&EPA
United Stales
Envirai menial Protection
Agency
Policy Assessment for the Review of the Lead
National Ambient Air Quality Standards
-------
This page is intentionally blank.
-------
EPA-452/R-14-001
May 2014
Policy Assessment
for the Review of the Lead
National Ambient Air Quality Standards
U.S. Environmental Protection Agency
Office of Air Quality Planning and Standards
Health and Environmental Impacts Division
Research Triangle Park, North Carolina
-------
DISCLAIMER
This document has been reviewed by the Office of Air Quality Planning and Standards
(OAQPS), U.S. Environmental Protection Agency (EPA), and approved for publication. This
OAQPS Policy Assessment contains conclusions of the staff of the OAQPS and does not
necessarily reflect the views of the Agency. Mention of trade names or commercial products is
not intended to constitute endorsement or recommendation for use.
-------
ACKNOWLEDGMENTS
This Policy Assessment is the product of the Office of Air Quality Planning and
Standards. It has been developed as part of the Environmental Protection Agency's (EPA)
ongoing review of the national ambient air quality standards (NAAQS) for lead (Pb). The Pb
NAAQS review team has been led by Dr. Deirdre Murphy. For the chapter on the health effects
evidence and exposure/risk information, the principal authors include Dr. Deirdre Murphy and
Dr. Zach Pekar, and Dr. Murphy served as the principal author for the chapter on the primary Pb
standard. For the chapters on welfare effects evidence and exposure/risk information and the
secondary Pb standard, the principal author is Ms. Ginger Tennant. The principal author on the
section discussing ambient air monitoring is Mr. Kevin Cavender. Contributors of emissions
information and air quality analyses are Mr. Marc Houyoux, Mr. Josh Drukenbrod, Dr. Halil
Cakir and Mr. Mark Schmidt. Staff from other EPA offices, including the Office of Research
and Development and the Office of General Counsel, also provided valuable comments and
contributions.
-------
This page is intentionally blank
-------
TABLE OF CONTENTS
List of Figures iv
List of Tables v
EXECUTIVE SUMMARY ES-1
1 INTRODUCTION 1-1
1.1 PURPOSE 1-1
1.2 BACKGROUND 1-3
1.2.1 Legislative Requirements 1-3
1.2.2 History of Lead NAAQS Reviews 1-5
1.2.3 Current Lead NAAQS Review 1-7
1.2.4 Related Lead Control Programs 1-9
1.3 SCOPE OF CURRENT REVIEW: FATE AND MULTIMEDIA PATHWAYS
OF AMBIENT AIR LEAD 1-14
1.3.1 Environmental Distribution and Exposure Pathways 1-14
1.3.1.1 Human Exposure Pathways 1-16
1.3.1.2 Ecosystem Exposure Pathways 1-18
1.3.2 Considerations Related to Historically Emitted Lead 1-18
1.4 GENERAL ORGANIZATION OF THE DOCUMENT 1-20
1.5 REFERENCES 1-21
2 AMBIENT AIR LEAD 2-1
2.1 SOURCES AND EMISSIONS TO AMBIENT AIR 2-1
2.1.1 Temporal Trends on aNational Scale 2-2
2.1.2 Sources and Emissions on National Scale - 2008 2-3
2.1.2.1 Stationary Sources 2-5
2.1.2.2 Mobile Sources 2-6
2.1.2.3 Natural Sources and Long-range Transport 2-7
2.1.2.4 Previously Deposited Lead 2-7
2.1.3 Sources and Emissions on Local Scale 2-9
2.2 AMBIENT AIR QUALITY 2-12
2.2.1 Air Monitoring 2-12
2.2.1.1 Lead NAAQS Surveillance Network 2-12
2.2.1.2 Other Lead Monitoring Networks 2-16
2.2.1.3 NAAQS Surveillance Monitoring Considerations 2-19
2.2.1.3.1 Sampling Considerations 2-19
2.2.1.3.2 Analysis Considerations 2-21
2.2.1.3.3 Network Design Considerations 2-21
2.2.2 Ambient Concentrations 2-24
2.2.2.1 Temporal Trends 2-24
2.2.2.2 Current Concentrations 2-26
2.3 AMBIENT AIR LEAD IN OTHER MEDIA 2-32
2.3.1 Atmospheric Deposition 2-32
i
-------
2.3.2 Terrestrial Media 2-34
2.3.2.1 Indoor Household Dust 2-34
2.3.2.2 Outdoor Dust in Areas of Human Activity 2-35
2.3.2.3 Soil 2-36
2.3.2.4 Biota 2-38
2.3.3 Aquatic Media 2-39
2.3.3.1 Surface Waters 2-39
2.3.3.2 Sediments 2-40
2.3.3.3 Biota 2-42
2.4 REFERENCES 2-42
3 HEALTH EFFECTS AND EXPOSURE/RISK INFORMATION 3-1
3.1 INTERNAL DISPOSITION AND BIOMARKERS OF EXPOSURE AND DOSE.. 3-1
3.2 NATURE OF EFFECTS 3-15
3.3 PUBLIC HEALTH IMPLICATIONS AND AT-RISK POPULATIONS 3-29
3.4 EXPOSURE AND RISK 3-38
3.4.1 Conceptual Model for Air-Related Lead Exposure and Risk 3-39
3.4.2 Case Studies 3-42
3.4.3 Analysis Approach 3-43
3.4.3.1 Estimating Exposure 3-46
3.4.3.2 Air Quality Scenarios Included in 2007 Assessment 3-49
3.4.3.3 Methods for Deriving Risk Estimates 3-51
3.4.3.3.1 Full Risk Model in 2007 REA 3-52
3.4.3.3.2 Air Quality Scenarios Reflecting the Current Standard 3-55
3.4.4 Challenges in Characterizing Air-related Exposure and Risk 3-56
3.4.5 Risk Estimates 3-58
3.4.6 Treatment of Variability 3-63
3.4.7 Characterizing Uncertainty 3-64
3.4.8 Updated Interpretation of Risk Estimates 3-67
3.5 REFERENCES 3-68
4 REVIEW OF THE PRIMARY STANDARD FOR LEAD 4-1
4.1 APPROACH 4-1
4.1.1 Approach Used in the Last Review 4-2
4.1.1.1 Approach Regarding the Need for Revision 4-3
4.1.1.2 Approach Regarding Elements of Revised Standard 4-5
4.1.2 Approach for the Current Review 4-11
4.2 ADEQUACY OF THE CURRENT STANDARD 4-14
4.2.1 Evidence-based Considerations 4-14
4.2.2 Exposure/Risk-based Considerations 4-22
4.2.3 CASAC Advice 4-26
4.3 STAFF CONCLUSIONS ON THE PRIMARY STANDARD 4-28
4.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND
DATA COLLECTION 4-36
4.5 REFERENCES 4-39
ii
-------
5 WELFARE EFFECTS AND EXPOSURE/RISK INFORMATION 5-1
5.1 WELFARE EFFECTS INFORMATION 5-1
5.2 EXPOSURE AND RISK INFORMATION 5-16
5.2.1 Screening Assessment from Last Review 5-17
5.2.2 Screening Assessment Results and Interpretation 5-20
5.3 REFERENCES 5-25
6 REVIEW OF THE SECONDARY STANDARD FOR LEAD 6-1
6.1 APPROACH 6-1
6.1.1 Approach Used in the Last Review 6-2
6.1.2 Approach for the Current Review 6-3
6.2 ADEQUACY OF THE CURRENT STANDARD 6-5
6.2.1 Evidence-based Considerations 6-5
6.2.2 Exposure/Risk-based Considerations 6-9
6.2.3 CASAC Advice 6-11
6.3 STAFF CONCLUSIONS ON THE SECONDARY
STANDARD 6-12
6.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND
DATA COLLECTION 6-13
6.5 REFERENCES 6-15
CHAPTER APPENDICES
Appendix 2A. The 2008 NEI: Data Sources, Limitations and Confidence 2A-1
Appendix 2B. Recent Regulatory Actions on Stationary Sources of Lead 2B-1
Appendix 2C. Criteria for Air Quality Data Analysis 2C-1
Appendix 2D. Air Quality Data Analysis Summary 2D-1
Appendix 3 A. Interpolated Risk Estimates for the Generalized (Local) Urban Case Study.. 3A-1
Appendix 5 A. Additional Detail on 2006 Ecological Screening Assessment 5 A-1
ATTACHMENT
Clean Air Scientific Advisory Committee Letter (June 4, 2013)
in
-------
LIST OF FIGURES
Figure 1 -1. Pathways of human and ecosystem exposure to lead from ambient air 1-16
Figure 2-1. Temporal trend in U.S. air emissions of Pb: 1970-2008 2-3
Figure 2-2. Geographic distribution of facilities and airports estimated to emit at least
0.50tpyofPbin2008 2-11
Figure 2-3. Map of Pb-TSP monitoring sites in current Pb NAAQS monitoring network 2-15
Figure 2-4. Sites near airports for which one year of Pb-TSP monitoring is required 2-16
Figure 2-5. Pb-PMio monitoring sites 2-17
Figure 2-6. Pb-PM2.5 monitoring sites in CSN and IMPROVE networks (2012) 2-19
Figure 2-7. Temporal trend in Pb -TSP concentrations: 1980-2010(31 sites) 2-24
Figure 2-8. Temporal trend in Pb-TSP concentrations: 2000-2012 (50 sites) 2-25
Figure 2-9. Airborne Pb -TSP concentrations (3-month average) at five sites near
roadways: 1979-2010 2-26
Figure 2-10. Pb-TSP maximum 3-month means (215 sites), 2010-2012 2-27
Figure 2-11. Distribution of maximum 3-month mean concentrations of Pb-TSP, Pb-PMio
and Pb-PM2.s at different site types, 2010-2012 2-29
Figure 2-12. Distribution of annual mean concentrations of Pb-TSP, Pb-PMio and Pb-PM2.s
at different site types, 2010-2012 2-30
Figure 2-13. Distribution of maximum monthly mean concentrations of Pb-TSP, Pb-PMio
and Pb-PM2.s at different site types, 2010-2012 2-31
Figure 2-14. Temporal trend in sediment Pb concentration from core samples in 12 lakes at
eight National Parks or Preserves 2-41
Figure 3-1. Temporal trend in mean blood Pb levels for NHANES cohorts 3-4
Figure 3-2. Human exposure pathways for air-related Pb 3-40
Figure 3-3. Overview of analysis approach 3-45
Figure 3-4. Comparison of four concentration-response functions used in risk assessment.. 3-53
Figure 3-5. Parsing of air-related risk estimates 3-57
Figure 4-1. Overview of approach for review of current primary standard 4-13
Figure 5-1. Analytical approach for screening-level ecological risk assessment in the last
review (2006 REA, Exhibit 2-6) 5-19
Figure 6-1. Overview of approach for review of current secondary standard 6-4
IV
-------
LIST OF TABLES
Table 2-1. U.S. Pb emissions by source categories estimated to emit at least 4 tpy 2-4
Table 2-2. Facilities estimated to emit at least 0.50 tpy of Pb in 2008 2-10
Table 2-3. Dry deposition of Pb in large metropolitan areas 2-36
Table 3-1. Empirically derived air-to-blood ratios for populations inclusive of children 3-13
Table 3-2. Associations with neurocognitive function measures in analyses with child
study group blood Pb levels <5 |ig/dL 3-23
Table 3-3. Summary of quantitative relationships of IQ and blood Pb for analyses with
blood Pb levels closest to those of young children in the U.S. today 3-29
Table 3-4. Number of children aged 5 and under in areas of elevated ambient air Pb
concentrations relative to theNAAQS 3-37
Table 3-5. Population size near larger sources of Pb emissions 3-38
Table 3-6. Types of population exposures assessed 3-43
Table 3-7. Summary of approaches used to estimate case study media concentrations 3-47
Table 3-8. Air quality scenarios assessed 3-51
Table 3-9. Comparison of total and incremental IQ loss estimates for blood Pb below
10 |ig/dL based on the four concentration-response functions 3-53
Table 3-10. Estimates of air-related risk from 2007 risk assessment 3-60
Table 3-11. Estimates of air-related risk for the generalized (local) urban case study,
including interpolated estimates for current standard 3-61
-------
This page is intentionally blank
-------
EXECUTIVE SUMMARY
This Policy Assessment (PA) has been prepared by staff in the Environmental Protection
Agency's (EPA) Office of Air Quality Planning and Standards (OAQPS) as part of the Agency's
ongoing review of the primary (health-based) and secondary (welfare-based) national ambient air
quality standards (NAAQS) for lead (Pb). It presents analyses and staff conclusions regarding
the policy implications of the key scientific and technical information that informs this review.
The PA is intended to "bridge the gap" between the relevant scientific evidence and technical
information and the judgments required of the EPA Administrator in determining whether to
retain or revise the current standards. Development of the PA is also intended to facilitate advice
and recommendations on the standards to the Administrator from an independent scientific
review committee, the Clean Air Scientific Advisory Committee (CASAC), as provided for in
the Clean Air Act (CAA).
Staff analyses in this PA are based on the scientific assessment presented in the
Integrated Science Assessment for Lead (ISA) prepared for this review by the EPA's Office of
Research and Development (ORD) as well as scientific and technical assessments from prior Pb
NAAQS reviews. Such assessments include quantitative human health and ecological risk and
exposure assessments (REAs) developed in the last review as new health and ecological REAs
were not warranted based on staffs and CASAC's consideration of the evidence newly available
in this review with regard to risk and exposure assessment. For the purpose of review of the
NAAQS in considering the scientific evidence and other technical information available in this
review, emphasis is given to consideration of the extent to which the evidence newly available
since the last review alters conclusions drawn in the last review with regard to health and welfare
effects of Pb, the exposure levels at which they occur and the associated at-risk populations and
ecological receptors or ecosystems.
The overarching questions in this review, as in all NAAQS reviews, regard the support
provided by the currently available scientific evidence and exposure/risk-based information for
the adequacy of the current standards and the extent to which the scientific evidence and
technical information provides support for concluding that consideration of alternative standards
may be appropriate. The analyses presented in this PA to address such questions lead to staff
conclusions that it is appropriate to consider retaining the current primary and secondary
standards without revision; accordingly, no potential alternative standards have been identified
by staff for consideration in this review. Comments and recommendations from CASAC, and
public comments, based on review of the draft PA, have informed staff conclusions and the
presentation of information in this final document.
ES-1
-------
Current Lead NAAQS and Scope of Review
The NAAQS for Pb was initially set in 1978. Review of the 1978 NAAQS for Pb,
completed in October 2008, resulted in substantial revision based on the large body of evidence
accumulated over the intervening three decades. In terms of the basic elements of the NAAQS,
the level of the primary standard was lowered by an order of magnitude from 1.5 |ig/m3 to 0.15
|ig/m3 and the averaging time was revised to a rolling three-month period (from a period based
on calendar quarters) with a maximum (not-to-be exceeded) form, evaluated over a 3-year
period. The indicator of Pb in total suspended particles (Pb-TSP) was retained, reflecting the
evidence that Pb particles of all sizes pose health risks. The secondary standard was revised to
be identical in all respects to the revised primary standard.
The multimedia and persistent nature of Pb contributes complexities to the review of the
Pb NAAQS unlike issues addressed in other NAAQS reviews. Air-related Pb distributes from
air to other media, including indoor and outdoor dusts, soil, food, drinking water, as well as
surface water and sediments. As a result, review of the Pb NAAQS considers the protection
provided against the health and environmental effects of air-related Pb associated both with
exposures to Pb in ambient air and with exposures to Pb that makes its way from ambient air into
other media. Additional complexity derives from the recognition that exposure to Pb also results
from nonair sources, including Pb in paint, tap water affected by plumbing containing Pb, lead-
tainted products, as well as surface water discharges and runoff from industrial sites. Such
nonair sources contribute to the total burden of Pb in the human body and in the environment,
making it much more difficult to assess independently the health and welfare effects attributable
to air-related Pb that are the focus of the NAAQS. Further, the persistence of Pb in the human
body and the environment is another important consideration in assessing the adequacy of the
current Pb standards. In so doing, staff is mindful of the history of the greater and more
widespread atmospheric emissions that occurred in previous years (e.g., under the previous Pb
standard, and prior to establishment of any Pb NAAQS) and that contributed to the Pb that exists
in human populations and ecosystems today. Likewise, staff also recognizes the role of nonair
sources of Pb, now and in the past, that also contribute to the Pb that exists in human populations
and ecosystems today. As in the last Pb NAAQS review, this backdrop of environmental Pb
exposure, and its impact on the populations and ecosystems which may be the subjects of the
currently available scientific evidence, complicates our consideration of the health and welfare
protection afforded by the current NAAQS.
ES-2
-------
Characterization of Ambient Air Lead
Emissions to ambient air and associated air Pb concentrations have declined substantially
over the past several decades. The most dramatic reductions in Pb emissions occurred prior to
1990 in the transportation sector due to the removal of Pb from gasoline. Lead emissions were
further reduced substantially between 1990 and 2008, with significant reductions occurring in the
metals industries at least in part as a result of national emissions standards for hazardous air
pollutants issued under Section 112 of the CAA. Additional reductions in stationary source
emissions are also anticipated from further regulations which have been promulgated since 2008
under Section 112 of the CAA.
As at the time of the last review, the majority of Pb emissions nationally is associated
with combustion of leaded aviation gasoline by piston-driven aircraft. The largest sources on a
local scale are generally associated with metals industries. As a result of revisions to monitoring
regulations stemming from the last Pb NAAQS review, Pb NAAQS monitors are required near
the largest Pb emissions sources, as well as at sites distant from such sources in large population
areas. Ambient air Pb monitoring data available thus far from this expanded network continue to
illustrate the source-related aspect of airborne Pb, with highest concentrations near large sources
and lowest in areas removed from sources. In addition, Pb monitoring data are also being
collected over at least a one-year period near a set of airports identified as most likely to have
elevated Pb concentrations due to leaded aviation gasoline usage. These data will improve our
understanding of Pb concentrations in ambient air near airports and conditions influencing these
concentrations. These data will also inform EPA's ongoing investigation into Pb emissions from
piston-engine aircraft under Section 231 of the CAA, separate from this Pb NAAQS review.
Lead occurs in ambient air in particulate form and, with characteristics and spatial
patterns influenced by a number of factors, deposits from air to surfaces in natural and human-
made environments. By this deposition process and subsequent transfer processes, ambient air
Pb is distributed into multiple human exposure pathways and environmental media in aquatic
and terrestrial ecosystems. In areas removed from large air emissions sources, currently
available information on Pb concentrations in nonair media includes numerous examples of
declines in surface concentrations reflective of the reductions in deposition over the past several
decades. In areas near large air sources where emissions reductions have occurred, only very
limited information is available, such as for reductions in air and surface dust concentrations,
with even less information available on trends for other media such as surface soils.
ES-3
-------
Health Effects and Review of the Primary Standard
Lead has long been recognized to exert an array of deleterious effects on multiple organ
systems as described in the ISA for this review and consistent with conclusions of prior scientific
assessments. Over the three decades from the time the standard was initially set in 1978 through
its revision with the NAAQS review completed in 2008, the evidence base expanded
considerably in a number of areas, including with regard to effects on neurocognitive function in
young children at increasingly lower blood Pb levels. These effects formed the primary basis for
the 2008 revisions to the primary standard. The current standard was set most specifically to
provide appropriate public health protection from the effects of air-related Pb on cognitive
function (e.g., IQ loss) in young children. In so doing, the standard was judged to provide the
requisite public health protection from the full array of health effects of Pb, consistent with the
CAA requirement that the primary standard, in the judgment of the Administrator, based on the
latest scientific knowledge, be requisite to protect public health with an adequate margin of
safely.
The health effects evidence newly available in this review, as critically assessed in the
ISA in conjunction with the full body of evidence, reaffirms conclusions on the broad array of
effects recognized for Pb in the last review. Further, staff observes the general consistency of the
current evidence with the evidence available in the last review, particularly with regard to key
aspects of the evidence on which the current standard is based. These key aspects include those
regarding the relationships between air Pb concentrations and the associated Pb in the blood of
young children (i.e., air-to-blood ratios) as well as between total blood Pb levels and effects on
neurocognitive function (i.e., concentration-response (C-R) functions for IQ loss). Factors
characterizing these two relationships are the key inputs to the framework developed in the last
review to translate the available evidence into a basis for considering a primary Pb standard that
would be requisite to protect against this and other Pb-related health endpoints. This framework
is again considered in light of the currently available evidence. This Pb NAAQS review, like
any NAAQS review, requires public health policy judgments. The public health policy
judgments for this review include the public health significance of a given magnitude of IQ loss
in a small subset of highly exposed children (i.e., those likely to experience air-related Pb
exposures at the level of the standard), as well as how to consider the nature and magnitude of
the array of uncertainties that are inherent in the evidence and in the application of this specific
framework.
In also considering the quantitative risk estimates associated with the current standard,
based on the risk assessment conducted in the last review, staff observes that these estimates
indicate a level of risk that is roughly consistent with and generally supportive of conclusions
drawn from the evidence using the evidence-based air-related IQ loss framework. Staff
ES-4
-------
additionally recognizes the complexity of the modeling done as part of that assessment and the
substantial limitations and uncertainties in the resulting risk estimates.
Based on the above considerations, staff concludes that the currently available
information supports a primary standard as protective as the current standard and that it is
appropriate to consider retaining the current standard without revision. In so doing, staff
additionally notes that the final decision on the adequacy of the current standard is largely a
public health policy judgment to be made by the Administrator, drawing upon the scientific
information as well as judgments about how to consider the range and magnitude of uncertainties
that are inherent in the scientific evidence and technical analyses. In this context, staff
recognizes that the uncertainties and limitations associated with the many aspects of the
relationship between air Pb concentrations and blood Pb levels and associated health effects are
amplified with consideration of increasingly lower air concentrations. In staffs view, based on
the current evidence there is appreciable uncertainty associated with drawing conclusions
regarding whether there would be reductions in blood Pb levels and risk to public health from
alternative lower levels as compared to the level of the current standard. Thus, staff concludes
that the basis for any consideration of alternative lower standard levels would reflect different
public health policy judgments as to the appropriate approach for weighing uncertainties in the
evidence and for providing requisite protection of public health with an adequate margin of
safety. Accordingly, and in light of the staff conclusion that it is appropriate to consider the
current standard to be adequate, this document does not identify potential alternative standards
for consideration in this review.
Welfare Effects and Review of the Secondary Standard
Consideration of the welfare effects evidence and screening-level risk information in the
last review (completed in 2008) led to the conclusion that there was a potential for adverse
welfare effects occurring under the then-current Pb standard (set in 1978), although there were
insufficient data to provide a quantitative basis for setting a secondary standard different from
the primary standard. Accordingly, the secondary standard was substantially revised to be
identical in all respects to the newly revised primary standard.
In assessing the currently available scientific evidence and the exposure/risk information
with regard to support for the adequacy of the protection afforded by the current standard, staff
observes the general consistency of the current evidence with that available in the last review,
including that with regard to ecological effects associated with Pb exposure and the substantial
limitations in the current evidence that complicate conclusions regarding the potential for Pb
emissions under the current, much lower standard to contribute to welfare effects. Such
complications include the significant difficulties in interpreting effects evidence from laboratory
ES-5
-------
studies to the natural environment and linking those effects to ambient air Pb concentrations.
Based on staff analysis, including the above considerations, staff concludes that the currently
available evidence and exposure/risk information do not call into question the adequacy of the
current standard to provide the requisite protection for public welfare. Thus, staff concludes that
consideration should be given to retaining the current standard, without revision, and this
document does not identify potential alternative standards for consideration in this review.
ES-6
-------
1 INTRODUCTION
1.1 PURPOSE
The U.S. Environmental Protection Agency (EPA) is presently conducting a review of
the primary (health-based) and secondary (welfare-based) national ambient air quality standards
(NAAQS) for lead (Pb). The overall plan and schedule for this review were presented in the
Integrated Review Plan for the National Ambient Air Quality Standards for Lead (IRP; USEPA,
201 la). The IRP also identified key policy-relevant issues to be addressed in this review and
discussed the key documents that generally inform NAAQS reviews, including an Integrated
Science Assessment (ISA), Risk and Exposure Assessments (REAs), and a Policy Assessment
(PA). The PA presents a staff evaluation of the policy implications of the key scientific and
technical information in the ISA and REAs for EPA's consideration.1 The PA generally
provides a transparent evaluation and staff conclusions regarding policy considerations related to
reaching judgments about the adequacy of the current standards and, if revision is considered,
what revisions may be appropriate to consider.
The PA is intended to help "bridge the gap" between the Agency's scientific assessments
presented in the ISA and REAs and the judgments required of the EPA Administrator in
determining whether it is appropriate to retain or revise the NAAQS. In evaluating the adequacy
of current standards and whether it is appropriate to consider alternative standards, the PA
focuses on information that is most pertinent to evaluating the basic elements of the NAAQS:
indicator,2 averaging time, form,3 and level. These elements, which together serve to define each
standard, must be considered collectively in evaluating the health and welfare protection
afforded by the Pb standards. The PA integrates and interprets the information from the ISA and
REAs to frame policy options for consideration by the Administrator. In so doing, the PA
recognizes that the selection of a specific approach to reaching final decisions on primary and
secondary NAAQS will reflect the judgments of the Administrator.
1 The terms "staff and "we" throughout this document refer to staff in the EPA's Office of Air Quality
Planning and Standards (OAQPS). In past NAAQS reviews, this document was referred to as the OAQPS Staff
Paper.
2 The "indicator" of a standard defines the chemical species or mixture that is to be measured in
determining whether an area attains the standard. The indicator for the Pb NAAQS is lead in total suspended
particles.
3 The "form" of a standard defines the air quality statistic that is to be compared to the level of the standard
in determining whether an area attains the standard. For example, the form of the annual NAAQS for fine
paniculate matter (PM2 5) is the average of annual mean PM2 5 concentrations for three consecutive years, while the
form of the 8-hour NAAQS for carbon monoxide is the second-highest 8-hour average in a year.
1-1
-------
The development of the PA is also intended to facilitate advice to the Agency and
recommendations to the Administrator from an independent scientific review committee, the
Clean Air Scientific Advisory Committee (CASAC), as provided for in the Clean Air Act. As
discussed below in section 1.2.1, the CASAC is to advise not only on the Agency's assessment
of the relevant scientific information, but also on the adequacy of the existing standards, and to
make recommendations as to any revisions of the standards that may be appropriate. The EPA
facilitates CASAC advice and recommendations, as well as public input and comment, by
requesting CASAC review and public comment on one or more drafts of the PA.4 In this PA for
this review of the Pb NAAQS, we consider the scientific and technical information available in
this review as assessed in the Integrated Science Assessment for Lead (henceforth referred to as
the ISA [USEPA, 2013a]), prepared by EPA's National Center for Environmental Assessment
(NCEA), and the quantitative human exposure and health risk and screening-level ecological risk
assessments performed in the last review. As discussed below in section 1.2.3, upon
consideration of the evidence newly available in this review with regard to risk and exposure
assessment, staff concluded that new health and welfare REAs were not warranted. Accordingly,
the quantitative risk information considered in this PA is based on the quantitative human
exposure and health risk and screening-level ecological risk assessments performed in the last
review (the 2007 Health Risk Assessment Report or 2007 REA [USEPA, 2007a] and the 2006
screening-level Ecological Risk Assessment or 2006 REA [ICF, 2006]) and is interpreted in the
context of newly available evidence in this review. The evaluation and staff conclusions
presented in this PA for the Pb NAAQS have been informed by comments and advice received
from CASAC in their reviews of the draft PA and of other draft Agency documents prepared in
this NAAQS review.
Beyond informing the EPA Administrator and facilitating the advice and
recommendations of CASAC and the public, the PA is also intended to be a useful reference to
all parties interested in the Pb NAAQS review. In these roles, it is intended to serve as a single
source of the most policy-relevant information that informs the Agency's review of the Pb
NAAQS, and it is written to be understandable to a broad audience.
4 The decision whether to prepare one or more drafts of the PA is influenced by preliminary staff
conclusions and associated CASAC advice and public comment, among other factors. Typically, a second draft PA
has been prepared in cases where the available information calls into question the adequacy of the current standard
and analyses of potential alternative standards are developed taking into consideration CASAC advice and public
comment. In such cases, a second draft PA includes preliminary staff conclusions regarding potential alternative
standards and undergoes CASAC review and public comment prior to preparation of the final PA. When such
analyses are not undertaken, a second draft PA may not be warranted.
1-2
-------
1.2 BACKGROUND
1.2.1 Legislative Requirements
Two sections of the Clean Air Act (CAA or the Act) govern the establishment and
revision of the NAAQS. Section 108 (42 U.S.C. section 7408) directs the Administrator to
identify and list certain air pollutants and then to issue air quality criteria for those pollutants.
The Administrator is to list those air pollutants that in her "judgment, cause or contribute to air
pollution which may reasonably be anticipated to endanger public health or welfare;" "the
presence of which in the ambient air results from numerous or diverse mobile or stationary
sources;" and "for which . . . [the Administrator] plans to issue air quality criteria..." Air quality
criteria are intended to "accurately reflect the latest scientific knowledge useful in indicating the
kind and extent of all identifiable effects on public health or welfare which may be expected
from the presence of [a] pollutant in the ambient air . . ." 42 U.S.C. § 7408(b). Section 109 (42
U.S.C. 7409) directs the Administrator to propose and promulgate "primary" and "secondary"
NAAQS for pollutants for which air quality criteria are issued. Section 109(b)(l) defines a
primary standard as one "the attainment and maintenance of which in the judgment of the
Administrator, based on such criteria and allowing an adequate margin of safety, are requisite to
protect the public health."5 A secondary standard, as defined in section 109(b)(2), must "specify
a level of air quality the attainment and maintenance of which, in the judgment of the
Administrator, based on such criteria, is requisite to protect the public welfare from any known
or anticipated adverse effects associated with the presence of [the] pollutant in the ambient air."6
The requirement that primary standards provide an adequate margin of safety was
intended to address uncertainties associated with inconclusive scientific and technical
information available at the time of standard setting. It was also intended to provide a reasonable
degree of protection against hazards that research has not yet identified. See Lead Industries
Association v. EPA, 647 F.2d 1130, 1154 (D.C. Cir 1980), cert, denied, 449 U.S. 1042 (1980);
American Petroleum Institute v. Costle, 665 F.2d 1176, 1186 (D.C. Cir. 1981), cert, denied, 455
U.S. 1034 (1982); American Farm Bureau Federation v. EPA, 559 F. 3d 512, 533 (D.C. Cir.
2009); Association of Battery Re cyclers v. EPA, 604 F. 3d 613, 617-18 (D.C. Cir. 2010). Both
kinds of uncertainties are components of the risk associated with pollution at levels below those
5 The legislative history of section 109 indicates that a primary standard is to be set at "the maximum
permissible ambient air level. . . which will protect the health of any [sensitive] group of the population," and that
for this purpose "reference should be made to a representative sample of persons comprising the sensitive group
rather than to a single person in such a group" S. Rep. No. 91-1196, 91st Cong., 2d Sess. 10 (1970).
6 Welfare effects as defined in section 302(h) (42 U.S.C. § 7602(h)) include, but are not limited to, "effects
on soils, water, crops, vegetation, man-made materials, animals, wildlife, weather, visibility and climate, damage to
and deterioration of property, and hazards to transportation, as well as effects on economic values and on personal
comfort and well-being."
1-3
-------
at which human health effects can be said to occur with reasonable scientific certainty. Thus, in
selecting primary standards that provide an adequate margin of safety, the Administrator is
seeking not only to prevent pollution levels that have been demonstrated to be harmful but also
to prevent lower pollutant levels that may pose an unacceptable risk of harm, even if the risk is
not precisely identified as to nature or degree. The CAA does not require the Administrator to
establish a primary NAAQS at a zero-risk level or at background concentration levels, see Lead
Industries v. EPA., 647 F.2d at 1156 n.51, but rather at a level that reduces risk sufficiently so as
to protect public health with an adequate margin of safety.
In addressing the requirement for an adequate margin of safety, the EPA considers such
factors as the nature and severity of the health effects involved, the size of sensitive population(s)
at risk,7 and the kind and degree of the uncertainties that must be addressed. The selection of any
particular approach to providing an adequate margin of safety is a policy choice left specifically
to the Administrator's judgment. See Lead Industries Association v. EPA, 647 F.2d at 1161-62.
In setting primary and secondary standards that are "requisite" to protect public health
and welfare, respectively, as provided in section 109(b), EPA's task is to establish standards that
are neither more nor less stringent than necessary for these purposes. In so doing, the EPA may
not consider the costs of implementing the standards. See generally, Whitman v. American
Trucking Associations, 531 U.S. 457, 465-472, 475-76 (2001). Likewise, "[a]ttainability and
technological feasibility are not relevant considerations in the promulgation of national ambient
air quality standards." American Petroleum Institute v. Costle, 665 F. 2d at 1185.
Section 109(d)(l) requires that "not later than December 31, 1980, and at 5-year
intervals thereafter, the Administrator shall complete a thorough review of the criteria
published under section 108 and the national ambient air quality standards . . . and shall make
such revisions in such criteria and standards and promulgate such new standards as may be
appropriate . . . ." Section 109(d)(2) requires that an independent scientific review committee
"shall complete a review of the criteria . . . and the national primary and secondary ambient air
quality standards . . . and shall recommend to the Administrator any new . . . standards and
revisions of existing criteria and standards as may be appropriate . . . ." Since the early 1980s,
this independent review function has been performed by the Clean Air Scientific Advisory
Committee (CASAC).8
7 As used here and similarly throughout this document, the term population (or group) refers to persons
having a quality or characteristic in common, such as a specific pre-existing illness or a specific age or life stage. As
discussed more fully in section 3.3 below, the identification of sensitive groups (called at-risk groups or at-risk
populations) involves consideration of susceptibility and vulnerability.
8 Lists of CAS AC members and of members of the CAS AC Pb Review Panel are available at:
http://vosemite.epa.gov/sab/sabproduct.nsfAVebCASAC/CommitteesandMembership7OpenDocument.
1-4
-------
1.2.2 History of Lead NAAQS Reviews
Unlike pollutants such as particulate matter and carbon monoxide, air quality criteria had
not been issued for Pb as of the enactment of the Clean Air Act of 1970, which first set forth the
requirement to set national ambient air quality standards based on air quality criteria. In the
years just after enactment of the CAA, the EPA did not intend to issue air quality criteria for Pb
and accordingly had not listed Pb under Section 108 of the Act. The EPA had determined to
control Pb air pollution through regulations to phase out the use of Pb additives in gasoline and
the EPA viewed those controls, and possibly additional federal controls, as the best approach to
controlling Pb emissions (See 41 FR 14921 (April 8, 1976). However, the decision not to list Pb
under Section 108 was challenged by environmental and public health groups and the U.S.
District Court for the Southern District of New York concluded that the EPA was required to list
Pb under Section 108. Natural Resources Defense Council v. EPA, 411 F. Supp. 864 21 (S.D.
N.Y. 1976), qff'd, 545 F.2d 320 (2d Cir. 1978).
Accordingly, on April 8, 1976, the EPA published a notice in the Federal Register that
Pb had been listed under Section 108 as a criteria pollutant (41 FR 14921) and on October 5,
1978, the EPA promulgated primary and secondary NAAQS for Pb under Section 109 of the Act
(43 FR 46246). Both primary and secondary standards were set at a level of 1.5 micrograms per
cubic meter (ug/m3), measured as Pb in total suspended particles (Pb-TSP), not to be exceeded
by the maximum arithmetic mean concentration averaged over a calendar quarter. These
standards were based on the 1977 Air Quality Criteria for Lead (USEPA, 1977).
The first review of the Pb standards was initiated in the mid-1980s. The scientific
assessment for that review is described in the 1986 Air Quality Criteria for Lead (USEPA,
1986a), the associated Addendum (USEPA, 1986b) and the 1990 Supplement (USEPA, 1990a).
As part of the review, the Agency designed and performed human exposure and health risk
analyses (USEPA, 1989), the results of which were presented in a 1990 Staff Paper (USEPA,
1990b). Based on the scientific assessment and the human exposure and health risk analyses, the
1990 Staff Paper presented recommendations for consideration by the Administrator (USEPA,
1990b). After consideration of the documents developed during the review and the significantly
changed circumstances since Pb was listed in 1976, the Agency did not propose any revisions to
the 1978 Pb NAAQS. In a parallel effort, the Agency developed the broad, multi-program,
multimedia, integrated U.S. Strategy for Reducing Lead Exposure (USEPA, 1991). As part of
implementing this strategy, the Agency focused efforts primarily on regulatory and remedial
clean-up actions aimed at reducing Pb exposures from a variety of nonair sources judged to pose
more extensive public health risks to U.S. populations, as well as on actions to reduce Pb
emissions to air, such as bringing more areas into compliance with the existing Pb NAAQS
1-5
-------
(USEPA, 1991). EPA continues this broad, multi-program, multimedia approach to reducing Pb
exposures today, as described in section 1.2.4 below.
The last review of the Pb air quality criteria and standards was initiated in November
2004 (69 FR 64926) and the Agency's plans for preparation of the Air Quality Criteria
Document and conduct of the NAAQS review were presented in documents completed in 2005
and early 2006 (USEPAa, 2005; USEPA 2006a).9 The schedule for completion of the review
was governed by a judicial order in Missouri Coalition for the Environment v. EPA (No.
4:04CV00660 ERW, Sept. 14, 2005; and amended on April 29, 2008 and July 1, 2008), which
specified a schedule for the review of duration substantially shorter than five years.
The scientific assessment for the review is described in the 2006 Air Quality Criteria for
Lead (USEPA, 2006b; henceforth referred to as the 2006 CD), multiple drafts of which received
review by CASAC and the public. The EPA also conducted human exposure and health risk
assessments and a pilot ecological risk assessment for the review, after consultation with
CASAC and receiving public comment on a draft analysis plan (USEPA, 2006c). Drafts of these
quantitative assessments were reviewed by CASAC and the public. The pilot ecological risk
assessment was released in December 2006 (ICF, 2006) and the final health risk assessment
report was released in November 2007 (USEPA, 2007a). The policy assessment, based on both
of these assessments, air quality analyses and key evidence from the 2006 CD, was presented in
the Staff Paper (USEPA, 2007b), a draft of which also received CASAC and public review. The
final Staff Paper presented OAQPS staffs evaluation of the public health and welfare policy
implications of the key studies and scientific information contained in the 2006 CD and
presented and interpreted results from the quantitative risk/exposure analyses conducted for this
review. Based on this evaluation, the Staff Paper presented OAQPS staff recommendations that
the Administrator give consideration to substantially revising the primary and secondary
standards to a range of levels at or below 0.2 jig/m3.
Immediately subsequent to completion of the Staff Paper, the EPA issued an advance
notice of proposed rulemaking (ANPR) that was signed by the Administrator on December 5,
2007 (72 FR 71488).10 CASAC provided advice and recommendations to the Administrator with
regard to the Pb NAAQS based on its review of the ANPR and the previously released final Staff
Paper and risk assessment reports. The proposed decision on revisions to the Pb NAAQS was
signed on May 1, 2008 and published in the Federal Register on May 20, 2008 (73 FR 29184).
Members of the public provided both written and, at two public hearings, oral comments and the
9 In the current review, these two documents have been combined in the IRP.
10 The ANPR was one of the features of the revised NAAQS review process that EPA instituted in 2006. In
2009 (Jackson, 2009), this component of the process was replaced by reinstatement of a policy assessment prepared
by OAQPS staff (previously termed the OAQPS Staff Paper).
1-6
-------
CASAC Pb Panel also provided advice and recommendations to the Administrator based on its
review of the proposal notice. The final decision on revisions to the Pb NAAQS was signed on
October 15, 2008 and published in the Federal Register on November 12, 2008 (73 FR 66964).
The November 2008 notice described EPA's decision to revise the primary and
secondary NAAQS for Pb, as discussed more fully in section 4.1.1 below. In consideration of
the much-expanded health effects evidence on neurocognitive effects of Pb in children, the EPA
substantially revised the primary standard from a level of 1.5 |ig/m3 to a level of 0.15 |ig/m3.
The averaging time was revised to a rolling three-month period with a maximum (not-to-be-
exceeded) form, evaluated over a three-year period. The indicator of Pb-TSP was retained,
reflecting the evidence that Pb particles of all sizes pose health risks. The secondary standard
was revised to be identical in all respects to the revised primary standards.11 Revisions to the
NAAQS were accompanied by revisions to the data handling procedures, the treatment of
exceptional events and the ambient air monitoring and reporting requirements, as well as
emissions inventory reporting requirements.12 One aspect of the new data handling requirements
is the allowance for the use of Pb-PMio monitoring for Pb NAAQS attainment purposes in
certain limited circumstances at non-source-oriented sites. Subsequent to the 2008 rulemaking,
additional revisions were made to the monitoring network requirements as described in chapter 2
below.
1.2.3 Current Lead NAAQS Review
On February 26, 2010, the EPA formally initiated its current review of the air quality
criteria and standards for Pb, requesting the submission of recent scientific information on
specified topics (75 FR 8934). Soon after this, the EPA held a science policy workshop to
discuss the policy-relevant scientific information, which informed identification of key policy
issues and questions to frame the review of the Pb NAAQS (75 FR 20843). Drawing from the
workshop discussions, the EPA developed the draft IRP (USEPA, 201 Ib). The draft IRP was
made available in late March 2011 for consultation with the CASAC Pb Review Panel and for
public comment (76 FR 20347). This document was discussed by the Panel via a publicly
accessible teleconference consultation on May 5, 2011 (76 FR 21346; Frey, 201 la). The final
IRP, developed in consideration of the CASAC consultation and public comment, was released
in November, 2011 (USEPA, 201 la; 76 FR 76972).
11 The current NAAQS for Pb are specified at 40 CFR 50.16.
12 The current federal regulatory measurement methods for Pb are specified in 40 CFR 50, Appendix G and
40 CFR part 53. Consideration of ambient air measurements with regard to judging attainment of the standards is
specified in 40 CFR 50, Appendix R. The Pb monitoring network requirements are specified in 40 CFR 58,
Appendix D, section 4.5. Guidance on the approach for implementation of the new standards was described in the
Federal Register notices forthe proposed and final rules (73 FR 29184; 73 FR 66964).
1-7
-------
In developing the ISA for this review, the EPA held a workshop in December 2010 to
discuss with invited scientific experts preliminary draft materials and released the first external
review draft of the document for CAS AC review and public comment on May 6, 2011 (USEPA,
201 Ic; 76 FR 26284). The CAS AC Pb Review Panel met at a public meeting on July 20, 2011
to review the draft ISA (76 FR 36120). The CASAC provided comments in a December 9, 2011
letter to the EPA Administrator (Frey and Samet, 2011). The second external review draft ISA
was released for CASAC review and public comment in February 2012 (USEPA, 2012b; 77 FR
5247) and was the subject of a public meeting on April 10-11, 2012 (77 FR 14783). The
CASAC provided comments in a July 20, 2012 letter (Samet and Frey, 2012). The third external
review draft was released for CASAC review and public comment in November 2012 (USEPA,
2012a; 77 FR 70776) and was the subject of a public meeting on February 5-6, 2013 (78 FR
938). The CASAC provided comments in a June 4, 2013 letter (Frey, 2013a). The final ISA was
released in late June 2013 (USEPA, 2013a; 78 FR 38318).
In June 2011, the EPA developed and released the REA Planning Document for
consultation with CASAC and public comment (USEPA, 201 Id; 76 FR 58509). This document
presented a critical evaluation of the information related to Pb human and ecological exposure
and risk (e.g., data, modeling approaches) newly available in this review, with a focus on
consideration of the extent to which new or substantially revised REAs for health and ecological
risk are warranted by the newly available evidence. Evaluation of the newly available
information with regard to designing and implementing health and ecological REAs for this
review led us to conclude that the currently available information did not provide a basis for
developing new quantitative risk and exposure assessments that would have substantially
improved utility for informing the Agency's consideration of health and welfare effects and
evaluation of the adequacy of the current primary and secondary standards, respectively (REA
Planning Document, sections 2.3 and 3.3, respectively). The CASAC Pb Panel provided
consultative advice on that document and its conclusions at a public meeting on July 21,2011
(76 FR 36120; Frey, 201 Ib). Based on their consideration of the REA Planning Document
analysis, the CASAC Pb Review Panel generally concurred with the conclusion that a new REA
was not warranted in this review (Frey, 201 Ib; Frey, 2013b). In consideration of the conclusions
reached in the REA Planning Document and CASAC's consultative advice, the EPA has not
developed REAs for health and ecological risk for this review. Accordingly, this Policy
Assessment considers the risk assessment findings from the last review with regard to any
appropriate further interpretation in light of the evidence newly available in this review.
A draft of this Policy Assessment was released for public comment and review by
CASAC in January 2013 (USEPA, 2013b; 77 FR 70776) and was the subject of a public meeting
on February 5-6, 2013 (78 FR 938). Comments provided by the CASAC in a June 4, 2013 letter
1-8
-------
(Frey, 2013b), as well as public comments received on the draft PA were considered in preparing
the final PA.
1.2.4 Related Lead Control Programs
States are primarily responsible for ensuring attainment and maintenance of the NAAQS.
Under section 110 of the Act (42 U.S.C. 7410) and related provisions, states are to submit, for
EPA approval, state implementation plans (SIPs) that provide for the attainment and
maintenance of such standards through control programs directed to sources of the pollutants
involved. The states, in conjunction with EPA, also administer the prevention of significant
deterioration program (42 U.S.C. 7470-7479) for these pollutants. In addition, federal programs
provide for nationwide reductions in emissions of these and other air pollutants through the
Federal Motor Vehicle Control Program under Title II of the Act (42 U.S.C. 7521-7574), which
involves controls for automobile, truck, bus, motorcycle, nonroad engine, and aircraft emissions;
the new source performance standards under section 111 of the Act (42 U.S.C. 7411); and the
national emission standards for hazardous air pollutants under section 112 of the Act (42 U.S.C.
7412).
As noted in section 1.2.2 above, the NAAQS is only one component of EPA's programs
to address Pb in the environment. Some recent actions expected to result in air Pb emissions
reductions that are associated with other EPA programs, such as those recognized above, are
more specifically recognized in section 2.1. The presentation below briefly summarizes
additional ongoing activities that, although not directly pertinent to the review of the NAAQS,
are associated with controlling environmental Pb levels and human Pb exposures more broadly.
Among those identified are EPA programs intended to encourage exposure reduction programs
in other countries.
Reducing Pb exposures has been recognized as a federal priority as environmental and
public health agencies continue to grapple with soil and dust Pb levels from the historical use of
Pb in paint and gasoline and from other sources.13 A broad range of federal programs beyond
those that focus on air pollution control provide for nationwide reductions in environmental
releases and human exposures. For example, pursuant to Section 1412 of the Safe Drinking
Water Act (SDWA), EPA regulates lead in public drinking water systems through corrosion
13 In 1991, the Secretary of the Health and Human Services (HHS) characterized Pb poisoning as the
"number one environmental threat to the health of children in the United States" (Alliance to End Childhood Lead
Poisoning. 1991). In 1997, President Clinton created, by Executive Order 13045, the President's Task Force on
Environmental Health Risks and Safety Risks to Children in response to increased awareness that children face
disproportionate risks from environmental health and safety hazards (62 FR 19885). By Executive Orders issued in
October 2001 and April 2003, President Bush extended the work for the Task Force beyond its original charter (66
FR52013 and68FR 19931). Reducing Pb poisoning in children was identified as the Task Force'stop priority.
1-9
-------
control and other utility actions which work together to minimize lead levels at the tap. (40 CFR
141.80-141.91). In addition, under Section 1417 of the Safe Drinking Water Act, pipes, fittings
and fixtures for potable water applications may not be used or introduced into commerce unless
they are considered "lead free" as defined by that Act (40 CFR 141.43).14 Additionally, federal
Pb abatement programs provide for the reduction in human exposures and environmental
releases from in-place materials containing Pb (e.g., Pb-based paint, urban soil and dust, and
contaminated waste sites). Federal regulations on disposal of Pb-based paint waste help facilitate
the removal of Pb-based paint from residences (68 FR 36487).
