hours flown in single-
engine piston-powered aircraft is projected to increase 0.5% yearly
from 2008 to 2025); the number of hours flown in twin-engine piston-
powered aircraft is projected to decrease 1.5% annually and the number
of hours flown in piston-powered rotocraft is projected to increase
3.9% annually. The changes in numbers of piston aircraft and hours
flown is generally reflected in the consumption of leaded avgas. For
the years 2008 through 2025, DOT's FAA estimates no change in the
volume of leaded avgas consumed by single-engine aircraft in the U.S.
(204 million gallons in 2008 and 2025), a 1.9% decrease in leaded avgas
consumed by multi-engine aircraft (from a baseline of 108 million
gallons in 2008 to 78 million gallons in 2025), and a 3.8% annual
increase in the volume of leaded avgas consumed by piston-powered
helicopters (from a baseline of 13 million gallons in 2008 to 24
million gallons in 2025). For 2025, the forecast volume of leaded avgas
is 348 million gallons. Consumption of this volume of fuel would
release 773 tons of lead to the air in 2025.
    The number of active pilots flying general aviation aircraft
(excluding air transport pilots) is projected to be slightly over half
a million in 2025, representing a yearly increase of 0.7% over the
forecast period.\125\ The student pilot population is forecast to
increase at a slightly higher rate of 1.0% yearly for a 2025 total
slightly over 100,000. Private pilots and sport pilots are also
projected to increase yearly (0.2% yearly increase in the number of