Federal programs to reduce exposure to Pb in paint, dust, and soil are specified under the
comprehensive federal regulatory framework developed under the Residential Lead-Based Paint
Hazard Reduction Act (Title X). Under Title X (codified as Title IV of the Toxic Substances
Control Act [TSCA]), EPA has established regulations and associated programs in the following
six categories: (1) training, certification and work practice requirements for persons engaged in
lead-based paint activities (abatement, inspection and risk assessment); accreditation of training
providers; and authorization of state and tribal lead-based paint programs; (2) training,
certification, and work practice requirements for persons engaged in home renovation, repair and
painting (RRP) activities; accreditation of RRP training providers; and authorization of state and
tribal RRP programs; (3) ensuring that, for most housing constructed before 1978, information
about lead-based paint and lead-based paint hazards flows from sellers to purchasers, from
landlords to tenants, and from renovators to owners and occupants; (4) establishing standards for
identifying dangerous levels of Pb in paint, dust and soil; (5) providing grant funding to establish
and maintain state and tribal lead-based paint programs; and, (6) providing information on Pb
hazards to the public, including steps that people can take to protect themselves and their
families from lead-based paint hazards.
Under Title IV of TSCA, EPA established standards identifying hazardous levels of Pb in
residential paint, dust, and soil in 2001. This regulation supports the implementation of other
regulations which deal with worker training and certification, Pb hazard disclosure in real estate
transactions, Pb hazard evaluation and control in federally-owned housing prior to sale and
housing receiving federal assistance, and U.S. Department of Housing and Urban Development
grants to local jurisdictions to perform Pb hazard control. The TSCA Title IV term "lead-based
paint hazard" implemented through this regulation identifies lead-based paint and all residential
lead-containing dust and soil regardless of the source of Pb, which, due to their condition and
14 In 2011, revisions to this section of the Safe Drinking Water Act lowered the amount of Pb permitted in
pipes, fittings, and fixtures; the changes became effective in January 2014. More information is provided in
" Summary of the Reduction of Lead in Drinking Water Act and Frequently Asked Questions" at
http://water.epa.gov/drink/info/lead/index.cfm)
1-10
-------
location, would result in adverse human health effects. One of the underlying principles of Title
X is to move the focus of public and private decision makers away from the mere presence of
lead-based paint to the presence of lead-based paint hazards, for which more substantive action
should be undertaken to control exposures, especially to young children. In addition, the success
of the program relies on the voluntary participation of states and tribes as well as counties and
cities to implement the programs and on property owners to follow the standards and EPA's
requirements.
On March 31, 2008, the EPA issued a new rule (Lead: Renovation, Repair and Painting
[RRP] Program, 73 FR 21692) to protect children from lead-based paint hazards. This rule
applies to compensated renovators and maintenance professionals who perform renovation,
repair, or painting in housing and child-care facilities built prior to 1978. Among its
requirements is one that requires that firms that conduct RRP activities be certified; that their
employees be trained; and that they follow protective work practice standards. These standards
prohibit certain dangerous work practices, such as open flame burning or torching of lead-based
paint. The required work practices also include posting warning signs, restricting occupants
from work areas, containing work areas to prevent dust and debris from spreading, conducting a
thorough cleanup, and verifying that cleanup was effective. The rule became fully effective in
April 2010. The rule also specifies procedures for the authorization of states, territories, and
tribes to administer and enforce these standards and regulations in lieu of a federal program. In
announcing this rule, EPA noted that approximately 37 million homes in the United States
contain some lead-based paint, and that this rule's requirements are key components of a
comprehensive effort to eliminate childhood Pb poisoning. To foster adoption of the rule's
measures, EPA has been conducting an extensive education and outreach campaign to promote
awareness of these new requirements among both the regulated entities and the consumers who
hire them. In addition, the EPA is investigating whether lead hazards are also created by RRP
activities in public and commercial buildings, and if appropriate, to issue RRP requirements for
this class of buildings.
Programs associated with the Comprehensive Environmental Response, Compensation,
and Liability Act (CERCLA or Superfund) and Resource Conservation Recovery Act (RCRA)
also implement abatement programs, reducing exposures to Pb and other pollutants. For
example, EPA determines and implements protective levels for Pb in soil at Superfund sites and
RCRA corrective action facilities. Federal programs, including those implementing RCRA,
provide for management of hazardous substances in hazardous and municipal solid waste (see,
e.g., 66 FR 58258). Federal regulations concerning batteries in municipal solid waste facilitate
1-11
-------
the collection and recycling or proper disposal of batteries containing Pb.15 Similarly, federal
programs provide for the reduction in environmental releases of hazardous substances such as Pb
in the management of wastewater (http://www.epa.gov/owm/).
A variety of federal nonregulatory programs also provide for reduced environmental
release of Pb-containing materials by encouraging pollution prevention, promotion of reuse and
recycling, reduction of priority and toxic chemicals in products and waste, and conservation of
energy and materials. These include the Resource Conservation Challenge
(http://www.epa.gov/epaoswer/osw/conserve/index.htm), the National Waste Minimization
Program (http://www.epa.gov/epaoswer/hazwaste/minimize/leadtire.htm), "Plug in to eCycling"
(a partnership between EPA and consumer electronics manufacturers and retailers;
http://www.epa.gov/epaoswer/hazwaste/recvcle/electron/crt.htmtfcrts), and activities to reduce
the practice of backyard trash burning (http://www.epa.gov/msw/backyard/pubs.htm).
In addition to the Pb control programs summarized above, EPA's research program
identifies, encourages and conducts research needed to locate and assess serious risks and to
develop methods and tools to characterize and help reduce risks. For example, EPA's Integrated
Exposure Uptake Biokinetic Model for Lead in Children (IEUBK model) is widely used and
accepted as a tool that informs the evaluation of site-specific data. More recently, in recognition
of the need for a single model that predicts Pb concentrations in tissues for children and adults,
EPA has been developing the All Ages Lead Model (AALM) to provide researchers and risk
assessors with a pharmacokinetic model capable of estimating blood, tissue, and bone
concentrations of Pb based on estimates of exposure over the lifetime of the individual (ISA,
section 3.6). EPA research activities on substances including Pb, such as those identified here,
focus on improving our characterization of health and environmental effects, exposure, and
control or management of environmental releases (see http://www.epa.gov/research/).
Other federal agencies also participate in programs intended to reduce Pb exposures. For
examples programs of the Centers for Disease Control and Prevention (CDC) provide for the
tracking of children's blood Pb levels in the U.S. and provide guidance on levels at which
medical and environmental case management activities should be implemented (CDC, 2012;
ACCLPP, 2012).16 As a result of coordinated, intensive efforts at the national, state and local
levels, including those programs described above, blood Pb levels in all segments of the
population have continued to decline from levels observed in the past. For example, blood Pb
15 See, e.g., "Implementation of the Mercury-Containing and Rechargeable Battery Management Act"
http://www.epa.gov/epaoswer/hazwaste/recycle/battery.pdfand "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.
16 The CDC guidance on blood Pb levels is described further in section 3.1 below.
1-12
-------
levels for the general population of children 1 to 5 years of age have dropped to a geometric
mean level of 1.17 ug/dL in the 2009-2010 National Health and Nutrition Examination Survey
(NHANES) as compared to the geometric mean in 1999-2000 of 2.23 jig/dL and in 1988-1991 of
3.6 ug/dL (ISA, section 3.4.1; CD, AX4-2). Similarly, blood Pb levels in non-hispanic black,
Mexican American and lower socioeconomic groups, which are generally higher than those for
the general population, have also declined (ISA, section 3.4.1; Jones et al, 2009).
The EPA also participates in a broad range of international programs focused on reducing
environmental releases and human exposures in other countries. For example, the Partnership
for Clean Fuels and Vehicles program engages governments and stakeholders in developing
countries to eliminate Pb in gasoline globally.17 From 2007 to 2011, the number of countries
known to still be using leaded gasoline was reduced from just over 20 to six, with three of the six
also offering unleaded fuel. All six were expected to eliminate Pb from fuel in the subsequent
few years (USEPA, 201 le). The U.S. EPA is a contributor to the Global Alliance to Eliminate
Lead Paint, which is a cooperative initiative jointly led by the World Health Organization and
the United Nations Environment Programme (UNEP) to focus and catalyze the efforts to achieve
international goals to prevent children's Pb exposure from paints containing Pb and to minimize
occupational exposures to Pb paint. This alliance has the broad objective of promoting a phase-
out of the manufacture and sale of paints containing Pb and eventually to eliminate the risks that
such paints pose. The UNEP is also engaged on the problem of managing wastes containing Pb,
including lead-containing batteries. The Governing Council of the UNEP, of which the U.S. is a
member, has adopted decisions focused on promoting the environmentally sound management of
products, wastes and contaminated sites containing Pb and reducing risks to human health and
the environment from Pb and cadmium throughout the life cycles of those substances (UNEP
Governing Council, 2011, 2013). EPA is also engaged in the issue of environmental impacts of
spent lead-acid batteries internationally through the Commission for Environmental Cooperation
(CEC), where the EPA Administrator along with the cabinet-level or equivalent representatives
of Mexico and Canada comprise the CEC's senior governing body (CEC Council).18
17 International programs in which the U.S. participates, including those identified here, are described at
several web sites: http://epa.gov/international/air/pcfV.html, http://www.unep.org/transport/pcfVA
http://www.unep.org/hazardoussubstances/Home/tabid/197/hazardoussubstances/LeadCadmium/PrioritiesforAction/
GAELP/tabid/6176/Default.aspx
18 The CEC was established to support cooperation among the North American Free Trade Agreement
partners to address environmental issues of continental concern, including the environmental challenges and
opportunities presented by continent-wide free trade.
1-13
-------
1.3 SCOPE OF CURRENT REVIEW: FATE AND MULTIMEDIA PATHWAYS OF
AMBIENT AIR LEAD
The multimedia and persistent nature of Pb contributes complexities to the review of the
Pb NAAQS unlike issues addressed in other NAAQS reviews.19 As described in section 1.1,
NAAQS are established to protect public health with an adequate margin of safety, and public
welfare from known or anticipated adverse effects, from air pollutants (substances emitted to
ambient air). Since Pb distributes from air to other media and is persistent, our review of the
NAAQS for Pb considers the protection provided against such effects associated both with
exposures to Pb in ambient air and with exposures to Pb that makes its way into other media
from ambient air. Additionally, in assessing the adequacy of protection afforded by the current
NAAQS, we are mindful of the long history of greater and more widespread atmospheric
emissions that occurred in previous years (both before and after establishment of the 1978
NAAQS) and that contributed to the Pb that exists in human populations and ecosystems today.
Likewise, we also recognize the role of other, nonair sources of Pb now and in the past that also
contribute to the Pb that exists in human populations and ecosystems today. As in the last Pb
NAAQS review, this backdrop of environmental Pb exposure, and its impact on the populations
and ecosystems which may be the subjects of the currently available scientific evidence,
complicates our consideration of the health and welfare protection afforded by the current
NAAQS. In the first section below, we summarize the environmental pathways of human and
ecosystem exposures to Pb emitted to ambient air and associated complexities. The subsequent
section briefly discusses the role of historically emitted Pb in our consideration of the adequacy
of the current NAAQS for Pb.
1.3.1 Environmental Distribution and Exposure Pathways
Lead emitted to ambient air is transported through the air and is also distributed to other
media through the process of deposition, which may occur in dry conditions or in association
with precipitation, as summarized further in section 2.3 below (ISA, section 2.7.2). Once
deposited, the fate of Pb is influenced by the type of surface onto which the particles deposit and
by the type and activity level of transport processes in that location. Precipitation and other
natural, as well as human-influenced, processes contribute to the fate of such particles, which
affects the likelihood of subsequent human and ecological exposures, e.g., tracking into nearby
houses or transport with surface runoff into nearby water bodies (ISA, sections 2.3 and 3.1). For
19 Some aspects of the review of the secondary standard for oxides of nitrogen and sulfur (completed in
2012), which involved consideration of pollutant transport and fate in nonair media with a focus on impacts to
aquatic ecosystems, have some similarity to considerations for Pb, while the Pb review also differs in other
important aspects.
1-14
-------
example, Pb particles deposited onto impervious surfaces, such as roadway, sidewalk or other
urban surfaces, may be more available for human contact while they remain on such surfaces or
are transferred to other human environments, such as on clothing or through resuspension and
infiltration (ISA, section 3.1.1.1). Deposited Pb can also be transported (by direct deposition or
stormwater runoff) to water bodies and into associated sediments, which may provide a storage
function for Pb in aquatic ecosystems (ISA, sections 2.3.2 and 6.2.1). Lead deposited in
terrestrial ecosystems can also be incorporated into vegetation and soil matrices (ISA, sections
2.3.3 and 6.2.1).
Figure 1-1 illustrates, in summary fashion, the pathways by which Pb emitted into
ambient air can be distributed in the environment, contributing to human and ecosystem
exposures. As shown in this figure, the multimedia distribution of Pb emitted into ambient air
(air-related Pb) contributes to multiple air-related pathways of human and ecosystem exposure
(ISA, sections 3.1.1 and 3.7.1).20 Figure 1-1 additionally illustrates that air-related pathways
may involve media other than air, including indoor and outdoor dust, soil, surface water and
sediments, vegetation and biota. As recognized by the figure and discussed more completely in
the subsections below, Pb occurring in indoor and outdoor environments that has not passed
through ambient air (nonair Pb) may complicate our consideration of ambient air related Pb
exposures. Further, the persistence of Pb and the associated environmental legacy of historical
releases pose an additional complication, also discussed below, with regard to consideration of
exposures associated with current Pb emissions.
20 The exposure assessment for children performed for the review completed in 2008 employed available
data and methods to develop estimates intended to inform a characterization of these pathways, as described in the
rulemaking notices for that review (73 FR 29184; 73 FR 66964) and the associated health risk assessment report
(USEPA, 2007).
1-15
-------
Current Pb Emissions
to Ambient Air
Ecosystem
Exposures
Human Exposures
(Inhalation and Ingestion)
Wildlife, Livestock, Crops
Human Population
(body burden)*
Compartments marked by asterisk may also include Pb emitted to air in the past
and Pb from nonair sources (released now and in the past). Depending on the
compartment, nonair sources may include wastewater releases to surface water or
Pb usage in paint, drinking water distribution or food processing/packaging.
Note: Arrows indicate general pathways by which Pb distributes in environment and human populations. Individual
pathway significance varies with location- and receptor-specific factors.
Figure 1-1. Pathways of human and ecosystem exposure to lead from ambient air.
1.3.1.1 Human Exposure Pathways
Air-related Pb exposure pathways for humans include inhalation of ambient air or
ingestion of food, water or other materials, including dust and soil, that have been contaminated
through a pathway involving Pb deposition from ambient air (ISA, section 3.1.1.1). Ambient air
inhalation pathways include both inhalation of air outdoors and inhalation of ambient air that has
infiltrated into indoor environments. The air-related ingestion pathways occur as a result of Pb
passing through the ambient air, being distributed to other environmental media and contributing
to human exposures via contact with and ingestion of indoor and outdoor dusts, outdoor soil,
food and drinking water. The various inhalation and ingestion air-related pathways may vary
with regard to the time in which they respond to changes in air Pb concentrations. For example,
human exposure pathways most directly involving Pb in ambient air and exchanges of ambient
air with indoor air (e.g., inhalation) can respond most quickly, while pathways involving
1-16
-------
exposure to Pb deposited from ambient air into the environment (e.g., diet) may be expected to
respond more slowly. The extent of this will be influenced by the magnitude of change, as well
as - for deposition-related pathways - the extent of prior deposition and environment
characteristics influencing availability of prior deposited Pb (section 1.3.1.2 below).
Lead currently occurring in nonair media may also derive from sources other than
ambient air (nonair Pb sources), as summarized further in section 2.3 below (ISA, section 3.7.1).
For example, Pb in dust inside some houses or outdoors in some urban areas may derive from the
common past usage of leaded paint, while Pb in drinking water may derive from the use of
leaded pipe or solder in drinking water distribution systems (ISA, section 3.1.3.3). We also
recognize the history of much greater air emissions of Pb in the past, such as that associated with
leaded gasoline usage and higher industrial emissions (as summarized in section 2.1.1 below)
which have left a legacy of Pb in other (nonair) media.
The relative importance of different pathways of human exposure to Pb, as well as the
relative contributions from Pb resulting from recent and historic air emissions and from nonair
sources, vary across the U.S. population as a result of both extrinsic factors, such as a home's
proximity to industrial Pb sources or its history of leaded paint usage, and intrinsic factors, such
as a person's age and nutritional status (ISA, sections 5.1, 5.2, 5.2.1, 5.2.5 and 5.2.6). Thus, the
relative contributions from specific pathways is situation specific (ISA, p. 1-11), although a
predominant Pb exposure pathway for very young children is the incidental ingestion of indoor
dust by hand-to-mouth activity (ISA, section 3.1.1.1). For adults, however, diet may be the
primary Pb exposure pathway (2006 CD, section 3.4). Similarly, the relative importance of air-
related and nonair-related Pb also varies with the relative magnitudes of exposure by those
pathways, which may vary with different circumstances. For example, relative contributions to a
child's total Pb exposure from air-related exposure pathways compared to other (nonair) Pb
exposures depend on many factors, including ambient air concentrations and air deposition in the
area where the child resides (as well as in the area from which the child's food derives), as well
as access to other sources of Pb exposure such as Pb paint, tap water affected by plumbing
containing Pb, and lead-tainted products. Studies indicate that in the absence of paint-related
exposures, Pb from other sources such as nearby stationary sources of Pb emissions may
dominate a child's Pb exposures (ISA, sections 3.1 and 3.1.3.2; 2006 CD, section 3.2.3). In
other cases, such as children living in older housing with peeling paint or where renovations have
occurred, the dominant source of Pb exposure may be dust from leaded paint used in the house in
the past. Depending on Pb levels in a home's tap water, drinking water can sometimes be a
significant source. Lead exposure may also be the result of a mixture of contributions from
multiple sources, with no one source dominating. Our understanding of the relative contribution
of air-related Pb to ingestion exposure pathways is limited by the paucity of studies that parse
1-17
-------
ingestion exposure pathways with regard to air-related and nonair Pb. Our understanding of the
relative contribution of air-related Pb associated with historical emissions and that from recent
emissions is similarly limited, as discussed further in section 1.3.2 below.
1.3.1.2 Ecosystem Exposure Pathways
The distribution of Pb from ambient air to other environmental media also influences the
exposure pathways in terrestrial and aquatic ecosystems. Exposure of terrestrial animals and
vegetation to air-related Pb can occur by contact with ambient air or by contact with soil, water
or food items that have been contaminated by Pb from ambient air (ISA, section 6.2). Transport
of Pb into aquatic systems similarly provides for exposure of biota in those systems, and
exposures may vary among systems as a result of differences in sources and levels of
contamination, as well as characteristics of the systems themselves. In addition to Pb contributed
by current atmospheric deposition, Pb may occur in aquatic systems as a result of nonair sources
such as industrial discharges or mine-related drainage, of historical air Pb emissions (e.g.,
contributing to deposition to a water body or via runoff from soils near historical air sources) or
combinations of different types of sources (e.g., resuspension of sediments contaminated by
urban runoff and surface water discharges).
The persistence of Pb contributes an important temporal aspect to lead's environmental
pathways, and the time (or lag) associated with realization of the impact of air Pb concentrations
on concentrations in other media can vary with the media (e.g., ISA, section 6.2.2). For example,
exposure pathways most directly involving Pb in ambient air or surface waters can respond more
quickly to changes in ambient air Pb concentrations while pathways involving exposure to Pb in
soil or sediments generally respond more slowly. An additional influence on the response time
for nonair media is the environmental presence of Pb associated with past, generally higher, air
concentrations. For example, after a reduction in air Pb concentrations, the time needed for
sediment or surface soil concentrations to indicate a response to reduced air Pb concentrations
might be expected to be longer in areas of more substantial past contamination than in areas with
lesser past contamination. Thus, considering the Pb concentrations occurring in nonair media as
a result of air quality conditions that meet the current NAAQS is a complexity of this review, as
it also was, although to a lesser degree, with regard to the prior standard in the last review.
1.3.2 Considerations Related to Historically Emitted Lead
In reviews of NAAQS, the overarching consideration of each review is first focused on
the general question as to whether the currently available information supports or calls into
question the adequacy of the current standard(s). In addressing that consideration for the
NAAQS for Pb, our focus is on Pb emitted to ambient air under conditions meeting the current
standard and its potential to cause health or welfare effects as a result of exposures to Pb in air or
1-18
-------
in other media. Our framing of the focus in this way differs from that for NAAQS reviews
involving other pollutants. We frame the focus in this way in consideration of the multiple
exposure pathways for Pb currently being emitted and in consideration of the persistence of Pb in
the environment over time, a characteristic which does not affect reviews of other NAAQS. In
considering the case for Pb, however, we recognize that, because of its persistence, both recent
emissions to ambient air and the substantial emissions of the past contribute to current Pb
exposures (via multiple exposure pathways, as summarized in section 1.4.1 above). And we
recognize that past Pb emissions contributed to many situations where air concentrations were
well in excess of the current Pb standard, and may continue to contribute to exposures even
where air concentrations are below the current standard. Yet our task in this and every NAAQS
review is focused on assessing the adequacy of the current standard.
The substantial historical emissions to air and releases to nonair media contributed to
human and environmental exposures in the past (e.g., 1978 CD, 1986 CD, 2006 CD, ISA).
Because of the persistence of Pb, historical exposures associated with both air-related and
nonair-related sources have contributed a legacy of Pb that is now stored within older humans
and ecosystems. For example, concentrations of Pb in the bone and blood of older members of
the U.S. population, who lived during the time of widespread air emissions associated with
leaded gasoline usage (as well as higher industrial emissions) under the previous Pb NAAQS or
prior to establishment of any Pb NAAQS, are greater than what would result from air quality
conditions allowed by the current, more restrictive NAAQS. Epidemiological studies of these
populations, in which this exposure history is represented by current bone or blood Pb
concentrations, contribute to the overall evidence base regarding lead-related health effects (as
discussed in chapter 3 below). Such studies of these historically exposed populations, however,
are generally less informative in judging the adequacy of the current primary standard (as
discussed in chapter 3 below). This is in contrast to epidemiological studies of very young
populations with much shorter and more recent exposure histories (also discussed in chapter 3).
Substantial and widespread atmospheric emissions of Pb in the U.S. (as well as releases
to other media) extend back through the 19th century (Yohn et al, 2004; Jackson et al., 2004;
Graney et al., 1995). These historical emissions contributed to the distribution of Pb within and
well beyond the U.S. (ISA, section 2.5.5; Reuer and Weiss, 2002; McConnell and Edwards,
2008). Although it has not been completely and totally characterized, multiple aspects of the
legacy of this widespread distribution have been documented and described. The current
concentrations of Pb in U.S. ecosystems thus reflect the influence of greater air emissions that
occurred in the past, under the prior Pb NAAQS and prior to establishment of any Pb NAAQS.21
21 The current distribution of Pb in U.S. ecosystems also reflects historical nonair releases.
1-19
-------
As described further in section 2.3 below, media in ecosystems across the U.S. are still
recovering from the past period of greater atmospheric emissions and deposition that is
documented in media such as soil, aquatic sediments and peat bogs (2006 CD, section 2.3.1;
ISA, section 2.6.2). Core samples of these media show a pattern of Pb concentrations in
deposited material that peaks around the 1970s followed by marked decline in more recent years
(2006 CD, section 2.3.1; ISA section 2.6.2). Individual ecosystem responses differ with regard
to their rates of change in media concentrations due to the extent of contamination in individual
systems as well as the influence of ecosystem-specific characteristics (further described in
section 2.3 below). Thus, the time required for these ecosystem media to come to a condition
that is relatively stable with time (i.e., "steady-state") will also vary, and the resulting range of
"steady-state" media concentrations in U.S. ecosystems under ambient air concentrations
consistent with the current NAAQS are unknown. Future research may better inform our
understanding in this area.
In considering the array of ecological effects evidence in this review, we recognize that
evidence of effects pertaining to the concentrations associated with the past, higher emissions (as
well as from nonair sources), while generally informative to our understanding of welfare effects
associated with environmental Pb, does not directly inform our consideration of welfare effects
that might be anticipated under the current secondary standard and thus may be generally less
informative in judging the adequacy of the current standard. The availability of information on
whether adverse effects could be anticipated from the Pb in terrestrial and aquatic ecosystems
that results from air quality conditions allowed by the current, more restrictive NAAQS is
discussed in chapter 5, with consideration of the current NAAQS discussed in chapter 6.
1.4 GENERAL ORGANIZATION OF THE DOCUMENT
Following this introductory chapter, this document is organized into three main parts: the
characterization of ambient Pb; lead-related health effects and the primary Pb NAAQS; and lead-
related welfare effects and the secondary Pb NAAQS. The characterization of ambient Pb is
presented in Chapter 2 and includes information on Pb properties in ambient air, current Pb
emissions and air quality patterns, historic trends, and background levels. Chapter 2 also
describes the Pb NAAQS surveillance and other Pb monitoring networks. In recognition of the
multimedia nature of Pb and the distribution into other media of Pb emitted into the air, Chapter
2 also includes information on Pb in media other than air including outdoor dust, soil, surface
water and sediment. This chapter provides a frame of reference for exposure and risk-related
considerations and subsequent discussion of the Pb NAAQS.
Chapters 3 and 4 comprise the second main part of this document, dealing with human
health and the primary standard. These chapters are organized around a series of questions,
1-20
-------
building on those identified in the IRP, that address the key policy-relevant issues related to the
primary standard. Chapter 3 presents an overview of key policy-relevant health effects evidence
and major health-related conclusions from the ISA; an examination of issues related to the
quantitative assessment of health risks; key results from quantitative assessments together with a
discussion of uncertainty and variability in the results; and discussion of the public health
implications of the evidence and exposure/risk information. Chapter 4 includes staffs
consideration of the scientific evidence and exposure/risk information related to the primary
standard and associated conclusions related to the adequacy of the current primary standard.
Chapters 5 and 6 comprise the third main part of this document. These chapters are
similarly organized around a series of questions, building on those identified in the IRP, that
address the key policy-relevant issues related to the secondary standard. Chapter 5 presents an
overview of welfare effects evidence related to these key policy-relevant issues and major
welfare effects-related conclusions from the ISA; an examination of issues related to the
screening-level ecological risk assessment; and key results from the risk assessment together
with a discussion of uncertainty and variability in the results; and discussion of the public
welfare implications of the quantitative assessment with regard to the current standard. The final
chapter, chapter 6, includes staffs conclusions related to the adequacy of the current secondary
standard.
1.5 REFERENCES
ACCLPP (2012) Low Level Lead Exposure Harms Children: A Renewed Call for Primary Prevention. Report of
the Advisory Committee on Childhood Lead Poisoning Prevention of the Centers for Disease Control and
Prevention. January 4, 2012. Available at: http://www.cdc.gov/nceh/lead/ACCLPP/blood lead levels.htm
CDC. (2012) CDC Response to Advisory Committee on Childhood Lead Poisoning Prevention Recommendations
in "Low Level Lead Exposure Harms Children: A Renewed Call of Primary Prevention." Available at:
http://www.cdc.gov/nceh/lead/ACCLPP/blood lead levels.htm
Frey, H.C. (201 la) Letter from Dr. H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee Lead
Review Panel, to Administrator Lisa P. Jackson. Re: Consultation on EPA's Draft Integrated Review Plan
for the National Ambient Air Quality Standards for Lead. May 25, 2011.
Frey, H.C. (20 lib) Letter from Dr. H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee Lead
Review Panel, to Administrator Lisa P. Jackson. Re: Consultation on EPA's Review of the National
Ambient Air Quality Standards for Lead: Risk and Exposure Assessment Planning Document. October 14,
2011.
Frey, H.C. (2013a) Letter from Dr. H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee and Clean
Air Scientific Advisory Committee Lead Review Panel, to Acting Administrator Bob Perciasepe. Re:
CAS AC Review of the EPA's Integrated Science Assessment for Lead (Third External Review Draft -
November 2012). June 4, 2013.
Frey, H.C. (2013b) Letter from Dr. H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee and Clean
Air Scientific Advisory Committee Lead Review Panel, to Acting Administrator Bob Perciasepe. Re:
1-21
-------
CASAC Review of the EPA's Policy Assessment for Lead (External Review Draft - January 2013). June 4,
2013.
Frey, H.C. and Samet, J.M. (2011) Letter from Drs. H. Christopher Frey, Chair, Clean Air Scientific Advisory
Committee Lead Review Panel, and Jonathan M. Samet, Chair, Clean Air Scientific Advisory Committee,
to Administrator Lisa P. Jackson. Re: CASAC Review of the EPA's Integrated Science Assessment for
Lead (First External Review Draft - May 2011). December 9, 2011.
ICF International. (2006) Lead Human Exposure and Health Risk Assessments and Ecological Risk Assessment for
Selected Areas. Pilot Phase. Draft Technical Report. Prepared for the U.S. EPA's Office of Air Quality
Planning and Standards, Research Triangle Park, NC. December.
Jackson, L. (2009) Memorandum from Administrator Lisa Jackson, Subject: Development of regulations and
policies. September 11, 2009. Available at:
http://www.epa.gov/ttn/naaqs/pdfs/NAAQSReviewProcessMemo52109.pdf
Samet, J.M. and Frey, H.C. (2012) Letter from Drs. Jonathan M. Samet, Chair, Clean Air Scientific Advisory
Committee and H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee Lead Review Panel,
to Administrator Lisa P. Jackson. Re: CASAC Review of the EPA's Integrated Science Assessment for
Lead (Second External Review Draft - February 2012). July 20, 2012.
UNEP Governing Council (2011) Proceedings of the Governing Council/Global Ministerial Environment Forum at
its twenty-sixth session. Decision number 26/3. UNEP/GC.26/19. 24 February 2011. Available at:
http://www.unep.org/gc/gc26/docs/Proceedings/K1170817 E-GC26-19 Proceedings.pdf
UNEP Governing Council (2013) Decisions adopted by the Governing Council at its twenty-seventh session and
first universal session. Decision 27/12: Chemicals and waste management. February 2013. Available at:
http://www.unep.org/GC/GC27/Docs/decisions/GC 27 decisions-English.pdf
U.S. Environmental Protection Agency. (1977) Air quality criteria for lead. Research Triangle Park, NC: Health
Effects Research Laboratory, Criteria and Special Studies Office; EPA report no. EPA-600/8-77-017.
Available from: NTIS, Springfield, VA; PB-280411.
U.S. Environmental Protection Agency. (1986a) 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.
U.S. Environmental Protection Agency. (1986b) Lead effects on cardiovascular function, early development, and
stature: an addendum to U.S. EPA Air Quality Criteria for Lead (1986). In: Air quality criteria for lead, v.
1. Research Triangle Park, NC: Office of Health and Environmental Assessment, Environmental Criteria
and Assessment Office; pp. A1-A67; EPA report no. EPA-600/8-83/028aF. Available from: NTIS,
Springfield, VA; PB87-142378.
U.S. Environmental Protection Agency. (1989) Review of the national ambient air quality standards for lead:
Exposure analysis methodology and validation: OAQPS staff report. Research Triangle Park, NC: Office of
Air Quality Planning and Standards; report no. EPA-450/2-89/011. Available on the web:
http://www.epa.gov/ttn/naaqs/standards/pb/data/rnaaqsl eamv.pdf
U.S. Environmental Protection Agency. (1990a) Air quality criteria for lead: supplement to the 1986 addendum.
Research Triangle Park, NC: Office of Health and Environmental Assessment, Environmental Criteria and
Assessment Office; report no. EPA/600/8-89/049F. Available from: NTIS, Springfield, VA; PB91-138420.
U.S. Environmental Protection Agency. (1990b) Review of the national ambient air quality standards for lead:
assessment of scientific and technical information: OAQPS staff paper. Research Triangle Park, NC: Office
1-22
-------
of Air Quality Planning and Standards; report no. EPA-450/2-89/022. Available from: NTIS, Springfield,
VA; PB91-206185. Available on the web: http://www.epa.gov/ttn/naaqs/standards/pb/data/rnaaqsl asti.pdf
U.S. Environmental Protection Agency. (1991) U.S. EPA Strategy for Reducing Lead Exposure. Available from
U.S. EPA Headquarters Library/Washington, D.C. (Library Code EJBD; Item Call Number: EAP
100/1991.6; OCLC Number 2346675). http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_pr.html
U.S. Environmental Protection Agency. (2005a) Project Work Plan for Revised Air Quality Criteria for Lead.
CASAC Review Draft. National Center for Environmental Assessment, Research Triangle Park, NC.
NCEA-R-1465. Available at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb cr_pd.html
U.S. EPA (U.S. Environmental Protection Agency). (2005b). All ages lead model (AALM) (Version Draft 1.05)
[Computer Program]. Research Triangle Park, NC: U.S. Environmental Protection Agency, National
Center for Environmental Assessment.
U.S. Environmental Protection Agency. (2006a) Plan for Review of the National Ambient Air Quality Standards for
Lead. Office of Air Quality Planning and Standards, Research Triangle Park, NC. Available at:
http://www.epa.gov/ttn/naaqs/standards/pb/s_pb cr_pd.html
U.S. Environmental Protection Agency. (2006b) Air Quality Criteria for Lead. Washington, DC, EPA/600/R-
5/144aF. Available online at: http://www.epa. gov/ttn/naaqs/standards/pb/s jb cr.html
U.S. Environmental Protection Agency. (2006c) Analysis Plan for Human Health and Ecological Risk Assessment
for the Review of the Lead National Ambient Air Quality Standards. Office of Air Quality Planning and
Standards, Research Triangle Park, NC. Available at:
http://www.epa.gov/ttn/naaqs/standards/pb/s_pb cr_pd.html
U.S. Environmental Protection Agency. (2007a) Lead: Human Exposure and Health Risk Assessments for Selected
Case Studies, Volume I. Human Exposure and Health Risk Assessments - Full-Scale and Volume II.
Appendices. Office of Air Quality Planning and Standards, Research Triangle Park, NC. EPA-452/R-07-
014a and EPA-452/R-07-014b. http://www.epa.gov/ttn/naaqs/standards/pb/sjb crtd.html
U.S. Environmental Protection Agency. (2007b) Review of the National Ambient Air Quality Standards for Lead:
Policy Assessment of Scientific and Technical Information, OAQPS Staff Paper. Office of Air Quality
Planning and Standards, Research Triangle Park, NC. EPA-452/R-07-013. Available at:
http://www.epa.gov/ttn/naaqs/standards/pb/sjb crsp.html
U.S. Environmental Protection Agency. (201 la) Integrated Review Plan for the National Ambient Air Quality
Standards for Lead. Research Triangle, NC. EPA-452/R-11-008. Available online at:
http://www.epa.gov/ttn/naaqs/standards/pb/sjb index.html
U.S. Environmental Protection Agency. (201 Ib) Integrated Review Plan for the National Ambient Air Quality
Standards for Lead. External Review Draft. Research Triangle, NC. EPA-452/D-11-001. Available online
at: http://www.epa.gov/ttn/naaqs/standards/pb/sjb index.html
U.S. Environmental Protection Agency. (201 Ic) Integrated Science Assessment for Lead (First External Review
Draft). Washington, DC, EPA/600/R-10/075A. Available online at:
http://www.epa.gov/ttn/naaqs/standards/pb/sjb index.html
U.S. Environmental Protection Agency. (201 Id) Review of the National Ambient Air Quality Standards for Lead:
Risk and Exposure Assessment Planning Document. Office of Air Quality Planning and Standards,
Research Triangle Park, NC. EPA/452/P-11-003. Available at:
http://www.epa.gOv/ttn/naaqs/standards/pb/s pb 2010 pd.html
1-23
-------
U.S. Environmental Protection Agency. (201 le) Partnership for Clean Fuels and Vehicles: Evaluation of the Design
and Implementation of the Lead Campaign. Final Report. Document number EPA-100-R-11-008. Office of
Policy, Washington, DC. December 2011.
U.S. Environmental Protection Agency. (2012a) Integrated Science Assessment for Lead (Third External Review
Draft). Washington, DC, EPA/600/R-10/075C. Available online at:
http://www.epa.gov/ttn/naaqs/standards/pb/sjb 2010 isa.html
U.S. Environmental Protection Agency. (2012b) Integrated Science Assessment for Lead (Second External Review
Draft). Washington, DC, EPA/600/R-10/075B. Available online at:
http://www.epa.gov/ttn/naaqs/standards/pb/s_pb index.html
U.S. Environmental Protection Agency. (2013a) Integrated Science Assessment for Lead. Washington, DC,
EPA/600/R-10/075F. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb 2010 isa.html
U.S. Environmental Protection Agency. (2013b) Policy Assessment for for the National Ambient Air Quality
Standards for Lead. External Review Draft. Research Triangle, NC. EPA-452/P-13-001. Available online
at: http://www.epa.gOv/ttn/naaqs/standards/pb/s pb 2010 pa.html.
1-24
-------
2 AMBIENT AIR LEAD
The focus for this Pb NAAQS review is on Pb derived from sources emitting Pb to
ambient air. As noted in section 1.3, air emissions contribute to concentrations in multiple
environmental media, and the role of nonair media is enhanced by the persistent nature of Pb.
Consequently this chapter discusses our current understanding of both Pb in ambient air and of
ambient air-related Pb in other media.
Lead emitted to the air is predominantly in particulate form, with the particles occurring
in various sizes (ISA, section 2.3).1 Once emitted, particle-bound Pb can be transported long or
short distances depending on particle size, which influences the amount of time spent in the
aerosol phase. Consistent with previous evidence, recent research on particulate matter with
mass median diameter of 2.5 and of 10 micrometers (PM2.5 and PMio) confirms the transport of
airborne Pb in smaller particles appreciable distances from its sources. For example, samples
collected at altitude over the Pacific Ocean, as well as the seasonal pattern of Pb-PlVfo.s at rural
sites in the western U.S., indicate transport of Pb from sources in Asia, although such sources
have been estimated to contribute less than 1 ng/m3 to western U.S. Pb concentrations (ISA,
sections 2.3.1 and 2.5.5; Murphy et al., 2007). In general, larger particles tend to deposit more
quickly, within shorter distances from emissions points, while smaller particles remain in aerosol
phase and travel longer distances before depositing (ISA, section 1.2.1). As summarized in
section 2.2.2 below, airborne concentrations of Pb near sources are much higher, and the
representation of larger particles generally greater, than at sites not directly influenced by
sources.
In this chapter, we discuss the current information on on sources and emissions of Pb to
ambient air (section 2.1), current ambient air monitoring methods and networks and associated
measurements (section 2.2) and the contribution of ambient air Pb to Pb in other media (section
2.3).
2.1 SOURCES AND EMISSIONS TO AMBIENT AIR
In this section we describe the most recently available information on sources and
emissions of Pb into the ambient air. The section does not provide a comprehensive list of all
sources of Pb, nor does it provide estimates of emission rates or emission factors for all source
categories. Rather, the discussion here is intended to identify the larger source categories, either
1 While in some circumstances Pb can be emitted in gaseous form, the Pb compounds that may be produced
initially in vapor phase can be expected to condense into particles upon cooling to ambient temperature and/or upon
oxidizing with mixing into the atmosphere (ISA, section 2.2.2.1; Gidney et al., 2010).
2-1
-------
on a national or local scale, and generally describe their emissions and distribution within the
U.S.
The primary data source for this discussion is the National Emissions Inventory (NEI) for
20082. The NEI is a comprehensive and detailed estimate of air emissions of both criteria and
hazardous air pollutants from air emissions sources. The NEI is generally prepared at three-year
intervals, such that the next NEI, for 2011, is currently under development. The NEI is prepared
by the EPA based primarily upon emission estimates and emission model inputs provided by
state, local, and tribal air agencies for sources in their jurisdictions, supplemented by data
developed by the EPA. Some of these estimates are required by regulation, while some are
voluntarily reported. For example, states are required to report Pb emissions from facilities
emitting more than 5 tons of Pb per year (tpy) and from facilities emitting greater than threshold
amounts for other criteria pollutants (e.g., 100 tpy of particulate matter or volatile organic
compounds; CFR 51, subpart A). Estimates of Pb emissions presented in this document (and in
the ISA) are drawn from the 2008 NEI version 3.3 As a result of various Clean Air Act
requirements, emissions standards implemented since 2008 for a number of industrial source
categories represented in the NEI are projected to result in considerably lower emissions at the
current time or in the near future. (Appendix 2A)
The following sections present information relative to 2008 Pb emissions on a national
and local scale. Lead is emitted from a wide variety of source types, some of which are small
individually but for which the cumulative emissions are large, and some for which the opposite is
true. For example, a source category may be composed of many small (i.e., low-emitting)
sources or of just a few very large (high-emitting) sources. Temporal trends in the national totals
of Pb emissions are presented in Section 2.1.1. Information about the emissions source types or
categories that are large on a national scale as of 2008 is presented in Section 2.1.2, while
information on the sources that are large at the local scale is presented in Section 2.1.3.
Additional information on data sources for, limitations of and our confidence in the information
summarized here is described in Appendix 2B.
2.1.1 Temporal Trends on a National Scale
Figure 2-1 shows the substantial downward trend in Pb emissions that has occurred over
the past several decades. The most dramatic reductions in Pb emissions occurred prior to 1990
in the transportation sector due to the removal of Pb from gasoline used in on-road vehicles.
Lead emissions were further reduced substantially between 1990 and 2008, with significant
2 http://www.epa.gov/ttn/chief/net/2008inventory.html
3 With regard to Pb emissions, the 2008 NEI, version 3 (January 2013) has been augmented with sources
not included in the 2008 NEI, version 2.
2-2
-------
reductions occurring in the metals industries at least in part as a result of national emissions
standards for hazardous air pollutants.
Highway Vehicles
Metal Working and Mining
Fuel Combustion
Piston Engine Aircraft
Miscellaneous
250 -i
200 -
1- 150
o
o
o
E 100 -
1970 1975 1980 1985 1990 1995 1999 2002 2005 2008
Figure 2-1. Temporal trend in U.S. air emissions of Pb: 1970-2008.
2.1.2 Sources and Emissions on National Scale - 2008
As indicated in Figure 2-1, the largest source sector emitting Pb into the atmosphere on a
national scale is aviation gasoline usage by piston engine driven aircraft. The next largest
nationally is metal working and mining. Considering the national estimates at a more detailed
scale, the largest source categories emitting Pb into the atmosphere on a national scale, after
emissions from aircraft operating on leaded fuel, are boilers and process heaters (fuel
combustion). The latter individually are generally small sources, which comprise a large
category when aggregated nationally (Table 2-1). The next largest categories are various metals
industries, including lead-specific industries (Table 2-1). Together these and other sources were
estimated to emit just under a thousand tpy of Pb in the U.S. in 2008.
2-3
-------
Table 2-1. U.S. Pb emissions by source categories estimated to emit at least 4 tpy.
Source Category Description
ALLCATEGORIESA
Aircraft operating on leaded fuel B
Industrial/Commercial/lnstitutional Boilers & Process Heaters
Utility Boilers
Iron and Steel Foundries
Integrated Iron and Steel Manufacturing
Steel Manufacturing: Electric Arc Furnaces
Secondary Lead Smelting
Primary Lead Smelting
Primary Copper Smelting
Mining
Military Base
Cement Production
Glass Manufacturing
Battery Manufacturing
Secondary Non-ferrous Metals (other)
Primary Non-ferrous Metals (other)
Carbon Manufacturing
Pulp and Paper Production
Secondary Copper Smelting
Commercial Marine Vessels
Fabricated Metal Products Manufacturing
Residential Heating
Municipal Waste Incineration
Sewage Sludge Incineration
Mineral Products Manufacturing
2008
Emissions (tons)
950
550
63
51
30
27
22
20
19 =
17
15
13
8
8
8
7
7
6
6
5
5
5
5
4
4
4
A - Emissions estimate totals from 2008 National Emissions Inventory, version 3 (January 2013) for point sources and
2008 NEI version 2 for nonpoint sources (residential heating).
B - This category includes Pb emitted at or near airports as well as Pb emitted in-flight. Lead emissions at or near
airports comprise 46% of the total aircraft Pb emissions inventory. Emissions value based on EPA estimates.
C - There is some uncertainty regarding the total emissions estimate for this source category in which there is one
operational smelter, which ceased smelter operations at this site at the end of 2013 (USEPA, 2012).
2-4
-------
Explanation of aggregation approaches used for Tables 2-1 and 2-2:
Facilities have numerous processes that can fall into different source categories and the NEI includes process-specific
emissions estimates. Source categories are groups of facilities that can be considered as the same type of emissions
source. In order to present the emissions for source categories (e.g., secondary copper smelting) rather than for processes
(e.g., Secondary Metal Production, Copper or Rotary Furnace) in Table 2-1, we aggregated processes for each facility and
then present national estimates for source categories. The source categories used were assigned using a three-tiered
approach. First, processes known to be affected by sector-specific rules were set to the source categories. This was done
for Utility Boilers, Portland Cement plants, Electric Arc Furnaces, Municipal Waste Combustors, and Taconite Ore facilities
(mapped to Integrated Iron and Steel Manufacturing). Other source categories did not use this first tier because the
processes in the inventory have not yet been mapped to other rules. Second, for processes that clearly map to source
categories, the inventory process descriptions (Source Classification Codes) were used to assign the source category. A
good example of this is for Industrial, Commercial, and Institutional Boilers and Process Heaters. For all remaining
processes, the Facility Type inventory field was mapped to a source category. Facility Types are the basis for aggregation
used in Table 2-2. Facility Types in the NEI were set manually by EPA staff for facilities greater than 0.5 tons of Pb and
using the North American Industrial Classification System (NAICS) codes for smaller facilities. This (setting of the facility
type) was done with consideration of the primary activity identified for the facility, which usually confirmed the NAICS code.
A facility only has a single Facility Type but can have multiple processes and source categories. For example, some
facilities are secondary metal processing plants for copper, aluminum, and non-ferrous metals, which divides their
emissions into Secondary Copper and Secondary Non-Ferrous metal source categories. In these cases, the facility
website was reviewed to try to assess the predominant activity and the NAICS code was considered as well, and a Facility
Type was set using the best judgement of EPA staff. However, the emissions for these facilities are split across multiple
processes as summed in Table 2-1. To prevent double counting of facility and state counts in Table 2-2, the Facility Type
was used so that each facility shows up only once in this table.
2.1.2.1 Stationary Sources
Since the last review of the Pb NAAQS, the EPA has completed a number of regulations
which will result in reduced Pb emissions from stationary sources regulated under the Clean Air
Act sections 112 and 129. For example, in January 2012, the EPA updated the National
Emission Standards for Hazardous Air Pollutants (NESHAP) for Secondary Lead Smelting (77
FR 555). These amendments to the original maximum achievable control technology standards
apply to facilities nationwide that use furnaces to recover Pb from lead-bearing scrap, mainly
from automobile batteries (15 existing facilities, one under construction). By the effective date
in 2014, this action is estimated to result in a Pb emissions reduction of 13.6 tpy across the
category (a 68% reduction). Also, the NESHAPs for Primary and Secondary Lead Smelting
were revised in 2011 and 2012, respectively (76 FR 70834, 77 FR 555), as well as more than a
dozen additional EPA actions taken in the past 5 years, which would not be reflected in the 2008
NEI estimates, will result in Pb emissions reductions (Appendix 2A).
2-5
-------
2.1.2.2 Mobile Sources
Forty years ago, combustion of leaded gasoline was the main contributor of Pb to the air.
In the early 1970s, the EPA set national regulations to gradually reduce the Pb content in
gasoline. In 1975, unleaded gasoline was introduced for motor vehicles equipped with catalytic
converters. The EPA banned the use of leaded gasoline in highway vehicles after December
1995.
Lead emissions from piston-engine aircraft operating on leaded fuel are currently the
largest source of Pb air emissions on a national scale. Lead is added to aviation gasoline
(commonly referred to as "avgas") used in most piston-engine aircraft in order to boost octane
and prevent engine knock.4 The most commonly used avgas, 100 Octane Low Lead, contains up
to 2.12 grams Pb per gallon (ASTM D 910). The Federal Aviation Administration estimates that
in 2008, 248 million gallons of avgas were consumed in the U.S.5 contributing an estimated 550
tons of Pb to the air that comprise 58% of the national Pb inventory.6 Leaded avgas is used at
approximately 20,000 airport facilities in the United States.
The EPA is currently collecting and evaluating information regarding emissions and air
concentrations of Pb resulting from avgas combustion by piston-engine aircraft (including
monitoring data described in section 2.2.1.1 below). This is part of an ongoing investigation
under section 231 of the Clean Air Act into the potential for these emissions to cause or
contribute to air pollution that may reasonably be anticipated to endanger public health or
welfare. This evaluation by the EPA is occurring separate from the NAAQS review. The EPA's
investigation includes substantial analytical work. The timeline for completion of this
investigation and possible issuance of a final endangerment determination includes completion
of necessary modeling and monitoring information and other data, development of a proposal
which will be published for public comment, review and analysis of comments received and
issuance of the final determination. If the EPA issues a positive determination that Pb emissions
from aircraft engines cause or contribute to air pollution that may reasonably be anticipated to
endanger public health or welfare, the EPA would then be required to propose and promulgate
emissions standards to control aircraft engine Pb emissions, and the Federal Aviation
4 Lead is not added to jet fuel used in commercial aircraft, military aircraft, or other turbine engine aircraft.
5 U.S. Department of Transportation Federal Aviation Administration Aviation Policy and Plans. FAA
Aerospace Forecast Fiscal Years 2010-2030. p.99. Available at:
http://www.faa.gov/about/office org/headquartersoffices/apl/aviation forecasts/aerospace forecasts/2010-
2030/media/2010%20Forecast%20Doc.pdf This document provides historical data for 2000-2008 as well as
forecast data.
6 EPA (2010) Calculating Piston-Engine Aircraft Airport Inventories for Lead for the 2008 National
Emissions Inventory. EPA-420-B-10-044. Available at:
http://www.epa.gov/otaq/regs/nonroad/aviation/420bl0044.pdf
2-6
-------
Administration would be required to promulgate regulations addressing the fuel used by those
aircraft. More information about EPA's actions is available at www.epa.gov/otaq/aviation.htm.
Vehicles used in racing are not regulated by the EPA under the Clean Air Act and can
therefore use alkyl-Pb additives to boost octane. The National Association for Stock Car Auto
Racing (NASCAR) formed a voluntary partnership with the EPA with the goal of permanently
removing alkyl-Pb from racing fuels used in the racing series now known as the Sprint Cup, the
Nationwide Series and the Camping World Truck Series. The major NASCAR race series now
use unleaded fuels.
Due to the presence of Pb as a trace contaminant in gasoline, diesel fuel and lubricating
oil, cars, trucks, and engines operating in nonroad equipment, marine engines and jet aircraft
emit small amounts of Pb (ISA, Section 2.2.2.6). Additional mobile sources of Pb include brake
wear, tire wear, and loss of Pb wheel weights (ISA, Section 2.2.2.6).
2.1.2.3 Natural Sources and Long-range Transport
Some amount of Pb in the air in the U.S. derives from natural sources, such as volcanoes,
sea salt, and windborne soil particles from areas free of anthropogenic activity and some may
also derive from anthropogenic sources of airborne Pb located outside of the U.S. (ISA, section
2.5.5). Emissions estimates for these sources, as well as forest wildfires and biogenic sources,
have not been developed for the NEI. Quantitative estimates for these processes remain an area
of significant uncertainty. Based on several different approaches, the ISA identifies several
estimates of the concentration of airborne Pb derived from natural sources. The estimates extend
no higher than 1 nanogram per cubic meter (ng/m3), and extend down as low as 0.02 ng/m3 (ISA,
section 2.5.5). The data available to derive such an estimate are limited and such a value might
be expected to vary geographically with the natural distribution of Pb.
Another contribution to U.S. airborne Pb concentrations is long-range transport such as
that associated with air masses carrying Pb from sources in Asia, where controls on Pb emissions
have lagged those in the U.S. and Canada (ISA, section 2.5.5; Osterberg et al., 2008). The most
recent estimates of contributions from Asia, however, conclude that the Asian contribution to
U.S. airborne Pb concentrations is generally less than 1 ng/m3 (ISA, section 2.5.5; Murphy,
2007; Ewing et al., 2010).
2.1.2.4 Previously Deposited Lead
Lead-bearing particles that occur in outdoor dust on soil or built surfaces (e.g., streets and
sidewalks) can be a source of airborne Pb as a result of particle resuspension (ISA, section
2.3.1.3). Proximity to major sources of Pb emissions, the extent of previous or historic
deposition, and the effectiveness of natural and human removal processes dictate how important
resuspension may be as a contribution to air Pb concentrations. In addition to resuspension and
2-7
-------
subsequent dispersion, surface water runoff (e.g., associated with rainfall) also plays a role in the
movement of Pb-bearing particles from outdoor surfaces to human-made or natural stormwater
sediment catchments (ISA, sections 1.2.1, 2.3.1.3, 2.3.2 and 2.3.2.4; Wong et al., 2006). Mean
residence time of street dust has been estimated for a low-traffic street (approximately 30
vehicles/hour) to be several months but less than a year (ISA, section 2.3.1.3; Allott et al 1990).
Outdoor dust may be resuspended into the air by wind or human-induced mechanical
forces, such that the main drivers of particle resuspension are typically mechanical stressors such
as vehicular traffic, construction and agricultural operations, and, generally to a lesser extent, the
wind (ISA, section 2.3.1.3; 2006 CD, section 2.3.3). Wind resuspension, often defined in terms
of a resuspension rate (the fraction of a surface contaminant released per unit time) is dependent
on many factors, including wind speed, soil/surface moisture, particle size, presence of saltating
particles and presence of vegetation; typical values range over several orders of magnitude (ISA,
section 3.3.1.3; 2006 CD, section 2.3.3). Vehicular resuspension results from shearing stress of
tires or turbulence generated by a passing vehicle and can be affected by a number of factors
including vehicle size, vehicle speed, soil or surface moisture, and particle size (ISA, section
2.3.1.3; 2006 CD, section 2.3.3). Variability and uncertainty in these factors, and with regard to
surface soil/dust composition, affect quantitative emissions estimates for these processes (2006
CD, section 2.3.3).7
The relative importance of resuspension of previously deposited dust particles as an
influence on airborne Pb concentrations will depend on site-specific circumstances, such as the
magnitude of Pb concentrations in the surface dust and air Pb contributions from nearby sources
of new Pb emissions, as well as with variation in the forces that influence particle resuspension.
For example, the highest air Pb concentrations associated with resuspension appear to occur in
areas of highly contaminated surface dust associated with historically active industrial sites,
which may or may not be currently active (ISA, sections 2.3.1.3). Air concentrations near such
sites with currently active facilities (e.g., metals industries) will reflect the impact of emissions
from the current industrial activity in addition to that from resuspension of any previously
deposited material (often a component of "fugitive" emissions estimates8). Accordingly, as
might be expected, the limited data available for comparison indicate the relative magnitude of
7 Quantitative estimates of resuspension-related emissions associated with many active industrial sources
(particularly metals sources) are included within the NEI, although such emissions associated with previously and
no longer active Pb sources are not as generally included in the NEI.
8 For example, emissions factors have been established to estimate fugitive emissions from resuspension of
previously deposited material as a result of vehicular traffic on facility roadways (USEPA, 1996-2011). Where used,
these estimates are combined with estimates for "process fugitives" (emissions that escape capture by control
devices) to estimate total fugitive emissions from a facility. Accordingly, control of resuspension resulting from
facility roadways, buildings or other property may be part of a strategy to meet regulatory emissions requirements
(e.g., national emissions standards for hazardous air pollutants for secondary lead smelting, 77 FR 556).
2-8
-------
air Pb concentrations associated with no-longer-active industrial sites to be generally lower than
that for active sites yet greater than that in locations somewhat removed from industrial sources
(section 2.2.2.2 below).
Lead-bearing particulate matter in other, non-industrial, locations of appreciable historic
Pb contamination, such as in soils or on surfaces in older urban areas or near older transportation
corridors may, if disturbed, also become suspended into the air and contribute to air Pb
concentrations, although the availability of such material for resuspension might be expected to
decline over time in most locations due to transport and removal processes. In older
transportation corridors or other locations not influenced by active industries, the significance of
resuspension (e.g., in terms of resultant air Pb concentrations) appears to be much less than that
associated with active industries or now-closed industries with substantial emissions in the past.9
For example, the available data indicate that current Pb concentrations near roadways are
substantially lower than those near large, currently active industrial sources (see ISA, sections
2.3.1.3 and 2.5.1.2 and Figures 2-9 and 2-11 below). In general, air Pb concentrations at sites
described as not influenced by an active industry are much lower than those near active sources
(see ISA, section 2.5.1.2 and Figure 2-11 below).
2.1.3 Sources and Emissions on Local Scale
Based on the 2008 estimates, the highest emissions in specific situations locally are from
different types of metals industries, 23 of which had 2008 estimates greater than or equal to 1.0
tpy Pb (Table 2-2). The geographic distribution of the facilities summarized in Table 2-2 is
presented in Figure 2-2.
9 Mass-balance analyses of emissions in southern California newly available in the last review suggested
that Pb in resuspended road dust may represent between 40% and 90% of Pb emissions in some areas (2006 CD, p.
2-65; ISA, section 3.2.2.7). Air Pb monitoring data near roadways, however, including those in California, indicate
Pb concentrations well below those near significant industrial sources and below the current Pb NAAQS (e.g., ISA,
section 3.5.1.2).
2-9
-------
Table 2-2. Facilities estimated to emit at least 0.50 tpy of Pb in 2008.
Facility Type
Primary Lead Smelting Plant
Steel Mill
Primary Copper Smelting/Refining Plant
Military Base
Secondary Lead Smelting Plant
Carbon or Graphite Plant
Primary Non-ferrous Metal Smelting/Refining Plant (not
Lead, Gold, Aluminum, or Copper)
Mines/Quarries
Ethanol Biorefineries
Portland Cement Manufacturing
Pulp and Paper Plant
Calcined Pet Coke Plant
Battery Plant
Wood Board Manufacturing Plant
Foundries, Iron and Steel
Foundries, Non-ferrous
Secondary Non-ferrous Metal Smelting/Refining Plant
(not Lead, Aluminum, or Copper)
Coke Battery
Electricity Generation via Combustion
Chemical Plant
Airport
Automobile/Truck or Parts Plant
Wastewater Treatment Facility
Munition or Explosives Plant
Glass Plant
Fabricated Metal Products Plant
Municipal Waste Combustor
Lumber/Sawmill
Plastic, Resin, or Rubber Products Plant
Taconite Processing Plant
Petroleum Storage Facility (Bulk Station)
Facilitk
No.
Facilities
1
14
4
4
5
1
1
5
2
1
2
1
3
1
3
3
2
2
2
1
6
1
1
1
;s emitting
No.
States
1
8
3
3
5
1
1
2
2
1
2
1
3
1
3
2
2
2
2
1
4
1
1
1
>1.0tpyA.B
Facility
Emissions
19.2°
1.0-9.8
2.3-8.8
1.4-7.2
1.4-7.1
6.3
5.4
1.6-3.8
1.5-3.8
3.3
2.5-3.0
2.5
1.5-2.5
2.3
1.1-2.3
1.2-2.0
1.2-2.0
1.0-1.8
1.0-1.7
1.7
1.0-1.3
1.2
1.0
1.0
Facilities c
< 1.0 and >
No.
Facilities
10
3
3
2
1
10
2
1
7
2
52
3
2
2
2
5
3
2
1
1
1
imitting
:0.50A.C
No.
States
9
3
2
2
1
8
2
1
5
2
17
2
2
2
2
4
3
1
1
1
1
A- Emissions totals from 2008 National Emissions Inventory, version 3 (January 2013), except in the case of airports for which EPA-specific
estimates were used.
B - This category includes facilities with total emissions estimates greater than or equal to 0.95 tpy.
C - This category includes facilities with total emissions estimates greater than or equal to 0.495 and less than 0.95 tpy.
D - There is additional uncertainty regarding this total emissions estimate for this facility, the only remaining operational primary Pb smelter in
the U.S., which ceased smelter operations at this site at the end of 2013 (USEPA, 2012).
2-10
-------
Airports with estimates <1.0 and =>0.50 tpy"
Airports with estimates <5.0 and =>1.0 tpy*
Study Airports
Facilities with estimates <1.0 and =>0.50 tpy**
^ Facilities with estimates <5.0 and =>1.0 tpy*
• Facilities with estimates => 5,0 tpy
Figure 2-2. Geographic distribution of facilities and airports estimated to emit at least 0.50 tpy of Pb in 2008.
2-11
-------
2.2 AMBIENT AIR QUALITY
The EPA and state and local agencies have been measuring Pb in the atmosphere since
the 1970s. In response to reduced emissions (see section 2.1), Pb concentrations have decreased
dramatically over that period. Currently, the highest concentrations occur near some metals
industries where some individual locations have concentrations that exceed the NAAQS. This
section describes the ambient Pb measurement methods, the sites and networks where these
measurements are made, and how the ambient Pb concentrations vary geographically and
temporally.
2.2.1 Air Monitoring
Ambient air Pb concentrations are measured by five national monitoring networks. The
networks include the State and Local Air Monitoring Sites (SLAMS) intended for Pb NAAQS
surveillance, the PM2.5 Chemical Speciation Network (CSN), the Interagency Monitoring of
Protected Visual Environments (IMPROVE) network, the National Air Toxics Trends Stations
(NATTS) network, and the Urban Air Toxics Monitoring program. All of the data from these
networks are accessible via EPA's Air Quality System (AQS):
http://www.epa.gov/ttn/airs/airsaqs/. In addition to these networks, various environmental
organizations have operated other sampling sites yielding data (which may or may not be
accessible via AQS) on ambient air concentrations of Pb, often for limited periods and/or for
primary purposes other than quantification of Pb itself. The subsections below describe each
network and the Pb measurements made at these sites.
2.2.1.1 Lead NAAQS Surveillance Network
This section describes sample collection, analysis and network aspects for the Pb SLAMS
network, the main purpose of which is surveillance for the Pb NAAQS. As such, the EPA
regulates how this monitoring is conducted in order to ensure accurate and comparable data for
determining compliance with the NAAQS. The code of federal regulations (CFR) at parts 50, 53
and 58 specifies required aspects of the ambient monitoring program for NAAQS pollutants.10
In order to be used in NAAQS attainment designations, ambient Pb concentration data must be
obtained using either the federal reference method (FRM) or a federal equivalent method (FEM).
The indicator for the current Pb NAAQS is Pb-TSP. However, in some situations,11 ambient Pb-
10 The FRMs for sample collection and analysis are specified in 40 CFR part 50, the procedures for
approval of FRMs and federal equivalent methods are specified in 40 CFR part 53 and the rules specifying
requirements for the planning and operations of the ambient monitoring network are specified in 40 CFR part 58.
11 The Pb-PMio measurements may be used for NAAQS monitoring as an alternative to Pb-TSP
measurements in certain conditions defined in 40 CFR part 58 Appendix C, section 2.10.1.2. These conditions
include where Pb concentrations are not expected to equal or exceed 0.10 micrograms per cubic meter as an
2-12
-------
PMio concentrations may be used in judging nonattainment. Accordingly, FRMs have been
established for Pb-TSP and for Pb-PMio. The current FRM for the measurement of Pb-TSP is
provided in 40 CFR part 50 Appendix G. This FRM includes sampling using a high-volume
TSP sampler that meets the design criteria identified in 40 CFR part 50 Appendix B and sample
analysis for Pb content using flame atomic absorption. There are 24 FEMs currently approved
for Pb-TSP.12 All 24 FEMs are based on the use of high-volume TSP samplers and a variety of
approved equivalent analysis methods.
A new FRM for Pb-PMio was promulgated as part of the 2008 review (40 CFR part 50
Appendix Q). This FRM is based on the PMio sampler defined in 40 CFR part 50 Appendix J
coupled with x-ray fluorescence (XRF) analysis. In addition, one FEM for Pb-PMio has been
finalized for the analysis of Pb-PMio based on inductively coupled plasma mass spectroscopy
(ICP-MS).
The current Pb monitoring network design requirements for NAAQS compliance
purposes (40 CFR part 58, Appendix D, paragraph 4.5) include two types of monitoring sites -
source-oriented monitoring sites and non-source-oriented monitoring sites. Source-oriented
monitoring sites are required near sources of air Pb emissions which are expected to or have been
shown to contribute to ambient air Pb concentrations in excess of the NAAQS. At a minimum,
there must be one source-oriented site located to measure the maximum Pb concentration in
ambient air resulting from each non-airport Pb source estimated to emit 0.50 or more tons of Pb
per year and from each airport estimated to emit 1.0 or more tons of Pb per year.13 The EPA
Regional Administrators may require additional monitoring beyond the minimum requirements
where the likelihood of Pb air quality violations is significant. Such locations may include those
near additional industrial Pb sources, recently closed industrial sources and other sources of
resuspended Pb dust, as well as airports where piston-engine aircraft emit Pb (40 CFR, part 58,
Appendix D, section 4.5(c)).
Monitoring agencies are also required, under 40 CFR, part 58, Appendix D, to conduct
non-source-oriented Pb monitoring at the NCore sites required in metropolitan areas with a
population of 500,000 or more.14 NCore is a network of multipollutant monitoring stations
arithmetic three-month mean and where the source of Pb emissions is expected to emit a substantial majority of its
Pb in the size fraction captured by PMio monitors.
12 A complete list of FEM can be found at the following webpage -
http://www.epa.gov/ttn/amtic/files/ambient/criteria/reference-equivalent-methods-list.pdf
13 The Regional Administrator may waive the requirement in paragraph 4.5(a) for monitoring near Pb
sources if the State or, where appropriate, local agency can demonstrate the Pb source will not contribute to a
maximum three-month average Pb concentration in ambient air in excess of 50 percent of the NAAQS level based
on historical monitoring data, modeling, or other means (40 CFR, part 58, Appendix D, section 4.5(a)(ii)).
14 Defined by the US Census Bureau - http://www.census.gov/population/www/metroareas/metroarea.html
2-13
-------
intended to meet multiple monitoring objectives that formally began in January 2011. The NCore
stations are a subset of the state and local air monitoring stations network and are intended to
support long-term trends analysis, model evaluation, health and ecosystem studies, as well as
NAAQS compliance. The complete NCore network consists of approximately 60 urban and 20
rural stations, including some existing SLAMS sites that have been modified for additional
measurements. Each state will contain at least one NCore station, and 46 of the states plus
Washington, DC, will have at least one urban station.
Either Pb-TSP or Pb-PMio monitoring may be performed at these sites. Of 50 NCore
sites measuring Pb concentrations as of April 2014, 28 are measuring Pb in TSP and 24 are
measuring Pb in PMio (two sites are measuring both Pb in TSP and Pb in PMio). While non-
source-oriented monitoring data can be used for purposes of NAAQS attainment designations, a
main objective for non-source-oriented monitoring is to gather information on neighborhood-
scale Pb concentrations that are typical in urban areas in order to better understand ambient air-
related Pb exposures for populations in these areas.
Source-oriented monitors near sources estimated to emit 1.0 tpy Pb were required to be
operational by January 1, 2010, and the remainder of the newly required source-oriented
monitors were required to be operational by December 27, 2011 (75 FR 81126). Currently,
approximately 260 Pb-TSP monitors are in operation; these are a mixture of source- and non-
source-oriented monitors. Figure 2-3 shows the geographic distribution of these monitors (in
addition to the airport study monitors described below) in the Pb NAAQS surveillance
network,15 with the Pb-TSP monitors existing at the time of the 2008 rulemaking indicated
separately from the newly sited Pb-TSP monitors.
; This figure reflects Pb-TSP monitors in AQS as of September 2012.
2-14
-------
Guam
Hawaii
o
2008 and earlier
2009 and later
Puerto Rico
Figure 2-3. Map of Pb-TSP monitoring sites in current Pb NAAQS monitoring network.
The current regulations also required one year of Pb-TSP monitoring (using FRM or
FEM methods) near 15 specific airports in order to gather additional information on the
likelihood of NAAQS exceedances near airports due to the combustion of leaded aviation
gasoline (75 FR 81126). These airports were selected based on three criteria: annual Pb
inventory between 0.5 ton/year and 1.0 ton/year, ambient air within 150 meters of the location of
maximum emissions (e.g., the end of the runway or run-up location), and airport configuration
and meteorological scenario that leads to a greater frequency of operations from one runway.
These characteristics were selected because they are expected, collectively, to identify airports
with the highest potential to have ambient Pb concentrations approaching or exceeding the Pb
NAAQS. Data from this monitoring study will be used to assess the need for additional Pb
monitoring at airports. These 15 sites (Figure 2-4) were intended to be operational no later than
December 27, 2011, although delays in monitor siting extended the installation of some of these
monitors into late 2012.
2-15
-------
Figure 2-4. Sites near airports at which one year of Pb-TSP monitoring is required.16
2.2.1.2 Other Lead Monitoring Networks
The NATTS network, designed to monitor concentrations of hazardous air pollutants
including Pb compounds, included 25 sites measuring Pb-PMio as of 2012. Most of these sites
(20) are in urban areas (Figure 2-5). In addition to the NATTS network, as of 2012, states were
collecting Pb-PMio at an additional 22 sites (most as part of the Urban Air Toxics Monitoring
program). All collect particulate matter as PMio for toxic metals analysis using either a high-
volume PMio sampler or a low volume PMio sampler, typically on a 1 in 6 day sampling
schedule. Most of these monitoring locations are not measuring using FRM/FEM methods at
this time. Lead in the collected sample is generally quantified via an ICP/MS method. The
standard operating procedure for metals by ICP/MS is available at:
16 The 15 Airports are: Merrill Field (Anchorage, AK), Pryor Field Regional (Limestone, AL), Palo Alto
Airport of Santa Clara County and Reid-Hillview (both in Santa Clara, CA), McClellan-Palomar and Gillespie Field
(both in San Diego, CA), San Carlos (San Mateo, CA), Nantucket Memorial (Nantucket, MA), Oakland County
International (Oakland, MI), Republic and Brookhaven (both in Suffolk, NY), Stinson Municipal (Bexar, TX),
Northwest Regional (Denton, TX), Harvey Field (Snohomish, WA), and Auburn Municipal (King, WA).
2-16
-------
http://www.epa.gov/ttn/atntic/airtox.httnl . As noted in section 2.2.1.1 above, non-source-
oriented Pb monitoring using FRM/FEMs that is required at the 51 NCore sites with a population
of 500,000 or more (shown in Figure 2-5) may be Pb-PMio. As shown in Figure 2-5, there are
some cases where states have addressed their NATTS and NCore Pb monitoring needs with the
use of a single monitoring site or may have nearby sites.
Alaska
Guam Hawaii
* NCore/NATTS
^ NCore
* NATTS
• Other
Puerto Rico
Figure 2-5. Pb-PMio monitoring sites.
17
17 Presented on this map are all NCore sites where FRM/FEM Pb monitoring is required along with other
sites actively monitoring Pb-PMio (by any method) based on having 2012 data in AQS as of September 2012.
2-17
-------
Two networks measure Pb in PM2.5, the EPA CSN and the IMPROVE network. The
CSN consists of 53 long-term trends sites (commonly referred to as the Speciation Trends
Network or STN sites) and approximately 150 supplemental sites, all operated by state and local
monitoring agencies. Most STN sites operate on a 1 in 3 day sampling schedule, while most
supplemental sites operate on a 1 in 6 day sampling schedule. All sites in the CSN network
determine Pb concentrations in PM2.5 samples. Lead is quantified via the XRF method.18 Data
are accessible through AQS. The locations of the CSN are shown in Figure 2-6. Nearly all of the
CSN sites are in urban areas, often at the location of highest known PM2.5 concentrations. The
first CSN sites began operation around 2000.
The IMPROVE network is administered by the National Park Service, largely with
funding by the EPA, on behalf of federal land management agencies and state air agencies that
use the data to track trends in rural visibility. Lead in PM2.5 is quantified via the XRF method, as
in the CSN. Data are managed and made accessible mainly through the VIEWS website
(http://vista.cira.colostate.edu/views/) but are also available via AQS. Samplers are operated by
several different federal, state, and tribal host agencies on the same 1 in 3 day schedule as the
STN. In the IMPROVE network, PM2.5 monitors are placed in "Class I" areas (including
National Parks and wilderness areas) and are mostly in rural locations (Figure 2-6). The oldest
of these sites began operation in 1988, while many others began in the mid 1990s. There are 110
formally designated IMPROVE sites, which are located in or near national parks and other Class
I visibility areas, virtually all of these being rural. Approximately 80 additional sites at various
urban and rural locations, requested and funded by various parties, are also informally treated as
part of the network.
18 The standard operating procedure for metals by XRF is available at:
http://www.epa.gov/ttnamtil/files/ambient/pm25/spec/xrfsop.pdf.
2-18
-------
A- v v •
5 .v^--_
V > W^/"
• ^ ;**^ A \ J9
IMPROVE
Alaska
D 25D 5DD I ,000 Miles 1 7l'l '±ri T'Rn M||P = D 245 490
0 25 50 100 Miles
Figure 2-6. Pb-PM2.s monitoring sites in CSN and IMPROVE networks (2012).
2.2.1.3 NAAQS Surveillance Monitoring Considerations
In this section, aspects of the methods for sampling and analysis of the Pb are reviewed,
and the current NAAQS surveillance network of monitoring locations are considered. The
methods for sampling and analysis are considered in light of the indicator for the Pb NAAQS,
and conclusions regarding the current NAAQS and associated indicator appear in chapter 4.
Consideration of the ambient air monitoring network generally informs the interpretation of
current data on ambient air concentrations and helps identify whether the monitoring network is
adequate to determine compliance with the NAAQS. This section discusses considerations
related to these aspects of the ambient air monitoring program for Pb.19
2.2.1.3.1 Sampling Considerations
As described in section 2.2.1.1 above, consistent with the Pb NAAQS indicator being Pb-
TSP, the FRM for Pb, which is required at all source-oriented sites, is measurement of Pb-TSP
using a high-volume TSP sampler meeting the design criteria specified in 40 CFR part 50
19 The code of federal regulations (CFR) at parts 50, 53 and 58 specifies required aspects of the ambient
monitoring program for NAAQS pollutants. The FRMs for sample collection and analysis are specified in 40 CFR
part 50, the procedures for approval of FRMs and FEMs are specified in 40 CFR part 53 and the rules specifying
requirements for the planning and operations of the ambient monitoring network are specified in 40 CFR part 58.
2-19
-------
Appendix B. During the review of the Pb NAAQS completed in 2008, CASAC noted the
variability in high-volume TSP sample measurements associated with the effects of wind speed
and wind direction on collection efficiency in their comments regarding the indicator. However,
at the time of the 2008 review, no alternative TSP sampler designs were identified that had an
adequate characterization of their collection efficiency over a wide range of particle sizes. The
existing high-volume sampler was retained as the sampling approach for the Pb-TSP FRM and
FEMs.
Since promulgation of the 2008 Pb NAAQS, the EPA has initiated an effort to review
alternative sampler designs in an effort to develop a new sampler to replace the current high-
volume Pb-TSP sampler. Efficient collection of particles much larger than 10 |im is
considerably more challenging because the greater inertia and higher settling velocities of Pb
particles hinder their efficient intake by samplers. The sampling difficulties and the long history
of research to develop adequate sampling technology for large particles have been thoroughly
reviewed (Garland and Nicholson, 1991). Some existing commercially available sampler inlets
are designed to collect particles larger than 10 jim with greater than 50% efficiency (Kenny et
al., 2005), and these inlets can be tested as potential replacements for TSP sampling. However,
no alternatives to the FRM TSP sampler have been identified that have been adequately
characterized.
The EPA has initiated efforts to characterize the collection efficiency of alternative
sampler designs through wind tunnel testing as a necessary step towards the development of a
new sampler capable of sampling particles larger than PMio without the noted wind speed and
wind direction biases. Important considerations in specifying a sampler design with these
desired features include the feasibility and challenges to collection of particles much larger than
10 |im; some existing alternative sample collection methods are discussed in ISA (ISA, section
2.4.1.1). Also important to consider are physical limitations in the ability to generate and
transport ultra-coarse particles that affect the ability to adequately characterize the new sampler.
Although all sizes of airborne Pb particles are of interest, the factors identified above are
expected to ultimately limit the upper cut-point of potential samplers to the range of 18-20
micrometers. Following characterization in a wind tunnel, field testing of promising candidates
would be required to evaluate performance and to make comparisons to the existing Pb-TSP
samplers. This effort is expected to take several years to complete, and, as such, it is unlikely
that this new sampler will be available in time for consideration during this NAAQS review due
to the activities which will need to be completed to adequately characterize its performance both
in the laboratory and the field. We expect the new sampler to be available for consideration in a
future review and consequently do not expect to consider new alternatives for sampling methods
for Pb-TSP as part of this review.
2-20
-------
In addition to the FRM for Pb-TSP, there is also, as noted in section 2.2.1.1 above, a
FRM for Pb-PMio (40 CFR part 50 Appendix Q), based on the PMio sampler defined in 40 CFR
part 50 Appendix J coupled with XRF analysis. The Pb-PMio measurements may be used as an
alternative to Pb-TSP measurements in certain conditions defined in 40 CFR part 58 Appendix C
paragraph 2.10. These conditions include where Pb concentrations are not expected to equal or
exceed 0.10 micrograms per cubic meter on an arithmetic 3-month mean and where the source of
Pb emissions is expected to emit a substantial majority of its Pb in the PMio size fraction. At this
time, we believe the low-volume FRM sampler for Pb-PMio to be adequate for this application.
Hence, we do not expect to consider new sampling methods for Pb-PMio as part of this review.
2.2.1.3.2 Analysis Considerations
Due to reduced availability of laboratories capable of performing flame atomic
absorption analyses and general advances in analysis methods, the EPA has initiated an effort to
expand FRM analysis methods beyond atomic absorption to include the more modern analysis
method, ICP-MS. A consultation with the CASAC Ambient Air Monitoring and Methods
Subcommittee was held on September 15, 2010 (Russell and Samet, 2010), and the EPA plans to
propose a new FRM for Pb-TSP based on this more modern analysis method in 2013. In
addition, the EPA has approved several new FEMs (for ICP-MS and other analysis methods)
since the last Pb NAAQS review was completed in 2008.
With regard to Pb-PMio samples, in addition to the FRM analysis method (XRF), two
FEMs have been accepted for Pb-PMio analysis since the 2008 Pb NAAQS rulemaking. These
methods are based on ICP-MS and are consistent with analysis methods used for the NATTS
network. The EPA will continue to consider new FEMs for analysis of Pb-PMio and Pb-TSP as
applications are received, although no new FRMs (beyond the Pb-TSP FRM for ICP-MS
discussed above) are expected during this NAAQS review.
2.2.1.3.3 Network Design Considerations
Significant revisions to the Pb network design requirements (40 CFR part 58, Appendix
D) were made as part of the 2008 Pb NAAQS review and an associated revision to the
requirements in 2010. As summarized in section 2.1.1.1 above, the current Pb monitoring
network design requirements (40 CFR part 58, Appendix D, paragraph 4.5) include two types of
monitoring sites - source-oriented monitoring sites and non-source-oriented monitoring sites - as
well as the collection of a year of Pb-TSP measurements at 15 specific airports. This section
describes the design considerations for the Pb NAAQS surveillance network.
Source-Oriented Monitoring. Since the phase out of Pb in on-road gasoline, Pb is
widely recognized as a source-oriented air pollutant. As summarized in the ISA, variability in
air Pb concentrations is highest in areas including a Pb source, "with high concentrations
2-21
-------
downwind of the sources and low concentration at areas far from sources" (ISA, p. 2-92).
Recent data summarized in section 2.2.2.2 below indicates that the highest ambient Pb
concentrations are found near large Pb sources, usually metals industries (see, for example,
Figures 2-11 through 2-13 below). Analysis of the monitoring network during the last Pb
NAAQS review with regard to adequacy of monitoring near such sources found that monitors
were lacking near many of the larger Pb emissions sources, leading the EPA to conclude that the
monitoring network existing at that time was inadequate to determine compliance with the
revised Pb NAAQS (73 FR 29262). Findings and conclusions of that analysis led to revisions of
network design requirements for source-oriented monitoring, begun with the 2008 Pb NAAQS
rulemaking (73 FR 66964). Additional revisions were completed as part of a reconsideration of
the monitoring requirements in December 2010 (75 FR 81126).
The current requirements for source-oriented monitoring include placement of monitor
sites near sources of air Pb emissions which are expected to or have been shown to contribute to
ambient air Pb concentrations in excess of the NAAQS. At a minimum, there must be one
source-oriented site located to measure the maximum Pb concentration in ambient air resulting
from each non-airport Pb source which emits 0.50 or more tons of Pb per year and from each
airport which emits 1.0 or more tons of Pb per year.20 The expansion of the network, including
these source-oriented sites, is shown in Figure 2-3. Comparison of Figure 2-3 (monitors) with
Figure 2-2 (sources) illustrates the coverage which the monitoring network provides, as of 2012,
of large Pb emissions sources.
The emissions threshold for source-oriented monitoring sites, 0.50 tpy, was developed
based on an analysis intended to estimate the lowest emission rate that under reasonable worst-
case conditions (e.g., meteorological and emission release conditions that lead to poor dispersion
and associated elevations in Pb concentrations) could lead to Pb concentrations exceeding the Pb
NAAQS (Cavender, 2008). This analysis included three approaches. The first two of the three
approaches included a simple scaling of the historic 5 tpy emission threshold applied to the old
1.5 |ig/m3 Pb NAAQS, and a simplified modeling effort using a screening model. The third
approach relied on design values based on Pb monitoring data surrounding large sources (1 tpy
or greater) of Pb. At the time of the 2008 review, complete 3-year design values were only
available for seven source-monitor pairs.
As more recent data become available, analysis of the updated and expanded dataset will
inform evaluation of the appropriateness of the current requirements. Since the analysis
20 The Regional Administrator may waive the requirement in paragraph 4.5(a) for monitoring near Pb
sources if the State or, where appropriate, local agency can demonstrate the Pb source will not contribute to a
maximum Pb concentration in ambient air in excess of 50 percent of the NAAQS (based on historical monitoring
data, modeling, or other means).
2-22
-------
performed during the 2008 review, over 150 additional source-oriented monitors have been
installed. At this time, the full set of these new monitors have not collected a complete 3-year
dataset, which is needed for the development of complete design values for the new source-
oriented monitors. For monitors installed in response to the 2008 revisions (near sources
estimated to emit 1.0 tpy or more of Pb), 3-years of certified data would be expected to have
been available in spring 2013. Three-years of certified data for the monitors required in the 2010
regulations will be available in spring 2015. As is seen from Figures 2-11 through 2-13 below,
Pb concentrations very widely across the source oriented monitors. This variation is not
unexpected given potential for appreciable differences in source characteristics beyond
estimated annual Pb emissions that would be expected to affect airborne Pb concentrations.
Such characteristics include source or industry type and associated processes and work practices,
proximity of emissions points to source boundaries, extent of fugitive emissions.
One-year Airport Monitoring. In addition to the above source-oriented monitoring
requirement for airports estimated to emit more than 1 tpy of Pb (40 CFR part 58, Appendix D,
4.5(a)) and the Regional authority to require monitoring near airports where piston-engine
aircraft emit Pb (40 CFR part 58, Appendix D, 4.5(c)), one year of monitoring was required near
15 specific airports in order to gather additional information on the likelihood of NAAQS
exceedances due to the combustion of leaded aviation gasoline (75 FR 81126; 40 CFR part 58,
Appendix D, 4.5(a)(iii)). Given delays in monitor siting, monitor installation at some of these
sites extended into late 2012. Accordingly, the timing for completion of the year of monitoring
has varied across the 15 locations. As described further in section 2.1.2.2 above, these airport
monitoring data along with other data gathering and analyses will inform EPA's ongoing
investigation into the potential for Pb emissions from piston-engine aircraft to cause or
contribute to air pollution that may reasonably be anticipated to endanger public health or
welfare. This investigation is occurring under Section 231 of the Clean Air Act (CAA), separate
from the Pb NAAQS review. As a whole, the various data gathering and analyses are expected to
improve our understanding of Pb concentrations in ambient air near airports and conditions
influencing these concentrations.
Non-Source-Oriented Monitoring. Monitoring agencies are also required to conduct
non-source-oriented monitoring NCore sites with a population of 500,000 or more, as noted
above.21 Currently, all 50 NCore sites are operational and measuring Pb concentrations, with 28
measuring Pb in TSP and 24 measuring Pb in PMio (2 sites are measuring both Pb in TSP and Pb
in PMio). While non-source-oriented monitoring data can be used for designation purposes, an
alternative objective stated for these sites is the collection of data on neighborhood-scale Pb
21 Defined by the US Census Bureau - http://www.census.gov/population/www/metroareas/metroarea.html
2-23
-------
concentrations that are typical in urban areas to inform our understanding of ambient air-related
Pb exposures for the general population. The data available as of April 2014 for these sites
indicate little variation in concentrations, with a range from less than 0.01 to 0.06 |ig/m3 in terms
of maximum 3-month average concentration (of Pb-PMio or Pb-TSP), with the vast majority of
sites showing concentrations less than 0.03 |ig/m3. In recognition of the limited extent of this
data analysis, we have not drawn conclusions here on the usefulness of these data for purposes of
characterizing neighborhood-scale concentrations. We additionally note the existence of other
monitoring networks that, although not required by regulation, provide data on Pb in PMio, and
also in PM2.5, at non-source-oriented urban sites. These include the NATTS for PMio and the
CSN for PM2.5, as described in section 2.2.1.2 above.
2.2.2 Ambient Concentrations
2.2.2.1 Temporal Trends
Ambient air concentrations of Pb in the U.S. have declined substantially over the past 30
years. Figure 2-7 illustrates this decline in terms of site-specific maximum 3-month average
concentrations at the set of 31 monitoring sites that have been operating across this period. The
median of this dataset has declined by more than 90% over the 30-year period, and the average
by 89%. Over the past 12 years, a larger dataset of 50 sites operating across that period also
indicates a decline, which is on the order of 50% for the average of that dataset (Figure 2-8).22
5.0-
111 11111 1111 11111 11122222222222
9999999999999999999900000000000
8888888888939998989900000000001
012345678901 2345678901 234567890
Note: Based on annual maximum 3-month average at 31 sites.
Figure 2-7. Temporal trend in Pb -TSP concentrations: 1980-2010 (31 sites).
22 In Figures 2-7 and 2-8, the top of the blue band is the 90th percentile among sites, the bottom is the 10th
percentile, and the white line is the average, http://www.epa.gov/air/airtrends/lead.html
2-24
-------
5.0
4.5-
n 4.0-
01 3.5"
ZJ
H 3.0 •
i i i i i i i i i i r
2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 2012
Note: Based on annual maximum 3-month average at 50 sites.
Figure 2-8. Temporal trend in Pb-TSP concentrations: 2000-2012 (50 sites).
The role of the phase-out of leaded gasoline for on-road vehicles on declining
concentrations is evident from temporal trends in air Pb concentrations near roadways, as
illustrated in Figure 2-9 which presents data for five monitors sited near roadways during the
years 1979 through 2010.23 These sites additionally indicate the concentrations currently
common at such sites, with the maximum 3-month average concentrations at all five sites falling
below 0.03 |ig/m3 in the most recent years.
23 In selecting these sites, the objective was to identify sites near roadways that do not appear to be near
other (stationary) sources of Pb emissions. In addition to consideration of information in national emissions
inventories, the areas around the sites were examined using satellite pictures (in Google Maps) for signs of current
or historical industrial activity.
2-25
-------
OOOOOOOOCOOOMCTlCTlCTlCTlCTlCTlCTlCTlCTlCTlCTlCTlCTlOOOOOOOOOOOOOOrH
i ^ fr i i ^ fr i i ^ fr i i ^ t is i ^ t i i ^ t i i ^ t i i ^ t i i ^ t i i ^ tii
Monitor locations: Los Angeles, CA (06-037-4002), Riverside, CA (06-065-1003), Cook, IL (17-031-0052,17-031-6003), Suffolk, MA (25-025-0002).
Figure 2-9. Airborne Pb -TSP concentrations (3-month average) at five sites near
roadways: 1979-2010.
2.2.2.2 Current Concentrations
As a result of revisions to the Pb NAAQS surveillance monitoring requirements
(described in section 2.2.1 above), Pb monitoring sites have been in transition over the last few
years as indicated by Figure 2-3. For presentation in this document, we have focused on the
most recent period for which adequately complete data are available, 2010-2012, recognizing
that the dataset developed for this period includes many but not all of the monitors newly
required by the December 2010 regulations described in section 2.2.1.1 above.
Lead concentrations, in terms of maximum 3-month average Pb-TSP concentration, at
monitoring sites active across the U.S. during the period 2010-2012, and for which sufficient
data are available to meet completeness criteria described in Appendix 2C, are presented in
Figure 2-10.24 Highest concentrations occur in the vicinity of large metals industries, as
discussed in section 2.1.2.1,25 Note that due to differences in data completeness criteria which
reflect the different purposes of the analyses (characterization of air quality at different types of
monitoring sites vs identification of sites exceeding the NAAQS), Figure 2-10 (and Figures 2-11
through 2-13) do not include some sites which may have been reported elsewhere (e.g., with
"design values" which are used for comparison to the NAAQS level).26
24 Criteria for development of the 2010-2012 air Pb-TSP, Pb-PMio and Pb-PM2 5 datasets discussed in this
section are described in Appendix 2C. Data summaries are included in Appendix 2D.
25 Information regarding areas of U.S. designated nonattainment with the Pb NAAQS is available at:
http://www.epa.gov/air/oaqps/greenbk/mindex.html.
26 Design values for the 2010-2012 period are available at: http://www.epa.gov/airtrends/values.html
2-26
-------
2010-2012 Pb-TSP
• highest 3-month average <= 0.05 |jg/m3
O highest 3-month average > 0.05 and <= 0.15 Mg/m3
• highest 3-month average > 0.15 and <= 0.5 |jg/m3
• highest 3-month average > 0.5 [jg/m3
Figure 2-10. Pb-TSP maximum 3-month means (215 sites), 2010-2012.
2-27
-------
Figures 2-11 through 2-13 illustrate differences in Pb-TSP concentrations, in terms of
three different metrics (maximum 3-month mean, annual mean, and maximum monthly mean),
among sites near and more distant from emissions sources.27 The Pb-TSP sites indicate the much
greater site and temporal variability in concentrations at source-oriented and previous source-
oriented sites as compared to non-source-oriented sites. Across the Pb-TSP sites, as would be
expected, the highest concentrations are observed at the source-oriented sites, followed by the
previous source-oriented sites. This is the case for all three metrics analyzed (maximum 3-
month mean, maximum monthly mean and annual mean).
Figures 2-11 through 2-13 additionally present distributions of Pb-PMio and Pb-PM2.s
concentrations in urban and rural locations where they are monitored. The Pb-PMio and Pb-
PM2.5 networks are described in section 2.2.1.2 and shown in Figures 2-5 and 2-6, respectively. It
is important to note that there are few sites in these recent datasets with colocated monitors for
the different size fractions. As described in the ISA, at 18 urban sites (without specification as to
proximity to Pb sources) with at least 30 co-located Pb-TSP and Pb-PMio samples collected
during various time periods (nearly all between 1990 and 2000), approximately 80% of the Pb
mass, on average, is captured by the Pb-PMio measurements (ISA, sections 2.5.3.1 and 2.8.4).
The data distributions in Figures 2-11 through 2-13 indicate reduced variability in concentration
for non-source-oriented sites and for particulate Pb of smaller size fractions.28
27 In the Figures 2-11 through 2-13, the whiskers indicate the 5th and 95th percentiles, the box indicates the
25th 50th and 75th percentiles and the star indicates the arithmetic mean.
28 The number of observations for some categories of monitoring site varies among the three figures due to
the impact of data completeness criteria used for the three different concentration metrics (see Appendix 2C).
2-28
-------
CO
E
c
_o
'-I—<
(D
s_
-I—<
C
CD
O
c
O
O
1.3-
1.2-
1.1-
1.0-
0.9-
0.8-
0.7-
0.6-
0.5-
0.4-
0.3-
0.2-
0.1-
0.0-
«
•
Pb-TSP
all sites
(n=236)
*
\
d
a m =
I I
Pb-TSP Pb-TSP Pb-TSP Pb-TSP
source-oriented source-oriented previous source- not source-oriented
(non-airport) sites (airport) sites oriented sites sites (n=93)
(n=119) (n=13) (n=11)
i
Pb-PM10
urban sites
(n=45)
I I
Pb-PM25 Pb-PM25
urban CSN non-urban
sites (n=1 93) IMPROVE sites
(n=102)
Figure 2-11. Distribution of maximum 3-month mean concentrations of Pb-TSP, Pb-PMio and Pb-PMi.5 at different site types,
2010-2012.
2-29
-------
co
E
c
o
"ro
§
g
o
0.6 H
0.5-
0.4-
0.3-
0.2 J
0.1-
0.0-
I I I I I
Pb-TSP Pb-TSP Pb-TSP Pb-TSP Pb-TSP
all sites source-oriented source-oriented previous source- not source-oriented
(n=242) (non-airport) sites (airport) sites oriented sites sites (n=96)
(n=121) (n=15) (n=11)
\
Pb-PM
10
urban sites
(n=54)
T
Pb-PM
2.5
urban CSN
sites (n=195)
I
Pb-PM25
non-urban
IMPROVE sites
(n=104)
Figure 2-12. Distribution of annual mean concentrations of Pb-TSP, Pb-PMio and Pb-PMi.s at different site types, 2010-2012.
2-30
-------
CO
E
"B)
c
o
'-I—<
03
-i—<
c
CD
O
c
o
O
1.8-
1.7-
1.6-
1.5-
1.4-
1.3-
1.2-
1.1-
1.0-
0.9-
0.8-
0.7-
0.6-
0.5-
0.4-
0.3-
0.2-
0.1-
0.0-
I 1
Pb-TSP
all sites
(n=243)
*
I
- — |
— '
1 1 fIS 1
I
Pb-TSP Pb-TSP Pb-TSP Pb-TSP
source-oriented source-oriented previous source- not source-oriented
(non-airport) sites (airport) sites oriented sites sites (n=96)
(n=121) (n=15) (n=11)
1
Pb-PM10
urban sites
(n=54)
Pb-PM25 Pb-PMh-
urban CSN , "?"
., , .... MPROVE sites
sites(n=184) [n=^
Figure 2-13. Distribution of maximum monthly mean concentrations of Pb-TSP, Pb-PMio and Pb-PMi.s at different site types,
2010-2012.
2-31
-------
2.3 AMBIENT AIR LEAD IN OTHER MEDIA
Lead emitted into the ambient air, depending on its chemical and physical characteristics,
deposits out of air onto surfaces in the environment. The environmental fate of atmospherically
emitted Pb, once deposited, is influenced by the type of surface onto which the particles deposit
and by the type and activity level of transport forces in that location. Deposited Pb can be
incorporated into soil matrices in terrestrial ecosystems or transported (by direct deposition or
stormwater runoff) to water bodies and into aquatic sediments, which may serve as aquatic
ecosystem sinks. Particles deposited onto impervious surfaces, such as urban surfaces or
roadways, are more available for human contact while they remain on such surfaces. For
example, particles on urban surfaces may be available for adherence onto skin or they may be
resuspended into the air and inhaled. Precipitation and other natural, as well as human-
influenced, processes contribute to the fate of such particles and their potential transport to areas
or environments of lesser or greater likelihood for human contact, e.g., transport with surface
runoff into nearby water bodies or tracking into nearby houses (ISA, section 2.3).
Lead from current and historical air emissions sources, in addition to a range of nonair
sources (e.g., land disposal of wastes as well as surface runoff and releases to surface waters),
contribute to Pb in outdoor dust, soil and aquatic systems. Because of its persistence, Pb from all
of these sources can contribute to media concentrations into the future. The pattern of resulting
Pb concentrations changes over time in response to changes in new Pb contributions to the
systems (e.g., in types and rates of addition), as well as environmental processes (chemical,
biological and physical) particular to each type of media and ecosystem. Accordingly, media
and ecosystems differ with regard to Pb concentrations and the changes in those concentrations
in response to airborne Pb. These differences relate to ecosystem processes as well as Pb source
or emissions characteristics and proximity.
The initial section below (section 2.3.1) summarizes salient information regarding
atmospheric deposition and how it is monitored. Subsequent sections describe the current
information related to the presence of ambient air Pb in nonair media and what it indicates
regarding impacts of current patterns of Pb in and being emitted to ambient air, including
relationships to impacts in the past and to other Pb sources. Section 2.3.2 focuses on terrestrial
media, while section 2.3.3 discusses aquatic media.
2.3.1 Atmospheric Deposition
Deposition is the pathway by which Pb particles are removed from the atmosphere and
transferred to other environmental media. There are several approaches by which atmospheric
deposition, or the transfer of Pb from the atmosphere to soil or water bodies, can be assessed.
These include measurements of Pb in rainfall (wet deposition) and on collection surfaces during
2-32
-------
dry periods (dry deposition); dry deposition is also estimated from measurements of airborne Pb
particles coupled with estimates of deposition velocity (see 2006 CD, Section 2.3.2). Less direct
approaches include monitoring changes in Pb concentration in various biological or physical
media such as lichen or mosses, snowpack, soil and aquatic sediments (ISA, sections 2.6.2, 2.6.4
and 2.6.6). Approaches for the latter three media may involve repeated measurements of surface
samples over time or core samples coupled with isotope dating. To gain information on
atmospheric deposition unaffected by contributions from direct nonair environmental releases,
such studies are generally conducted in somewhat remote areas. As there are currently no
nationwide Pb atmospheric deposition monitoring programs, the discussion of atmospheric
deposition in this and subsequent sections is drawn from this range of approaches (2006 CD,
sections 2.3, 8.2.2 and AX7.1.2.3; ISA, sections 2.3.1.2 and 2.6 ). Geographic differences in
deposition generally relate to differences in the amount and size distribution of airborne Pb
particles in that location, as well as meteorology and other site-specific factors. For example, the
size of particles, as well as solubility in rainwater, can also influence wet deposition rates (ISA,
section 2.3.1.2; 2006 CD, p. 2-59). Factors that particularly influence dry deposition are the
level of atmospheric turbulence, especially in the layer nearest the ground, particle size
distributions and density, and the nature of the surface itself, such as smooth or rough (2006 CD,
pp. 2-55 to 2-57).
Evidence for the temporal pattern of U.S. Pb deposition generally indicates a peak during
the middle twentieth century (e.g., 1940s through 1970s) followed by substantial declines in the
latter part of the century (ISA, section 2.3.1; 2006 CD section 2.3.1; Jackson et al., 2004). This
pattern reflects the increased use of Pb in the industrial age (including its use in gasoline in the
twentieth century) and declines in response to environmental controls on gasoline and metals
industries in the latter part of the twentieth century. Studies continue to document declines in
atmospheric deposition since the 1980s in locations remote from industrial areas (e.g.,
Watmough and Dillon, 2007). As would be expected, stationary sources of Pb continue to
contribute to relatively higher deposition rates in industrial areas as compared to other areas,
although rates in those areas appear to have also declined since the 1970s-80s (ISA, section
2.3.1.2; Sabin and Schiff, 2008).
In addition to records of atmospheric deposition in the U.S., evidence also documents the
long-range atmospheric transport and distribution of the substantial emissions of Pb from the
U.S. and other developed countries to regions well beyond those source countries. For example,
evidence provided by isotopic analyses of rainwater and surface water in the North Atlantic and
ice cores in Greenland have documented the long-range transport and distribution of Pb from
North American and European sources (ISA, section 2.5.5; 2006 CD, p. AX7-141; 1977 CD,
section 6.3.1; Veron et al., 1998). The historical record provided by those cores indicate the
2-33
-------
period of most substantial deposition to that remote region during the 1960s and 1970s followed
by a dramatic decline (ISA, section 2.5.5; McConnell and Edwards, 2008). These and other
records of long-range transport indicate the widespread distribution of historically emitted Pb
(e.g., 2006 CD, section 2.3.1).
2.3.2 Terrestrial Media
Lead in the terrestrial media discussed here may originate from current or historical air
emissions or other sources. Other sources to these media include historical use of indoor and
outdoor leaded paint, more prevalent in areas with older buildings, and the processing of lead-
containing materials. Further, the concentrations of Pb in each media, as well as the relative
contributions from various types of sources to those concentrations, vary among media and
among locations for any one media. Differences among locations in media concentrations of air-
related Pb are generally related to the current and historical magnitude of Pb emissions and
deposition at that location, as well as location- and media-specific removal factors.
2.3.2.1 Indoor Household Dust
Household dust arises from particulate matter generated indoors and outdoors, and Pb in
household dust can reflect a combination of these sources.29 Airborne particles can be
transported indoors with ambient air, while particles deposited outdoors from ambient air may be
carried in on humans and their clothing or other items transported indoors. Depending on factors
such as the proximity of the residence to current or historical metals industries, leaded paint
usage, and age of the residence (which informs consideration of potential for presence of leaded
paint), Pb in indoor residential dust can reflect current or historical atmospheric Pb or nonair-
related sources, such as leaded paint. Another indoor source is tobacco smoking (ISA, section
3.1.3.2; Gaitens et al., 2009; 2006 CD, p. 3-15; Mannino et al., 2003). The age of the residence
may be an indicator of the potential for the presence of leaded paint and, in areas of significant
levels of airborne Pb in the past, such as near mining or smelting industries, may also indicate
the potential for the residual presence of historically emitted Pb (ISA, sections 3.1.1 and 3.1.3.2;
2006 CD section 3.2.3). A study of households in the Baltimore metropolitan area (in which
there are no areas designated non-attainment for the current Pb NAAQS)30 indicated indoor air
Pb concentrations to be significantly associated with outdoor air Pb concentrations but did not
show a statistically significant relationship of outdoor air Pb with indoor dustPb (ISA, 3.1.3.2;
Egeghy et al., 2005). Rather, indoor dust Pb was associated with Pb concentration in soil and
29 As discussed in chapter 4 below, indoor dust is a major pathway for air-related Pb exposure for pre-
school children, largely related to prevalent hand-to-mouth behavior at that age.
30 http://www.epa.gov/air/oaqps/greenbk/mnc.html
2-34
-------
several factors related to housing age, perhaps indicating the greater role of sources other than air
Pb for those households (Egeghy et al., 2005).
2.3.2.2 Outdoor Dust in Areas of Human Activity
Lead in particulate matter occurring on outdoor surfaces (outdoor dust) may reflect
current or historical Pb emissions, as well as the historical uses of Pb in products on buildings
and infrastructure in surrounding areas. The concentrations of air-related Pb in outdoor dust and
the relative contribution of air-related Pb to the total Pb concentrations in outdoor dust vary
depending on the location-specific characteristics of air-related (and other) Pb sources. The role
of air-related sources in outdoor dust Pb has been documented in areas near industrial sources,
such as smelters, where Pb concentrations in outdoor dust have been documented to decline in
response to reduced emissions. For example, outdoor dust Pb concentrations in a long-time
Canadian smelter town were found to track smelter Pb emissions, as a new smelting technology
which reduced airborne Pb concentrations by 75% resulted in a 50% reduction in outdoor dust
Pb loading rate and concentrations (2006 CD, p. 3-23; Hilts, 2003). The residence time of settled
dust Pb (e.g., on sidewalks and other public surfaces) and thus the response of settled dust Pb
concentrations to changes in emissions and associated atmospheric deposition of Pb particles are
expected to reflect site-specific rates of transport or removal processes, such as stormwater
runoff and atmospheric resuspension and transport (ISA, sections 2.3.1.3 and 2.3.2.4; Allott et
al., 1990; Wong etal., 2006).
Rates of dry deposition of Pb in large metropolitan areas during the past decade are much
lower than those reported for the 1970s (ISA, sections 2.3.1 and 2.6.1; Table 2-4, below). For
example, dry deposition of Pb into Los Angeles harbor during 2002-2006 was more than an
order of magnitude lower than rates reported for the same location in 1975 (ISA section 2.3.1.2;
Sabin and Schiff, 2008; Lim et al., 2006). Across the Los Angeles metropolitan area, average
rates generally ranged from 10 to 32 micrograms per square meter per day (|ig/m2/day) and down
to 0.3 |ig/m2/day for the non-urban site of Malibu during 2002-2003 (Lim et al., 2006). Rates
within this range are reported from studies in Manhattan and a non-industrial area of New Jersey,
with a somewhat higher rate reported for a major industrial location within the New York City
metropolitan area (Yi et al., 2006; Caravanos et al., 2006a). Although rates have not been
reported recently for smelter locations in the U.S., the outdoor dustfall deposition rate reported in
a smelter town in British Columbia, Canada, after the installation of new technology that reduced
average airborne Pb-TSP concentrations to a level still at least twice the current U.S. NAAQS
(0.3 |ig/m3 from prior average of 1.1 |ig/m3) was several orders of magnitude higher than those
reported for New York, Los Angeles and Chicago urban areas (Hilts, 2003; Lim et al., 2006;
Sabin et al., 2006; Yi et al., 2006; Caravanos et al., 2006a).
2-35
-------
From the few studies reporting levels of Pb loading or concentration in outdoor dust
within the past decade or so, loading to surfaces of pedestrian traffic signals in New York City
was on average approximately 15% of the loading reported on sidewalks in older, residential
areas of downtown Baltimore (e.g., approximately 250 ug/ft2 as compared to 1500 ug/ft2) and an
order of magnitude or more below that reported in the long-time Canadian smelter town
(Caravanos et al., 2006b; Farfel et al 2005; Hilts, 2003).
Table 2-3. Dry deposition of Pb in large metropolitan areas.
Description
Los Angeles Harbor, June-Nov 2006
Los Angeles Harbor, 2002-2003°
Los Angeles Harbor, 1975
Los Angeles, metropolitan area urban sites, 2002-2003 c
Los Angeles, metropolitan area, non-urban site Malibu, 2002- 2003 c
Los Angeles, I-405, near Westwood (downwind side), spring 2003 D
Los Angeles, I-405, near Westwood (upwind side), spring 2003°
Jersey City, NJ, 2001-2002
New Brunswick, NJ, 2001- 2002
Manhattan, NYC, 2nd story rooftop (unprotected), 2003-2005
Chicago, 1993-95E
Average (or
Median*) Dry
Deposition Rate
(ngPb/m2/day)A
14*B
15
300*
10-32
0.3
24
7.3
50
8
27
38-71
Study
Sabin and Schiff, 2008
Limetal.,2006
Sabin and Schiff, 2008
Limetal.,2006
«
Sabin etal, 2006
«
Yi etal., 2006
«
Caravanos etal., 2006a
Yi etal 2001 ; Paode etal., 1998
A - Methods generally involved collection and analysis of samples of deposited particulate matter; details provided in references cited.
B - Rates for rest of off-shore transact from Santa Barbara to San Diego Bay ranged from 0.52 (Oxnard) - 3.3 (San Diego Bay) |ig/m3.
C - Average Pb-TSP range= 0.0056-0.017 |jg/m3 for urban sites; 0.0022 at Malibu site.
D - Average Pb-TSP at downwind site over sampling period -0.02 pg/m3.
E - This time period is the most recent for which such data are reported for this metropolitan area.
2.3.2.3 Soil
As is the case for Pb in outdoor dust, Pb occurring in surface soils can be derived from
current or historical emissions, as well as leaded paint usage on older buildings and other
structures. The relative role of these sources may vary with the type of environment and
proximity to industry and population centers.
In forested areas away from old urban areas, the role of leaded gasoline in soil
contamination is illustrated by the documented reductions in Pb in surface soils subsequent to the
phase-out of leaded gasoline for on-road vehicles. For example, forest surface soil (litter)
concentrations in a transect from Vermont through Maine and up to Gaspe in Quebec, which in
1979 exhibited a significant spatial trend ranging from 200 milligrams per kilogram, dry weight
2-36
-------
(mg/kg dw) at its southernmost point down to 60 mg/kg dw at its northernmost and most remote
point in Quebec, declined to 32-66 mg/kg dw (with no spatial trend) by 1996 (ISA, section 2.6.1;
Evans, 2005). In forests from the mid-Atlantic to southern New England, a reduction in litter Pb
concentration was observed between 1978 and 2004-05 (ISA, section 2.6.1; Johnson and Richter,
2010). In the latter study, the authors observed less change in concentration in the more northern
sampling sites, which they attribute to reduced rates of organic matter decomposition in those
colder temperature areas. Similarly, an additional New England study by Kaste et al (2006) also
documented a pattern in temporal reductions in soil Pb (O-horizon) related to decomposition
activity. These recent findings are generally consistent with findings reported in the last review
which indicated the gradual migration of deposited Pb into mineral soils (e.g., Miller and
Friedland, 1994; Kaste et al., 2003; Wang and Benoit, 1997; Johnson et al., 1995; Zhang, 2003).
Few studies have investigated temporal trends of surface soil Pb concentrations in more
populated areas in relation to reductions in usage of leaded gasoline and paint. Current
concentrations in areas of past heavy traffic powered by leaded gasoline are generally elevated
above areas more distant from these areas (ISA, section 2.6.1). Current roadway-related sources
of Pb (e.g., wear of vehicle parts), while substantially less significant than the historic use of
leaded gasoline, may continue to provide some contribution to surface dust/soil in these areas
(ISA, section 2.2.2.6). Surface soil and dust concentrations are much higher in such areas in
large, older cities than surrounding suburban areas (ISA, section 2.6.1). In older residential
areas, the presence of leaded house paint is another contributor to surface soil concentrations
(ISA, sections 2.6.1; Yesilonis et al., 2008; Brown et al., 2008; Clark et al., 2006).
Areas of long-term Pb emissions from point sources appear to be the areas of highest
surface soil Pb concentrations (ISA, sections 2.6 and 2.6.1). For example, Pb surface soil
concentrations within approximately 100-250 meters of long-established Pb smelters have been
five to ten times higher than those at 3-5 km distance (ISA, section 2.6.1; 2006 CD, Table 3-4).
Surface soil concentrations of Pb near U.S. mines that are no longer active have also been found
to be elevated above more distant areas (2006 CD, Table 3-6). Information described in the 2006
CD for areas surrounding smelters after implementation of pollution controls, although showing
declines in Pb concentrations in outdoor dustfall, street dust and indoor dustfall, has not indicated
a noticeable decline in soil Pb concentrations (2006 CD, pp. 3-23 to 3-24). The continued Pb
emissions in such industrial areas likely influence the dynamics of Pb concentrations in the soil,
affecting any response to emissions reductions. Estimates of associated steady-state surface soil
Pb concentrations or the expected longer-term temporal pattern for this situation have not been
made.
In summary, findings to date indicate that many of those systems less influenced by
current point sources have and may still be responding to reduced Pb deposition rates associated
2-37
-------
with reduced atmospheric emissions of Pb, including those associated with the phase-out of
leaded gasoline for on-road vehicles, while potential responses of soils near point sources and
those involving historically deposited Pb near roadways are less well characterized, but might be
expected to have longer time horizons.
2.3.2.4 Biota
Terrestrial plants can take up Pb from soils into roots and then transport it to other plant
tissues, as well as absorb deposited Pb into above-ground plant tissues (ISA, section 3.1.3.3;
2006 CD, section 2.3.7; 1986 CD, sections 6.5.3 and 7.2.2.2.1). The relative contributions of
these pathways to the different plant tissues differ with the physiology of different plants, the
chemical and physical characteristics of the soil, and the relative levels of Pb in soil and
atmospheric deposition (ISA, section 3.1.3.3). Terrestrial animals may take in Pb through
ingestion of vegetation, vegetation-consuming animals or soil, as well as directly from air. The
relative contributions from these terrestrial animal exposure pathways vary with contamination
level of the different items, as well as with species-specific factors, including intake rates.
The availability of data to document temporal trends in Pb concentrations in terrestrial
biota is somewhat limited. Measurements of Pb in some biota indicate reductions in biologically
available Pb over the past 30 years in some remote locations. For example, measurements of Pb
in lichen from Golden Lake in Mount Ranier National Park (2005) and Emerald Lake basin in
Sequoia/Kings Canyon National Parks (2004) indicate significant reductions (approximately 3-5-
fold) since samples were previously collected in those locations in 1984 (ISA, section 2.6.6;
Landers et al., 2008). Further, Pb in teeth of juvenile and adult moose in Isle Royale National
Park in northern Michigan have also declined substantially (ISA, section 2.6.8; Vucetich et al.,
2009).
Few recent data are available to characterize terrestrial biota Pb contamination levels
associated with current air Pb deposition. In one example, however, Pb deposition associated
with hauling mining materials has substantially increased Pb concentrations in moss within 10
meters of a road in the remote wilderness areas of Cape Krusenstern National Monument,
Alaska.31 In this example, the median Pb concentration measured within 10 meters of the haul
road in summer 2001 was more than 20 times higher than at sites at greater distance from the
road and nearly three orders of magnitude greater than those reported for this moss in other
Alaska locations in 1990-1992 (ISA, section 2.3.1.2; Hasselbach et al., 2005).
The composition of human and wildlife diets (and associated contamination levels)
influences the relative magnitude of dietary Pb intake, which may derive from currently existing
31 Red Dog mine is a zinc and Pb mine initiated in 1987. The materials are transported from the mine to a
port on the Chukchi Sea via a 52-mile long haul road.
2-38
-------
or historic air sources in the U.S. or in countries that export food to the U.S. As noted in section
1.3.1.1 above, U.S. dietary Pb may also derive from nonair sources, such as through processing
steps.
2.3.3 Aquatic Media
2.3.3.1 Surface Waters
In addition to delivery by atmospheric deposition directly to surface waters, Pb is also
carried into surface waters via wastewater effluent from municipalities and industry, stormwater
runoff, erosion, and accidental discharges (2006 CD, p. AX7-142; ISA section 2.3.2). As a result
of the phasing out of leaded gasoline for use in on-road vehicles, reductions in Pb concentrations
have been documented in surface waters of the North Atlantic Ocean, as well as the relatively
less remote areas of the Great Lakes (2006 CD, p. 7-23). The availability of studies investigating
historical trends in surface waters is limited, in part due to analytical issues that challenged many
monitoring programs in the past (2006 CD, AX7.2.2.2). Thus, temporal trends reported in many
aquatic systems are based on sediment analyses (see section 2.3.3.2 below).
Most Pb occurring in aquatic systems is associated with particles, with the distribution
between particle-bound and dissolved form being influenced by water chemistry as well as
suspended sediment levels (ISA, 2.3.2; 2006 CD, pp. AX7-117 to AX7-118, Section AX7.2.2).
Water columns have been described as "transient reservoirs" for pollutants (2006 CD, p. 2-75).
Once deposited to sediments, whether Pb is available for resuspension back into the water
column with potential transport further down a watershed versus being buried into deeper
sediments depends on the aquatic system (ISA, section 2.7.2). In open ocean waters (generally
characterized by depth and distance from continental sources), resuspension to surface waters is
unlikely. In more shallow systems, and those influenced by land sources (e.g., stormwater runoff
as well as point sources), resuspension may play a role in water column concentrations. For
example, studies in San Francisco Bay, the southern arm of which has an average depth of 2 m,
have indicated that Pb particles may be remobilized from surface sediments into the water
column (2006 CD, AX7-141).
The distribution of Pb dissolved in many U.S. surface waters has been reported by the
United States Geological Survey (USGS) National Water-Quality Assessment (NAWQA)
program. The NAWQA data set referenced in the ISA (ISA, section 2.6) encompasses data
collected from 1991-2003 on Pb concentrations in flowing surface waters for more than 50 river
basins and aquifers throughout the country (2006 CD, Section AX7.2.2.3). These data indicate a
mean dissolved Pb concentration in U.S. surface waters of 0.66 ug/L (range 0.04 to 30 ug/L) in
waters affected by a combined contribution of natural and anthropogenic sources, as compared to
a mean of 0.52 ug/L (range 0.04 to 8.4 ug/L) for waters in "forest", "rangeland", and "reference"
2-39
-------
sites (2006 CD, Section AX7.2.2.3). The highest surface water Pb concentrations were observed
in sites impacted by land uses such as mining (2006 CD, p. AX7-131). The role of surface
runoff in delivering contamination to waters near such land uses, as well as near metals
industries, presents a challenge to the task of disentangling the relative contributions from
atmospheric deposition as compared to those associated with surface runoff.
2.3.3.2 Sediments
Many studies have investigated temporal trends in sediment Pb concentrations, using
sediment cores or surface sediment Pb concentration, with declines documented in many systems
and usually attributed to the phasing out of leaded gasoline for on-road vehicles and industrial
emissions reductions (ISA, sections 2.6.2 and 2.7.5; 2006 CD, section AX7.2.2). Several studies
documenting the increased Pb deposition of the industrial age, including specifically leaded
gasoline usage, and the subsequent declines associated with on-road leaded gasoline phase-out
were reported in the 2006 CD. They include investigations involving sediment cores from the
Okefenokee Swamp in Georgia as well as from 35 reservoirs and lakes in urban and reference
locations (ISA, section 2.6.2; 2006 CD, p. AX7-141). In the latter, the median reduction in Pb
mass accumulation rate in the cores, adjusted for background concentrations, was 246%, with the
largest decreases in lakes located in dense urban watersheds (ISA, section 2.6.2; 2006 CD, p.
AX7-141; Mahler et al, 2006). A third study of sediment cores in 12 lakes in the Great Lakes
area also documented a peak in Pb concentrations consistent with peak use of leaded gasoline in
the U.S. in the mid 1970s and declining concentrations in most lake sediments through the mid
1990s (2006 CD, p. 2-55; Yohn et al., 2004). Sediment surveys by the USGS NAWQA have
reported the highest Pb concentrations in Idaho, Utah, and Colorado, with seven of the highest
concentrations at sites classified as mining land use (2006 CD, p. AX7-133).
Among the more recent investigation of temporal trends in aquatic sediments described in
the ISA is that associated with the Western Airborne Contaminants Assessment Project which
documented Pb in sediment cores from 14 lakes in eight U.S. national parks in western states,
including three in Alaska (ISA, section 2.6.2; Landers et al., 2010). Among the Alaska cores, in
which concentrations were generally on the order of 20 |ig/kg dw, there was little variation in Pb
concentration, flux or enrichment factor. The other park cores, with few exceptions, generally
exhibited an increase in concentration commencing in the mid-nineteenth century, which
transitioned to declining trends in the past few decades, with lower concentrations in more
recent, surface material. The highest concentration was recorded at core depth corresponding to
2-40
-------
the mid-1970s, in one of the Sequoia/Kings Canyon lake cores (Figure 2-16; ISA, section 2.6.2;
Landers et al., 201032).
125 -•
100 -•
25
Sequoia/Kings Canyon-Pear (mid California)
Sequoia/Kings Canyon-Emerald (mid California)
Mt Ranier-Golden (mid Washington)
Mt Ranier-LP19 (mid Washington)
Glacier-Snyder (Montana)
Glacier-Oldman (Montana)
Rocky Mnt-Lone Pine (Colorado)
Rocky Mtn-Mills (Colorado)
Olympic (Washington)
Oenali (mid Alaska)
Gates of the Arctic (n. Alaska)
Noatak (n. Alaska)
1800
1830
1860
1890 1920
Year Material Deposited
1950
1980
2010
Figure 2-14. Temporal trend in sediment Pb concentration from core samples in twelve
lakes at eight National Parks or Preserves.
Analyses of cores taken in several lakes and reservoirs along the Apalachicola,
Chattahoochee, and Flint River Basin from north of the Atlanta, GA metropolitan area to the
Gulf of Mexico indicate changes in sediment concentration both with time and in relation to
influence of the large metropolitan area of Atlanta (ISA, section 2.6.2; Callender and Rice,
2000). Highest concentrations were documented just downstream from Atlanta at the core depth
corresponding to the 1975-1980 time period; the corresponding concentration for the most
recent time period (1990-1995) at that location was approximately 50% lower (ISA, section
2.6.2; Callender and Rice, 2000). These data may reflect changes in surface water discharges of
Pb in the Atlanta area, during this time period, as well as changes in air deposition. The smaller
32 Figure created from database for Landers et al (1980);
http://www.nature.nps.gov/air/Studies/air toxics/wacap.cfm.
2-41
-------
reduction (on the order of 20%) observed across the 20-year time period at the upstream site is
likely more generally reflective of changes in air deposition.
2.3.3.3 Biota
Aquatic biota can contain Pb that may be derived from historic or current atmospheric
deposition in the watershed, from historic or current direct water discharges or from natural
sources (ISA, section 6.2.1). In near-shore systems and populated watersheds, all of these
sources may play a role in observed Pb concentrations, complicating consideration of the role of
ambient air Pb deposition. Additional challenges are presented by available data for mobile
species such as fish (e.g., ISA, section 2.6.8; 2006 CD, section AX7.2.2.2). A 20-year record of
Pb concentrations in blue and zebra mussels and oysters in U.S. coastal waters provides varying
evidence on temporal trends that may reflect patterns in site-specific environmental releases as
well as other ecosystem impacts on Pb fate and transport over that period (ISA, section 2.6.7;
Kimbrough et al., 2008).
2.4 REFERENCES
Allott, RW; Hewitt, CN; Kelly, MR. (1989). The environmental half-lives and mean residence times of
contaminants in dust for an urban environment: Barrow-in-Furness. Sci Total Environ 93: 403-410.
http://dx.doi.org/10.1016/0048-9697(90190131-0
Brown, RW; Gonzales, C; Hooper, MJ; Bayat, AC; Fornerette, AM; McBride, TJ; Longoria, T; Mielke, HW.
(2008). Soil lead (Pb) in residential transects through Lubbock, Texas: A preliminary assessment. Environ
GeochemHealth 30: 541-547. http://dx.doi.org/10.1007/sl0653-008-9180-Y .
Callender, E; Rice, KC. (2000). The urban environmental gradient: Anthropogenic influences on the spatial and
temporal distributions of lead and zinc in sediments. Environ Sci Technol 34: 232-238.
http://dx.doi.org/10.1021/es990380s .
Caravanos, I; Weiss, A.L.; Jaeger, RJ. (2006a) An exterior and interior leaded dust deposition survey in New York
City: results of a 2-year study. Environ. Res. 100: 159-164.
Caravanos, J; Weiss, AL; Blaise, MJ; Jaeger, RJ. (2006b). A survey of spatially distributed exterior dust lead
loadings in New York City. Environ Res 100: 165-172. http://dx.doi.0rg/10.1016/i.envres.2005.05.001.
Cavender, K. (2008). Update of Analysis of Proposed Source-Oriented Monitoring Emission Threshold.
Memorandum to Lead NAAQS Review Docket (OAQ-2006-0735)
http://www.epa.gov/ttnnaaqs/standards/pb/data/20081015Cavender.pdf
Clark, HF; Brabander, DJ; Erdil, RM. (2006). Sources, sinks, and exposure pathways of lead in urban garden soil. J
Environ Qua! 35: 2066-2074. http://dx.doi.org/10.2134/ieq2005.0464.
Egeghy, P. P.; Quackenboss, J. J.; Catlin, S.; Ryan, P. B. (2005) Determinants of temporal variability in
NHEXASMaryland environmental concentrations, exposures, and biomarkers. J. Exposure Anal. Environ.
Epidemiol. 15: 388-397.
2-42
-------
Evans, GC; Norton, SA; Fernandez, IJ; Kahl, JS; Hanson, D. (2005). Changes in concentrations of major elements
and trace metals in northeastern US-Canadian sub-alpine forest floors. Water Air Soil Pollut 163: 245-267.
Farfel, MR; Orlova, AO; Lees, PSJ; Rohde, C; Ashley, PJ; Chisolm, JJ, Jr. (2005). A study of urban housing
demolition as a source of lead in ambient dust on sidewalks, streets, and alleys. Environ Res 99: 204-213.
http://dx.doi.0rg/10.1016/j.envres.2004.10.005 .
Gaitens, JM; Dixon, SL; Jacobs, DE; Nagaraja, J; Strauss, W; Wilson, JW; Ashley, PJ. (2009). Exposure of US
children to residential dust lead, 1999-2004:1. Housing and demographic factors. Environ Health Perspect
117: 461-467. http://dx.doi.org/10.1289/ehp.11917.
Garland, JA, Nicholson, KW 1991. A review of methods for sampling large airborne particles and associated
radioactivity. J. Aerosol Sci. Vol.22 (4):479-499.
Gidney, J; Twigg, M; Kittelson, D. (2010). Effect of organometallic fuel additives on nanoparticle emissions from a
gasoline passenger car. Environ Sci Technol 44: 2562-2569.
Hasselbach, L; VerHoef, JM; Ford, J; Neitlich, P; Crecelius, E; Berryman, S; Wolk, B; Bohle, T. (2005). Spatial
patterns of cadmium and lead deposition on and adjacent to National Park Service lands in the vicinity of
Red Dog Mine, Alaska. Sci Total Environ 348: 211-230. http://dx.doi.0rg/10.1016/i.scitotenv.2004.12.084 .
Hilts, S. R. (2003) Effect of smelter emission reductions on children's blood lead levels. Sci. Total Environ. 303: 51-
58.
Jackson, B.P., P.V. Winger, PJ. Lasier (2004) Atmospheric lead deposition to Okefenokee Swamp, Georgia, USA.
Environ Poll. 130:445-451.
Johnson, C. E.; Siccama, T. G.; Driscoll, C. T.; Likens, G. E.; Moeller, R. E. (1995) Changes in lead
biogeochemistry in response to decreasing atmospheric inputs. Ecol. Appl. 5: 813-822.
Johnson, AH; Richter, SL. (2010). Organic-horizon lead, copper, and zinc contents of Mid-Atlantic forest soils,
1978-2004. Soil Sci Soc Am J 74: 1001-1009. http://dx.doi.org/10.2136/sssaj2008.0337.
Kaste, JM; Bostick, BC; Friedland, AJ; Schroth, AW; Siccama, TG. (2006). Fate and speciation of gasoline-derived
lead in organic horizons of the northeastern USA. Soil Sci Soc Am J 70: 1688-1698.
http://dx.doi.org/10.2136/sssai2005.0321.
Kaste, J.; Friedland, A.; Stirrup, S. (2003) Using stable and radioactive isotopes to trace atmospherically deposited
Pb in montane forest soils. Environ. Sci. Technol. 37: 3560-3567.
Kenny L; Beaumont G, Gudmundsson A, Thorpe A, Koch W. (2005) Aspiration and sampling efficiencies of the
TSP and louvered particulate matter inlets. J Environ Monit. May 2005. 7 481-487.
Kimbrough, KL; Lauenstein, GG; Christensen, JD; Apeti, DA. (2008). An assessment of two decades of
contaminant monitoring in the nation's coastal zone. Silver Spring, MD: National Centers for Coastal
Ocean Science, http://aquaticcommons.org/2232/
Landers, DH; Simonich, SL; Jaffe, DA; Geiser, LH; Campbell, DH; Schwindt, AR; Schreck, CB; Kent, ML; Hafner,
WD; Taylor, HE; Hageman, KJ; Usenko, S; Ackerman, LK; Schrlau, JE; Rose, NL; Blett, TF; Erway, MM.
(2008). The fate, transport, and ecological impacts of airborne contaminants in western national parks
(USA). (EPA/600/R-07/138). Corvallis, Oregon: U.S. Environmental Protection Agency, NHEERL,
Western Ecology Division, http://www.nature.nps.gov/air/studies/air toxics/WACAPreport.cfm.
Landers, DH; Simonich, SM; Jaffe, D; Geiser, L; Campbell, DH; Schwindt, A; Schreck, C; Kent, M; Hafner, W;
Taylor, HE; Hageman, K; Usenko, S; Ackerman, L; Schrlau, J; Rose, N; Blett, T; Erway, MM. (2010). The
2-43
-------
Western Airborne Contaminant Assessment Project (WACAP): An interdisciplinary evaluation of the
impacts of airborne contaminants in western U.S. National Parks. Environ Sci Technol 44: 855-859.
http://dx.doi.org/10.1021/es901866e .
Lim, JH; Sabin, LD; Schiff, KC; Stolzenbach, KD. (2006). Concentration, size distribution, and dry deposition rate
of particle-associated metals in the Los Angeles region. Atmos Environ 40: 7810-7823.
http://dx.doi.0rg/10.1016/i.atmosenv.2006.07.025.
McConnell, JR; Edwards, R. (2008). Coal burning leaves toxic heavy metal legacy in the Arctic. PNAS 105: 12140-
12144. http://dx.doi.org/10.1073/pnas.0803564105
Mahler, B. J.; Van Metre, P. C.; Callender, E. (2006) Trends in metals in urban and reference lake sediments across
the United States, 1970 to 2001. Environ. Toxicol. Chem. 25: 1698-1709.
Mannino, D.M.; Albalak, R.; Grosse, S.; Repace, J. (2003) Second-hand smoke exposure and blood lead levels in
U.S. children. Epidemiology 14(6): 719-727.
Miller, E. K.; Friedland, A. J. (1994) Lead migration in forest soils: response to changing atmospheric inputs.
Environ. Sci. Technol. 28: 662-669.
Osterberg, E; Mayewski, P; Kreutz, K; Fisher, D; Handley, M; Sneed, S; Zdanowicz, C; Zheng, J; Demuth, M;
Waskiewicz, M; Bourgeois, J. (2008). Ice core record of rising lead pollution in the North Pacific
atmosphere. Geophys Res Lett 35: L05810. http://dx.doi.org/10.1029/2007gl032680
Paode, RD; Sofuoglu, SC; Sivadechathep, J; Noll, KE; Holsen, TM; Keeler, GJ. (1998). Dry deposition fluxes and
mass size distributions of Pb, Cu, and Zn measured in southern Lake Michigan during AEOLOS. Environ
Sci Technol 32: 16291635. http://dx.doi.org/10.1021/es970892b.
Russell A. and Samet, J.M. (2010) Letter from Dr. A. Russell, Chair, Clean Air Scientific Advisory Committee,
Ambient Air Monitoring Methods Subcommittee and J.M. Samet, Chair, Clean Air Scientific Advisory
Committee, to Administrator Lisa P. Jackson. Re: CASAC Review of EPA's White Paper Approach for
the Development of a new Federal Reference Method (FROM) for Lead in Total Suspended Particulates
(Pb-TSP). November 30, 2010.
Sabin, LD; Schiff, KC. (2008). Dry atmospheric deposition rates of metals along a coastal transect in southern
California. Atmos Environ 42: 6606-6613. http://dx.doi.0rg/10.1016/i.atmosenv.2008.04.042
U.S. Environmental Protection Agency. (1996-2011). AP-42, Compilation of Air Pollutant Emission Factors, 5th
Edition. Volume 1: Stationary Point and Area Sources, Chapter 13: Miscellaneous Sources. Available at:
http://www.epa.gov/ttn/chief/ap42/chl3/index.html
U.S. Environmental Protection Agency. (2012) Modification of Administrative Order on Consent in the matter of
Doe Run Resources Corporation. U.S. Environmental Protection Agency, Region 7, Kansas City, KS. Jan
9, 2012.
Veron, A. J., Church, T.M., Flegal, A.R. (1998) Lead isotopes in the western North Atlantic: transient tracers of
pollutant lead inputs. Environ. Res. 78: 104-111.
Vucetich, JA; Outridge, PM; Peterson, RO; Eide, R; Isrenn, R. (2009). Mercury, lead and lead isotope ratios in the
teeth of moose (Alces alces) from Isle Royale, U.S. Upper Midwest, from 1952 to 2002. J Environ Monit.
Wang, E. X.; Benoit, G. (1997) Fate and transport of contaminant lead in spodosols: a simple box model analysis.
Water Air Soil Pollut. 95: 381-397.
2-44
-------
Watmough, SA; Dillon, PJ. (2007). Lead biogeochemistry in a central Ontario forested watershed. Biogeochemistry
84: 143-159. http://dx.doi.org/10.1007/sl0533-007-9110-6
Wong, CSC; Li, XD; Thornton, I. (2006). Urban environmental geochemistry of trace metals [Review]. Environ
Pollut 142: 1-16. http://dx.doi.0rg/10.1016/i.envpol.2005.09.004
Yesilonis, ID; Pouyat, RV; Neerchal, NK. (2008). Spatial distribution of metals in soils in Baltimore, Maryland:
Role of native parent material, proximity to major roads, housing age and screening guidelines. Environ
Pollut 156: 723-731. http://dx.doi.0rg/10.1016/j.envpol.2008.06.010 .
Yi, SM; Totten, LA; Thota, S; Yan, S; Offenberg, JH; Eisenreich, SJ; Graney, J; Holsen, TM. (2006). Atmospheric
dry deposition of trace elements measured around the urban and industrially impacted NY-NJ harbor.
Atmos Environ 40: 6626-6637. http://dx.doi.0rg/10.1016/j.atmosenv.2006.05.062 .
Yohn, S., Long, D., Fett, J., Patino, L. (2004) Regional versus local influences on lead and cadmium loading to the
Great Lakes region. Appl. Geochem. 19: 1157-1175.
Zhang, Y.-H. (2003) 100 years of Pb deposition and transport in soils in Champaign, Illinois, U.S.A. Water Air Soil
Pollut. 146: 197-210.
2-45
-------
3 HEALTH EFFECTS AND EXPOSURE/RISK INFORMATION
This chapter presents key aspects of the current evidence of lead-related health effects
and presents exposure/risk information from the quantitative assessment performed in the last
review in the context of the currently available evidence. Staff has drawn from EPA's synthesis
of the scientific evidence presented in the Integrated Science Assessment for Lead (USEP A,
2013; henceforth referred to as the ISA) and 2006 Air Quality Criteria Document for Lead
(USEP A, 2006; henceforth referred to as the 2006 CD), and from the documentation of the 2007
human exposure and health risk assessment (documented in USEP A, 2007a; henceforth referred
to as the 2007 REA). The chapter is organized into sections considering the information on
blood Pb as a biomarker (section 3.1), the nature of Pb effects on health (section 3.2), public
health implications and at-risk populations (section 3.3), and exposure and risk information
(section 3.4). Presentation within these sections is organized to address key policy-relevant
questions for this review concerning the evidence and exposure/risk information, building upon
the questions included in the IRP (IRP, section 3.1).
3.1 INTERNAL DISPOSITION AND BIOMARKERS OF EXPOSURE AND DOSE
The health effects of Pb, discussed in detail in the ISA and summarized in section 3.2
below, are remote from the portals of entry to the body (i.e., the respiratory system and
gastrointestinal tract). Consequently, the internal disposition and distribution of Pb is an integral
aspect of the relationship between exposure and effect. As discussed below, blood Pb has
traditionally been used as a biomarker of Pb exposure and of internal dose, with relationships
between air Pb concentrations and blood Pb concentrations informing consideration of the
NAAQS for Pb. Information available in this review continues to support conclusions in the last
review with regard to these relationships.
Lead associated with inhaled particles may, depending on particle size and Pb solubility,
be absorbed into the systemic circulation or transported with particles to the gastrointestinal tract
(ISA, section 3.2.1.1). The absorption efficiency of Pb from the gastrointestinal (GI) tract varies
with characteristics associated with the ingested Pb (e.g., particle size and chemical form or
matrix), as well as with an individual's physiology (e.g., maturity of the GI tract), nutritional
status (e.g., iron, calcium, and zinc deficiencies increase absorption), and the presence of food in
the GI tract (ISA, section 3.2.1.2). Once in the blood stream, where approximately 99% of the
Pb is associated with red blood cells (mostly bound to aminolevulinic acid dehydratase, the
predominant ligand), Pb is quickly distributed throughout the body (e.g., within days) and is
available for exchange with the soft and skeletal tissues, conceptually viewed as the fast and
slow turnover pools, respectively (ISA, section 3.2.2). Skeletal tissue serves as the largest
3-1
-------
storage compartment, with much less Pb stored in soft tissues (e.g., kidney, liver, brain, etc.)
(ISA, section 3.2.2.2).
The role of the bone as the main storage compartment is related to the ability of Pb to
form stable complexes with phosphate and replace calcium in the salt comprising the primary
crystalline matrix of bone (ISA, section 3.2.2.2). In infants less than a year old, the bone is
estimated to contain approximately 60% of the total body burden of Pb (ISA, section 3.2.2.2;
Barry, 1975). Circulating Pb is taken up into the bone regions of active calcification.
Accordingly, during early childhood there is rapid uptake of Pb into mineralizing bone, with
somewhat more than 70% of total body burden Pb estimated to reside in bone of children aged 2
to 16, increasing up to more than 90% by adulthood (ISA, section 3.2.2.2; Barry, 1975). The net
accumulation of Pb in bone over a person's lifetime results in bone lead concentrations generally
increasing with age (ISA, section 3.2.2.2).
The distribution of Pb in the body is dynamic. Throughout life, Pb in the body is
exchanged between blood and bone and between blood and soft tissues (ISA, sections 3.3.5 and
3.2.2; 2006 CD, section 4.3.2). The rates of these exchanges vary with age, exposure and
various physiological variables. For example, resorption of bone, which results in the
mobilization of Pb from bone into the blood, is a somewhat rapid and ongoing process during
childhood and a more gradual process in later adulthood (ISA, sections 3.2.2.2, 3.3.5 and 3.7.2).
Resorption rate is appreciably increased in pregnant or nursing women and in association with
osteoporosis in postmenopausal women or, to a lesser magnitude, in older men (ISA, sections
3.3.5.2). Changes in Pb exposure circumstances can also influence these exchanges, e.g., when
exposure levels are substantially reduced, the relative contribution of Pb from bone to blood Pb
concentration increases (ISA, section 3.3.5). The studies that address the relative contributions
of bone Pb and current Pb exposure to blood Pb are limited to a few human studies during the
1980s and early 1990s, when leaded gasoline usage was common, and a study in non-human
primates. These studies indicate an appreciable contribution from bone Pb stores to Pb in blood,
on the order of 40-70% of blood Pb contributed from bone, under circumstances with higher
concurrent exposure than exposures common today (ISA, section 3.3.5; Smith et al., 1996;
Gulson et al., 1995; Manton, 1985; Franklin et al., 1997).
During bone resorption that occurs in pregnancy, Pb is released from bone, increasing the
bone contribution to maternal blood Pb levels, and maternal Pb circulates across the placenta,
posing risk to the developing fetus and providing the fetal body burden (ISA, sections 3.2.2.4,
3.3.5, 3.7.2 and 3.7.3; 2006 CD, 6.6.2; Chuang et al., 2001). The relative size of contributions of
maternal bone Pb and current maternal exposure to maternal blood Pb and fetal body burden are
influenced by the relative magnitude of current and historical exposures. In various study
populations with mean maternal blood Pb levels ranging from 1.7 to 8.6 |ig/dL, average blood Pb
O O
3-2
-------
concentration in the umbilical cord (as representative of newborn blood) has been reported to
range from 70% to 100% of average maternal blood Pb (ISA, section 3.2.2.4); the range is
similar for four study populations with mean maternal blood Pb level below 4 |ig/dL (Amaral et
al., 2010; Patel and Prabhu, 2009; Lagerkvist et al., 1996; Jedrychowski et al., 2011). The
relationship between cord blood Pb and maternal blood Pb concentrations is more variable for
individual mother-child pairs. In a low-income population with mean maternal blood Pb of 1.9
|ig/dL, factors associated with occurrences of relatively higher cord-to-maternal blood Pb ratios
included higher maternal blood pressure and alcohol consumption, while factors associated with
relatively lower cord-to-maternal blood Pb ratios included higher maternal hemoglobin and
sickle cell trait presence (Harville et al., 2005). As a result of the contributions of maternal bone
Pb to maternal blood Pb during pregnancy, the contribution to fetal body burden from maternal
bone Pb relative to maternal concurrent exposure can be appreciable. This maternal bone Pb
contribution to fetal body burden is likely to vary, however, in response to differences between
maternal historical exposures and those during pregnancy, among other factors (2006 CD,
sections 4.3.1.5 and 4.3.2.5; ISA, section 5.1; Chuang et al., 2001; Gulson et al., 1999; Gulson et
al., 2003; Gulson et al., 2004a; Rothenberg et al., 2000).
Limited data indicate that blood Pb levels in some newborns may decline during the
period extending through the first few months of life; the extent to which this may occur may be
influenced by the magnitude of blood Pb level at birth and of subsequent exposure during early
infancy (ISA, section 3.4.1; Carbone et al., 1998; Simon et al., 2007; Gulson et al., 1999, 2001).
As infants become more mobile and engage in hand-to-mouth behavior, blood Pb levels then
commonly increase to a peak around one to two years of age (ISA, sections 3.4.1 and 5.2.1.1).
• Does the current evidence continue to support blood Pb level as a useful indicator
of Pb exposure and dose for purposes of characterizing Pb health effects, with
well-recognized strengths and limitations? To what extent does the evidence
suggest alternatives?
As discussed in past CDs and in the ISA, blood Pb is the most commonly used indicator
of human Pb exposure. Given the association with exposure and the relative ease of collection,
blood Pb levels are extensively used as an index or biomarker of exposure by national and
international health agencies, as well as in epidemiological and toxicological studies of Pb health
effects and dose-response relationships (ISA, sections 3.3.2, 3.4.1, 4.3, 4.4, 4.5, 4.6, 4.7, and
4.8). While bone Pb measurements are also used in epidemiological studies as an indicator of
cumulative Pb exposure, blood Pb measurements remain the predominant, well-established and
well-characterized exposure approach.
5-3
-------
Since 1976, the U.S. Centers for Disease Control and Prevention (CDC) has been
monitoring blood Pb levels nationally through the National Health and Nutrition Examination
Survey (NHANES). This survey has documented the dramatic decline in mean blood Pb levels
in all ages of the U.S. population that has occurred since the 1970s, as shown in Figure 3-1, and
that coincides with actions on leaded fuels, leaded paint, lead in food packaging, and lead-
containing plumbing materials that have reduced Pb exposure in the U.S. (ISA, section 3.4.1;
Pirkle et al., 1994; Schwemberger et al., 2005). This decline has continued over the more recent
past. For example, the 2009-2010 geometric mean blood Pb level in U.S. children aged 1-5
years is 1.17 |ig/dL, as compared to 1.51 |ig/dL in 2007-2008 (ISA, section 3.4.1) and 1.8 |ig/dL
in 2003-2004, the most recent data available at the time of the last review (73 FR 67002).
Somewhat less dramatic declines have been reported in the upper tails of the distribution and in
different groups with higher blood Pb levels than the general child population (ISA, Figures 3-17
and 3-19).
o
-------
The CDC, and its predecessor agencies, have for many years used blood Pb level as a
metric for identifying highly exposed children at risk of adverse health effects for whom
recommendations might be made for their protection (e.g., CDC, 1991; CDC, 2005). In 1978,
when the Pb NAAQS was initially established, the CDC recognized a blood Pb level of 30 ug/dL
as a level warranting individual intervention (CDC, 1991). In 1985, the CDC recognized a level
of 25 ug/dL for intervention, and in 1991, they adopted a multi-tier approach that recommended
individual intervention actions at a level of 15 ug/dL and implementation of more general
community-wide prevention activities if many children in a community have blood Pb at or
above 10 ug/dL (CDC, 1991; CDC, 2005). In 2005, CDC revised their statement on Preventing
Lead Poisoning in Young Children, specifically recognizing the evidence of adverse health
effects in children with blood Pb levels below 10 ug/dL and emphasizing the importance of
preventive measures (CDC, 2005).l Consistent with this statement, the CDC revised their
approach in 2012 to one that relies on the 97.5th percentile of blood Pb concentrations in U.S.
children aged one to five years of age (currently 5 jig/dL)2 as a reference level for identifying
young children for whom they recommend particular follow-up actions (CDC, 2012).
Unless influenced by a recent elevation in exposure, blood Pb measurements are a
reflection of total body burden. Accordingly, Figure 3-1 illustrates the reduction in Pb body
burden in the U.S. population over the past 40 years. Associations of health effects with blood
Pb measurements indicate relationships with body burden and may, in some cases, indicate
relationships with recent exposures. The extent to which blood Pb measurements represent
current or recent exposure circumstances, however, may be uncertain, particularly where
histories include exposures largely different from those occurring more recently (ISA, sections
3.3 and 3.3.2). This uncertainty may be greater for blood Pb measurements taken in older
children3 and adults than those for young children as a result of their longer exposure histories.
For example, the Pb in bone of adults may have accumulated over decades of Pb exposure (with
past exposures often greater than current ones for current U.S. populations) such that the bone
may be a significant source of Pb in blood in later years of life, after exposure has ended or been
appreciably reduced. Thus, in adult and older child populations with past exposures that were
1 With the 2005 statement, CDC identified a variety of reasons, reflecting both scientific and practical
considerations, for not lowering the 1991 level of concern, including a lack of effective clinical or public health
interventions to reliably and consistently reduce blood Pb levels that are already below 10 ug/dL, the lack of a
demonstrated threshold for adverse effects, and concerns for deflecting resources from children with higher blood
Pb levels (CDC, 2005).
2 CDC intends to update the value every 4 years using the two most recent NHANES surveys (CDC, 2012).
3 There is a paucity of experimental measurements of Pb biomarkers during adolescence to inform our
characterization of Pb biokinetics (and relative roles of recent vs historic exposure on blood Pb levels) during this
lifestage, in which individuals undergo rapid changes in sexual development, growth, food and water intake, bone
growth and turnover, behavior, etc. (ISA, section 3.3).
3-5
-------
appreciably elevated in comparison to more recent exposures, current blood Pb levels may
predominantly reflect their exposure history rather than their current exposures (ISA, sections
3.3.5, 3.3.5.2 and 3.4.1). Accordingly, the extent to which studies using cross-sectional blood Pb
measurements as the exposure biomarker inform our understanding of relationships between
recent Pb exposures and various health effects can differ across age groups and is greatest for
very young children, as discussed in section 3.3 below.
The relationship of children's blood Pb to recent exposure may reflect their labile bone
pool, with their rapid bone turnover in response to rapid childhood growth rates (ISA, section
3.3.5). The relatively smaller skeletal compartment of Pb in children (particularly very young
children) compared to adults is subject to more rapid turnover. As a result the blood Pb
concentration of children can more quickly reflect changes in their total body burden (associated
with their shorter exposure history) and can also reflect changes in recent exposures (ISA,
section 3.3.5).
Multiple studies of the relationship between Pb exposure and blood Pb in children (e.g.,
Lanphear and Roghmann 1997; Lanphear et al., 1998) have shown young children's blood Pb
levels to reflect Pb exposures, including exposures to Pb in surface dust. These and studies of
child populations near sources of air Pb emissions, such as metal smelters, further demonstrate
the effect of airborne Pb on interior dust and on blood Pb (ISA, sections 3.4.1, 3.5.1 and 3.5.3;
Hilts, 2003; Gulson et al., 2004b). Accordingly, blood Pb level was the index of exposure for
children in the risk assessment performed in the last Pb NAAQS review (described in section 3.4
below).
A well-recognized strength of using children's blood Pb to investigate relationships
between Pb exposure and health effects is the relatively lesser uncertainty in the causality aspects
of such relationships than might be associated with such relationships based, for example, on
media concentration. Blood Pb is an integrated marker of aggregate Pb exposure across all
pathways. The blood Pb concentration-response relationships described in epidemiological
studies of lead-exposed populations do not distinguish among different sources of Pb or
pathways of Pb exposure (e.g., inhalation, ingestion of indoor dust, ingestion of dust containing
leaded paint). Given our focus on ambient air contributions to Pb exposures, discussion in
response to the question below considers the available information regarding relationships
between Pb in ambient air and the associated Pb in blood. Additionally, the exposure component
of the risk assessment performed for the last Pb NAAQS review (and described in section 3.4
below) employed biokinetic modeling to estimate blood Pb levels associated with aggregate Pb
exposure to inform our estimates of contributions to blood Pb arising from ambient air-related
Pb.
-------
Alternative biomarkers of Pb exposure include bone Pb, teeth Pb, and hair Pb (ISA,
section 3.3.1, 3.3.3 and 3.3.4). Given the role of bone as the repository of more than 90% of an
adult body's Pb burden, bone Pb levels are recognized as indicators of body burden and
cumulative lifetime exposure (ISA, sections 3.2.2.2, 3.3 and 3.3.5). The currently available
evidence does not, however, indicate these or any other alternatives to be superior to blood Pb in
young children or as commonly used for the purposes of tracking recent Pb exposures and for
assessing potential health risk for this age group (ISA, section 3.7.3). In summary, the current
evidence continues to support our conclusions from the last review regarding the use of blood Pb
levels as an internal biomarker of Pb exposure and dose informative to characterize Pb health
effects in young children.
• To what extent has new information altered scientific conclusions regarding the
relationships between Pb in ambient air and Pb in children's blood?
As described above, blood Pb is an integrated marker of aggregate exposure across all
pathways and a reflection of exposure history. Thus, our interpretation of the health effects
evidence for purposes of this review necessitates characterization of the relationships between Pb
from those sources and pathways of interest in this review (i.e., those related to Pb emitted into
the air) and blood Pb. The evidence in this regard derives from analyses of datasets for
populations residing in areas with differing air Pb concentrations, including datasets for
circumstances in which blood Pb levels have changed in response to changes in air Pb. The
control for variables other than air Pb that can affect blood Pb varies across these analyses.
Lead in ambient air contributes to Pb in blood by multiple exposure pathways by both
inhalation and ingestion exposure routes (ISA, section 3.1.1). The quantitative relationship
between ambient air Pb and blood Pb, which is often termed a slope or ratio, describes the
increase in blood Pb (in |ig/dL) estimated to be associated with each unit increase of air Pb (in
|ig/m3). Ratios are presented in the form of 1 :x, with the 1 representing air Pb (in |ig/m3) and x
representing blood Pb (in |ig/dL). Description of ratios as higher or lower refers to the values for
x (i.e., the change in blood Pb per unit of air Pb). Slopes are presented as simply the value of x.
At the conclusion of the last review in 2008, the EPA interpreted the evidence as
providing support for use (in informing the Administrator's decision on standard level) of a
range "inclusive at the upper end of estimates on the order of 1:10 and at the lower end on the
order of 1:5" (73 FR 67002). This conclusion reflected consideration of the air-to-blood ratios
presented in the 1986 CD4 and associated observations regarding factors contributing to variation
in such ratios, ratios reported subsequently and ratios estimated based on modeling performed in
the REA, as well as advice from CASAC (73 FR 66973-66975, 67001-67002). The information
4 The 2006 CD did not include an assessment of then-current evidence on air-to-blood ratios.
3-7
-------
available in this review, which is assessed in the ISA and largely, although not completely,
comprises studies that were available in the last review, does not alter the primary scientific
conclusions drawn in the last review regarding the relationships between Pb in ambient air and
Pb in children's blood. The ratios summarized in the ISA in this review span a range generally
consistent with the range concluded in 2008 (ISA, section 3.5.1).
The air-to-blood ratios for children, or for populations inclusive of children, discussed in
the ISA for this review are summarized in Table 3-1. The evidence pertaining to this
quantitative relationship between air Pb and children's blood Pb is now, as in the past, limited by
the circumstances in which the data are collected. These estimates are generally developed from
studies of populations in a variety of Pb exposure circumstances. Accordingly, there is
significant variability in air-to-blood ratios among the different study populations exposed to Pb
through different air-related exposure pathways and at different exposure levels. This variability
in air-to-blood estimates can relate to the representation of air-related pathways and study
populations, including, for example, relatively narrow age ranges for the population in order to
reduce age-related variability in blood Pb, or including populations with narrowly specified
dietary sources. It can relate to the study population exposure and blood Pb levels (ISA, section
3.7.4). It can also relate to the precision of air and blood measurements and of the study
circumstances, such as with regard to spatial and temporal aspects. Additionally, in situations
where exposure to nonair sources covaries with air-related exposures that are not accounted for
in deriving ratio estimates, uncertainties may relate to the potential for confounding by nonair
exposure covariance (ISA, section 3.5). Most studies have reported the relationship as either
log-log or linear (Table 3-1; ISA, section 3.7.4).
As was noted in the last review, age is an important influence on the magnitude of air-to-
blood ratio estimates derived. Ratios for children are generally higher than those for adults, and
higher for young children than older children, perhaps due to behavioral differences between the
age groups, as well as their shorter exposure history. Similarly, given the common pattern of
higher blood Pb levels in pre-school aged children than during the rest of childhood, related to
behaviors that increase environmental exposures (e.g., hand-to-mouth activity), ratios would be
expected to be highest in earlier childhood. Additionally, estimates of air-to-blood ratios that
include air-related ingestion pathways in addition to the inhalation pathway are "necessarily
higher," in terms of blood Pb response, than those estimates based on inhalation alone (USEPA
1986, p. 11-106). Thus, the extent to which studies account for the full set of air-related
inhalation and ingestion exposure pathways affects the magnitude of the resultant air-to-blood
estimates, such that including fewer pathways as "air-related" yields lower ratios. Estimates of
air-to-blood ratios can also be influenced by population characteristics that may influence blood
-------
Pb; accordingly, some analyses include adjustments. Most of the studies in Table 3-1 include
ratios derived from linear analyses, while a subset are derived from nonlinear models.
Given the recognition of young children as a key at-risk population in section 3.3 below,
as well as the influence of age on blood Pb levels, the studies presented in Table 3-1 are grouped
with regard to the extent of their inclusion of children younger than or barely school age (less
than or equal to five years of age). Among the first group of studies, focused exclusively on
young children, only one study dates from the end of or after the phase-out of leaded gasoline
usage (namely, Hilts, 2003). This study reports changes in children's blood Pb levels associated
with reduced Pb emissions and associated air concentrations near a Pb smelter in Canada (for
children through age five). Given the timing of this study, after the leaded gasoline phase-out,
and its setting near a smelter, the ambient air Pb in this study may be somewhat more
comparable to that near sources in the U.S. today than other studies discussed herein. The study
authors report an air-to-blood ratio of 1:6.5 An EPA analysis of the air and blood data reported
for 1996, 1999 and 2001 results in a ratio of 1:6.5, and the analysis focused only on the 1996 and
1999 data (pre- and post- the new technology) yields a ratio of 1:7 (ISA, section 3.5.1; Hilts,
2003).6 The two other studies that focused on children of age 5 or younger analyzed variations
in air Pb as a result of variations in leaded gasoline usage in Chicago, Illinois. The study by
Hayes et al. (1994) compared patterns of ambient air Pb reductions and blood Pb reductions for
large numbers of children, aged 6 months to 5 years, in Chicago between 1974 and 1988, a
period when significant reductions occurred in both measures. The study reported a better fit for
the log-log model which describes a pattern of higher ratios with lower ambient air Pb and blood
Pb levels (Hayes et al., 1994). Based on the log-log model, the ratio derived for the relationship
of quarterly mean air concentration with blood Pb during the period is 1:8 (Table 3-1). Another
analysis for a Chicago dataset, performed by Schwartz and Pitcher (1989) focused on the
5 Sources of uncertainty include the role of factors other than ambient air Pb reduction in influencing
decreases in blood Pb (ISA, section 3.5.1). The author cited remedial programs (e.g., community and home-based
dust control and education) as potentially responsible for some of the blood Pb reduction seen during the study
period (1997 to 2001), although the author notes that these programs were in place in 1992, suggesting they are
unlikely to have contributed to the sudden drop in blood Pb levels occurring after 1997 (Hilts, 2003). Other aspects
with potential implications for ratios include the potential for children with lower blood Pb levels not to return for
subsequent testing, and the age range of 6 to 36 months in the 2001 blood screening compared to ages up to 60
months in earlier years of the study (Hilts, 2003).
6 This study considered changes in ambient air Pb levels and associated blood Pb levels over a five-year
period which included closure of an older Pb smelter and subsequent opening of a newer facility in 1997 and a
temporary (3 month) shutdown of all smelting activity in the summer of 2001. The author observed that the air-to-
blood ratio for children in the area over the full period was approximately 1:6. The author noted limitations in the
dataset associated with exposures in the second time period, after the temporary shutdown of the facility in 2001,
including sampling of a different age group at that time and a shorter time period (3 months) at these lower ambient
air Pb levels prior to collection of blood Pb levels. Consequently, EPA calculated an alternate air-to-blood Pb ratio
based on ambient air Pb and blood Pb reductions in the first time period, after opening of the new facility in 1997
(ISA, section 3.5.1).
3-9
-------
association of blood Pb in black children (aged < 5 years) with the use of leaded gasoline from
1976 through 1980. Given that leaded gasoline exposure occurs by air-related pathways,
additional analyses have related the leaded gasoline usage for this period to air concentrations.
The resulting relationship of blood Pb with air Pb (adjusted for age and a number of other
covariates) yields a ratio of 1:8.6 (ISA, table 3-12, section 3.5.1). The blood Pb concentrations
in the two leaded gasoline studies are appreciably higher (a factor of two or more) than those in
the study near the smelter (Hilts, 2003).
The second group of studies in Table 3-1 (comprising studies including but not limited to
children less than or equal to five years of age) includes a complex statistical analysis and
associated dataset for a cohort of children born in Mexico City from 1987 through 1992 (Schnaas
et al., 2004). This study, which was not assessed in the last review, encompasses the period of
leaded gasoline usage and further informs our understanding of factors influencing the
quantitative relationship between air Pb and children's blood Pb. Air-to-blood ratios developed
from this study are influenced by a number of factors and appear to range from roughly 2 to 6, in
addition to an estimate of 9 (ISA, section 3.5.1), although the latter is derived from a data set
restricted to the latter years of the study when little change in air Pb concentration occurred, such
that the role of air Pb may be more uncertain. Estimates associated with the developmental
period of highest exposure (e.g., age 2 years) range up to approximately 6, illustrating the
influence of age on the ratio (ISA, section 3.5.1). Also in the second group in Table 3-1 are two
much older studies of populations with age ranges extending well beyond 6 years. The first is
the review and meta-analysis by Brunekreef (1984) using datasets available at the time for
variously aged children as old as 18 years with identified air monitoring methods and reliable
blood Pb data for 18 locations in the U.S. and internationally.7 The author discusses potential
confounders of the relationship between air Pb and blood Pb, recognizing the desirability of
taking them into account when deriving an air-to-blood relationship from a community study but
noting that was not feasible in such an analysis. Two models were produced, one based on the
full pooled dataset and a second limited to blood Pb-air Pb data pairs with blood Pb levels below
20 |ig/dL (r2 values were 0.692 and 0.331, respectively). From these two logn-logn models, air-
to-blood ratio estimates were derived for air concentrations corresponding to the geometric
means of the two sets of data pairs. At those concentrations (1.5 and 0.54 |ig/m3, respectively),
the resultant ratios both round to 5. The study by Schwartz and Pitcher (1989) described above
also analyzed the relationship between U.S. NHANES II blood Pb levels for white subjects, aged
7 In the dataset reviewed by Brunekreef (1984), air-to-blood ratios from the subset of those studies that
used quality control protocols and presented adjusted slopes include values of 3.6 (Zielhuis et al., 1979), 5.2 (Billick
et al., 1979, 1980); 2.9 (Billick et al., 1983), and 8.5 (Brunekreef et al, 1983). The studies cited here adjusted for
parental education (Zielhuis et al., 1979), age and race (Billick et al., 1979, 1980) and air Pb monitor height (Billick
et al., 1983); Brunekreef (1984) used multiple regression to control for several confounders (73 FR 66974).
3-10
-------
<74 years, and national usage of leaded gasoline. A separate, less specifically described, air Pb
dataset was used to convert the relationship of blood Pb with gas Pb to one for blood Pb with air
Pb, with a resultant ratio on the order of 9, adjusted for age and other covariates (Henderson,
2007a, pp. D-2 to D-3; ISA, Table 3-12).
The last two studies included in Table 3-1 are focused on older children (ages 6-11). The
methods for characterization of air Pb concentrations (and soil Pb for Ranft et al., 2008) also
differ from other studies in Table 3-1. The first study regressed average blood Pb concentrations
for multiple locations around Mumbai, India on average air Pb concentrations at those locations
(Tripathi et al., 2001). The values in the linear regression were 13 pairs of location-specific
geometric means of all the data collected over the 13-year period from 1984 to 1996; the
reported slope was 3.6 (Tripathi et al., 2001). The location-specific geometric mean blood Pb
levels in this study (8.6-14.4 |ig/dL) indicate blood Pb distributions in this age group much
higher than those pertinent to similarly aged children in the U.S. today. The second study
analyzed air, soil and children's blood Pb concentrations in Duisburg, Germany, during the
leaded gasoline phase-out (Ranft et al., 2008). Average blood Pb levels declined over the nearly
20-year study period from 9 |ig/dL in 1983 (345 children average age of 9 years) to 3 |ig/dL in
2000 (162 children average of 6 years).8 Average air Pb concentration declined from 0.45 |ig/m3
to 0.06 |ig/m3 over the same period, with the largest reduction occurring between the first study
year (derived from two monitoring sites for full study area) and the second study year, 1991, for
which air concentrations were derived from a combination of dispersion modeling and the two
monitoring sites.9 For a mean air Pb concentration of 0.1 |ig/m3, the study's multivariate log-
linear regression model predicted air-to-blood ratios of 3.2 and 6.4 for "background" blood Pb
concentrations of 1.5 and 3 |ig/dL, respectively. In this study, background referred to Pb in
blood from other sources; the blood Pb distribution over the study period, including levels when
air Pb concentrations are lowest, indicates 3 |ig/dL may be the better estimate of background for
this study population. Inclusion of soil Pb as a variable in the model may have contributed to an
underestimation of the these blood Pb-air Pb ratios for this study because some of the Pb in soil
likely originated in air and the blood Pb-air Pb slope does not include the portion of the soil/dust
Pb ingestion pathway that derives from air Pb. Using univariate linear, log-log and log-linear
models on the median air and blood Pb concentrations reported for the five years included in this
study, the ISA also derived air-to-blood ratio estimates ranging from 9 to 17 (ISA, p. 3-126;
8 Blood Pb measurements were available on a total of 843 children across five time periods, in the first of
which the average child age was 9 years while it was approximately 6 years in each of the latter years: 1983
(n=356), 1991 (n=147), 1994 (n=122), 1997 (n=56), and 2000 (n=162) (Ranft et al., 2008).
9 The 1983 air Pb concentrations were based on two monitoring stations, while a combination of dispersion
modeling and monitoring data was used in the later years. Surface soil Pb measurements were from 2000-2001, but
geo-matched to blood Pb measurements across full study period (Ranft et al., 2008).
3-11
-------
Ranft et al., 2008, Table 2). Uncertainties related to this study's estimates include those related
to the bulk of air concentration reduction occurring between the first two time points (1983 and
1991) and the difference among the year's air datasets (e.g., two data sources [air monitors] in
1983 and multiple geographical points from a combination of the monitors and modeling in
subsequent years).
3-12
-------
Table 3-1. Empirically derived air-to-blood ratios for populations inclusive of children.
Study Information
Quantitative Analysis
Air-to-Blood
Ratio A
Focused on children < 5 years old
Children, 0.5-5 yr (n = 9,604), average age 2.5 yr
Chicago, IL, 1974-1988
Urban area with lead-emitting industries, leaded gasoline usage
Hayes etal. (1994)
Children, 0.5-5 yr (1996-1999), 0.5-3 yr (2001) (n = 200-500)
Trail, BC, 1996-2001;
Small town before/after cleaner technology on large metals
smelter (at end of/after leaded gasoline phase-out)
Hilts (2003)
Black children, <5 yr (n = 5,476)
Chicago, IL, Feb 1976- Feb 1980
Area with lead-emitting industries, leaded gasoline usage
Schwartz and Pitcher (1989), U.S. EPA (1986a)
ogn-logn regression: quarterly median PbB and quarterly
mean PbA
[unadjusted]
PbB: 10-28 pg/dL (quarterly median)
PbA: 0.05-1 .2 pg/m3 (quarterly mean)
linear regression: annual GM PbB and AM PbA
[unadjusted]
PbB: 4.7-11. 5 pg/dL (annual GM)
PbA: 0.03-1 .1 |jg/m3 (annual AM)
linear regression: quarterly mean PbB with gasoline Pb
(usage) [ adjusted for demographic covariates]
combined with gasoline Pb - air Pb relationship.
PbB: 18-27 pg/dL (quarterly mean, adjusted)
PbA- gas Pb relationship based on annual U.S. means
of per-site maximum quarterly means (0.36-1 .22 |jg/m3)
8.2 (@ 0.62) B
6-7.0°
8.6°
Larger age range, inclusive of children < 5 years old
Children, 96 groups of various age ranges, (n>1 90,000)
Various countries (18 locations), 1974-1983
urban or near lead-emitting industries, leaded gasoline usage
Brunekreef (1984)
Children, born 1987-92 (n = 321); Mexico City, 1987-2002
Average age increased over study period: <3yrs (1987-1992),
and increased by a year each year after that
Urban area during/after leaded gasoline usage
Schnaas etal. (2004)
U.S. NHANES II white subjects, 0.5-74 yr, Feb 1976-1980
National survey during time of leaded gasoline usage
Schwartz and Pitcher (1989), U.S. EPA (1986a)
Meta-analyses (logn-logn regression of group means):
(1) all children, (2) children <20 pg/dL [unadjusted]
PbB: 5-76 pg/dL (study group means)
PbA: 0.1-24 pg/m3 (location means)
Linear , logn-logn regressions: annual mean PbB and
PbA [unadjusted]
PbB: 5-12 |jg/dL (annual GM), aged 0.5-10 yr
PbA: 0.07-2.8 |jg/m3 (AM); 0.1-0.4 over last 6 years
Linear regression: PbB with mass Pb in gasoline as
described above, [adjusted for demographic covariates]
PbB: 11-18 pg/dL (mean per gas Pb, adjusted)
PbA- gas Pb relationship based on annual U.S. means
of per-site maximum quarterly means (0.36-1 .22 pg/m3)
Full dataset:
4.6(@1.5)E
<20|jg/dL:
4.8(@0.54)F
Linear:
9.0(0.1-0.4)
2.5 (full range)
Log-log: 4.5
(@0.4)c
9.3°
Focused on children > 6 years old
Children, 6-10 yr(n = 544)
Mumbai, India, 1984-1996
Large urban area, leaded gasoline usage
Tripathi etal. (2001)
Children, 6-1 1 yr (n=843); average: -9.5 yr (1983), -6.5 (others)
Duisburg, Germany-5 areas: 1983, 1991, 1994, 1997, 2000
Industrial urban area during/after leaded gasoline usage
Ranft etal. (2008)
Linear regression: 13-vear location-specific GM PbB and
PbA [unadjusted]
PbB: 8.6-14.4 |jg/dL (location GM)
PbA: 0.11-1.18 |jg/m3 (location GM); 0.45 (overall GM)
Linear, logn-logn. log-linear regressions: annual mean
PbB and air Pb [unadjusted]
PbB: 3.33-9.13 |jg/dL (AMs of 5 study years)
PbA: 0.06-0.45 |jg/m3 (5 AMs), 0.10 (overall median)
3.6
Log-linear G
6.4, 3.2
A - Predicted change in blood Pb (|jg/dL per |jg/m3) over range ± 0.01 |jg/m3 from study's central air Pb, which is provided in |jg/m3 in parentheses.
For linear models, this is simply the air Pb coefficient.
B - In(PbB) = In(PbA) x 0.24 +3.17 (ISA, Table 3-12; Hayes et al., 1994)
C - See discussion in text and ISA, section 3.5.1.
D - Based on data for U.S. (1986 CD). See ISA, section 3.5.1. Log-lin = log-linear model.
E - In(PbB) = In(PbA) x 0.3485 +2.853
F - In(PbB) = In(PbA) x 0.21 59 + 2.620
G -Derived from regressions with separate soil Pb variable, contributing to underestimation of contribution from air Pb (see text and ISA, section 3.5.1).
GM, geometric mean; AM, arithmetic mean; GSD, geometric standard deviation; PbB, blood Pb concentration, |jg/dL; PbA, air Pb concentration, |jg/m3
3-13
-------
In the 2008 Pb NAAQS review, in addition to considering the evidence presented in the
published literature and that reviewed in the 1986 CD, we also considered air-to-blood ratios
derived from the exposure assessment (73 FR 66974; 2007 REA, section 5.2.5.2). In the
exposure assessment (summarized in section 3.4 below), current modeling tools and information
on children's activity patterns, behavior and physiology were used to estimate blood Pb levels
associated with multimedia and multipathway Pb exposure. The results from the various case
studies assessed, with consideration of the context in which they were derived (e.g., the extent to
which the range of air-related pathways was simulated, and the limitations associated with those
simulations), and the multiple sources of uncertainty (see section 3.4.7 below) are also
informative to our understanding of air-to-blood ratios. Estimates of air-to-blood ratios for the
two REA case studies that represent localized population exposures exhibited an increasing trend
across air quality scenarios representing decreasing air concentrations. For example, across the
alternative standard levels assessed, which ranged from a calendar quarter average of 1.5 jig/m3
down to a monthly average of 0.02 |ig/m3, the ratios ranged from 1:2 to 1:9 for the general urban
case study, with a similar trend although of generally higher ratio for the primary smelter case
study subarea. This pattern of model-derived ratios is generally consistent with the range of
ratios obtained from the literature. We continue to recognize a number of sources of uncertainty
associated with these model-derived ratios which may contribute to high or low biases.10
The evidence on the quantitative relationship between air Pb and air-related Pb in blood
is now, as in the past, limited by the circumstances (such as those related to Pb exposure) in
which the data were collected. Previous reviews have recognized the significant variability in
air-to-blood ratios for different populations exposed to Pb through different air-related exposure
pathways and at different air and blood levels, with the 1986 CD noting that ratios derived from
studies involving the higher blood and air Pb levels pertaining to occupationally exposed
workers are generally smaller than ratios from studies involving lower blood and air Pb levels
(ISA, p. 3-132; 1986 CD, p. 11-99). Consistent with this observation, slopes in the range of 3 to
10 For example, the limited number of air-related pathways (inhalation and indoor dust ingestion) simulated
to change in response to changes in ambient air Pb reductions in these case studies could have implications for the
air-to-blood ratios. Additionally, with regard to the urban case study, the relationship between dust loading and
concentration, a key component in the hybrid dust model used in estimating indoor dust Pb levels, is based largely
on a housing survey dataset reflecting dust Pb in housing constructed before 1980 (as described in the 2007 REA,
Volume II, Appendix G, Attachment G-l). The use of leaded paint in some housing constructed before 1980
contributes some uncertainty due to the potential role of indoor Pb paint (compared to ambient air Pb) in the
relationship. The empirically-based ambient air Pb - dust Pb relationships used in the primary Pb smelter (subarea)
case study may contribute to a potential for the ratios from this case study to more fully capture the impact of
changes in ambient air Pb on indoor dust Pb, and consequently on blood Pb. Some have suggested, however, that
the regression used may not accurately reflect the temporal relationship between reductions in ambient air Pb and
indoor dust Pb and as a result may overestimate the dust Pb reduction per ambient air Pb reduction, thus contributing
a potential high bias to the air-to-blood Pb ratios.
3-14
-------
5 were estimated for child population datasets assessed in the 1986 CD (ISA, p. 3-132; 1986 CD
p. 11-100; Brunekreef, 1984; Tripathi et al., 2004). Additional studies considered in the last
review and those assessed in the ISA provide evidence of ratios above this older range (ISA, p.
3-133). For example a ratio of 6.5-7 is indicated by the study by Hilts (2003), one of the few
studies that evaluate the air Pb-blood Pb relationship in conditions that are closer to the current
state in the U.S. (ISA, p. 3-132). We additionally note the variety of factors identified in the
ISA that may potentially affect estimates of various ratios (including potentially coincident
reductions in nonair Pb sources during the course of the studies), and for which a lack of
complete information may preclude any adjustment of estimates to account for their role (ISA,
section 3.5).
In summary, as at the time of the last review of the NAAQS for Pb, the currently
available evidence includes estimates of air-to-blood ratios, both empirically- and model-derived,
with associated limitations and related uncertainties. These limitations and uncertainties, which
are summarized here and also noted in the ISA, usually include uncertainty associated with
reductions in other Pb sources during the study period. The limited amount of new information
available in this review has not appreciably altered the scientific conclusions reached in the last
review regarding relationships between Pb in ambient air and Pb in children's blood or with
regard to the range of ratios. The currently available evidence continues to indicate ratios
relevant to the population of young children in the U.S. today, reflecting multiple air-related
pathways in addition to inhalation, to be generally consistent with the approximate range of 1:5
to 1:10 given particular attention in the 2008 NAAQS decision, including the "generally central
estimate" of 1:7 (73 FR 67002, 67004; ISA, pp. 3-132 to 3-133).
3.2 NATURE OF EFFECTS
Lead has been demonstrated to exert a broad array of deleterious effects on multiple
organ systems as described in the assessment of the evidence available in this review and
consistent with conclusions of past CDs (ISA, section 1.6; 2006 CD, section 8.4.1). A sizeable
number of studies on Pb health effects are newly available in this review and are critically
assessed in the ISA as part of the full body of evidence. The newly available evidence reaffirms
conclusions on the broad array of effects recognized for Pb in the last review (see ISA, section
1.10).11 Consistent with those conclusions, in the context of pollutant exposures considered
11 Since the last Pb NAAQS review, the IS As which have replaced CDs in documenting each review of the
scientific evidence (or air quality criteria) employ a systematic framework for weighing the evidence and describing
associated conclusions with regard to causality, using established descriptors ("causal" relationship with relevant
exposure, "likely" to be causal, evidence is "suggestive" of causality, "inadequate" evidence to infer causality, "not
likely") (ISA, Preamble).
3-15
-------
relevant to the Pb NAAQS review,12 the ISA determines that causal relationships13 exist for
Pbwith effects on the nervous system in children (cognitive function decrements and the group of
externalizing behaviors comprising attention, impulsivity and hyperactivity), the hematological
system (altered heme synthesis and decreased red blood cell survival and function), and the
cardiovascular system (hypertension and coronary heart disease), and on reproduction and
development (postnatal development and male reproductive function) (ISA, table 1-2).
Additionally, the ISA describes relationships between Pb and effects on the nervous system in
adults, on immune system function and with cancer14 as likely to be causal15 (ISA, table 1-2,
sections 1.6.4 and 1.6.7).
In some categories of health effects, there is newly available evidence regarding some
aspects of the effects described in the last review or that strengthens our conclusions regarding
aspects of Pb toxicity on a particular physiological system. Among the nervous system effects of
Pb, the newly available evidence is consistent with conclusions in the previous review which
recognized that "[t]he neurotoxic effects of Pb exposure are among those most studied and most
extensively documented among human population groups" (2006 CD, p. 8-25). Nervous system
effects that receive prominence in the current review, as in previous reviews, include those
12 With regard to consideration of pollutant exposures for studies included in the ISA, the ISA states the
following (ISA, pp. Ix-lxi).
In draw ing judgments regarding causality for the criteria air pollutants, the ISA focuses on
evidence of effects in the range of relevant pollutant exposures or doses, and not on determination
of causality at any dose. Emphasis is placed on evidence of effects at doses (e.g., blood Pb
concentration) or exposures (e.g., air concentrations) that are relevant to, or somewhat above,
those currently experienced by the population. The extent to which studies of higher
concentrations are considered varies by pollutant and major outcome category, but generally
includes those with doses or exposures in the range of one to two orders of magnitude above
current or ambient conditions. Studies that use higher doses or exposures may also be considered
to the extent that they provide useful information to inform understanding of mode of action,
interspecies differences, or factors that may increase risk of effects for a population. Thus, a
causality determination is based on weight of evidence evaluation for health, ecological or
welfare effects, focusing on the evidence from exposures or doses generally ranging from current
levels to one or two orders of magnitude above current levels.
13 In determining there to be a causal relationship for Pb with specific health effects, EPA has concluded
that "[e]vidence is sufficient to conclude that there is a causal relationship with relevant pollutant exposures (i.e.,
doses or exposures generally within one to two orders of magnitude of current levels)" (ISA, p. Ixii)
14 Lead has been classified as a probable human carcinogen by the International Agency for Research on
Cancer, based mainly on sufficient animal evidence, and as reasonably anticipated to be a human carcinogen by the
U.S. National Toxicology Program (ISA, section 4.10). In this assessment, EPA concludes that a causal relationship
is likely to exist between Pb exposure and cancer, based primarily on consistent, strong evidence from experimental
animal studies, but inconsistent epidemiological evidence (ISA, section 4.10.5).
15 In determining that there is likely to be a causal relationship for Pb with specific health effects, EPA has
concluded that "[e]vidence is sufficient to conclude that a causal relationship is likely to exist with relevant pollutant
exposures, but important uncertainties remain" (ISA, p. Ixii).
3-16
-------
affecting cognitive function and behavior in children (ISA, section 4.3), with conclusions that are
consistent with findings of the last review.
Across the broad array of Pb effects for systems and processes other than the nervous
system, the evidence base has been augmented with additional epidemiological investigations in
a number of areas, including developmental outcomes, such as puberty onset, and adult outcomes
related to cardiovascular function, for which several large cohorts have been analyzed (ISA,
Table 1-8 and sections 4.4 and 4.8). Conclusions on these other systems and processes are
consistent with conclusions reached in the last review, while also extending our conclusions on
some aspects of these effects. For example, evidence in this review for the cardiovascular
system includes information on the role of interactions of cumulative Pb exposure with other
factors, such as stress in contributing to hypertension, and on a role for Pb in contributing to
coronary heart disease (ISA, section 4.4 and Table 1-8).
Based on the extensive assessment of the full body of evidence available in this review,
the major conclusions drawn by the ISA regarding health effects of Pb in children include the
following (ISA, p. Ixxxvii).
Multiple epidemiologic studies conducted in diverse populations of children
consistently demonstrate the harmful effects ofPb exposure on cognitive function
(as measured by IQ decrements, decreased academic performance and poorer
performance on tests of executive function).... Evidence suggests that some Pb-
related cognitive effects may be irreversible and that the neurodevelopmental
effects ofPb exposure may persist into adulthood (Section 1.9.4). Epidemiologic
studies also demonstrate that Pb exposure is associated with decreased attention,
and increased impulsivity and hyper activity in children (externalizing behaviors).
This is supported by findings in animal studies demonstrating both analogous
effects and biological plausibility at relevant exposure levels. Pb exposure can
also exert harmful effects on blood cells and blood producing organs, and is likely
to cause an increased risk of symptoms of depression and anxiety and withdrawn
behavior (internalizing behaviors),deer eases in auditory and motor function,
asthma and allergy, as well as conduct disorders in children and young adults.
There is some uncertainty about the Pb exposures contributing to the effects and
blood Pb levels observed in epidemiologic studies; however, these uncertainties
are greater in studies of older children and adults than in studies of young
children (Section 1.9.5).
Based on the extensive assessment of the full body of evidence available in this review,
the major conclusions drawn by the ISA regarding health effects of Pb in adults include the
following (ISA, p. Ixxxviii).
A large body of evidence from both epidemiologic studies of adults and
experimental studies in animals demonstrates the effect of long-term Pb exposure
on increased blood pressure (BP) and hypertension (Section 1.6.2). In addition to
its effect on BP, Pb exposure can also lead to coronary heart disease and death
3-17
-------
from cardiovascular causes and is associated with cognitive function decrements,
symptoms of depression and anxiety, and immune effects in adult humans. The
extent to which the effects ofPb on the cardiovascular system are reversible is not
well-characterized. Additionally, the frequency, timing, level, and duration of Pb
exposure causing the effects observed in adults has not been pinpointed, and
higher past exposures may contribute to the development of health effects
measured later in life.
As in prior reviews of the Pb NAAQS, this review is focused on those effects most
pertinent to ambient air Pb exposures. Given the reductions in ambient air Pb levels over the
past decades, these effects are generally those associated with the lowest levels of Pb exposure
that have been evaluated. Additionally, we recognize the limitations on our ability to draw
conclusions regarding the exposure conditions contributing to the findings from epidemiological
analyses of blood Pb levels in populations of older children and adults, particularly in light of
their history of higher Pb exposures. In the last review, while recognizing the range of health
effects in variously aged populations related to Pb exposure, we focused on the health effects for
which the evidence was strongest with regard to relationships with the lowest exposure levels,
neurocognitive effects in young children. The policy-relevant questions on health effects for this
review (identified in the IRP) were framed in recognition of the conclusions of the last review.
Our consideration of the health effects evidence in this review is framed by policy-relevant
questions building on those identified in the IRP.
• To what extent is there new scientific evidence available to improve our
understanding of the health effects associated with various time periods of Pb
exposures at various stages of life?
As in the last review, we base our current understanding of health effects associated with
different Pb exposure circumstances at various stages of life on the full body of available
evidence which includes epidemiological studies of health effects associated with population Pb
biomarker levels as well as laboratory animal studies in which the effects of different exposures
on different lifestages are assessed under controlled conditions. The epidemiological evidence is
overwhelmingly comprised of studies that rely on blood Pb for the exposure metric, with the
remainder largely including a focus on bone Pb. Because these metrics reflect Pb in the body
(e.g., as compared to Pb exposure concentrations) and, in the case of blood Pb, reflect Pb
available for distribution to target sites, they strengthen the evidence base for purposes of
drawing causal conclusions with regard to Pb generally. The complexity of Pb exposure
pathways and internal dosimetry tends to limit the extent to which these types of studies inform
our more specific understanding of the Pb exposure circumstances (e.g., timing, duration,
frequency and magnitude) eliciting the various effects.
3-18
-------
The specific exposure circumstances, including timing during the lifetime, that contribute
to the blood Pb (or bone Pb) measurements with which associations have been analyzed in
epidemiological studies are unknown. This is particularly the case with regard to the
contributing role of recent exposures for which uncertainty is greater in adults and older children
than in younger children (ISA, sections 1.9.4). For example, a critical aspect of much of the
epidemiological evidence, particularly that focused on older adults in the U.S. today, is the
backdrop of generally declining environmental Pb exposure (from higher exposures during their
younger years) that is common across many study populations (ISA, p. 4-2). An additional
factor complicating the interpretation of health effect associations with blood Pb measurements
in older children and younger adults is the common behaviors of younger children (e.g., hand-to-
mouth contact) which generally contribute to relatively greater environmental exposures earlier
in life (ISA, sections 3.1.1, 4.2.1). Such exposure histories complicate our ability to draw
conclusions regarding critical time periods and lifestages for Pb exposures eliciting the effects
with which associations with Pb biomarkers have been observed in populations of adults and
older children (e.g., ISA, section 1.9.6).16
As at the time of the last review, assessment of the full evidence base, including evidence
newly available in this review, demonstrates that Pb exposure prenatally and also in early
childhood can contribute to neurocognitive impacts in childhood, with evidence also indicating
the potential for effects persisting into adulthood (ISA, sections 1.9.5, 1.9.6, and 1.10). In
addition to the observed associations of prenatal and childhood blood Pb with effects at various
ages in childhood, there is also evidence of lead-related cognitive function effects in non-
occupationally exposed adults (ISA, section 4.3.11). This includes evidence of associations of
such effects in adulthood with childhood blood Pb levels and, in other cohorts, with concurrent
(adult) blood Pb levels (ISA, sections 4.3.2.1, 4.3.2.7 and 4.3.11). As the studies finding
associations of adult effects with childhood blood Pb levels did not examine adult blood Pb
levels, the relative influence of adult Pb exposure cannot be ascertained, and a corresponding
lack of early life exposure or biomarker measurements for the latter studies limit our ability to
draw conclusions regarding specific Pb exposure circumstances eliciting the observed effects
(4.3.11). Findings of stronger associations for adult neurocognitive effects with bone Pb,
16 The evidence from experimental animal studies can be informative with regard to key aspects of
exposure circumstances in eliciting specific effects which can inform our interpretation of the epidemiological
evidence. For example, the animal evidence base with regard to Pb effects on blood pressure demonstrates the
etiologically-relevant role of long-term (as compared to short-term) exposure (ISA, section 4.4.1). This finding then
informs consideration of epidemiological studies of adult populations for whom historical exposures were likely
more substantial than concurrent ones to suggest that the observed effects may be related to the past exposure (ISA,
section 4.4.1). For other health effects, the animal evidence base may or may not be informative with regard to the
role of specific exposure circumstances in eliciting those effects.
3-19
-------
however, indicate the role of historical or cumulative exposures for those effects (ISA, section
4.3).
Given the relatively short exposure histories of young children, there is relatively reduced
uncertainty regarding the lifestages in which exposures contribute to effects for associations of
early childhood effects with early childhood blood Pb levels (ISA, sections 1.9.4, 1.9.6 and
4.3.11). In considering our understanding of the relative impact on neurocognitive function of
additional Pb exposure of children by school age or later we recognize increasing uncertainty
associated with limitations of the currently available evidence, including epidemiological cohorts
with generally similar temporal patterns of exposure. We take note, additionally, of evidence
from experimental animal studies and a small body of epidemiological studies that indicates that
Pb exposures during different lifestages can induce cognitive impairments. The limited
epidemiological evidence is of populations with blood Pb levels that are not strongly correlated
over time and that can, accordingly, address the issue of the role of exposure subsequent to the
earliest lifestages (ISA, section 4.3.11; Hornung et al., 2009). Some animal evidence
demonstrates impaired learning with infancy only, from infancy into adulthood, and postinfancy
only Pb exposure (Rice, 1990; Rice and Gilbert 1990; Rice, 1992). Further, evidence thatPb
exposure presents a risk during different lifestages is also consistent with our broader
understanding that nervous system development continues throughout childhood. The limited
analyses of this issue that are newly available in this review do not appreciably change our
understanding or conclusions on this from those of the prior review (ISA, section 4.3.11).
As in the last review, there is also substantial evidence of other neurobehavioral effects in
children, such as reduced attention span, increased impulsivity, hyperactivity, conduct disorders
and effects on internalizing behaviors. The evidence for many of these endpoints, as with
neurocognitive effects, also includes associations of effects at various ages in childhood and, for
some effects, into adulthood, with blood Pb levels reflective of several different lifestages (e.g.,
prenatal and several different ages in childhood) (ISA, sections 4.3.3 and 4.3.4). There is similar
or relatively less extensive evidence to inform our understanding of such effects associated with
specific time periods of exposure at specific lifestages than is the case for effects on cognitive
function.
Across the range of Pb effects on physiological systems and processes other than the
nervous system, the full body of evidence on etiologically relevant circumstances of Pb exposure
eliciting increases in blood pressure and hypertension is somewhat more informative than is the
case with regard to many other effects. In the case of lead-induced increases in blood pressure,
the evidence indicates an importance of long-term exposure (ISA, sections 1.6.2 and 4.4.7.1).
In summary, as in the last review, we continue to recognize a number of uncertainties
regarding the circumstances of Pb exposure, including timing or lifestages, eliciting specific
3-20
-------
health effects. Consideration of the evidence newly available in this review has not appreciably
changed our understanding on this topic. The relationship of long-term exposure to Pb with
hypertension and increased blood pressure in adults is substantiated despite some uncertainty
regarding the exposures circumstances (e.g., magnitude and timing) contributing to blood Pb
levels measured in epidemiological studies. Across the full evidence base, the effects for which
our understanding of relevant exposure circumstances is greatest are neurocognitive effects in
young children. Thus, we continue to recognize and give particular attention to the role of Pb
exposures relatively early in childhood in contributing to neurocognitive effects which may
persist into adulthood.
• At what levels of Pb exposure do health effects of concern occur? Is there
evidence of effects at exposure levels lower than previously observed and what
are important uncertainties in that evidence?
In considering the question posed here, we recognize, as discussed in section 3.1 above,
that the epidemiological evidence base for our consideration in this review, as in the past,
includes substantial focus on internal biomarkers of exposure, such as blood Pb, with relatively
less information specific to exposure levels, including those derived from air-related pathways.
Given that blood and bone Pb are integrated markers of aggregate exposure across all sources
and exposure pathways, our interpretation of studies relying on them is informed by what is
known regarding the historical context and exposure circumstances of the study populations. For
example, a critical aspect of much of the epidemiological evidence is the backdrop of generally
declining Pb exposure over the past several decades. Thus as a generality, recent
epidemiological studies of populations with similar characteristics as those studied in the past
tend to involve lower overall Pb exposures and accordingly lower blood Pb levels (e.g., ISA,
sections 2.5 and 3.4.1; 2006 CD, section 3.4). This has been of particular note in the evidence of
blood Pb associations with nervous system effects, particularly impacts on cognitive function in
children, for which we have seen associations with progressively lower childhood blood Pb
levels across past reviews (ISA, section 4.3.12; 1986 CD; USEPA, 1990; 2006 CD; 73 FR
66976).
The evidence currently available with regard to the magnitude of blood Pb levels
associated with neurocognitive effects in children is generally consistent with that available in
the review completed in 2008. Nervous system effects in children, specifically effects on
cognitive function, continue to be the effects that are best substantiated as occurring at the lowest
blood Pb concentrations (ISA, pp. Ixxxvii-lxxxviii). Associations of blood Pb with effects on
cognitive function measures in children have been reported in many studies across a range of
3-21
-------
childhood blood Pb levels, including study group (mean/median) levels ranging down to 2 |ig/dL
(e.g., ISA, p. Ixxxvii and section 4.3.2).17
Studies in which such findings were reported for childhood study group blood Pb levels
below 5 |ig/dL are summarized in Table 3-2.18 In recognition of the influence of age on blood
Pb levels, the analyses in Table 3-2 are listed in order of age at which the blood Pb
measurements were taken. Findings for studies newly available in this review are indicated in
bold text. Although the analyses from Lanphear et al (2005) listed in Table 3-2 were available in
the last review, the information presented in Table 3-2 for sample size and mean blood Pb
concentration has been updated to reflect recalculations using data corrected for recently
identified errors, as described further in the next section below (Kirrane and Patel, 2014).
17 The value of 2 ug/dL refers to the regression analysis of blood Pb and end-of-grade test scores, in which
blood Pb was represented by categories for integer values of blood Pb from 1 ug/dL to 9 and >10 ug/dL from large
statewide database. A significant effect estimate was reported for test scores with all blood Pb categories in
comparison to the reference category (1 ug/dL), which included results at and below the limit of detection. Mean
levels are not provided for any of the categories (Miranda et al., 2009).
18 Two additional studies (both newly available) that report such associations with blood Pb levels for
which the mean is equal to 5.0 ug/dL. The first is a study of 506 children in Detroit, MI (born, 1982-1984) at age 7
years which observed a significant negative association with concurrent blood Pb levels for which the mean equals
5.0 ug/dL (8.9% of childen with concurrent blood Pb above 10 ug/dL) (ISA, sections 4.3.2.1 and 4.3.3.1; Chiodo et
al., 2007). The second study focuses on 174 of the Rochester cohort children at age 6 years, reporting significant
negative associations with FSIQ for four different blood Pb metrics: concurrent (mean = 5.0 ug/dL), lifetime
average (mean=7.2 ug/dL), infancy average (mean =7.1 ug/dL) and peak (mean =11.4 ug/dL) (Jusko et al., 2008).
3-22
-------
Table 3-2. Associations with neurocognitive function measures in analyses with child study group blood Pb levels <5 ug/dL.
Measure*
Study Group Dataset Description
Blood Pb Levels
Age
Mean6
(Mg/dL)
Range5
(Mg/dL)
N
Additional Information on Analyses
cStudies discussed in ISA (section 4.3.2) with findings of effects on neurocognitive measures reported for childhood study group PbB < 5 jjg/dL
(ordered by age of blood Pb measurements)
FSIQ
BSID/MDI
AcadPerf
AcadPerf
FSIQ
FSIQ
FSIQ
LM, EF
AcadPerf
FSIQ
LM
AcadPerf
LM
AcadPerf
Boston, prospective, age 5 yr
Subgroup with peak PbB <10 pg/dL
Bellinger and Needleman 2003
Mexico City, age 24 mo,Tellez-Rojo et al., 2006
Subgroup with PbB<5 pg/dL
Full dataset
North Carolina, 4th graders
4th grade reading scores, Full dataset
Miranda et al., 2009
Avon, United Kingdom, age 7-8 yr
standard assessment scores, Full dataset,
Chandramouli et al., 2009
Rochester, prospective cohort, age 5 yr
Subgroup with peak PbB <10 pg/dL
Canfield etal., 2003
Pooled International, age 6-10 yr
Subgroup with peak PbB <7.5 pg/dL
Lanphear et al 2005 E
New England, 2 areas, age 6-10, ,
Full dataset,
Surkan et al., 2007
Korea, 4 areas, age 8-1 1 yr
Full dataset
Kim et al., 2009
NHANES 111(1988-1994)
Lanphear etal. ,2000
NHANES III (1991-1994)
Krieg etal., 2010
24 mo
24 mo
9-36 mo
30 mo
Syr
5-7 yr
6-1 Oyr
8-1 1yr
6-1 6 yr
12-1 6 yr
3.8
2.9
4.3
4.8
4.22
3.32
3.3
2.3
1.73
1.9
1.95
1-9.3
0.8-4.9
0.8-9.8
1-16
21%<2
52% 2-5
21% 5-10
0.5-8.4
(LOD=1)
0.9-7.4
1-10
0.4-4.9
48
193
294
57,678
488°
71
118
389
261
4,853
766-80
Regression, PbB as continuous variable; statistically significant negative
association
Regression, PbB as continuous variable; statistically significant negative
association
Linear and quantal regressions with integer PbB as categorical variable (PbB-1
reference category, includes LOD). Linear analysis: statistically significant effect
for all comparison categories. Quantal analysis: statistically significant effect in all
reading score quantiles for PbB categories greater than integer PbB=3; largest
effect in lower quantiles. Means not reported for PbB categories.
Regressions with PbB as continuous and categorical variables: continuous
analysis (statistically significant negative association); categorical (significantly
reduced scores for 5-10 |jg/dL vs reference group [ 0-2 M9/dL])
Regression, PbB as continuous variable; statistically significant negative
association
Regression, PbB as continuous variable; statistically significant negative
association
Regression, PbB grouped into categories; statistically significant negative
association for high subgroup (5-10 ug/dL, n=32) compared to reference PbB
subgroup (1-2 ug/dL, n=286).
Regression, PbB analyzed as quartiles; statistically significant difference among
quartiles; statistically significant negative association in continuous analysis of full
dataset and high blood manganese group
Continuous (unadjusted) and categorical (adjusted) analysis; significant difference
among PbB quartiles (< 1, 1.1-1.9, 2.0-3.0, >3.0 ug/dL), and neg assoc PbB <5.0.
Regression analysis; PbB as continuous variable; statistically significant negative
association.
A - FSIQ = Full Scale Intelligence Quotient; BSD = Bayley Scales of Development; MDI= Mental Development Index; LM=Learning and Memory; EF= Executive Function; AcadPerf= Academic Performance.
B - Blood Pb level (PbB) information provided here is in some cases augmented by study authors (Bellinger, 2008; Canfield, 2008a,b; Hornung, 2008a,b; Tellez-Rojo, 2008; Kirrane and Patel, 2014).
C - Bolded measures and studies are newly available in this review. D - In practice, 337-425 cases were included in analysis (Chandramouli et al., 2009).
E - Blood Pb measurements of subgroup with peak PbB <7. 5 |ig/dl_ comprised of 24.6% age 5 (Boston, Cleveland), 58.5% age 6 (Rochester), 16.9% age 7 (Yugoslavia, Mexico, Cincinnati). IQ assessed at age 5 for the
single member of this subgroup from Cleveland cohort. This analysis includes blood Pb data from Rochester and Boston cohorts, although for different ages (6 and 5 years, respectively) than the ages analyzed in Canfield
et al 2003 and Bellinger and Needleman 2003. For full dataset analysis (n=1333), IQ assessed at ages 5-10 yr, median blood Pb (at ages 5-7 yr) of 9.7 pg/dL and 5th -95th percentile of 2.5-33.2 pg/dL.
5-23
-------
Among the analyses of lowest study group blood Pb levels at the youngest ages in Table
3-2 are analyses available in the last review of Pb associations with neurocognitive decrement in
study groups with mean levels on the order of 3-4 |ig/dL in children aged 24 months or ranging
from 5 to 7 years (73 FR 66978-66969; ISA, sections 4.3.2.1 and 4.3.2.2; Bellinger and
Needleman, 2003; Canfield et al., 2003; Lanphear et al., 2005; Tellez-Rojo et al., 2006;
Bellinger, 2008; Canfield, 2008; Tellez-Rojo, 2008; Kirrane and Patel, 2014).19 Newly available
in this review are two studies reporting association of blood Pb levels prior to three years of age
with academic performance on standardized tests in primary school; mean blood Pb levels in
these studies were 4.2 and 4.8 |ig/dL (ISA, section 4.3.2.5; Chandramouli et al., 2009; Miranda
et al., 2009). One of these two studies, which represented integer blood Pb levels as categorical
variables, indicated a small effect on end-of-grade reading score of blood Pb levels as low as 2
|ig/dL, after adjustment for age of measurement, race, sex, enrollment in free or reduced lunch
program, parental education, and school type (Miranda et al., 2009).
In a newly available study of blood Pb levels at primary school age, a significant
association of blood Pb in children aged 8-11 years and concurrently measured full scale IQ
(FSIQ) was reported for a cross-sectional cohort in Korea with a mean blood Pb level of 1.7
|ig/dL and range of 0.43-4.91 |ig/dL (Kim et al., 2009).20 In considering the blood Pb levels in
this study, we note that blood Pb levels in children aged 8-11 are generally lower than those in
pre-school children, for reasons related to behavioral and other factors (ISA, sections 3.3.5, 3.4.1
and 5.2.1.1).21 It is likely that the blood Pb levels of this study group at earlier ages, e.g., prior to
school entry, were higher and the available information does not provide a basis to judge whether
the blood Pb levels in this study represent lower exposure levels than those experienced by the
younger study groups. In still older children, a large cross-sectional investigation of blood Pb
association with effects on memory and learning that was available in the last review was
focused on children aged 6-16 years, born during 1972-1988, with a mean blood Pb of 1.9
|ig/dL. A study newly available in this review, focused on a subset of the earlier study cohort
19 The tests for cognitive function in these studies include age-appropriate Wechsler intelligence tests
(Lanphear et al., 2005; Bellinger and Needleman, 2003), the Stanford-Binet intelligence test (Canfield et al., 2003),
and the Bayley Scales of Infant Development (Tellez-Rojo et al., 2006). The Wechsler and Stanford-Binet tests are
widely used to assess neurocognitive function in children and adults. These tests,however, are not appropriate for
children under age three. For such children, studies generally use the age-appropriate Bayley Scales of Infant
Development as a measure of cognitive development.
20 Limitations of this study included a lack of consideration of potential confounding by parental caregiving
quality or IQ (ISA, Table 4-3).
21 This study also investigated the potential role of manganese (Mn) in the blood Pb associated effects.
When the cohort was subdivided based on Mn blood Pb levels, using the median Mn level (14 ug/L) as the break
point, the significant association of intelligence quotient (IQ) with Pb persisted in the higher Mn group but was no
longer significant in the lower Mn group (ISA, section 4.3.2). Separate analysis of the full study group found a
significant negative association of IQ with blood Mn (Kim et al., 2009).
3-24
-------
(ages 12-16, born during 1975-1982), also reports a significant negative association of blood Pb
with learning and memory test results with mean blood Pb levels of approximately 2 |ig/dL (ISA,
section 4.3.2.3; Lanphear et al., 2000; Krieg et al., 2010). In considering these study findings
with regard to the question of exposure levels eliciting effects, we recognize, however, that blood
Pb levels are, in general, lower among teenagers than young children and also that, for these
subjects specifically, the magnitude of blood Pb levels during the earlier childhood (e.g., pre-
school ages) was much higher. For example, the mean blood Pb levels for the 1-5 year old age
group in the NHANES 1976-80 sample was 15 |ig/dL, declining to 3.6 |ig/dL in the NHANES
1988-1991 sample (Pirkle et al., 1994; ISA, section 3.4.1).
With regard to other nervous system effects in children, the evidence base at lower blood
Pb levels is somewhat extended since the last review with regard to the evidence on Pb and
effects on externalizing behaviors, such as attention, impulsivity, hyperactivity and conduct
disorders (ISA, section 4.3.3 and table 4-17). Several newly available studies investigating the
role of blood Pb levels in older children (primary school age and older) have reported significant
associations for these effects with concurrent blood Pb levels, with mean levels generally on the
order of 5 |ig/dL or higher (ISA, section 4.3.3). One exception is the newly available cross-
sectional, categorical analysis of the NHANES 2001-2004 sample of children aged 8-15 years,
which found higher prevalence of conduct disorder in the subgroup with concurrent blood Pb
levels of 0.8-1.0 |ig/dL as compared to the <0.8 |ig/dL group (ISA, section 4.3.4 and Table 4-
12). As noted above, we recognize that many of these children, born between 1986 and 1996,
are likely to have had much higher Pb exposures (and associated blood Pb levels) in their earlier
years than those commonly experienced by young children today, thus precluding a conclusion
regarding evidence of effects associated with lower exposure levels than provided by evidence
previously available.
As summarized earlier in this section, blood Pb has been associated with a range of health
effects on multiple organ systems or processes. As is the case for studies of nervous system
effects in children, newly available studies of other effects in child and adult cohorts include
cohorts with similar or somewhat lower mean blood levels than in previously available studies.
Categories of effects for which a causal relationship has been concluded in the ISA and for
which there are a few newly available epidemiological studies indicating blood Pb associations
with effects in study groups with somewhat lower blood Pb levels than previously available for
these effects include effects on development (delayed puberty onset) and reproduction (male
reproductive function) and on the cardiovascular system (hypertension) (ISA, sections 4.4 and
4.8; 2006 CD, sections 6.5 and 6.6). With regard to the former category, study groups in the
newly available studies include groups comprised of older children ranging up to age 18 years,
for which there is increased uncertainty regarding historical exposures and their role in the
3-25
-------
observed effects.22 An additional factor that handicaps our consideration of exposure levels
associated with these findings is the appreciable uncertainty associated with our understanding of
Pb biokinetics during this lifestage (ISA, sections 3.2, 3.3, and 4.8.6). The evidence newly
available for Pb relationships with cardiovascular effects in adults include some studies with
somewhat lower blood Pb levels than in the last review. The long exposure histories of these
cohorts, as well as the generally higher Pb exposures of the past complicate conclusions
regarding exposure levels that may be eliciting observed effects (ISA, sections 4.4.2.4 and
4.4.7).23
In summary, our conclusions regarding exposure levels at which Pb health effects occur,
particularly with regard to such levels that might be common in the U.S. today, are complicated
now, as in the last review, by several factors. These factors include the scarcity of information in
epidemiological studies on cohort exposure histories, as well as by the backdrop of higher past
exposure levels which frame the history of some study cohorts. Recognizing the complexity, as
well as the potential role of higher exposure levels in the past, we continue to focus our
consideration of this question on the evidence of effects in young children for which our
understanding of exposure history is less uncertain.24 Within this evidence base, we recognize
the lowest study group blood Pb levels to be associated with effects on cognitive function
measures, indicating that to be the most sensitive endpoint. As described above, and
summarized in Table 3-2, the evidence available in this review is generally consistent with that
available in the last review with regard to blood Pb levels at which such effects had been
reported (ISA, section 4.3.2; 2006 CD, section 8.4.2.1; 73 FR 66976-66979). As blood Pb levels
are a reflection of exposure history, particularly in early childhood (ISA, section 3.3.2), we
conclude, by extension, that the currently available evidence does not indicate Pb effects at
exposure levels appreciably lower than recognized in the last review.
We additionally note that, as in the last review, a threshold blood Pb level with which
nervous system effects, and specifically neurocognitive effects, occur in young children cannot
be discerned from the currently available studies (ISA, sections 1.9.3 and 4.3.12).
Epidemiological analyses have reported blood Pb associations with neurocognitive effects (FSIQ
22 Several of these studies involve NHANES III cohorts for which early childhood exposures were
generally much higher than those common in the U.S. today (ISA, section 4.8.5).
23 Studies from the late 1960s and 1970s suggest that adult blood Pb levels during that period ranged from
roughly 13 to 16 ug/m3 and from 15 to 30 ug/dL in children aged six and younger (ISA, section 4.4.1).
24 In focusing on effects associated with blood Pb levels in early childhood, however, we additionally
recognize the evidence across categories of effects that relate to blood Pb levels in older child study groups (for
which early childhoood exposure may have had an influence) which provides additional support to an emphasis
nervous system effects (ISA, sections 4.3, 4.4, 4.5, 4.6, 4.7, 4.8).
3-26
-------
or BSID MDI25) for young child population subgroups (age five years or younger) with
individual blood Pb measurements as low as approximately 1 |ig/dL and mean concentrations as
low as 2.9 to 3.8 ng/dL (ISA, section 4.3.12; Bellinger and Needleman, 2003; Bellinger, 2008;
Canfield el al., 2003; Canfield, 2008; Tellez-Rojo et al., 2006; Tellez-Rojo et al., 2008). As
concluded in the ISA, however, "the current evidence does not preclude the possibility of a
threshold for neurodevelopmental effects in children existing with lower blood levels than those
currently examined" (ISA, section 4.3.13).
Important uncertainties associated with the evidence of effects at low exposure levels are
similar to those recognized in the last review, including the shape of the concentration-response
relationship for effects on neurocognitive function at low blood Pb levels in today's young
children. Also of note is our interpretation of associations between blood Pb levels and effects in
epidemiological studies, with which we recognize uncertainty with regard to the specific
exposure circumstances (timing, duration, magnitude and frequency) that have elicited the
observed effects, as well as uncertainties in relating ambient air concentrations (and associated
air-related exposures) to blood Pb levels in early childhood, as discussed in section 3.1 above.
We additionally recognize uncertainties associated with conclusions drawn with regard to the
nature of the epidemiological associations with blood Pb (e.g., ISA, section 4.3.13), but note that,
based on consideration of the full body of evidence for neurocognitive effects, the EPA has
determined a causal relationship to exist between relevant blood Pb levels and neurocognitive
impacts in children (ISA, section 4.3.15.1).
• To what extent does the newly available evidence alter our understanding of the
concentration-response relationship for neurocognitive effects (IQ) with blood Pb
levels in young children?
Based primarily on studies of FSIQ, the assessment of the currently available studies, as
was the case in the last review, continues to recognize a nonlinear relationship between blood Pb
and effects on cognitive function, with a greater incremental effect (greater slope) at lower
relative to higher blood Pb levels within the range thus far studied, extending from well above 10
|ig/dL to below 5 |ig/dL (ISA, section 4.3.12). This was supported by the evidence available in
the last review, including the analysis of the large pooled international dataset comprised of
blood Pb measurements and IQ test results from seven prospective cohorts (Lanphear et al.,
2005; Rothenberg and Rothenberg, 2005; ISA, section 4.3.12). The blood Pb measurements in
this pooled dataset that were concurrent with the IQ tests ranged from 2.5 |ig/dL to 33.2 |ig/dL.
The study by Lanphear et al (2005) additionally presented analyses that stratified the dataset
25 Bayley Scales of Infant Development, Mental Development Index. The Bayley MDI is a well-
standardized and widely used assessment measure of infant cognitive development. Scores earlier than 24 months
are not necessarily correlated with later FSIQ scores in children with normal development (ISA, section 4.3.15.1).
3-27
-------
based on peak blood Pb levels (e.g., with outpoints of 7.5 |ig/dL and 10 |ig/dL peak blood Pb)
and found that the coefficients from linear models of the association for IQ with concurrent
blood Pb were higher in the lower peak blood Pb level subsets than the higher groups (ISA,
section 4.3.12; Lanphear et al., 2005).
We note that since the completion of the ISA, two errors have been identified with the
pooled dataset analyzed by Lanphear et al (2005) (Kirrane and Patel, 2014). A recent
publication and EPA have separately recalculated the statistics and mathematical models of
Lanphear et al (2005) using the corrected pooled dataset (Kirrane and Patel, 2014). While the
magnitude of the loglinear and linear regression coefficients are modified slightly based on the
corrections, the conclusions drawn from these coefficients, including the finding of a steeper
slope at lower (as compared to higher) blood Pb concentrations are not affected (Kirrane and
Patel, 2014).
In other publications, stratified analyses of several individual cohorts also observed
higher coefficients for blood Pb relationships with measures of neurocognitive function in lower
as compared to higher blood Pb subgroups (ISA, section 4.3.12; Canfield et al., 2003; Bellinger
and Needleman, 2003; Kordas et al., 2006; Tellez-Rojo et al., 2006). Of these subgroup
analyses, those involving the lowest mean blood Pb levels and closest to the current mean for
U.S. preschool children are listed in Table 3-3 below (drawn from Table 3 of the 2008 final
rulemaking notice [73 FR 67003], and Kirrane and Patel, 2014). These analyses were important
inputs for the evidence-based, air-related IQ loss framework which informed decisions on a
revised standard in the last review (73 FR 67005), discussed in section 4.1.1 below. As the
framework focused on the median of the four slopes in Table 3-3, the change to the one from
Lanphear et al (2005) based on the recent recalculation described above has no impact.
3-28
-------
Table 3-3. Summary of quantitative relationships of IQ and blood Pb for analyses with
blood Pb levels closest to those of young children in the U.S. today.
Blood Pb Levels
(MQ/dL)
Geometric
Mean
2.9
3.3
3.32
3.8
Range
(min-max)
0.8-4.9
0.9-7.4
0.5-8.4
1-9.3
Study/Analysis
Tellez-Rojo et al (2006)B, subgroup with concurrent blood Pb <5 (ig/dL
Lanphear et al (2005)°, subgroup with peak blood Pb <7.5 (ig/dL
Canfield et al (2003) c, subgroup with peak blood Pb <10 (ig/dL
Bellinger and Needleman (2003)°, subgroup with peak blood Pb <10 (ig/dL
Median value
Average
Linear
SlopeA
(IQB points
per |jg/dL)
-1.71
-2.53
-1.79
-1.56
-1.75
A - Average linear slope estimates here are generally for relationship with IQ assessed concurrently with blood Pb measurement. As
exceptions, Bellinger & Needleman (2003) slope is relationship for 10 year old IQ with blood Pb levels at 24 months, and the data for Boston
cohort included in Lanphear et al 2005 slope are relationship for 10 year old IQ with blood Pb levels at 5 years.
B -The slope for Tellez-Rojo et al 2006 is for BSID (MDI), a measure of cognitive development appropriate to study population age (24-mos).
C - The Lanphear et al. (2005) pooled International study also includes blood Pb data from the Rochester and Boston cohorts, although for
different ages (6 and 5 years, respectively) than the ages analyzed in Canfield et al. (2003) and Bellinger and Needleman (2003). Thus, the
ages at the blood Pb measurements used in derivation of the linear slope for the Lanphear et al (2005) subgroup shown here are 5 to 7 years.
The blood Pb levels and coefficient presented here reflect the recalculation using the corrected pooled dataset (Kirrane and Patel, 2014).
Several studies newly available in the current review have, in all but one instance, also
found a nonlinear blood Pb-cognitive function relationship in nonparametric regression analyses
of the cohort blood Pb levels analyzed (ISA, section 4.3.12). These studies, however, used
statistical approaches that did not produce quantitative results for each blood Pb group (ISA,
section 4.3.12). Thus, newly available studies have not extended the range of observation for
quantitative estimates of this relationship to lower blood Pb levels than those of the previous
review. The ISA further notes that the potential for nonlinearity has not been examined in detail
within a lower, narrower range of blood Pb levels than those of the full cohorts thus far studied
in the currently available evidence base (ISA, section 4.3.12). Such an observation in the last
review supported the consideration of linear slopes with regard to blood Pb levels at and below
those represented in Table 3-3. In summary, the newly available evidence does not substantively
alter our understanding of the concentration-response relationship (including quantitative
aspects) for neurocognitive impact, such as IQ with blood Pb in young children.
3.3 PUBLIC HEALTH IMPLICATIONS AND AT-RISK POPULATIONS
There are several potential public health impacts associated with Pb exposure. In
recognition of effects causally related to blood Pb levels somewhat near those most recently
reported for today's population and for which the weight of the evidence is greatest, the potential
public health impacts most prominently recognized in the ISA are population IQ impacts
associated with childhood Pb exposure and prevalence of cardiovascular effects in adults (ISA,
3-29
-------
section 1.9.1). With regard to the latter category, as discussed above, the full body of evidence
indicates a role of long-term cumulative exposure, with uncertainty regarding the specific
exposure circumstances contributing to the effects in the epidemiological studies of adult
populations, for whom historical Pb exposures were likely much higher than exposures that
commonly occur today (ISA, section 4.4). There is less uncertainty regarding the exposure
patterns contributing to the blood Pb levels reported in studies of younger populations (ISA,
sections 1.9.4, 1.10). Accordingly, we focus the discussion of public health implications relevant
to this review predominantly on nervous system effects, including IQ decrements, in children.
We focus this discussion on IQ in recognition of IQ being a well-established, widely
recognized and rigorously standardized measure of neurocognitive function, as well as a global
measure reflecting the integration of numerous processes (ISA, section 4.3.2; 2006 CD, sections
6.2.2 and 8.4.2). We recognize, however, that IQ is one of several measures of cognitive
function negatively associated with Pb exposure. Other examples include other tests of
intelligence and cognitive development and tests of other cognitive abilities, such as learning,
memory, and executive functions, as well as academic performance and achievement (ISA,
section 4.3.2). In considering the public health significance of neurocognitive effects of Pb in
children, we recognize that, although some may be transient, some effects may persist into
adulthood (ISA, section 1.9.5).26 We also note that deficits in neurodevelopment early in life
may have lifetime consequences as "[njeurodevelopmental deficits measured in childhood may
set affected children on trajectories more prone toward lower educational attainment and
financial well-being" (ISA, section 4.3.14). Thus, population groups for which
neurodevelopment is affected by Pb exposure in early childhood are at risk of related impacts on
their success later in life.
There are important distinctions between population and individual risk such that
"[s]mall shifts in the population mean IQ can be highly significant from a public health
perspective" (ISA, p. xciii). For example, if lead-related decrements are manifested uniformly
across the range of IQ scores in a population, "a small shift in the population mean IQ may be
significant from a public health perspective because such a shift could yield a larger proportion
of individuals functioning in the low range of the IQ distribution, which is associated with
increased risk of educational, vocational, and social failure" as well as a decrease in the
proportion with high IQ scores (ISA, section 1.9.1).
26 The ISA states that the "persistence of effects appears to depend on the duration and window of exposure
as well as other factors that may affect an individual's ability to recover from an insult", with some evidence of
greater recovery in children reared in households with more optimal caregiving characteristics and low concurrent
blood Pb levels (ISA, p. 1-77; Bellinger et al., 1990).
3-30
-------
In the discussion below, we use the term at-risk populations27 to recognize populations
that have a greater likelihood of experiencing lead-related health effects, i.e., groups with
characteristics that contribute to an increased risk of Pb-related health effects. These populations
are also sometimes referred to as sensitive groups, as in section 1.2.1 above. This increased
likelihood of lead-related effects can result from many factors, including lifestage or age, sex,
race or ethnicity, diet, pre-existing disease state, or increased exposure (ISA, chapter 5).
Accordingly, in identifying factors that increase risk of lead-related health effects, there has been
consideration of evidence regarding factors contributing to increased susceptibility (i.e.,
physiological or intrinsic factors contributing to a greater response for the same exposure), and
those contributing to increased exposure (including that resulting from behavior leading to
increased contact with contaminated media). As noted in the ISA, "definitions of susceptibility
and vulnerability vary across studies, but in most instances 'susceptibility' refers to biological or
intrinsic factors (e.g., age, sex) while 'vulnerability' refers to nonbiological or extrinsic factors
(e.g., socioeconomic status [SES])" and the terms "at-risk" and "sensitive" populations have in
various instances been used to encompass these concepts more generally (ISA, p. 5-1). Although
we emphasize the term "at-risk", we rely on the other terms in particular instances below; in so
doing, our usage is consistent with these definitions.
Factors that increase risk of lead-related effects include, among others, behavioral and
physiological factors. A behavioral factor of great impact on Pb exposure is the incidence of
hand-to-mouth activity that is prevalent in very young children and by which they transfer Pb in
settled particles to their mouths (ISA, sections 3.7.1 and 5.2.1.1). Physiological factors include
both conditions contributing to a group's increased risk of effects at a given blood Pb level, and
those that contribute to blood Pb levels higher than those otherwise associated with a given Pb
exposure (ISA, sections 5.3 and 5.1, respectively). We also considered evidence encompassing
situations of elevated exposure, such as residing in old housing with Pb-containing paint or near
sources of ambient Pb, as well as socioeconomic factors, such as reduced access to health care or
low socioeconomic status (SES) that can contribute to increased risk of adverse health effects
from Pb (ISA, sections 1.9.7, 5.2, and 5.4).
• Has new information altered our understanding of human populations that are
particularly at risk of health effects from Pb exposures?
The information newly available in this review has not substantially altered our
understanding of at-risk populations. As in the last review, the factor most prominently
27 In the context of "at-risk populations", the term population refers to persons having one or more qualities
or characteristics including, for example, a specific pre-existing illness or a specific age or lifestage, with lifestage
referring to a distinguishable time frame in an individual's life characterized by unique and relatively stable
behavioral and/or physiological characteristics that are associated with development and growth.
3-31
-------
recognized to contribute to increased risk of Pb effects is age (ISA, section 1.9.6). As noted in
section 3.2 above, although the specific ages or lifestages of greatest susceptibility or risk have
not been established (e.g., ISA, section 4.3.11), the at-risk status of young children to the
neurodevelopmental effects of Pb is well recognized (e.g., ISA, sections 1.9.6, 4.3, 5.2.1, 5.3.1,
and 5.4). The evidence indicates that prenatal blood Pb levels are associated with nervous
system effects, including mental development in very young children and can also be associated
with cognitive decrements in older children (ISA, section 4.3). The coincidence during early
childhood of behaviors that increase exposure, such as hand-to-mouth contact, and the
development of the nervous system contributes increased risk during this time (ISA, sections
4.3.2.6, 5.2.1.1, and 5.3.1.1). The evidence also indicates a relationship of postnatal blood Pb
levels (through early childhood to school age) with cognitive function decrement in older
children and adolescents (ISA, section 4.3). In epidemiological studies, associations have been
observed of neurocognitive, and some other nervous system effects, at various ages from early
childhood to school age with prenatal, early-childhood, lifetime average, and concurrent blood
Pb levels as well as with childhood tooth Pb levels (ISA, section 4.3). Consideration of
epidemiological study results for different lifestages of exposure, particularly later in childhood,
is complicated by the fact that blood Pb levels in children, although highly affected by recent
exposure, are also influenced by their history of Pb exposure due to rapid growth-related bone
turnover in children (ISA, section 3.3.5). Thus, blood Pb level in children also may reflect past
Pb exposures and, to some extent, maternal Pb, with relative contributions varying with child and
maternal exposure history (ISA, section 3.2.2.4, 3.4.1 and 4.3.15; 2006 CD, section 6.6.2).
Collectively, however, the evidence indicates both the susceptibility of the developing fetus and
early postnatal years, as well as the potential for continued susceptibility through childhood as
the human central nervous system continues to mature and be vulnerable to neurotoxicants (ISA,
sections 1.9.5 and 4.3.15; 2006 CD, section 6.2.12).
In the collective body of evidence of nervous system effects in children, it is difficult to
distinguish exposure in later lifestages (e.g., school age) and its associated risk from risks
resulting from exposure in prenatal and early childhood (ISA, section 4.3.11). While early
childhood is recognized as a time of increased susceptibility, a difficulty in identifying a discrete
period of susceptibility from epidemiological studies has been that the period of peak exposure,
reflected in peak blood Pb levels, is around 18-27 months when hand-to-mouth activity is at its
maximum (ISA, section 3.4.1 and 5.2.1.1; 2006 CD, p. 6-60). The task is additionally
complicated by the role of maternal exposure history in contributing Pb to the developing fetus
(ISA, section 3.2.2.4.). Epidemiological analyses evaluating risk of neurocognitive impacts (e.g.,
reduced IQ) associated with different blood Pb metrics in cohorts with differing exposure
patterns (including those for which blood Pb levels at different ages were not highly correlated)
3-32
-------
indicate associations with blood Pb measurements concurrent with FSIQ tests at ages of
approximately 6-7 years, although the analyses did not conclusively demonstrate stronger
findings for early (e.g., age 2 years) or concurrent blood Pb (ISA, section 4.3.11). The
experimental animal evidence additionally indicates early life susceptibility (ISA, section 4.3.15
and p. 5-21). Thus, the full evidence base continues to indicate prenatal and early childhood
lifestages as periods of increased lead-related risk. In summary, while uncertainties remain with
regard to the role of Pb exposures during a particular age of life in eliciting nervous system
effects, such as cognitive function decrements, the evidence continues to indicate the at-risk
status of pre- and postnatal childhood lifestages (ISA, sections 4.3.11 and 4.3.15).
Several physiological factors increase risk of lead-related health effects by contributing to
increased blood Pb levels over those otherwise associated with a given Pb exposure (ISA,
sections 3.2, 3.3 and 5.1). These include nutritional status, which plays a role in Pb absorption
from the GI tract (ISA, section 3.2.1.2). For example, diets deficient in iron, calcium or zinc can
contribute to increased Pb absorption and associated higher blood Pb levels (ISA, sections
3.2.1.2, and 5.1). Evidence is suggestive of some genetic characteristics as potential risk factors,
such as presence of the 5-aminolevulinic acid dehydratase-2 (ALAD-2) allele which has been
indicated to increase blood Pb levels or lead-related risk (ISA, sections 3.3.2 and 5.1).
Risk factors based on increased exposure include spending time in proximity to sources
of Pb to ambient air or other environmental media (e.g., large active metals industries or
locations of historical Pb contamination) (ISA, sections 3.7.1 and 5.2.5). Residential factors
associated with other sources of Pb exposure (e.g., leaded paint or plumbing with Pb pipes or
solder) are another exposure-related risk factor (ISA, sections 3.7.1 and 5.2.6). The role of
socioeconomic status (SES) with regard to lead-related risk is somewhat complicated. SES often
serves as a marker term for one or a combination of unspecified or unknown environmental or
behavioral variables. Lower SES has been associated with higher Pb exposure and higher blood
Pb concentration (ISA, sections 5.3.16, 6.2.4 and 6.4). Further, it is independently associated
with an adverse impact on neurocognitive development, and a few studies have examined SES as
a potential modifier of the association of childhood Pb exposure with cognitive function with
inconsistent findings regarding low SES as a potential risk factor. Although the differences in
blood Pb levels among children of lower as compared to higher income levels have lessened,
blood Pb levels continue to be higher among lower-income children indicating higher exposure
and/or greater influence of factors independent of exposure, such as nutritional factors (ISA,
sections 1.9.6, 5.2.1.1 and 5.4).
In considering risk factors associated with increased Pb exposure or increased blood Pb
levels, we note that the currently available evidence continues to support a nonlinear relationship
between neurocognitive effects and blood Pb that indicates incrementally greater impacts at
3-33
-------
lower as compared to higher blood Pb levels (ISA, section 4.3.12), as described in section 3.2
above. An important implication of this finding is that while children with higher blood Pb
levels are at greater risk of lead-related effects than children with lower blood Pb levels, on an
incremental basis (e.g., per |ig/dL), the risk is greater for children at lower blood Pb levels. This
was given particular attention in the last review of the Pb NAAQS, in which the standard was
revised with consideration of the incremental impact of air-related Pb on young children in the
U.S and the recognition of greater impact for those children with lower absolute blood Pb levels
(73 FR 67002). Such consideration included a focus on those C-R studies involving the lowest
blood Pb levels, as described in section 4.1.1 below.
Some racial or ethnic backgrounds have been identified as factors that may increase risk
of lead-related health effects (ISA, sections 1.9.6, 5.2.3 and 5.3.7). For example, although blood
Pb levels in the U.S. general population (e.g., geometric mean level in children aged 1-5) have
declined, mean levels reported in recent NHANES samples continue to differ among children of
different ethnic backgrounds, with higher levels in non-white persons as compared to whites
(ISA, sections 3.4.1, 5.2.1.1 and 5.2.3). Additionally, a study of lead-related risk of hypertension
among adults reported greater risk associated with blood Pb levels above 1 |ig/dL among
Mexican Americans and non-Hispanic blacks than among non-Hispanic whites (ISA, section
5.3.7; Muntner et al., 2005). The evidence available in the current review, consistent with that in
the last, also suggests that health status or pre-existing disease is potentially a physiological risk
factor for lead-related effects (ISA, section 1.9.6). Populations with pre-existing health
conditions, such as hypertension, may be more susceptible than those without such conditions for
particular Pb-associated effects (ISA, section 5.3.4). For example, increased risks of lead-related
renal effects and heart rate variability have been reported among hypertensive individuals
compared to those that are normotensive (ISA, section 1.9.6). Additionally, African Americans,
as a group, have a higher frequency of hypertension than the larger U.S. population as a whole
and than other ethnic groups (NCHS, 2011) and, as a result, may face a greater risk of adverse
health impact from Pb-associated cardiovascular effects.
Older adulthood has been identified as a lifestage of potentially greater risk of lead-
related health effects based primarily on the evidence of increases in blood Pb levels during this
lifestage (ISA, sections 5.2.1.2, 5.3.1.2, and 5.4). Contributing to blood Pb levels in the studied
populations of older adults are likely to be their exposure histories, which included younger
years during the time of leaded gasoline usage and other sources of Pb exposures which were
more prevalent in the past than today (e.g., ISA, Figure 2-1 and section 2.5.2). Exposure history
has a contributing role to blood Pb levels throughout life, and the increased rate of bone
remodeling during later adulthood increases contributions of Pb from bone stores into the
systemic circulation during that lifestage (ISA, sections 3.3.5 and 5.2.1.2). Additionally, limited
3-34
-------
animal evidence has indicated specific brain pathology in older animals that had substantial Pb
exposures earlier in life (ISA, sections 4.3.9.1 and 5.3.1). Further, the full body of evidence
includes observed associations of some cardiovascular and neurological effects with bone and
blood Pb in older populations, with biological plausibility for the role of Pb provided by
experimental animal studies (ISA, sections 4.3.5, 4.3.7 and 4.4).
In summary, the information newly available in this review has not appreciably altered
our understanding of human populations that are particularly sensitive to Pb exposures. In the
current review, as at the time of the last review of the Pb NAAQS, we recognize young children
as an important at-risk population, with sensitivity extending to prenatal exposures and into
childhood development. Additional risk factors include deficiencies in dietary minerals (iron,
calcium and zinc), some racial or ethnic backgrounds, and spending time in proximity to
environmental sources of Pb or residing in older houses. The evidence for SES continues to
indicate increased blood Pb levels in lower income children, although its role with regard to an
increased health risk for same blood Pb level is unclear. Additionally, the currently available
evidence continues to suggest a potential for increased risk associated with several other factors,
including older adulthood, pre-existing disease (e.g., hypertension), variants for certain genes
and increased stress.
• Is there new evidence on health effects beyond neurocognitive endpoints in
children that suggest additional at-risk populations should be given increased
focus in this review?
The evidence newly available in this review supports or strengthens our previous
conclusions regarding the broad array of health effects of Pb (see ISA, section 1.10 which
compares key conclusions drawn in the last review with conclusions drawn in the current
assessment). Additionally, in some categories of health effects, the newly available studies
extend the evidence for some aspects of the health effects described in the last review. For
example, among the nervous system effects, the newly available evidence continues to support
the conclusions from the last review regarding Pb and neurocognitive and behavioral effects
(ISA, section 4.3). Across the array of neurocognitive and behavioral effects, we recognize the
sensitivity of the prenatal period and several lifestages of childhood, and we particularly
recognize young children as an important at-risk population in light of current environmental
exposure levels.
As discussed in section 3.2 above, the blood Pb levels of populations studied in newly
available epidemiological studies that report associations of blood Pb with effects for systems
and processes other than the nervous system (e.g., cardiovascular, developmental and
reproductive) are similar to or, in a few cases, somewhat lower than those assessed in the last
review (ISA, sections 4.4, 4.6, 4.7, and 4.8). The greater uncertainties regarding the time,
3-35
-------
duration and magnitude of exposure contributing to these observed health effects complicate
identification of sensitive lifestages and associated exposure patterns that might be compared
with our understanding of the sensitivity of young children to neurocognitive impacts of Pb.
Thus, while augmenting the evidence base on these additional endpoints, the newly available
evidence does not lead us to identify a health endpoint expected to be more sensitive to Pb
exposure than neurocognitive endpoints in children, leading us to continue to conclude that the
appropriate primary focus for our review is on neurocognitive endpoints in children.
In summary, there are a variety of ways in which lead-exposed populations might be
characterized and stratified for consideration of public health impacts. Age or lifestage was used
to distinguish potential groups on which to focus in the last review in recognition of its role in
exposure and susceptibility, and young children were selected as the priority population for the
risk assessment (see section 3.4 below) in consideration of the health effects evidence regarding
endpoints of greatest public health concern and in recognition of effects on the developing
nervous system as a sentinel endpoint for public health impacts of Pb. This identification
continues to be supported by the evidence available in the current review.
• What does the information about air Pb concentrations available in this review
indicate with regard to the size of at-risk populations and their distribution
across the U.S.?
The magnitude of a public health impact is dependent upon the size of populations
affected, as well as type or severity of the effect. As summarized above, the population group
that may be most at risk of health effects associated with exposure to Pb is young children. The
2010 census indicates nearly 310 million people residing in the U.S., approximately 74 million
of whom are children under the age of 18, with some 20 million under the age of five years.
Children at greatest risk from air-related Pb are those children with highest air-related Pb
exposure which are considered to be those living in areas of higher ambient air Pb
concentrations. The discussion below considers the information available to inform our
understanding of areas of children potentially at risk from air-related Pb.
In considering the extent of this at-risk population, we turn first to consideration of those
areas in the U.S. with air Pb concentrations above the current standard (e.g., section 2.2.2.2
above). Using the available monitoring data and U.S. census information, Table 3-4 summarizes
the size of populations within 0.5 km of monitors in our current Pb NAAQS surveillance
network at which Pb concentrations were higher than the current standard during the recent
period from 2009-2011. The distance to which concentrations exceeding the standard might
extend will vary with the magnitude of the Pb concentrations and particle size, among other
factors; a half-kilometer distance was selected for purposes of illustration here. This analysis
indicates that approximately 2,400 children aged 5 or under reside within 0.5 km of monitors
3-36
-------
exceeding the current standard. To also account for the population in areas with air
concentrations just at (or very near) the current standard, we have also identified an additional
nine Pb-TSP monitors with 3-month average concentrations within 10% of, but not exceeding,
the current standard (Appendix 2D). Based on the 2010 U.S. census, 265 children aged 5 or
under reside within 0.5 km of these additional sites.
Table 3-4. Number of children aged 5 and under in areas of elevated ambient air Pb
concentrations relative to the NAAQS.
Population within 0.5 km of monitors
with maximum 3-month Pb concentration greater than 0.15 jig/m3
(2009-2011)
Allsites>0.15ng/m3
Subset of sites >0.5 jig/m3
Number of
Counties
29
11
Number of States
or Territories
20
9
Total
population
25,344
11,753
Children,
5 and under
2,416
1,018
Data Sources: U.S. Bureau of the Census, 2010 Census of Population and Housing and recent Pb-TSP dataset
presented in Figure 2-10 above (dataset criteria and summaries included Appendices 2C and 2D, respectively).
Section 2.2.1.1 above describes the surveillance monitoring network required for identifying locations with the
potential to exceed the NAAQS.
As the air quality data set analyzed in section 2.2.2 above may not be inclusive of all of
the newly sited monitors, as discussed in section 2.2.1 above, we recognize there may be other
areas of the country where concentrations are above or just meet the current standard but for
which such data are not yet available. To consider the potential for there to be additional, not yet
identified, areas with elevated Pb concentrations, we have separately quantified the size of young
child populations residing in areas near large Pb sources in Table 3-5. In so doing, we recognize
uncertainties and potential limitations associated with these emissions estimates for these
purposes, uncertainties both with regard to the accuracy of such estimates and also with regard to
the role of specific source characteristics and meteorology, not explicitly considered here, in
influencing ambient air Pb concentrations and contributing to substantial variation in air Pb
concentrations at source locations (e.g., Figure 2-11 above). Accordingly, while the summary in
Table 3-5 is informative in considering the potential prevalence of airborne Pb emissions and
potential exposure of human populations, it is limited with regard to its ability to identify
populations living in areas of elevated ambient air Pb concentrations. We interpret this analysis
to indicate that fewer than about 7,800 young children (aged 5 or younger) live in areas with air
Pb concentrations near or above the current standard, with the current monitoring data indicating
the size of this population to be approximately 2,700.
3-37
-------
Table 3-5. Population size near larger sources of Pb emissions.
Facilities (other than airports)
Number of
Locations
Population,
all ages
Population,
aged 5 and
younger
Airports
Number of
Locations
Population,
all ages
Population,
aged 5 and
younger
All
Population,
aged 5 and
younger
Population Within 0.5 km of Sources Emitting at Least 0.5 tpy in 2008
Facilities/Airports estimated to emit > 5.0 tpy
484
61
I
0
0
61
Facilities/Airports estimated to emit 1.0-4.9 tpyf
53
12,143
731
I
6
6,261
266
I
997
Facilities/Airports estimated to emit 0.50 - 0.95 tpy B
63
12,934
1,143
I
52
76,105
6,699 I 7,842
A - Facilities estimated to emit at least 1.0 tpy (after rounding to 1 decimal place) and less than 5.0 (after rounding to 1 decimal place).
B - Facilities estimate to emit at least 0.50 tpy (after rounding to 2 decimal places) and less than 1.0 (after rounding to 1 decimal place).
Sources: Population counts from U.S. Bureau of the Census, 2010 Census of Population and Housing. Emissions estimates for facilities other
than airports drawn from 2008 NEI, version 3 (December 2012); estimates for airports reflect EPA's best estimates of piston-engine aircraft
emissions. Piston-engine aircraft emissions inventory is available at: http://www.epa.aov/ttn/chief/net/2008neiv2/2008 neiv2 ted draft.pdf.
3.4 EXPOSURE AND RISK
The risk information available for this review and described here is based primarily on
the exposure and risk assessment developed in the last review of the Pb NAAQS (henceforth
referred to as the 2007 REA [USEPA, 2007a]), as considered in the context of the evidence
newly available in this review (as presented in the ISA). As described in the REA Planning
Document, careful consideration of the information newly available in this review, with regard to
designing and implementing a full REA for this review, led us to conclude that performance of a
new REA for this review was not warranted. We did not find the information newly available in
this review to provide the means by which to develop an updated or enhanced risk model that
would substantially improve the utility of risk estimates in informing the current Pb NAAQS
review (REA Planning Document, section 2.3). Based on their consideration of the REA
Planning Document analysis, the CASAC Pb Review Panel generally concurred with the
conclusion that a new REA was not warranted in this review (Frey, 2011).28 Accordingly, the
information described here is drawn primarily from the 2007 REA, augmented by a limited new
case study-specific analysis focused on risk associated with the current standard, as described in
section 3.4.3.3 below.
28 In our evaluation presented in the REA Planning Document and in consultation with CASAC, we
indicated our conclusion that the information newly available in this review did not provide the means by which to
develop an updated or enhanced risk model that would substantially improve the utility of risk estimates in
informing the current Pb NAAQS review. In their review of the draft PA, the CASAC Pb Review Panel reenforced
their concurrence with EPA's decision not to develop a new REA (Frey, 2013).
3-38
-------
The focus for the risk assessment and associated estimates presented here is on Pb
derived from sources emitting Pb to ambient air. As discussed in section 1.3 above (and
conceptually illustrated in Figure 1-1), the multimedia and persistent nature of Pb, the role of
multiple exposure pathways, and the contributions of nonair sources of Pb to human exposure
media all present challenges and contribute significant additional complexity to the health risk
assessment that goes far beyond the situation for similar assessments typically performed for
other NAAQS pollutants (e.g., that focus only on the inhalation pathway). Limitations in the
available data and models affected our characterization of the various complexities associated
with exposure to ambient air Pb. As a result, the assessment includes a number of simplifying
assumptions in a number of areas and, as described in section 3.4.4 below, our estimates of air-
related Pb risk are approximate and are characterized by upper and lower bounds.
The conceptual model developed to inform planning for the 2007 REA, including
identification of key exposure media, target population, health endpoint and risk metric is
described in section 3.4.1. The 2007 REA relied on a case study approach to provide estimates
that inform our understanding of air-related exposure and risk in different types of air Pb
exposure situations; the case studies included are described in section 3.4.2. In section 3.4.3, the
analysis approach and general aspects of exposure and risk assessment methods are summarized,
and the air quality scenarios simulated are described. In section 3.4.3, we also summarize the
2007 REA risk model and the interpolation approach used in the limited new analyses performed
for purposes of this review. Section 3.4.4 identifies key aspects of the exposure assessment and
risk estimates are presented in section 3.4.5. Treatment of key sources of variability in exposure
and risk estimates is described in section 3.4.6 and the characterization of uncertainty is
summarized in 3.4.7. An updated interpretation of the risk estimates for our purposes in this Pb
NAAQS review section is presented in section 3.4.8.
3.4.1 Conceptual Model for Air-Related Lead Exposure and Risk
In considering public health risks associated with Pb from ambient air, the focus is on Pb
derived from those sources emitting Pb to ambient air. The multimedia and persistent nature of
Pb, illustrated in Figure 1-1 above, as well as the existence of many nonair sources of Pb to the
environment, contribute multiple complexities to the consideration of exposure and risk for
ambient air-related Pb. The conceptual model that informed planning for the 2007 REA
identified sources, pathways, routes, exposed populations, and health endpoints, focusing on
those aspects of Pb exposure most relevant to the review, while also recognizing the role of Pb
exposure pathways unrelated to Pb in ambient air (2007 REA, section 2.1).
3-39
-------
As recognized in section 1.3 above, sources of human Pb exposure include current and
historical air emissions sources, as well as miscellaneous nonair sources, which can contribute to
multiple exposure media and associated pathways (e.g., inhalation of ambient air, ingestion of
indoor dust, outdoor soil/dust and diet or drinking water).29 Figure 3-2 illustrates these human
exposure pathways from an analytical perspective, drawing on the conceptual model for the
assessment (2007 REA, Figure 2-1).30 As shown in Figure 3-2, in addition to airborne emissions
(recent or those in the past), sources of Pb to these pathways also include old leaded paint,
including Pb mobilized indoors during renovation/repair activities, and contaminated soils. Lead
in diet and drinking water may have air pathway-related contributions as well as contributions
from nonair sources (e.g., Pb solder on water distribution pipes and Pb in materials used in food
processing). Limitations in our data and modeling tools handicapped our ability to separate the
nonair contributions to Pb exposure from estimates of air-related Pb exposure and risk.31
1
+ r—
Inhalation of
ambient air Pb
(outdoors or
indoors)
V . J
Pb in ambient air
Infiltration
Indoor air
Deposition
indoors
\Resui
pension
n
" 0
\
\
\Resusp
\
\
\
\
\
°mtrMkina"in v
Indoor dust ^
\ ^
Ingestion of
indoor dust Pb
v y
fPaintN |
VPb^/
eposition
jtdoors
insion
i
Outdoor
soil/dust
(
/Histories
i^^x Food i
lives
/^LancT\
r \releases/
^PbfromN*
distribution J
processing/
V\_
crops/ | Drinl*
lock)
Ingestion of outdoor Ingestion of PI
soil/dust Pb J diet/drinking w
Jng water
f Water ^
ulischargesy
) in
ater
Sources unrelated to environmental pathways (e.g., jewety, mini-blinds) notshown.
Figure 3-2. Human exposure pathways for air-related Pb.
29 We did not explicitly consider Pb exposure related to consumer products (e.g., toys, cosmetics, dishes) in
the 2007 REA.
30 We additionally note that Pb in children at birth is from maternal exposures, recent or historical, as
recognized in section 3.1 above, and that ingestion of maternal breast milk may be a Pb exposure pathway for
infants in some cases (ISA, section 3.1.3.3).
31 The assessment grouped the exposure and risk estimates for Pb in diet and drinking water together and
combined them with the other pathways in estimates presented for "total Pb exposure". Characterization of the risk
assessment results in the rulemaking recognized the contribution, albeit unquantified, from air-related pathways
within this category.
3-40
-------
Identification of exposure populations, exposure/dose metric, health effects endpoint and
risk metric to be included in the 2007 REA were based on consideration of the then-currently
available evidence as assessed in detail in the 2006 CD. As discussed in the REA Planning
Document (USEPA, 2011), these selections continue to be supported by the evidence now
available in this review as described in the ISA.
In the REA, we focused on IQ loss in children exposed up to age 7 years. This focus
reflected the evidence for young children with regard to air-related exposure pathways and
susceptibility to Pb health impacts (e.g., ISA, sections 3.1.1, 4.3, 5.2.1.1, 5.3.1.1, and 5.4). For
example, the hand-to-mouth activity of young children contributes to their Pb exposure (i.e.,
incidental soil and indoor dust ingestion) and ambient air-related Pb has been shown to
contribute to Pb in outdoor soil and indoor house dust (ISA, sections 3.1.1 and 3.4.1; 2006 CD,
section 3.2.3).
Blood Pb is commonly used as an integrated index or biomarker of exposure due to both
its association with exposure, particularly recent exposure in young children, and the relative
ease of the measurements, as discussed in section 3.1 above. Although bone Pb measurements
have become easier to collect and consequently, their use has been more widespread,
epidemiological and toxicological studies of Pb health effects and dose-response relationships
(particularly for neurodevelopmental effects in children) tend to be dominated by blood Pb as the
exposure metric. Therefore, we focused on modeling blood Pb in young children, developing
estimates for two blood Pb metrics: "concurrent" and "lifetime average". For the former we
estimated blood Pb at age 7 years, while lifetime average was estimated as the average across the
7-year period.32
In addition, our focus on young children reflects the evidence that the developing nervous
system in children is among, if not, the most sensitive of the endpoints associated with Pb
exposure (ISA, sections 1.6 and 1.10). At the time of the last review, we noted that limitations
precluded prediction of changes in adult blood Pb levels (or bone Pb levels) given changes in
ambient Pb levels. This reflects the fact that the presence of substantial historic Pb stores in most
adults introduces uncertainty into the prediction of changes in blood or bone Pb in these adult
populations resulting from changes in ambient air Pb exposure. Additionally, in considering
concentration-response relationships for adult blood Pb and adult health outcomes, we
recognized the uncertainty with regard to the role of historic compared to recent exposures in
eliciting the observed outcomes. Based on conclusions regarding the scientific evidence
available in the last review (presented in the 2006 CD), the assessment focused on risk to the
32 The pathways represented in this modeling included childhood inhalation and ingestion pathways, as
well as maternal contributions to newborn body burden (2007 REA, Appendix H, Exhibit H-6).
3-41
-------
central nervous system in childhood as the most sensitive effect that could be quantitatively
assessed, with decrement in IQ used as the risk metric.
3.4.2 Case Studies
Lead exposure and associated risk were estimated for multiple case studies that generally
represent two types of residential population exposures to air-related Pb (see Table 3-6): (1)
location-specific urban populations of children with a broad range of air-related exposures,
reflecting existence of urban concentration gradients; and, (2) children residing in localized areas
with air-related exposures representing air concentrations specifically reflecting the standard
level being evaluated. Thus, the two types of case studies differed with regard to the extent to
which they represented population variability in air-related Pb exposure (as discussed further in
section 3.4.7 below). Three location-specific urban case studies focused on residential areas
within Cleveland, Chicago, and Los Angeles, providing representations of urban populations
with a broad range of air-related exposures due to spatial gradients in both ambient air Pb levels
and population density. For example, the highest air concentrations in these case studies (i.e.,
those closest to the standard being assessed) were found in very small parts of the study areas,
while a large majority of the case study populations resided in areas with much lower air
concentrations. The case studies representing the children most highly exposed via air-related
pathways were the generalized (local) urban case study (also referred to as general urban case
study) and the primary Pb smelter case study subarea. The generalized (local) urban case study
was not based on a specific geographic location and reflected several simplifying assumptions in
representing exposure including uniform ambient air Pb levels associated with the standard of
interest across the hypothetical study area and a uniform study population. The primary Pb
smelter case study provides risk estimates for children living in a specific area within which
some locations, at the time of the 2007 REA, were not meeting the then-current standard. In
addition to characterizing risks within a 10 km radius area surrounding the smelter (full area), we
focused particularly on a subarea within 1.5 km of the facility, where airborne Pb concentrations
were closest to the then-current standard (a maximum calendar quarter average concentration of
1.5 |ig/m3 Pb-TSP) and where children's air-related exposures are most impacted by emissions
associated with the Pb smelter from which air Pb concentrations were estimated. Based on the
nature of the population exposures represented by the two categories of case study, the
generalized (local) urban and primary Pb smelter case study subarea include populations that are
relatively more highly exposed by way of air pathways to air Pb concentrations near the standard
3-42
-------
level evaluated, compared with the populations in the three cities or the full area of the primary
smelter case study.33'34
Table 3-6. Types of population exposures assessed.
Type of Population Exposure
Broad range of
air-related
exposures
Generalized, high
end of air-related
exposure
Part of metropolitan area with spatially
varying air concentrations, inclusive of
location at standard or conditions
being evaluated
As above, with dominant, historically
active metals industry as ambient air
Pb source
Localized residential area with air
concentrations generally representing
the standard or conditions evaluated
Multiple exposure
zones, larger
populations
Single exposure
zone without
enumerated
population
A few exposure
zones with small
population
Case Study1
Location-specific urban:
Cleveland, Chicago, Los Angeles
Primary Pb smelter
(full area)
Generalized (local) urban
Primary Pb smelter (subarea)
3.4.3 Analysis Approach
The approach to assessing exposure and risk for the two categories of case studies was
comprised of four main analytical steps: (a) estimation of ambient air Pb concentrations, (b)
estimation of Pb concentrations in other key exposure media, including outdoor soil and indoor
dust, (c) use of exposure media Pb concentrations, with other pathway Pb intake rates (e.g., diet),
to estimate blood Pb levels in children using biokinetic modeling, and (d) use of concentration-
response functions derived from epidemiology studies to estimate IQ loss associated with the
blood Pb levels. In implementing these steps for the primary smelter case study, air
concentrations were estimated using dispersion modeling; indoor dust concentrations were
estimated for the case study subarea using a site-specific regression model. The approach for the
generalized (local) urban case study and location-specific urban case studies was somewhat
33 An additional case study (the secondary Pb smelter case study) was also developed in the 2007 REA,
however, significant limitations associated with the use of dispersion modeling to predict ambient air, dust and soil
Pb levels near the facility contributed to large uncertainties in the risk estimates (2007 REA, section 4.3.1).
34 In addition to the case studies included in the 2007 REA, the pilot phase of the 2007 REA also included a
near-roadway case study, focused on subset of urban population exposed immediately near roadways (ICF
International, 2006). Based on the pilot results and advice from CASAC, however, this case study was not carried
into the full-scale analysis. As an alternative, we developed the generalized (local) urban case study to represent
urban residents in a localized area exposed to air-related Pb associated with the standard being assessed.
3-43
-------
simpler, since it did not involve fate and transport modeling for air concentration estimates and,
instead, used ambient monitor levels to characterize the gradient in air Pb levels across the study
area. All steps are somewhat simpler in the generalized (local) urban case study which included
a single exposure zone. Figure 3-3 identifies the key input data sets, modeling steps and
intermediate model output in each of the four analytical steps. The first three steps were
employed in the exposure assessment (discussed in section 3.4.3.1), while the fourth is the risk
assessment step (discussed in section 3.4.3.3).
3-44
-------
H
W
t/5
t/5
w
t/5
1/5
<
w
&
1/5
§
5
N
3
w
o
^
<
ffi
o
w
1/5
3
Characterizing ambient
deposition to soil
air levels and
Ambient monitoring data
(general urban and location-specific urba
! Ambient
| concentrat
j for study a
Characterizing soil and indoor
dust concentrations
j
Combination of (a) statistical
(regression) and/or (b) mechanistic
(compartmental) indoor dust prediction <
models
(all case studies)
n)
Stack and
fugitive
emissions data
Air dispersion modeling L
(primaryPb smelter) P
air : 1
~ J
Nationally-representative
residential soil Pb value selected
from literature
(general urban and location-
specific urban)
_hL_ , ~
f '}
j Indoor residential dust j
I concentrations j
'•. ./
L
Characterizing blood Pb levels
Background Pb exposure levels
•diet
• drinking water
• indoor paint (actually reflected in
dust modeling)
t
Demographics (distribution of
children within study areas)
(primaryPb smelter and location- '
specific urban)
Characterizing risk (IQ lo
ss)
f
/" "\ Risk
Distribution of IQ loss for j ^
study populations ! / ,
(partitioned between policy- k-J ^
f •
| Outdoor res idential L
1 soil concentrations j
i '
Biokinetic blood Pb
i ^ modeling ^
| (all case studies)
\~ J
J— '
Probabilistic modeling of blood Pb r
levels for children within each case |
study location
(all case studies)
^ J
1 ' Concentration-r
estimation - IQ ") , based on log-no
nge estimation «— 1 (Lanphear poole
I case studies) from that study
J
relevant exposures and j
policy-relevant background) j
Site-specific soil
monitoring data
combined with
statistical
extrapolation
(primaryPb
smelter)
f N
| Ambient air j
j 1 concentrations 1
I (see above) !
.J
/- \
GSD reflecting inter-
individual variability
in behavior related to
Pb exposure and
biokinetics
;sponse functions
rmal functions
d analysis), or on data
Drawn from 2007 REA, Figure 3-3 (USEPA, 2007).
Figure 3-3. Overview of analysis approach.
3-45
-------
3.4.3.1 Estimating Exposure
Concentrations of Pb were estimated in ambient media and indoor dust using a
combination of empirical data and modeling projections. The use of empirical data brings with it
uncertainty related to the potential inclusion of nonair source signals in these measurements (e.g.,
house paint contributions to indoor dust and outdoor soil Pb). Conversely, the use of modeling
tools introduces other uncertainties (e.g., model and parameter uncertainties). The
characterization of uncertainty associated with the risk assessment is discussed in section 3.4.7.
Table 3-7 summarizes the exposure modeling approaches and data used to characterize Pb
concentrations or input associated with each exposure pathway for each of the case studies.
Characterization of Pb in ambient air relied on (a) dispersion modeling of facility-related
(including fugitive) Pb emissions for the primary Pb smelter case study, (b) the use of ambient
monitor data for the location-specific urban case studies, and (c) an assumption of uniform
ambient air Pb levels (matching the standard level being considered) for the generalized (local)
urban case study. The use of dispersion modeling for the primary Pb smelter case study allowed
us to capture more spatially refined patterns of ambient air Pb over residential areas in the
vicinity of the facility, where ambient Pb levels were dominated by Pb released from the facility.
For the location-specific urban case studies, we used Pb monitors within each of the urban study
areas to characterize spatial gradients. By contrast, the generalized (local) urban case study is
designed to assess exposure and risk for a smaller group of residents (e.g., neighborhood)
exposed at the level of the standard and therefore, did not rely on monitor data in characterizing
levels, since ambient air Pb was fixed at the standard being assessed. While ambient air Pb
concentrations in the primary Pb smelter case study reflected only contributions from direct and
fugitive emissions associated with the facility, concentrations in the location-specific urban study
areas, which relied on empirical (monitor-based) data to define ambient air Pb concentrations,
reflected contributions from all contributing sources, be they currently active stationary or
mobile sources, resuspension of previously deposited Pb or other. Additional detail on
estimation of ambient (outdoor) and indoor air concentrations is presented in section 5.2.2 and
Appendices A through D of the 2007 REA.
Characterization of Pb concentrations in outdoor surface soil/dust resulting from
deposition of airborne Pb was based on the use of (a) existing site-specific measurements
(primary Pb smelter case study) and (b) nationally representative residential soil measurements
obtained from the literature (general and location-specific urban case studies). In the case of the
primary Pb smelter case study, soil Pb concentration data were available for a zone close to the
facility and statistical extrapolation from these data was used to predict soil levels for portions of
the study area beyond this zone. Additional detail on estimation of Pb concentrations in outdoor
surface soil or dust is presented in sections 3.1.3 and 5.2.2.2 and Appendix F of 2007 REA.
3-46
-------
To predict concentrations of ambient Pb in indoor dust, we relied on a combination of (a)
regression-based models that relate indoor dust to outdoor air Pb and/or outdoor soil Pb and (b)
mechanistic models that predict indoor dust Pb based on key mechanisms (e.g., infiltration of
outdoor air indoors, deposition rates of Pb from indoor air to indoor surfaces, house cleaning
rates). For the point source case study, we used a combination of regression-based models
obtained from the literature and developed based on site-specific data and we developed a
customized hybrid empirical-mechanistic model for the general and location-specific urban case
studies. This reflected the fact that available regression-based models had been developed
largely based on residential exposures near large point sources and were not considered
representative of more general urban exposures. Consequently, a mechanistic model, augmented
with empirical data, was developed for the generalized (local) urban case study. Additional
detail on estimation of Pb concentrations in indoor dust is presented in sections 3.1.4 and 5.2.2.2
and Appendix G of 2007 REA.
Table 3-7. Summary of approaches used to estimate case study media concentrations.
Simulation of
air quality
impacts
Concentrations
for these
media were
varied across
air quality
scenarios
(see section
3.4.3.2).
Concentrations
were constant
across air
quality
scenarios
(data/modeling
limitations)
Media
category
Ambient air
Pb levels
Indoor dust
Pb levels
Outdoor soil
Pb levels
Dietary Pb
intake
Drinking
water Pb
intake
Generalized (local)
urban case study
Single ambient air Pb
level assumed across
entire study area
(single exposure zone)
Location-specific
urban case study
Source and non-source
monitors describe
concentration gradient (6
to 1 1 exposure zones
per case study)
Hybrid model: dynamic aspect relates ambient air
Pb concentrations to indoor dust Pb; empirical
aspect represents Pb from other sources (e.g.,
paint, historical air, Pb carried indoors with people)
National dataset (HUD, for houses constructed
between 1940 and 1998).
Primary Pb smelter case
study (1.5 km subarea
and 10 km full area)
Dispersion modeling of
smelter-related emissions
(22 census block groups
and 115 blocks)
For subarea - regression of
site-specific air, dust data.
For full area - regression of
air, dust, soil data from
other, historical locations.
Site-specific data (for
subarea)
National datasets for Pb residue data (US FDA Total Diet Study) and food
consumption data (NHANES)
US and Canada datasets for residential water Pb concentrations and ingestion
rates
Blood Pb levels were predicted from estimates of Pb contained in various media (e.g.,
ambient air, diet, water, indoor dust) and estimates of Pb intake from dietary and drinking water
pathways, using the Integrated Exposure and Uptake Biokinetic (IEUBK) model (2007 REA,
3-47
-------
sections 3.2.1.1 and S.2.4).35 Diet and drinking water intake and concentrations, as well as other
model inputs, were based on the most current information (2007 REA, Appendix H). Detail on
methods used to characterize media Pb concentrations and all IEUBK inputs for each case study
are in the 2007 REA, sections 3.1, 3.2, 5.2.3 and 5.2.4 and appendices C through H. As the
shortest temporal scale accepted for inputs to the IEUBK is a year, all model inputs, developed
for each exposure zone in each case study, were annual average values. For media concentration
inputs, the same values were used for each year of the seven-year simulation. Other model
inputs varied as appropriate with the age of the simulated child (2007 REA, Appendix H).
To simulate population variability in Pb intake and uptake, we used the IEUBK model to
first generate a central-tendency estimate of the blood Pb levels for the group of children within a
given exposure zone of a study area.36 Outside the IEUBK model, we then combined this central-
tendency estimate with a geometric standard deviation (GSD) reflecting variability in blood Pb
levels for groups of children to generate a distribution of blood Pb levels for a study area. The
procedure for combining the lEUBK-based central tendency blood Pb estimate with a GSD to
generate a population distribution of blood Pb levels differs somewhat for the categories of case
studies. The approach for the general urban case study is fairly simple in that we have a single
lEUBK-based estimate of blood Pb levels, and this is, in turn, combined with the GSD selected
for this study area to produce a population distribution of blood Pb levels. For both the primary
Pb smelter and the location-specific urban study areas, multiple polygons within the larger study
area (e.g., U.S. Census blocks for the location specific urban study areas) are used as the basis
for generating distributions of blood Pb levels for the child population in each study area. These
distributions are generated using a Monte Carlo-based population-weighted sampling method
with U.S. Census child counts for each polygon and an adjustment factor distribution based on
the chosen GSD (see 2007 REA, sections 3.2.2 and 5.2.2.3).
The GSD reflects a number of factors which operate together to produce interindividual
variability in blood Pb levels, including: (a) biokinetic variability (differences in the uptake,
distribution or clearance of Pb), (b) differences in behavior related to Pb exposure (e.g., varying
hand-to-mouth activity, tap water ingestion rates, and time spent playing indoors) and (c)
35 In predicting PbB levels, we assumed that Pb concentrations in exposure media remained constant
throughout the 7 year simulation period.
36 In typical IEUBK applications, the GSD is applied within the IEUBK model as part of the modeling
process in order to generate percentiles of PbB distribution for the population simulated. However, for the NAAQS
REA, we used IEUBK only for generating the central-tendency PbB value for a given exposure zone and then
probabilistically combined that estimate with the GSD outside of the IEUBK model. This allowed us, in the case of
the primary Pb smelter and the location-specific urban case studies (as noted below) to generate individual
population-level PbB distributions for each exposure zone which could then be population-weighted and combined
using Monte Carlo sampling to generate a single population-distribution for each study area. This was not possible
with the typical application of the GSD within the IEUBK model.
3-48
-------
differences in environmental Pb exposure concentrations (e.g., spatial gradients in ambient Pb
levels of a resolution beyond that simulated in each case study, differences in
cleaning/vacuuming rates and air exchanges rates).37 For all of the study areas, we assumed that
pathway apportionment of blood Pb levels based on the modeling of the central-tendency blood
Pb level (using IEUBK) holds for all percentiles of blood Pb levels derived by combining that
central tendency estimate with the GSD. Blood Pb modeling completed for all case studies
included estimates of both concurrent and lifetime-average blood Pb metrics, although ultimately
we focused on the concurrent blood Pb metric in estimating risk (2007 REA, section 2.1.5).38
3.4.3.2 Air Quality Scenarios Included in 2007 Assessment
The air quality scenarios assessed in the 2007 REA for the case studies identified in
Table 3-6 above included conditions just meeting the NAAQS that was current at the time of the
last review (1.5 ug/m3, maximum calendar quarter average) and conditions meeting several
alternative, lower standards. Additionally, scenarios for current conditions (2003-2005) were
also included for the three location-specific urban case studies.39 These air quality scenarios are
characterized by quarterly or monthly averaging times and a not-to-be-exceeded form. Once the
air quality dataset representing each scenario was developed, the associated annual average
concentrations for each exposure zone were derived for input to the IEUBK model, which does
not accept air quality inputs of a temporal scale shorter than a year (2007 REA, Appendix H).40
As a result of the differing air quality conditions of the location-specific case studies,
there were differences among them with regard to the scenarios assessing the then-existing or
alternative standards (see Table 3-8). To simulate the previous (1978) standard at the primary Pb
37 We specified GSDs for each of the case studies that reflected differences in the study areas and
underlying study populations, as well as the availability of blood Pb measurement data (see 2007 REA, sections
3.2.3 and 5.2.2.3).
38 As discussed in section 2.1.5 of the 2007 REA, the concurrent PbB measurement (i.e., PbB
measurements at the time of IQ test) and the lifetime-average blood level (i.e., average of measurements taken over
child's first 6-7 years) were considered stronger predictors of lead's effect on IQ than were peak and early childhood
levels.
39 For the location-specific urban case studies of Cleveland, Chicago and Los Angeles, the maximum
monthly average concentration was 0.56, 0.31 and 0.17 ug/m3, respectively, and the maximum calendar quarter
average concentration was 0.36, 0.14 and 0.09 ug/m3, respectively, (2003-2005 data; 2007 REA, Appendix O).
40 Although many different patterns of temporally varying air concentration will just meet a given potential
alternative standard, the shortest time step accommodated by the blood Pb model is a year. Thus, the air Pb
concentration inputs to the blood Pb model for each air quality scenario are annual average air Pb concentrations.
For the generalized (local) urban case study, the national Pb-TSP monitoring dataset was analyzed to characterize
the distribution of site-specific relationships between metrics reflecting the averaging time and form for the air
quality scenarios being assessed (Table 3-5) and the annual average. The IEUBK annual average input was then
derived by multiplying the level for a given air quality scenario by the ratio for the averaging time and form for that
air quality scenario. For the location-specific case studies, the full temporally varying air Pb concentration dataset
for each exposure zone was used to derive the average annual concentration for the IEUBK input.
3-49
-------
smelter location, at which then-current monitoring data indicated exceedance of that standard, a
proportional roll-down was performed across the area to achieve conditions that just met that
standard. Additionally, although it was considered an extremely unlikely scenario that air
concentrations in urban areas across the U.S. that were well below the previous NAAQS would
increase to just meet that standard (e.g., by way of expansion of existing sources or congregation
of multiple sources in adjacent locations), we simulated this scenario in all case studies. In so
doing, the air Pb concentrations were rolled up proportionally across the location-specific urban
study areas to conditions just meeting the standard. No other scenario simulations involved
rolling concentrations up. For the primary Pb smelter case study, air Pb concentrations were
proportionally rolled down to conditions just meeting each of the potential alternative standards
assessed. In the three location-specific urban case studies, the temporally and spatially varying
concentrations were rolled down to conditions just meeting each of the potential alternative
standards that they exceeded (2007 REA, section 5.2.2.1).41
For the generalized (local) urban case study, which has a single exposure zone in which
air Pb concentrations do not vary spatially, we derived a single air Pb concentration estimate to
meet the standard assessed (e.g., specified maximum monthly or quarterly average). To reflect
the variability in air Pb concentrations that occur over time scales less than a year as a result of
temporal changes in meteorology and source and emission characteristics, the annual average air
concentration (input for IEUBK and dust model) was derived for the maximum monthly and
quarterly average metrics assessed using relationships based on the available Pb-TSP monitoring
data for large U.S. urban areas (2007 REA, Appendix A).
41 When concentrations in the exposure zone (within the study area) that has the highest Pb concentrations
(in terms of the metric being assessed) achieve a maximum quarterly or monthly average of the specified level, the
potential standard is "just met".
3-50
-------
Table 3-8. Air quality scenarios assessed.
Air Quality Conditions Just Meeting ...
Maximum
Quarterly Average
(pg/m3)
1.5B
0.2C
Maximum
Monthly Average
(pg/m3)
0.5
0.2
0.05
0.02
Case Studies Where Simulated
Generalized
(local)
Urban*
V
V
V
V
V
V
Location Specific
Primary
Smelter
V
V
V
V
V
V
Cleveland
V
V
V
V
V
Chicago
V
V
V
V
Los
Angeles
V
V
V
A - Conditions were set to meet the standards assessed in the single exposure zone of this case study.
B - Concentrations were proportionally rolled down to conditions just meeting the previous standard in the primary Pb
smelter case study; concentrations in the three urban location-specific case studies were proportionally rolled up to just
meet this standard.
C - Concentrations were proportionally rolled down to just meet this and the other potential alternative standards.
The approaches for estimating Pb concentrations in other media varied depending on the
type of case study (see section 3.4.3.1 above). Limitations in the available data and modeling
tools precluded simulation of linkages between some media and air Pb, such that the full impact
of changes in air Pb conditions associated with attainment of lower standards was not simulated.
For example, dietary and drinking water Pb concentrations, as well as soil Pb concentrations,
were not varied across the air quality scenarios in any case study (see Table 3-7). For all case
studies, however, indoor dust Pb concentrations were simulated to change with the different air
quality scenarios that also provided differing ambient air Pb concentrations (outdoors and
indoors).
3.4.3.3 Methods for Deriving Risk Estimates
In this section, we first summarize the full risk model employed in the 2007 REA for
estimating risk for a broad range of air quality scenarios (section 3.4.3.3.1). Then, in section
3.4.3.3.2, we summarize approaches by which we have identified risk estimates pertaining to the
current standard, the second of which involves an analysis newly completed in this review in
which risk estimates are interpolated for the current standard based on the 2007 REA risk
estimates.
3-51
-------
3.4.3.3.1 Full Risk Model in 2007 REA
The risk characterization step employed in the 2007 REA involved generating a
distribution of IQ loss estimates for the set of children simulated in the exposure assessment.
Specifically, estimated blood Pb levels for the concurrent blood Pb metric42 were combined with
four blood Pb concentration-response (C-R) functions for IQ loss based on the analysis by
Lanphear et al (2005) of a pooled international dataset of blood Pb and IQ (see 2007 REA,
section 5.3.1.1). Four different C-R functions were selected to provide different
characterizations of behavior at low exposures. The decision to use four different functions is in
recognition of uncertainty related to modeling this endpoint, particularly at lower blood Pb levels
for which there is limited representation in the Lanphear et al (2005) pooled dataset; the 5th
percentile for the concurrent blood Pb measurements in that dataset is 2.5 |ig/dL, and the mean is
9.7 |ig/dL (73 FR 66978). The four different functions are either based directly on the lognormal
model described in Lanphear et al (2005), or they are derived from data presented in that study.43
The four functions are presented in Figure 3-4 and compared in Table 3-9 with regard to total IQ
loss and incremental IQ loss (IQ loss per |ig/dL blood Pb) across a range of concurrent blood Pb
levels. A brief description of each of the functions is also here:
• Log-linear with cutpoint: log-linear function derived from the pooled analysis applied
down to 1 |ig/dL (concurrent blood Pb metric) with no IQ loss projected below that
exposure level.
• Log-linear with low-exposure linearization: log-linear function applied down to 1 |ig/dL
(concurrent blood Pb metric) with linearization of the slope at that point which is used to
project IQ loss down to the origin.
• Dual linear - stratified at 10 |ig/dL: function developed by fitting a two-piece linear
function stratified at 10 |ig/dL (peak blood Pb concentration) to the log-linear function
developed from the pooled analysis.
• Dual linear-stratified at 7.5 |ig/dL: as above, but based on stratification of the two-piece
function at 7.5 |ig/dL (peak blood Pb concentration).
42 Risk estimates were also developed for lifetime average PbB levels using concentration-response
functions derived from the Lanphear et al (2005) analysis for lifetime average PbB levels. Estimates based on the
concurrent PbB metric are given primary emphasis, consistent with advice from CASAC (Henderson, 2007b).
43 The two log-linear C-R functions rely on the loglinear model in Lanphear et al (2005). The two dual
linear C-R functions rely on the linear models reported in Lanphear et al (2005) for concurrent blood Pb in four
groupings of children based on whether peak blood Pb levels were below or at/above 10 or 7.5 ug/dL. In order to
utilize the linear models in the REA, we considered the relationship between peak and concurrent blood Pb levels in
the pooled dataset, as well as in the cohort comprising the bulk of the low blood Pb subsets. In both cases, the
difference was approximately a factor of two (2007 REA, section 5.3.1.1). The "dual linear-stratified at 10 ug/dL"
function applies the Lanphear et al (2005) linear coefficient for children with peak blood Pb below 10 ug/dL to REA
concurrent blood Pb estimates below 5 ug/dL and the linear coefficient for children with peak blood Pb at or above
10 ug/dL to REA concurrent blood Pb estimates at or above 5 ug/dL (Figure 3-4). The "dual linear -stratified at 7.5
ug/dL" function applies the Lanphear et al (2005) linear coefficient for children with peak blood Pb below 7.5ug/dL
to REA concurrent blood Pb estimates below 3.75 ug/dL and the linear coefficient for children with peak blood Pb
at or above 7.5 ug/dL to REA concurrent blood Pb estimates at or above 3.75 ug/dL.
3-52
-------
14
12
10
8 -
°
8
0 6
4
2
o
/'
/
*
/ ----•• " "
f .--••'"
/' ..-••"'
/ .-•' . .^-•-""~
'•'"' ' ^^^^
f ,<^~^^
,£^7^
01 234567891
Concurrent blood Pb (ug/dL)
D
— log-linear w ith outpoint
10 ug/dL, peak
— dual linear - stratified at
7.5 ug/dL, peak
exposure linearization
Figure 3-4. Comparison of four concentration-response functions used in risk assessment.
Table 3-9. Comparison of total and incremental IQ loss estimates for blood Pb below 10
ug/dL based on the four concentration-response functions.
Performance Metric
Total IQ loss
Incremental IQ loss
(average # points
per |jg/dL)
at 2 |jg/dl_
at 5 pg/dL
at 7.5 |jg/dL
at 10 |jg/dL
<2 pg/dL
<5 pg/dL
<7.5 pg/dL
<10|jg/dL
Concentration-Response Function
Log-linear
with outpoint
Log-linear with
low-exposure
linearization
Dual linear -
stratified at 10
pg/dL peak
Dual linear -
stratified at 7.5
pg/dL peak
Points, IQ loss
1.9
4.3
5.4
6.2
0.94
0.87
0.73
0.62
4.6
7.0
8.1
8.9
2.29
1.41
1.09
0.89
1.6
3.9
4.3
4.6
0.80
0.80
0.58
0.47
5.9
11.1
11.5
11.9
2.94
2.24
1.55
1.20
Of the four C-R functions provided above, we have the greatest overall confidence in risk
estimates generated using the log-linear with low-exposure linearization (LLL) function because
this function (a) is nonlinear, describing greater response per unit blood Pb at lower blood Pb
levels consistent with multiple studies, (b) is based on fitting a function to the entire pooled
dataset (and hence uses all of the data in describing response across the range of exposures), (c)
is supported by sensitivity analyses showing the model coefficients to be robust (Lanphear et al.,
3-53
-------
2005), and (d) provides an approach for predicting IQ loss at the lowest exposures simulated in
the assessment (which for some simulated children yield blood Pb levels below those studied).
Risk estimates generated using the other three C-R functions are also presented to provide
perspective on the impact of uncertainty in this key modeling step. For additional detail on the
rationale for placing greater emphasis on the LLL function, see section 4.2.1 of the 2007 Pb Staff
Paper (USEPA, 2007b).
As noted in section 3.2 above, since the completion of the ISA in the current review, two
errors have been identified with the pooled dataset analyzed by Lanphear et al (2005) (Kirrane
and Patel, 2014). A recent publication and EPA have separately recalculated the statistics and
mathematical models of Lanphear et al (2005) using the corrected pooled dataset (Kirrane and
Patel, 2014). While the conclusions drawn from these coefficients, including the finding of a
steeper slope at lower (as compared to higher) blood Pb concentrations are unaffected, the
magnitude of the loglinear and linear regression coefficients are somewhat lower based on the
corrections. For example, the loglinear model coefficient used for the LLL function, which we
focused on in the last review and also focus on here, changed only negligibly from -2.7 to -2.65
when recalculated using the corrected pooled dataset (Kirrane and Patel, 2014). As a result, the
risk estimates for this function described below and presented in Tables 3-10 and 3-11 would be
expected to be very similar although slightly lower if derived using the recalculated loglinear
model coefficient for the corrected dataset.44'45
Two categories of risk metrics were generated for each of the location-specific case
studies:
• Population riskpercentiles: The IQ loss associated with policy-relevant exposure
pathways for specific percentiles of the child population (e.g., the 50th, 90th and 95th
percentile modeled child). This category of metric provides perspective on the
distribution of IQ loss resulting from policy-relevant exposure pathways, ranging from
the typical or average child (50th percentile, mean) to children experiencing higher
exposures (90th, 95th percentiles). Greater emphasis has been placed on the median IQ
loss estimates due to increased confidence in these estimates relative to the higher
percentile estimates, as noted in section 3.4.7.
44 Since the loglinear model coefficient calculated from the corrected dataset is unchanged at two
significant figures from that original reported, any change to the risk estimates would be very small and, particularly
in light of other uncertainties in the analysis, does not materially affect staff's consideration of the results.
45 We also note that risk estimates for the other three C-R functions would also be expected to change as a
result of corrections to two of the linear model coefficients (Kirrane and Patel, 2014), such that the upper end of the
risk estimates range presented parenthetically in Tables 3-10 and 3-11 for all four functions would also be expected
to be somewhat lower (the upper end is generally based on estimates from the dual linear-stratified at 7.5 ug/dL,
peak, function). As was the case in the last review, the ranges reflecting all four functions are not a focus in this
review.
3-54
-------
• Child frequency counts associated with specific risk percentiles: Number of children
associated with each of the population percentiles (e.g., the number of children predicted
to have risk levels at or above the 95th percentile). This risk metric provides a perspective
on the number of children associated with various levels of IQ loss for a particular case
study.
For the generalized (local) urban case study, only the first type of risk metric, population
risk percentiles, was developed because a specific location with associated demographic data
was not modeled. In summarizing risk estimates from the 2007 REA in this document, we have
focused on the first category of risk metric and,specifically, on the median IQ loss estimates.
3.4.3.3.2 Air Quality Scenarios Reflecting the Current Standard
As the 2007 REA did not include an air quality scenario simulated to just meet the
standard selected by the 2008 decision,46 we have considered two approaches for identifying risk
estimates pertaining to conditions just meeting the current Pb standard (set in 2008) for our
purposes in this review. We first reviewed all the scenarios analyzed in the 2007 REA and
recognize the similarity to the current standard of the then-current conditions scenario for the
Chicago case study. Accordingly, we consider the risk estimates for that scenario for our
purposes in this review of considering risk associated with the current standard (see section 3.4.5
below). Additionally, in recognition of the variation among specific locations and urban areas
with regard to air quality patterns and exposed population, we have also newly developed
estimates for an air quality scenario just meeting the current Pb NAAQS in the context of the
generalized (local) urban case study to augment the risk information available in this current
review. The newly developed estimates were derived based on interpolation from the risk
estimates available for scenarios previously assessed for the generalized (local) urban case study.
Such interpolated estimates were only developed for the generalized urban case study due to its
use of a single exposure zone which greatly simplified the method employed, thus contributing
relatively lesser uncertainty from the interpolation step.47
In newly developing estimates for the current standard in the generalized (local) urban
case study, the general approach we followed was to identify the two alternative standard
46 The 2008 decision on the level for the revised NAAQS was based primarily on consideration of the
evidence-based air-related IQ loss framework. Although the specific level, averaging time and form chosen for the
new standard were not among the air quality scenarios that had been simulated in that review, the risk estimates
available for the range of simulated scenarios were concluded to be roughly consistent with and generally supportive
of the evidence-based air-related IQ loss estimates (73 FR 67006; see section 4.1.1 below).
47 We did not complete interpolation of risk estimates for the current standard for the other case studies
(i.e., the primary Pb smelter and location-specific urban case studies) because those case studies utilized a more
complex, spatially-differentiated and population-based approach for which precludes application of the simple linear
interpolation approach described, without introduction of substantial added uncertainty. The simplicity of the
generalized (local) urban study area, however, with its single exposure zone, is amenable to the linear interpolation
of risk described here.
3-55
-------
scenarios simulated in the 2007 REA which represented air quality conditions bracketing those
for the current standard and then linearly interpolate an estimate of risk for the current standard
based on the slope created from the two bracketing estimates. In representing air quality
conditions for these purposes, we focused on the annual average air Pb concentration estimates
used as IEUBK model inputs for the various air quality scenarios. An annual average
concentration estimate to represent the current standard was identified in a manner consistent
with that employed in the 2007 REA for this case study (see section 3.4.3.2 above) with the use
of currently available monitoring data for relationships between air quality metrics for
representation of the current standard. By this method, the air quality scenario for the current
standard (0.15 |ig/m3, as a not-to-be-exceeded 3-month average) was found to be bracketed by
the scenarios for alternative standards of 0.20 jig/m3 (maximum calendar quarter average) and
0.20 |ig/m3 (maximum monthly average). A risk estimate for the current standard was then
derived using the slope relating general urban case study IQ loss to annual average Pb
concentration used for those two air quality scenarios. We used this interpolation approach to
develop median risk estimates for the current standard based on each of the four C-R functions.
Details on the method for the interpolation approach are provided in Appendix 3 A. The
interpolated median estimates of risk for the current standard for the generalized (local) urban
case study are provided below in Table 3-9.
3.4.4 Challenges in Characterizing Air-related Exposure and Risk
In estimating the portion of total (all-pathway) blood Pb and IQ loss attributable to air-
related pathways, we faced a variety of challenges. Although we parsed total estimates into
those for diet/drinking water and two air-related categories, referred to as "recent air" and "past
air", significant limitations in our modeling tools and data resulted in an inability to parse
specific risk estimates into specific pathways. Although Pb in diet and drinking water sources
may include Pb derived from Pb in the ambient air (as well as Pb from nonair sources),
limitations precluded explicit modeling of the contribution from air pathways to these exposure
pathways, such that the air-related component of these exposures was not estimated.48 As a result
we utilized the estimates from recent and past air categories to create bounds within which we
consider air-related risk to fall, as illustrated in Figure 3-5 and described further below.
48 Further, although paint is not an air-related source of Pb exposure, for this analysis, may be reflected
somewhat in estimates developed for the "past air" category, due to modeling constraints. Fore example, technical
limitations of the indoor dust Pb modeling may contribute to paint-related Pb in the "past air" component of indoor
dust Pb and limitations in the available data and modeling may contribute to paint-related Pb in estimates of soil Pb.
3-56
-------
"Recent air"
Ambient air
Indoor dust
1 newly emitted lead
1 resuspension of historically
emitted and deposited lead
"Past air"
Indoor dust (other)
Outdoor soil
• historically emitted Pb (still in home
and/or still available for contact in
external soil/dust)
• paint
• Diet
• Drinking water
• newly emitted Pb
•historically emitted Pb
Total Pb risk = recent air pathways+j
s, including nonair pathways
• 2007 REA simulated just meeting alternative NAAQS by changing recent air exposures.
• Although no changes were simulated for past air exposures or to diet and drinking water pathways, changes
to the NAAQS were expected to also influence those exposure pathways to some extent.
> Air-related risk estimated to fall within range bounded by estimates of recent air and recent air + past air.
Figure 3-5. Parsing of air-related risk estimates.
Those Pb exposure pathways tied most directly to ambient air, which consequently have
the potential to respond relatively more quickly to changes in air Pb (i.e., inhalation and
ingestion of indoor dust Pb derived from the infiltration of ambient air Pb indoors), were placed
into the "recent air" category. The other air-related Pb exposure pathways, all of which are
associated with atmospheric deposition, were placed into the "past air" category. These include
ingestion of Pb in outdoor dust/soil and ingestion of the portion of Pb in indoor dust that after
deposition from ambient air outdoors is carried indoors with humans. Additionally, while we
recognized the potential for these other air-related exposures to be affected (over some time
frame) by an adjustment to the Pb NAAQS, limitations in our date and tools precluded our
simulation of that relationship with air Pb levels.
Among the limitations affecting our estimates for the air-related categories is the
apportionment of nonair pathways. For example, while conceptually indoor Pb paint
contributions to indoor dust Pb would be considered background and included in a "background"
category for this assessment, due to technical limitations related to indoor dust Pb modeling, dust
from Pb paint was included as part of "other" indoor dust Pb (i.e., as part of past air exposure).
The inclusion of indoor paint Pb as a component of "other" indoor dust Pb (and consequently as
a component of the "past air" category) represents a source of potential high bias in our
prediction of exposure and risk associated with the "past air" category because indoor paint Pb is
a nonair Pb source. At the same time, Pb in ambient air does contribute to the drinking water
3-57
-------
and diet exposure pathways and is likely a substantial contribution to diet. We could not
separate the air contribution from the nonair contributions in the drinking water and diet
pathways. As a result, our risk estimate for the drinking water/diet category of pathways
includes some air-related risk representing a source of potential low bias in our predictions of
air-related risk.
Further, we note that in simulating reductions in exposure associated with reducing
ambient air Pb levels through alternative NAAQS (and increases in exposure if the current
NAAQS was reached in certain case studies) only the exposure pathways categorized as "recent
air" (inhalation and ingestion of that portion of indoor dust associated with outdoor ambient air)
were varied with changes in air concentration. The assessment from the previous review did not
simulate decreases in "past air" exposure pathways (e.g., reductions in outdoor soil Pb levels
following reduction in ambient air Pb levels and a subsequent decrease in exposure through
incidental soil ingestion and the contribution of outdoor soil to indoor dust). These exposures
were held constant across all air quality scenarios. This modeling/data limitation, accordingly,
precluded estimates for this category from reflecting any impact of changes in air quality
conditions and thus any impacts of the alternative standard levels simulated.
In summary, because of limitations in the assessment design, data and modeling tools,
our risk estimates for the "past air" category in the last review include both risks that are truly
air-related and potentially, some nonair risk. Because we could not sharply separate Pb linked to
ambient air from Pb from other (nonair) sources, some of the three categories of risk are
underestimated and others overestimated. On balance, we believe this limitation leads to a slight
overestimate of the risks in the "past air" category. At the same time, as discussed above, the
"recent air" category does not fully represent the risk associated with all air-related pathways.
Thus, we considered the risk attributable to air-related exposure pathways to be bounded on the
low end by the risk estimated for the "recent air" category and on the upper end by the risk
estimated for the "recent air" plus "past air" categories. With regard to the latter, we are
additionally cognizant of the modeling and data limitations which reduce the extent to which the
upper end of these bounds reflects impacts of alternative air quality conditions simulated.
3.4.5 Risk Estimates
This section summarizes air-related risk estimates generated for the previous review and
also risk estimates that have been newly derived in this review by interpolation from the previous
review estimates for the current standard (see section 3.4.3.3.2 above). Included in this summary
is consideration of the following question:
3-58
-------
• What is the nature and magnitude of air-related risks remaining upon just
meeting the current Pb standard?
The air-related risk quantified in the 2007 REA is for IQ loss associated with Pb
exposure. As discussed in section 3.2 above, the evidence in the last review, as well as in the
current review, supports identification of neurocognitive effects in young children as a
particularly sensitive endpoint for the exposure circumstances relevant to this review and which
addresses the important at-risk population, young children. With this support in the evidence for
quantification, the risk assessment quantified decrements in IQ, an established indicator of
neurocognitive function. With regard to the nature of the risks, in addition to recognizing the
role of IQ as an indicator of an array of neurocognitive function impacts, we additionally take
note of the evidence regarding implications of neurocognitive impacts in young children with
regard to potential future impacts as the children age, as recognized in section 3.2 above.
In presenting risk estimates here, we focus on the median estimates of air-related IQ loss
for each case study. Estimates of air-related risk are substantially more uncertain for extremes of
the risk distribution, such as the 95th percentile. Those estimates and estimates for other risk
metrics, including population incidence for IQ loss at those case studies with population
enumeration, are available elsewhere (2007 REA, sections 4.2 and 5.3.2). In this section, Table
3-10 presents air-related IQ loss estimates derived in the 2007 REA for the full set of case
studies. Table 3-11 provides a subset of these risk estimates for the generalized (local) urban case
study in addition to estimates for air quality conditions just meeting the current standard, derived
by interpolation. A number of details, listed here, should be kept in mind when reviewing the
estimates presented in Tables 3-9 and 3-10.
• The risk estimates represent IQ loss associated with air-related Pb exposure for the
median child (exposure is modeled through age seven years).
• Our estimation of risk attributable to air-related exposure pathways is approximate, as
described in sections 3.4.4 and 3.4.7. We consider the air-related risk to fall within the
ranges presented, bounded on the low end by estimates for the pathways categorized as
"recent air" and on the upper end by the sum of the estimates for both the "recent" and
"past air" pathways.49
• The bolded range of risk estimates is derived using the C-R function in which we have
the highest overall confidence (the log-linear with low-exposure linearization - see
section 3.4.3.3.1). The wider range of risk estimates presented within the parentheses in
both tables reflects the application of all four C-R functions (see discussion in section
3.4.3.3.1) to exposure estimates for the "recent" and "recent" plus "past" air categories.
49 The third category of pathways for which risk was estimated in the 2007 REA comprised diet and
drinking water pathways. As other (nonair) sources of Pb can be appreciable contributors of Pb to these pathways,
this category is referred to as "background" in the 2007 REA.
3-59
-------
Consequently, this range of risk estimates reflects both uncertainty in estimation of air-
related exposures as well as uncertainty in the C-R function for IQ loss in children.
Table 3-10. Estimates of air-related risk from 2007 risk assessment.
Air Quality Scenario
Just meeting specified
maximum quarterly/monthly
average (ug/m3)
Median air-related IQ loss A
Generalized
(local)
urban case
study
Primary Pb
smelter
(subarea) case
study B>c
Location-s
Cleveland
lecific urban ca
Chicago
se studies
Los Angeles
Alternative Standards Scenarios
1 .5, max quarterly D
(previous NAAQS)
0.5, max monthly
0.2, max quarterly
0.2, max monthly
0.05, max monthly
0.02, max monthly
3.5-4.8
(1.5-7.7)
1.9-3.6
(0.7 - 4.8)
1.5-3.4
(0.5-4.3)
1.2-3.2
(0.4 - 4.0)
0.5-2.8
(0.2 - 3.3)
0.3-2.6
(0.1-3.1)
<6
<(3.2 - 9.4)
<4.5
<(2.1-7.7)
<3.8
<(1.5-5.6)
<3.7
<(1.2-5.1)
<2.8
<(0.9 - 3.4)
<2.9
<(0.9 - 3.3)
2.8 - 3.9 E
(0.6 - 4.6)
0.6-2.9
(0.2 - 3.9)
0.43-2.8
(0.1-3.3)
0.6-2.8
(0.1-3.2)
0.1-2.6
(O.1-3.1)
<0.1-2.6
(<0. 1-3.0)
3.4- 4.7 E
(1.4-7.4)
F
F
0.6-2.9
(0.3-3.6)
0.2-2.6
(0.1-3.2)
0.1-2.6
(O.1-3.1)
2.7 - 4.2 E
(1.1-6.2)
F
F
0.7-2.9°
(0.2 - 3.5)
0.3-2.7
(0.1-3.2)
0.1-2.6
(O.1-3.1)
Then-current (2003-2005) Conditions
0.36, max quarterly
0.14, max quarterly
0.09, max quarterly
0.7-2.9
(0.2-3.6)
0.6 - 2.9
(0.3-3.5)
0.7-2.9
(0.2-3.5)
A - Air-related risk is bracketed by "recent air" (lower bound of presented range) and "recent" plus "past air" (upper bound of
presented range) (see section 3.4.4). Boldface estimates are generated using the C-R function in which we have the highest
overall confidence (the log-linear with low-exposure linearization). Values in parentheses reflect the range of estimates
associated with all four concentration-response functions (see discussion in section 3.4.3.3.1).
B - In the case of the primary Pb smelter case study, only recent plus past air estimates are available.
C - Median air-related IQ loss estimates for the primary Pb smelter (full study area) range from <1 .7 to <2.9 points, with no
consistent pattern across simulated NAAQS levels. This lack of a pattern reflects inclusion of a large fraction of the study
population with relatively low ambient air impacts such that there is lower variation (at the population median) across standard
levels (see section 4.2 of the Risk Assessment, Volume 1).
D - This corresponds to roughly 0.7 - 1 .0 ug/m3 maximum monthly mean, across the urban case studies
E - A "roll-up" was performed so that the highest monitor in the study area is increased to just meet this level.
F - A "roll-up" to this level was not performed.
G - A "roll-up" to this level was not performed; these estimates are based on current conditions in this area (0.17 max monthly).
The Information in this table is drawn from the 2007 REA, Table 5-9.
3-60
-------
Table 3-11. Estimates of air-related risk for the generalized (local) urban case study,
including interpolated estimates for current standard.
Air Quality Scenario
Just meeting specified metric (ug/m3)
Maximum
Quarterly
Average D
1.5
(previous
NAAQS)
0.2
Maximum
Monthly
Average
0.5
0.2
0.05
0.02
Maximum
3-month
Average
0.15B
(current
NAAQS)
Median Air-related IQ Loss A
for
Generalized (local)
Urban Case Study
3.5-4.8 (1.5-7.7)
1.9-3.6 (0.7-4.8)
1.5-3.4 (0.5-4.3)
1.5-3.4 (0.5-4.3)
1.2-3.2 (0.4-4.0)
0.5-2.8 (0.2-3.3)
0.3-2.6 (0.1-3.1)
A - Air-related risk is bracketed by "recent air" (lower bound of presented range) and
"recent" plus "past air" (upper bound of presented range) (see section 3.4.4 for additional
detail on these categories). Boldface estimates are generated using the C-R function in
which we have the highest overall confidence (the log-linear with low-exposure
linearization). Values in parentheses reflect the range of estimates associated with all
four concentration-response functions (see discussion in section 3.4.3.3.1). Values in
parentheses reflect the range of estimates associated with all four concentration-
response functions.
B - Risk estimates interpolated - see text.
Key observations regarding these air-related risk estimates across the array of air
quality scenarios include the following:
All Case Studies
• Relative to the previous Pb NAAQS, substantial reduction in estimates of air-related risk
is demonstrated across the full set of potential alternative standards simulated (Table 3-
10). This is particularly the case for the lower bound (the recent air estimates) which
reflects only the pathways simulated to respond to changes in air concentrations
associated with different air quality scenarios.
Generalized (local) Urban Case Study
• As described above, the general urban case study provides risk estimates for a single
group of children residing in a single area where air concentrations throughout area are
near the level of the standard being simulated. In this case study, air-related median IQ
3-61
-------
loss, based on the higher confidence C-R function (bold), ranged from roughly 2 to 4 IQ
points for the 0.5 |ig/m3, maximum monthly average scenario, to <1 to roughly 3 IQ
points for the 0.02 |ig/m3, maximum monthly average scenario. These ranges are
expanded somewhat with consideration of the full range of C-R functions considered in
the analysis.
Location-specific Case Studies
Compared to the other case studies, the air-related risk estimates for the location-specific
urban case studies are lower because of the broader range of air-related exposures and the
distribution of the population within the study areas. For example, the majority of the
populations in each of the location-specific case studies reside in areas with ambient air
Pb levels well below each standard assessed, particularly for standard levels above 0.05
|ig/m3, as a maximum monthly average. Consequently, risk estimates for these case
studies indicate little response to alternative standard levels above 0.05|ig/m3 maximum
monthly average (as shown in Table 3-10).
For the primary Pb smelter subarea, only an upper bound on risk attributable to air-
related exposures is provided due to uncertainties associated with the dust Pb model used
for this case study.50 For all air quality scenarios, the population median recent plus past
air risk estimate is generally similar to or slightly higher than those for the general urban
case study, likely due to differences in the indoor dust models used for the two case
studies (discussed in the 2007 REA, sections 3.1.4).
Key observations regarding air-related risk estimates for the current standard include
the following:
• The median air-related IQ loss estimate for then-current conditions in the Chicago study
area, which just met a level of 0.14 jig/m3 as a maximum calendar quarter average, falls
somewhere within the lower and upper bounds of 0.6 and 2.9 points IQ loss, respectively
(Table 3-10).
• The median air-related IQ loss estimate for the current standard in the Generalized (local)
Urban Case Study, newly derived by interpolation from 2007 REA results, falls
somewhere within the lower and upper bounds of 1.5 and 3.4 points IQ loss, respectively
(Table 3-11). This estimate is derived by interpolation between the estimates for the 0.2
|ig/m3 maximum quarterly and 0.2 |ig/m3 maximum monthly average scenarios that were
derived in 2007 REA. The newly interpolated estimate is essentially the same as the
estimate for 0.2 |ig/m3 maximum quarterly average scenario for this case study.
• Based on results from the last review for a location-specific urban study area and on
those newly derived in this review based on interpolation from 2007 REA results, median
air-related IQ loss for the current standard is estimated, with rounding, to generally fall
above a rough lower bound of 1 point IQ loss and below a rough upper bound of 3 points
IQ loss.
50 The regression model used for estimating dust Pb concentrations in the primary Pb smelter case study
does not lend itself to partitioning the recent air Pb from other contributions. Accordingly, this partitioning was not
done for this case study (2007 REA, sections 2.4.3 and 3.1.4.2).
3-62
-------
3.4.6 Treatment of Variability
This section discusses the degree to which the design of the previous risk assessment
reflected consideration for key sources of variability associated with the scenarios evaluated
(e.g., IQ loss in children associated with ambient Pb in various residential settings). In so doing,
we address the following question.
• How are key sources of variability treated in the assessment?
Key sources of variability associated with the risk assessment include:
• Variation in ambient air Pb levels among U.S. urban residential areas: The location-
specific urban study areas were chosen to provide coverage for diverse residential
populations in U.S. urban areas with relatively elevated ambient air Pb levels (as
characterized using monitoring). We believe that the three cities included in those case
studies capture the variability in spatial patterns of ambient air Pb concentrations within
and across such areas reasonably well. In addition, the generalized (local) urban case
study provides coverage for a residential population exposed in a localized area with air
concentrations somewhat near the standard being evaluated, providing coverage for a
higher-end population risk scenario where a subset of urban children are exposed without
any spatial gradient in ambient air Pb levels.
• Variation in the spatial distribution of children within an urban area and assignment of
ambient air Pb exposure: Exposure of populations within the three location-specific
urban study areas was characterized to the U.S. Census block group level. Each block
group was associated ambient air Pb exposure based on proximity to the monitor nearest
to block group centroid (2007 REA, section 5.2.2). While there is uncertainty associated
with these exposures (population weighted through use of census block groups) - for
example, we did not consider time spent by children away from their residential block
group - we believe that this approach provides reasonable coverage for the potential
pattern of interaction between resident children located in these urban study areas and the
associated spatial gradients of ambient air Pb levels.
• Variation among children in factors other than media concentrations that influence
Blood Pb levels: The inputs to the blood Pb model were central tendency estimates for
each exposure zone within each study area (pathway-specific estimates for central-
tendency child). The IEUBK model then generated blood Pb levels for that central-
tendency child within each exposure zone. These central-tendency blood Pb levels were
then combined with a GSD reflecting variability in blood Pb levels for young children
(at/near age 7 years) to generate a distribution of total blood Pb for a group of children
within each exposure zone in a given case study under the specific air quality scenario.
We have reasonable confidence that this modeling approach captures variability in total
Pb exposure (and consequently total blood Pb levels) for children modeled for a given
study area. As noted in section 3.4.7 below, however, there is uncertainty associated with
parsing individual pathway contributions to total blood Pb levels (and consequently to
3-63
-------
total Pb-attributable risk). This is particularly true for high-end population percentile
estimates of IQ loss.
• Inter-individual variability in IQ loss related to Pb exposure: The use of C-R functions
based on a pooled analysis (Lanphear et al., 2005) which combined study populations
from a number of different epidemiological studies of IQ loss in children likely provides
reasonable coverage for variation across children regarding IQ loss attributable to Pb
exposure. Furthermore, our estimation of risk based on several C-R functions provides
further coverage for that variability, as well as also addressing uncertainty in the
specification of that C-R functional form (see section 3.4.7 below).
3.4.7 Characterizing Uncertainty
Although the risk assessment utilized a number of innovative modeling elements in order
to generate representative estimates of risk for the various study area populations, like all risk
models there was uncertainty associated with the model and its output.
• What are the important uncertainties associated with any risk/exposure
estimates?
One overarching area of uncertainty concerns the precision of our estimation of the
neurocognitive risk (as represented by IQ loss) associated with ambient air Pb. For example,
because of the evidence for a nonlinear response of blood Pb to Pb exposure and also for
nonlinearity in the C-R relationship for Pb-associated IQ loss, the assessment first estimated
blood Pb levels and associated risk for total Pb exposure (i.e., including Pb from air-related and
nonair exposure pathways) and then separated out estimates for pathways of interest. We
separated out the estimates of total (all-pathway) blood Pb and IQ loss into three categories that
included two air-related categories ("past" and "recent"), in addition to a third category for diet
and drinking water. However, significant limitations in our modeling tools affected our ability to
develop precise estimates for air-related exposure pathways. As recognized in section 3.4.4
above, we believe these limitations led to a slight overestimation of the risks for the past air
category and to an under-representation of air-related pathways for the recent air category.
Thus, we characterized the risk attributable to air-related exposure pathways to be bounded by
the estimates developed for the past air category and the sum of estimates for the recent air and
past air categories. For air quality scenarios other than those for the previous NAAQS, this
upper bound is recognized as having a potential upward bias with regard to its reflection of the
simulated air quality conditions because modeling and data limitations precluded simulation of
the influence of lower air Pb concentrations on the outdoor dust and soil exposure pathways, as
noted in section 3.4.4 above.
Additional limitations, assumptions and uncertainties, recognized in various ways in the
assessment and presentation of results, along with a concise characterization of their expected
impact on results, are listed below. The list begins with factors related to design of the
3-64
-------
assessment or of the case studies, followed by those related to estimation of Pb concentrations in
ambient air, indoor dust, outdoor soil/dust, and blood, and estimation of Pb-related IQ loss.
• Temporal Aspects: During the 7-year exposure period, media concentrations remain
fixed and the simulated child resides at the same residence (although exposure factors,
including behavioral and physiological parameters, are adjusted to match the aging of the
child). While these aspects of simulation introduce uncertainty into the risk estimates, it
is not clear whether there is a directional bias. For example, failure to consider population
mobility during the simulation period could bias the overall risk distribution upwards
unless children move to or from a residential location with higher Pb exposure, in which
case this would not be the case.
• Generalized (local) Urban Case Study: The design for this case study employs
assumptions regarding uniformity that are reasonable in the context of a general
description of a small neighborhood population but would contribute significant
uncertainty to extrapolation of these estimates to a specific urban location, particularly a
relatively large one. Thus, the risk estimates for this case study, while generally
representative of an urban residential population exposed to the specified ambient air Pb
levels, cannot be readily related to a specific large urban population. As long as these
important caveats are considered in interpreting the risk estimates (i.e., these risk
estimates likely represent a relatively small portion of the resident child population in any
given city just meeting specific air quality conditions), then the potential error of
extrapolating these results to a larger child population can be avoided. An additional area
of uncertainty is with regard to the representation of variability in air quality. Given the
relatively greater variability common in areas of high Pb concentrations, the approach
used to reflect variability may bias the estimates high, although there is uncertainty with
regard to the representativeness of the monitoring dataset used to characterize this.
• Location-specific Urban Case Studies: Limitations in the spatial density of ambient air
monitors in the three metropolitan areas simulated limit our characterization of spatial
gradients of ambient air Pb levels in these case studies. While this factor introduces
uncertainty into the risk estimates for this category of case study, it is not clear whether
there is a directional bias.
• Air Quality Simulation: The proportional roll-up and roll-down procedures used in some
case studies to simulate air quality conditions just meeting the previous NAAQS and
alternative NAAQS, respectively, assume proportional changes in air concentrations
across those case study areas to create those air quality scenarios. The EPA recognizes
the uncertainty with our simulation of higher air Pb concentrations that would just meet
the previous (1978) NAAQS in the urban location-specific case studies, as well as the
uncertainty in simulation of conditions associated with the implementation of emissions
reduction actions to meet a lower standard. There is the potential that the use of the
proportional approach for adjusting monitor values introduced a degree of high bias into
estimates of risk reduction. This could result if we find that urban areas can target
specific Pb sources impacting individual monitors, thereby avoiding the need for more
generalized reduction strategies resulting in a uniform pattern of reduction across all
monitors in an urban area. It is important to point out, however, that the generalized
urban case study is not affected by this potential bias, since, given the single exposure
3-65
-------
zone involved, the single ambient air Pb level is fixed to reflect meeting the standard
being considered (i.e., no spatial gradient is simulated in the small, localized residential
area being modeled).
Outdoor Soil/Dust Pb Concentrations: Limitations in datasets on Pb levels in surface
soil/dust Pb in urban areas and in our ability to simulate the impact of reduced air Pb
levels related to lowering the NAAQS contribute uncertainty to air-related risk estimates.
In this case, it is likely that we have low biased our estimates of risk reduction associated
with alternative (lower) Pb NAAQS levels, since we have not simulated potential
changes in soil Pb related to changes in ambient air Pb.
Indoor DustPb Concentrations: Limitations and uncertainty in modeling of indoor dust
Pb levels, including the impact of reductions in ambient air Pb levels, contributes
uncertainty to air-related risk estimates. Although our modeling of indoor dust does link
changes in ambient air Pb to changes in indoor dust Pb (via air exchanges and indoor
deposition onto surfaces), the modeling does not include a link between ambient air Pb,
outdoor soil Pb and subsequent changes in the level of Pb carried (or "tracked") into the
house. This could introduce low bias into our total estimates of air-related Pb exposure
and risk.
Interindividual Variability in Blood Pb Levels: Uncertainty related to population
variability in blood Pb levels (i.e., interindividual variability in factors other than media
concentration that influence blood Pb) and limitations in modeling of this introduces
significant uncertainty into blood Pb and IQ loss estimates for the 95th percentile of the
population. We are not aware of any systematic bias introduced into the analysis from
this source of uncertainty.
Pathway Apportionment for Higher Percentile Blood Pb and risks: Limitations,
primarily in data, prevented us from characterizing the degree of correlation among high-
end Pb exposures for the various pathways (e.g., the degree to which an individual
experiencing high drinking water Pb exposure would also experience high Pb paint
exposure and high ambient air-related Pb exposure). Our inability to characterize
potential correlations between exposure pathways (particularly at the higher percentile
exposure levels) limited our ability to (a) effectively model high-end Pb risk and (b)
apportion that risk between different exposure pathways, including ambient air-related
pathways.
IQ Loss Concentration-response Functions: Specification of the quantitative relationship
between blood Pb level and IQ loss is subject to greater uncertainty at lower blood Pb
levels (e.g., particularly below 2.5 |ig/dL concurrent blood Pb). However, we believe that
by considering four different models (which each treat the response at low blood Pb
levels in a different manner), we have completed a reasonable characterization of this
source of uncertainty and its impact on risk estimates. Given comparison of risk estimates
generated using the four models, it would appear that this source of uncertainty has a
potentially significant impact on risk.
3-66
-------
3.4.8 Updated Interpretation of Risk Estimates
As summarized in prior sections, a range of information gaps and areas of uncertainty
were associated with the information available in the last review. In the REA Planning
Document, staff considered the degree to which information newly available since the last Pb
NAAQS review might address specific uncertainties associated with the 2007 REA, such that an
updated risk model might be developed with the potential to provide new exposure and risk
estimates substantially different51 from estimates generated in 2007 (USEPA, 2011). Staff
concluded that the newly available information did not provide the means by which to develop
an updated or enhanced risk model that would substantially improve the utility of risk estimates
in informing the Pb NAAQS review. Specifically it was concluded that none of the primary
sources of uncertainty identified to have the greatest impact on risk estimates would be
substantially reduced through the use of newly available information (USEPA, 2011).
Our ongoing review of the newly available information leads us to conclude at this time,
that the key observations regarding air-related Pb risk modeled for the set of standard levels
covered in the 2007 REA, as well as the risk estimates interpolated for the current standard (as
discussed in section 3.4.5) are not significantly affected by the new information. Our overall
characterization of uncertainty and variability associated with those estimates (as described
above in sections 3.4.6 and 3.4.7) is not appreciably affected by new information. As recognized
at the time of the last review, exposure and risk modeling conducted for this analysis was
complex and subject to significant uncertainties due to limitations in the data, and models,
among other aspects. Further, limitations in the assessment design, data and modeling tools
handicapped us from sharply separating Pb linked to ambient air from Pb that is not air related.
In summary, the estimates of risk attributable to air-related exposures, with which we
recognize a variety of sources of uncertainty, are considered to be approximate, falling within
upper and lower bounds, roughly estimated as 3 and 1 IQ points, which over- and underestimate
risk, respectively. In scenarios for more restrictive air quality conditions than those associated
with the previous Pb standard, substantial reductions in air-related risk were demonstrated.
Focusing on the results for the generalized (local) urban case study, the interpolated estimates for
the scenario representing the current standard are very similar to estimates for the two 0.2 |ig/m3
scenarios (maximum monthly and quarterly averages) simulated in the 2007 REA52 and are
51 In this context, "substantially different" has been intended to mean that the degree of uncertainty is
substantially reduced, or bias is addressed, such that the new risk estimates could convey a different message
regarding the magnitude of public health impacts associated with the current or potential alternative standards.
52 There is uncertainty associated with judging differences between the current standard and these potential
alternative standards due to the difference in air quality datasets used to estimate air concentration variability of the
2007 REA estimates versus the interpolated risk estimate.
3-67
-------
appreciably lower than those associated with the previous standard. In characterizing the
magnitude of air-related risk associated with the current standard, we focus on median estimates,
for which we have appreciably greater confidence than estimates for outer ends of risk
distribution (see section 3.4.7) and on risks derived using the C-R function in which we have
greatest confidence (see sections 3.4.3.3.1 and 3.4.7). The risk results for the current standard
estimated in the last review for one of the location-specific urban study area populations and
those newly derived in this review using interpolation of the estimates from the last review for
the generalized (local) urban case study, which is recognized to reflect a generalized high end of
air-related exposure for localized populations, provide approximate bounds for air-related risk,
with attendant uncertainties described above.
3.5 REFERENCES
Amaral et al., 2010; Amaral, JH; Rezende, VB; Quintana, SM; Gerlach, RF; Barbosa, F, Jr; Tanus-Santos, JE.
(2010). The relationship between blood and serum lead levels in peripartum women and their respective
umbilical cords. Basic Clin Pharmacol Toxicol 107: 971-975. http://dx.doi.org/10.1111/i. 1742-
7843.2010.00616.x
Barry, PSI. (1975). A comparison of concentrations of lead in human tissues. Occup Environ Med 32: 119-139.
Barry, PSI. (1981). Concentrations of lead in the tissues of children. Occup Environ Med 38: 61-71.
Bellinger, D. C. and Needleman, H. L. (2003) Intellectual impairment and blood lead levels [letter]. N. Engl. J. Med.
349: 500.
Bellinger, D. 2008. Email message to Jee-Young Kim, U.S. EPA. February 13, 2008. Docket number EPA-HQ-
OAR-2006-0735.
Billick, I.H.; Curran, A.S.; Shier, D.R. (1979) Analysis of pediatric blood lead levels in New York City for 1970-
1976. Environ. Health Perspect. 31: 183-190.
Billick, I.H.; Curran, A.S.; Shier, D.R. (1980) Relation of pediatric blood lead levels to lead in gasoline. Environ.
Health Perspect. 34: 213-217.
Billick, I.H. (1983) Sources of lead in the environment. In: Rutter, M.; Russell Jones, R., eds. Lead versus health:
sources and effects of low level lead exposure. New York, NY: John Wiley and Sons, Ltd; pp. 59-77.
Brunekreef, B.; Noy, D.; Biersteker, K.; Boleij, J. (1983) Blood lead levels of Dutch city children and their
relationship to lead in the environment. J. Air Pollut. Control Assoc. 33: 872-876.
Brunekreef, B. (1984) The relationship between air lead and blood lead in children: a critical review. Science of the
total environment, 38: 79-123.
Canfield, R. L.; Henderson, C. R., Jr.; Cory-Slechta, D. A.; Cox, C.; Jusko, T. A.; Lanphear, B. P. (2003)
Intellectual impairment in children with blood lead concentrations below 10 ug per deciliter. N. Engl. J.
Med. 348: 1517-1526.
Canfield, R.L. 2008a. Email message to Jee-Young Kim, U.S. EPA. February 7, 2008. Docket number EPA-HQ-
OAR-2006-0735.
3-68
-------
Canfield, R.L. 2008b. Email messages to Jee-Young Kim, U.S. EPA. August 11 and 12, 2008. Docket number
EPA-HQ-OAR-2006-073 5.
Carbone, R; Laforgia, N; Crollo, E; Mautone, A; lolascon, A. (1998). Maternal and neonatal lead exposure in
southern Italy. Neonatology 73: 362-366.
Centers for Disease Control (1991) Preventing lead poisoning in young children: a statement by the Centres for
Disease Control. Atlanta, GA: U.S. Department of health and Human Services, Public Health Service;
October 1. http://wonder.cdc.gov/wonder/prevguid/p0000029/p0000029.asp
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.
Centers for Disease Control and Prevention (2012) CDC Response to Advisory Committee on Childhood Lead
Poisoning Prevention Recommendations in "Low Level Lead Exposure Harms Children: A Renewed Call
of Primary Prevention". Atlanta, GA: U.S. Department of Health and Human Services, Public Health
Service. June 7.
Chandramouli, K; Steer, CD; Ellis, M; Emond, AM. (2009). Effects of early childhood lead exposure on academic
performance and behaviour of school age children. Arch Dis Child 94: 844-848.
http://dx.doi.org/10.1136/adc.2008.149955
Chuang, HY; Schwartz, J; Gonzales-Cossio, T; Lugo, MC; Palazuelos, E; Aro, A; Hu, H; Hernandez-Avila, M.
(2001). Interrelations of lead levels in bone, venous blood, and umbilical cord blood with exogenous lead
exposure through maternal plasma lead in peripartum women. Environ Health Perspect 109: 527-532.
http://dx.doi.org/10.1289/ehp.Ol 109527
Franklin, CA; Inskip, MJ; Baccanale, CL; Edwards, CM; Manton, WI; Edwards, E; O'Flaherty, EJ. (1997). Use of
sequentially administered stable lead isotopes to investigate changes in blood lead during pregnancy in a
nonhuman primate (Macaca fascicularis). Toxicol Sci 39: 109-119.
Frey, H.C. (2011) Letter from Dr. H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee Lead
Review Panel, to Administrator Lisa P. Jackson. Re: Consultation on EPA's Review of the National
Ambient Air Quality Standards for Lead: Risk and Exposure Assessment Planning Document. October 14,
2011.
Frey, H.C. (2013) Letter from Dr. H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee Lead
Review Panel, to Acting Administrator Bob Perciasepe. Re: Review of EPA's Policy Assessment for the
Review of the National Ambient Air Quality Standards for Lead. June 4, 2013.
Gulson, B; Mahaffey, KR; Mizon, KJ; Korsch, MJ; Cameron, MA; Vimpani, G. (1995). Contribution of tissue lead
to blood lead in adult female subjects based on stable lead isotope methods. Transl Res 125: 703-712.
Gulson, B; Mahaffey, KR; Jameson, CW; Patison, N; Law, AJ; Mizon, KJ; Korsch, MJ; Pederson, D. (1999).
Impact of diet on lead in blood and urine in female adults and relevance to mobilization of lead from bone
stores. Environ Health Perspect 107: 257-263. http://dx.doi.org/10.1289/ehp.99107257
Gulson, B; Mizon, KJ; Korsch, MJ; Palmer, JM; Donnelly, JB. (2003). Mobilization of lead from human bone tissue
during pregnancy and lactation: A summary of long-term research. Sci Total Environ 303: 79-104.
http://dx.doi.org/10.1016/S0048-9697(02)00355-8
Gulson, B; Mizon, KJ; Palmer, JM; Korsch, MJ; Taylor, AJ; Mahaffey, KR. (2004a). Blood lead changes during
pregnancy and postpartum with calcium supplementation. Environ Health Perspect 112: 1499-1507.
http://dx.doi.org/10.1289/ehp.6548
3-69
-------
Gulson, BL; Mizon, KJ; Davis, JD; Palmer, JM; Vimpani, G. (2004b). Identification of sources of lead in children in
a primary zinc-lead smelter environment. Environ Health Perspect 112: 52-60.
http://dx.doi.org/10.1289/ehp.6465
Harville, E. W.; Hertz-Picciotto, I.; Schramm, M; Watt-Morse, M.; Chantala, K.; Osterloh, J.; Parsons, P. J.;Rogan,
W. (2005) Factors influencing the difference between maternal and cord blood lead. Occup.Environ. Med.
62: 263-290.
Hayes, E.B.,; McElvaine, M.D.; Orbach, H.G.; Fernandez, A.M.; Lyne, S.; Matte, T.D. (1994) Long-term trends in
blood lead levels among children in Chicago: Relationship to air lead levels. Pediatrics 93:195-200.
Henderson, R. (2007a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to
Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee's (CASAC) Review of
the 1st Draft Lead Staff Paper and Draft Lead Exposure and Risk Assessments. March 27, 2007.
Henderson, R. (2007b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to
Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee's (CASAC) Review of
the 2nd Draft Lead Human Exposure and Health Risk Assessments Document. September 27, 2007.
Hilts, S. R. (2003) Effect of smelter emission reductions on children's blood lead levels. Sci. Total Environ. 303: 51-
58.
Hornung, R. 2008a. Email message to Jee-Young Kim, U.S. EPA. February 11, 2008. Docket number EPA-HQ-
OAR-2006-0735.
Hornung, R. 2008b. Email message to Jee-Young Kim, U.S. EPA. August 19, 2008. Docket number EPA-HQ-
OAR-2006-0735.
Hornung, RW; Lanphear, BP; Dietrich, KN. (2009). Age of greatest susceptibility to childhood lead exposure: A
new statistical approach. Environ Health Perspect 117: 1309-1312. http://dx.doi.org/10.1289/ehp.0800426
ICF International. (2006) Lead Human Exposure and Health Risk Assessments and Ecological Risk Assessment for
Selected Areas. Pilot Phase. Draft Technical Report. Prepared for the U. S. EPA's Office of Air Quality
Planning and Standards, Research Triangle Park, NC. December.
Jedrychowski, W; Perera, F; Maugeri, U; Miller, RL; Rembiasz, M; Flak, E; Mroz, E; Majewska, R; Zembala, M.
(2011). Intrauterine exposure to lead may enhance sensitization to common inhalant allergens in early
childhood: A prospective prebirth cohort study. Environ Res 111: 119-124.
http://dx.doi.0rg/10.1016/j.envres.2010.ll.002
Kim, Y; Kim, BN; Hong, YC; Shin, MS; Yoo, HJ; Kim, JW; Bhang, SY; Cho, SC. (2009). Co-exposure to
environmental lead and manganese affects the intelligence of school-aged children. Neurotoxicology 30:
564-571. http://dx.doi.0rg/10.1016/i.neuro.2009.03.012
Kirrane, E; Patel, M. (2014). Memorandum to Integrated Science Assessment for Lead Docket (EPA-HQ-ORD-
2011-0051).
Krieg, EF, Jr; Butler, MA; M-h, C; Liu, T; Yesupriya, A; Dowling, N; Lindegren, ML. (2010). Lead and cognitive
function in VDR genotypes in the Third National Health and Nutrition Examination Survey. Neurotoxicol
Teratol 32: 262-272. http://dx.doi.0rg/10.1016/i.ntt.2009.12.004
Lagerkvist, BJ; Ekesrydh, S; Englyst, V; Nordberg, GF; Soderberg, HA; Wiklund, DE. (1996). Increased blood lead
and decreased calcium levels during pregnancy: A prospective study of Swedish women living near a
smelter. Am J Public Health 86: 1247-1252.
3-70
-------
Lanphear, BP; Roghmann, KJ. (1997). Pathways of lead exposure in urban children. Environ Res 74: 67-73.
Lanphear, BP; Matte, TD; Rogers, J; Clickner, RP; Dietz, B; Bornschein, RL; Succop, P; Mahaffey, KR; Dixon, S;
Galke, W; Rabinowitz, M; Farfel, M; Rohde, C; Schwartz, J; Ashley, P; Jacobs, DE. (1998). The
contribution of lead-contaminated house dust and residential soil to children's blood lead levels: A pooled
analysis of 12 epidemiologic studies. Environ Res 79: 51-68. http://dx.doi.org/10.1006/enrs. 1998.3859
Lanphear, BP; Dietrich, K; Auinger, P; Cox, C. (2000). Cognitive deficits associated with blood lead concentrations
<10 microg/dL in US children and adolescents. Public Health Rep 115: 521-529.
Lanphear, B. P.; Hornung, R.; Khoury, J.; Yolton, K.; Baghurst, P.; Bellinger, D. C.; Canfield, R. L.; Dietrich, K.
N.; Bornschein, R.; Greene, T.; Rothenberg, S. J.; Needleman, H. L.; Schnaas, L.; Wasserman, G.;
Graziano, J.; Roberts, R. (2005) Low-level environmental lead exposure and children's intellectual
function: an international pooled analysis. Environ. Health Perspect. 113: 894-899.
Manton, WI. (1985). Total contribution of airborne lead to blood lead. Occup Environ Med 42: 168-172.
http://dx.doi.0rg/10.1136/oem.42.3.168
Miranda, ML; Kim, D; Reiter, J; Overstreet Galeano, MA; Maxson, P. (2009). Environmental contributors to the
achievement gap. Neurotoxicology 30: 1019-1024. http://dx.doi.0rg/10.1016/i.neuro.2009.07.012
National Center for Health Statistics. (2010) National health and nutrition examination survey: Questionnaires,
datasets, and related documentation.
National Center for Health Statistics. (2011) Health, United States, 2011: With Special Feature on Socioeconomic
Status and Health. Hyattsville, MD. http://www.cdc.gov/nchs/data/hus/husll.pdf
Patel, AB; Prabhu, AS. (2009). Determinants of lead level in umbilical cord blood. Indian Pediatr 46: 791-793.
Pirkle, JL; Brody, DJ; Gunter, EW; Kramer, RA; Paschal, DC; Flegal, KM; Matte, TD. (1994). The decline in blood
lead levels in the United States: The National Health and Nutrition Examination Surveys (NHANES).
JAMA 272: 284-291. http://dx.doi.org/10.1001/jama. 1994.03520040046039
Ranft, U; Delschen, T; Machtolf, M; Sugiri, D; Wilhelm, M. (2008). Lead concentration in the blood of children and
its association with lead in soil and ambient air: Trends between 1983 and 2000 in Duisburg. J Toxicol
Environ Health A 71: 710-715. http://dx.doi.org/10.1080/15287390801985117
Rice, DC. (1990). Lead-induced behavioral impairment on a spatial discrimination reversal task in monkeys exposed
during different periods of development. Toxicol Appl Pharmacol 106: 327-333.
http://dx.doi.org/10.1016/0041-008X(90)90251-O
Rice, DC. (1992). Lead exposure during different developmental periods produces different effects on FI
performance in monkeys tested as juveniles and adults. Neurotoxicology 13: 757-770.
Rice, DC; Gilbert, SG. (1990). Sensitive periods for lead-induced behavioral impairment (nonspatial discrimination
reversal) in monkeys. Toxicol Appl Pharmacol 102: 101-109. http://dx.doi.org/10.1016/0041-
008X(90)90087-B
Rothenberg, S. J.; Khan, F.; Manalo, M.; Jian, J.; Cuellar, R.; Reyes, S.; Acosta, S.; Jauregui, M.; Diaz, M.;
Sanchez, M.; Todd, A. C.; Johnson, C. (2000) Maternal bone lead contribution to blood lead during and
after pregnancy. Environ. Res. 82: 81-90.
Schnaas, L; Rothenberg, SJ; Flores, MF; Martinez, S; Hernandez, C; Osorio, E; Perroni, E. (2004). Blood lead
secular trend in a cohort of children in Mexico City (1987-2002). Environ Health Perspect 112:1110-1115.
http://dx.doi.org/10.1289/ehp.6636
3-71
-------
Schwartz, J., and Pitcher, H. (1989) The relationship between gasoline lead and blood lead in the United States. J
Official Statistics 5(4):421-431.
Schwemberger, MS, JE Mosby, MJ Doa, DE Jacobs, PJ Ashley, DJ Brody, MJ Brown, RL Jones, D Homa. (2005)
Mortality and Morbidity Weekly Report 54(20):513-516. May 27, 2005
Simon, DL; Maynard, EJ; Thomas, KD. (2007). Living in a sea of lead changes in blood- and hand-lead of infants
living near a smelter. J Expo Sci Environ Epidemiol 17: 248-259. http://dx.doi.org/10.1038/sj.jes.7500512
Smith, D. R.; Osterloh, J. D.; Flegal, A. R. (1996) Use of endogenous, stable lead isotopes to determine release of
lead from the skeleton. Environ. Health Perspect. 104: 60-66.
Surkan, PJ; Zhang, A; Trachtenberg, F; Daniel, DB; McKinlay, S; Bellinger, DC. (2007). Neuropsychological
function in children with blood lead levels <10 ug/dL. Neurotoxicology 28: 1170-1177.
http://dx.doi.0rg/10.1016/j.neuro.2007.07.007
Tellez-Rojo, M. M.; Bellinger, D. C.; Arroyo-Quiroz, C.; Lamadrid-Figueroa, H.; Mercado-Garcia, A.; Schnaas-
Arrieta, L.; Wright, R. O.; Hernandez-Avila, M.; Hu, H. (2006) Longitudinal associations between blood
lead concentrations < 10 ug/dL and neurobehavioral development in environmentally-exposed children in
Mexico City. Pediatrics 118: e323-e330.
Tellez-Rojo, M. 2008. Email message to Jee-Young Kim, U.S. EPA. February 11, 2008. Docket number EPA-HQ-
OAR-2006-0735.
Tripathi, R.M.; Raghunath, R.; A.V. Kumar; V.N. Sastry; S. Sadasivan. (2001) Atmospheric and children's blood
lead as indicators of vehicular traffic and other emission sources in Mumbai, India. Sci Total Enviro 267:
101-108.
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.
U.S. Environmental Protection Agency. (1989) Review of the national ambient air quality standards for lead:
Exposure analysis methodology and validation: OAQPS staff report. Research Triangle Park, NC: Office of
Air Quality Planning and Standards; report no. EPA-450/2-89/011. Available on the web:
http://www.epa.gov/ttn/naaqs/standards/pb/data/rnaaqsl eamv.pdf
U.S. Environmental Protection Agency. (1990) Air quality criteria for lead: supplement to the 1986 addendum.
Research Triangle Park, NC: Office of Health and Environmental Assessment, Environmental Criteria and
Assessment Office; report no. EPA/600/8-89/049F. Available from: NTIS, Springfield, VA; PB91-138420.
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/ttn/naaqs/standards/pb/s_pb cr.html
U.S. Environmental Protection Agency. (2007a) Lead: Human Exposure and Health Risk Assessments for Selected
Case Studies, Volume I. Human Exposure and Health Risk Assessments - Full-Scale and Volume II.
Appendices. Office of Air Quality Planning and Standards, Research Triangle Park, NC. EPA-452/R-07-
014a and EPA-452/R-07-014b.
U.S. Environmental Protection Agency. (2007b) Review of the National Ambient Air Quality Standards for Lead:
Policy Assessment of Scientific and Technical Information, OAQPS Staff Paper. Office of Air Quality
Planning and Standards, Research Triangle Park, NC. EPA-452/R-07-013. Available at:
http://www.epa.gOv/ttn/naaqs/standards/pb/s pb cr sp.html
3-72
-------
U.S. Environmental Protection Agency. (2011) Review of the National Ambient Air Quality Standards for Lead:
Risk and Exposure Assessment Planning Document. Office of Air Quality Planning and Standards,
Research Triangle Park, NC. EPA/452/P-11-003. Available at:
http://www.epa.gov/ttn/naaqs/standards/pb/s_pb 2010_pd.html
U.S. Environmental Protection Agency. (2013) Integrated Science Assessment for Lead. Washington, DC,
EPA/600/R-10/075F. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb 2010 isa.html
Zielhuis, R.L.; del Castilho, P.; Herber, R.F.M.; Wibowo, A.A.E.; Salle, H.J.A. (1979) Concentrations of lead and
other metals in blood of two and three year-old children living near a secondary smelter. Int. Arch. Occup.
Environ. Health 42: 231-239.
3-73
-------
4 REVIEW OF THE PRIMARY STANDARD FOR LEAD
This chapter presents staff conclusions regarding the primary Pb standard. These staff
conclusions are guided by consideration of key policy-relevant questions and based on the
assessment and integrative synthesis of information presented in the ISA and by staff analyses
and evaluations presented in chapters 2 and 3 herein. The evaluations and staff conclusions
presented in this chapter have also been developed with consideration of CASAC advice and
public comment on the external review draft of this document. These evaluations and staff
conclusions will inform the Administrator's decisions on whether to retain or revise the existing
primary standard for Pb.
Following an introductory section on the general approach for reviewing the primary
standard (section 4.1), including a summary of considerations in the last review, the discussion in
this chapter focuses on the central issue of whether the information available in this review
supports or calls into question the adequacy of the current primary standard. Building on the
responses to specific policy-relevant questions on the scientific evidence and exposure-risk
information in chapter 3 above, presentation in section 4.2 is also organized into consideration of
key policy-relevant questions framing evidence-based and exposure/risk-based considerations.
The policy-relevant questions in this document are based on those included in the IRP (TRP,
section 3.1). In section 4.3, staff conclusions are developed. Section 4.4 presents a brief
overview of key uncertainties and areas for future research.
4.1 APPROACH
Staffs approach in this review of the current primary standard takes into consideration
the approaches used in the last Pb NAAQS review addressing key policy-relevant questions in
light of currently available scientific and technical information. The past and current approaches
described below are both based, most fundamentally, on using EPA's assessment of the current
scientific evidence and associated quantitative analyses to inform the Administrator's judgment
regarding a primary standard for Pb that protects public health with an adequate margin of safety.
In drawing conclusions for consideration with regard to the primary standard, we note that the
final decision on the adequacy of the current standard is largely a public health policy judgment
to be made by the Administrator. The Administrator's final decision must draw upon scientific
information and analyses about health effects, population exposure and risks, as well as
judgments about how to consider the range and magnitude of uncertainties that are inherent in
the scientific evidence and analyses. Our approach to informing these judgments, discussed
more fully below, is based on the recognition that the available health effects evidence generally
reflects a continuum, consisting of levels at which scientists generally agree that health effects
4-1
-------
are likely to occur, through lower levels at which the likelihood and magnitude of the response
become increasingly uncertain. This approach is consistent with the requirements of the
NAAQS provisions of the Act and with how the EPA and the courts have historically interpreted
the Act. These provisions require the Administrator to establish primary standards that, in the
judgment of the Administrator, are requisite to protect public health with an adequate margin of
safety. In so doing, the Administrator seeks to establish standards that are neither more nor less
stringent than necessary for this purpose. The Act does not require that primary standards be set
at a zero-risk level, but rather at a level that avoids unacceptable risks to public health including
the health of sensitive groups.1 The four basic elements of the NAAQS (indicator, averaging
time, level, and form) are considered collectively in evaluating the health protection afforded by
the current standard.
The following subsections include background information on the approach used in the
previous review of the standard (section 4.1.1) and a discussion of the approach for the current
review (section 4.1.2).
4.1.1 Approach Used in the Last Review
The last review of the NAAQS for Pb was completed in 2008 (73 FR 66964). In
consideration of the much-expanded health effects evidence on neurocognitive effects of Pb in
children available at that time, the EPA substantially revised the primary standard from 1.5
|ig/m3, as a not-to-be exceeded average concentration over a calendar quarter, to a level of 0.15
|ig/m3, as a not-to-be-exceeded rolling 3-month average concentration. The 2008 decision to
revise the primary standard was based on the extensive body of scientific evidence published
over almost three decades, from the time the standard was originally set in 1978 through 2005-
2006. The 2008 decision considered the body of evidence as assessed in the 2006 CD (USEPA,
2006) as well as the 2007 Staff Paper assessment of the policy-relevant information contained in
the CD and the quantitative risk/exposure assessment (USEPA, 2007a, 2007b), the advice and
recommendations of CAS AC (Henderson 2007a, 2007b, 2008a, 2008b), and public comment.
While recognizing that Pb has been demonstrated to exert "a broad array of deleterious
effects on multiple organ systems", the review focused on the effects most pertinent to ambient
air exposures, which given ambient air Pb reductions over the past 30 years are those associated
with relatively lower exposures and associated blood Pb levels (73 FR 66975). In so doing, the
1 The at-risk population groups identified in a NAAQS review may include low income or minority groups.
Where low income/minority groups are among the at-risk populations, the rulemaking decision will be based on
providing protection for these and other at-risk populations and lifestages (e.g., children, older adults, persons with
pre-existing heart and lung disease). To the extent that low income/minority groups are not among the at-risk
populations identified in the ISA, a decision based on providing protection of the at-risk lifestages and populations
would be expected to provide protection for the low income/minority groups.
4-2
-------
EPA recognized the general consensus that the developing nervous system in children is among,
if not the most sensitive health endpoint associated with Pb exposures. Thus, primary attention
was given to consideration of nervous system effects, including neurocognitive and
neurobehavioral effects, in children (73 FR 66976). The body of evidence included associations
of such effects in study populations of variously-aged children with mean blood Pb levels below
10 |ig/dL, extending from 8 down to 2 |ig/dL (73 FR 66976). The public health implications of
effects of air-related Pb on cognitive function (e.g., IQ) in young children were given particular
focus in the review.
4.1.1.1 Approach Regarding the Need for Revision
The conclusions reached by the Administrator in the last review were based primarily on
the scientific evidence, with the risk- and exposure-based information providing support for
various aspects of the decision. In reaching his conclusion on the adequacy of the then-current
standard, which was set in 1978, the Administrator placed primary consideration on the large
body of scientific evidence available in the review including significant new evidence
concerning effects at blood Pb concentrations substantially below those identified when the
standard was initially set (73 FR 66987; 43 FR 46246). Given particular attention was the robust
evidence of neurotoxic effects of Pb exposure in children, recognizing: (1) that while blood Pb
levels in U.S. children had decreased notably since the late 1970s, newer epidemiological studies
had investigated and reported associations of effects on the neurodevelopment of children with
those more recent lower blood Pb levels and (2) that the toxicological evidence included
extensive experimental laboratory animal evidence substantiating well the plausibility of the
epidemiological findings observed in human children and expanding our understanding of likely
mechanisms underlying the neurotoxic effects (73 FR 66987). Additionally, within the range of
blood Pb levels investigated in the available evidence base, a threshold level for neurocognitive
effects was not identified (73 FR 66984; 2006 CD, p. 8-67). Further, the evidence indicated a
steeper dose-response relationship for effects on cognitive function at those lower blood Pb
levels than at higher blood Pb levels that were more common in the past, "indicating the
potential for greater incremental impact associated with exposure at these lower levels" (73 FR
66987). As at the time when the standard was initially set in 1978, the health effects evidence
and exposure/risk assessment available in the last review supported the conclusion that air-
related Pb exposure pathways contribute to blood Pb levels in young children by inhalation and
ingestion (73 FR 66987). The available information in the last review also indicated, however,
that the air-to-blood ratio was likely larger than the air-to-blood ratio (of 2 |ig/dL blood Pb to 1
|ig/m3 air Pb) estimated when the standard was initially set (73 FR 66987).
4-3
-------
In the Administrator's decision on the adequacy of the 1978 standard, the Administrator
considered the evidence using a very specifically defined framework, referred to as an air-related
IQ loss evidence-based framework. This framework integrates evidence for the relationship
between Pb in air and Pb in young children's blood with evidence for the relationship between
Pb in young children's blood and IQ loss (73 FR 77987), as described in more detail in section
4.1.1.2 below. This evidence-based approach considers air-related effects on neurocognitive
function (using the quantitative metric of IQ loss) associated with exposure in those areas with
elevated air concentrations equal to potential alternative levels for the Pb standard. Thus, the
conceptual context for the framework is that it provides estimates of air-related IQ loss for a
subset of the population of U.S. children (i.e., the subset living in close proximity to air Pb
sources that contribute to elevated air Pb concentrations that equal the current level of the
standard). This is the subset expected to experience air-related Pb exposures at the high end of
the national distribution of such exposures, not at the average. This is the case since when a
standard of a particular level is just met at a monitor sited to record the highest source-oriented
concentration in an area, the large majority of children in the larger surrounding area would
likely experience exposures to concentrations well below that level.
The two primary inputs to the evidence-based air-related IQ loss framework are air-to-
blood ratios and C-R functions for the relationship between blood Pb and IQ response in young
children. Additionally taken into consideration in applying and drawing conclusions from the
framework were the uncertainties inherent in these inputs. Application of the framework also
entailed consideration of an appropriate level of protection from air-related IQ loss to be used in
conjunction with the framework. In simplest terms, the framework provides for estimation of a
mean air-related IQ decrement for young children in the high end of the national distribution of
air-related exposures by focusing on children exposed to air-related Pb in those areas with
elevated air Pb concentrations equal to specific potential standard levels. The framework
estimates of mean air-related IQ loss are derived through multiplication of the following factors:
standard level (|ig/m3), air-to-blood ratio in terms of |ig/dL blood Pb per |ig/m3 air concentration
and slope for the C-R function in terms of points IQ decrement per |ig/dL blood Pb.
Based on the application of the air-related IQ loss framework to the evidence, the
Administrator concluded that, for exposures projected for air Pb concentrations at the level of the
1978 standard, the quantitative estimates of IQ loss associated with air-related Pb indicated risk
of a magnitude that in his judgment was significant from a public health perspective, and that the
evidence-based framework supported a conclusion that the 1978 standard did not protect public
health with an adequate margin of safety (73 FR 77987). The Administrator further concluded
that the evidence indicated the need for a substantially lower standard level to provide increased
public health protection, especially for at-risk groups (most notably children), against an array of
4-4
-------
effects, most importantly including effects on the developing nervous system (73 FR 77987). In
addition to giving primary consideration to the much expanded evidence base since the standard
was set, the Administrator also took into consideration the exposure/risk assessments. In so
doing, he observed that, while taking into consideration their inherent uncertainties and
limitations, the quantitative estimates of IQ loss associated with air-related Pb in air quality
scenarios just meeting the then-current standard also indicated risk of a magnitude that in his
judgment was significant from a public health perspective. Thus, the Administrator concluded
the exposure/risk estimates provided additional support to the evidence-based conclusion that the
standard needed revision (73 FR 66987).
4.1.1.2 Approach Regarding Elements of Revised Standard
In considering appropriate revisions to the prior standard in the review completed in
2008, each of the four basic elements of the NAAQS (indicator, averaging time, form and level)
was evaluated. The rationale for decisions on those elements is summarized below.
With regard to indicator, consideration was given to replacing Pb-TSP with Pb-PMio.
The EPA recognized, however, that Pb in all particle sizes contributes to Pb in blood and
associated health effects, additionally noting that the difference in particulate Pb captured by
TSP and PMio monitors may be on the order of a factor of two in some areas (73 FR 66991).
Further, the Administrator recognized uncertainty with regard to whether a Pb-PMio-based
standard would also effectively control ultra-coarse2 Pb particles, which may have a greater
presence in areas near sources where Pb concentrations are highest (73 FR 66991). The
Administrator decided to retain Pb-TSP as the indicator to provide sufficient public health
protection from the range of particle sizes of ambient air Pb, including ultra-coarse particles (73
FR 66991). Additionally, a role was provided for Pb-PMio in the monitoring required for a Pb-
TSP standard (73 FR 66991) based on the conclusion that use of Pb-PMio measurements at sites
not influenced by sources of ultra-coarse Pb, and where Pb concentrations are well below the
standard, would take advantage of the increased precision of these measurements and decreased
spatial variation of Pb-PMio concentrations, without raising the same concerns over a lack of
protection against health risks from all particulate Pb emitted to the ambient air that support
retention of Pb-TSP as the indicator (versus revision to Pb-PMio) (73 FR 66991). Accordingly,
allowance was made for the use of Pb-PMio monitoring for Pb NAAQS attainment purposes in
certain limited circumstances, at non-source-oriented sites, where the Pb concentrations are
2 The term ultra-coarse is used to refer to particles collected by a TSP sampler but not by a PMio sampler.
This terminology is consistent with the traditional usage of' 'fine'' to refer to particles collected by a PM2 5 sampler,
and ' 'coarse'' to refer to particles collected by a PMio sampler but not by a PM2 5 sampler, recognizing that there
will be some overlap in the particle sizes in the three types of collected material.
4-5
-------
expected to be substantially below the standard and ultra-coarse particles are not expected to be
present (73 FR 66991).
With regard to averaging time and form for the revised standard, consideration was given
to a monthly averaging time, with a form of second maximum, and a 3-month calendar quarter
averaging time, with not-to-be exceeded forms. While the Administrator recognized that there
were some factors that might imply support for a period as short as a month for averaging time,
he also noted other factors supporting use of a longer time. He additionally took note of the
complexity inherent in this consideration for the primary Pb standard, which is greater than in the
case of other criteria pollutants due to the multimedia nature of Pb and its multiple pathways of
human exposure.
In this situation for Pb, the Administrator emphasized the importance of considering all
of the relevant factors, both those pertaining to the human physiological response to changes in
Pb exposures and those pertaining to the response of air-related Pb exposure pathways to
changes in airborne Pb, in an integrated manner. With regard to the human physiological
response to changes in Pb exposures, the evidence discussed in the CD indicated that children's
blood Pb levels respond quickly to increased Pb exposures, such that an abrupt increase in Pb
uptake results in increased blood Pb levels. Contributing to this response is the absorption
through the lungs and the gastrointestinal tract and the rapid distribution, once absorbed,
throughout the body. With regard to the relationship between airborne Pb and children's blood
Pb, evidence collected during the time of leaded gasoline usage when airborne Pb was a
prominent Pb exposure pathway across the population indicated children's blood Pb to respond
to changes in airborne Pb over a month's time lag. The phase-out of on-road leaded gasoline,
however, has resulted in changed circumstances with regard to children's exposure pathways,
with accompanying temporal implications. Accordingly, EPA considered the limited evidence
indicating the more numerous factors influencing ingestion (versus inhalation) pathways, which
were considered likely to lessen the impact of month-to-month variations in airborne Pb
concentrations on levels of air-related Pb in children's blood. Such factors were considered
likely to lead to response times (e.g., for the response of blood to air Pb via these pathways)
extending longer than a month (73 FR 66996). The Administrator also recognized limitations
and uncertainties in the evidence including the limited available evidence specific to the
consideration of the particular duration of sustained airborne Pb levels having the potential to
contribute to the adverse health effects identified as most relevant to this review, as well as
variability in the response time of indoor dust Pb loading to ambient airborne Pb. Based on these
various considerations, the Administrator concluded that the information provided support for an
averaging time no longer than a 3-month period.
4-6
-------
With regard to a three-month averaging time, the EPA recognized that a rolling three-
month averaging time can provide (e.g., compared to a block calendar quarter) control on month-
to-month variability in air Pb concentrations and in associated exposures (73 FR 66996). The
rolling three-month average eliminates the possibility for two consecutive "high" months falling
in two separate calendar quarters to be considered independently (perhaps being mitigated by
"low" months falling in each of the same calendar quarters). Rather, in the rolling 3-month
approach, the same month would contribute to three different 3-month periods through separate
combinations with three different pairs of months, thus providing a more complete consideration
of air quality during that month and the 3-month periods in which it falls. The Administrator
additionally concluded it appropriate to modify the method by which the 3-month average metric
is derived, to be the average of three monthly average concentrations, as compared to the then-
current practice by which the average was derived across the full dataset for a quarter without
equally weighting each month within the quarter. Thus, in consideration of the uncertainty
associated with the evidence pertinent to averaging time discussed above, the Administrator
noted that the two changes in form for the standard (to a rolling 3-month average and to
providing equal weighting to each month in deriving the 3-month average) both afford greater
weight to each individual month than did the calendar quarter form of the 1978 standard, tending
to control both the likelihood that any month will exceed the level of the standard and the
magnitude of any such exceedance.
Based on this integrated consideration of the range of relevant factors, the averaging time
was revised to a rolling three-month period with a maximum (not-to-be-exceeded) form,
evaluated over a three-year period. As compared to the previous averaging time and form of
calendar quarter (not-to-be exceeded), this revision was considered to be more scientifically
appropriate and more health protective (73 FR 77996). The rolling average gives equal weight to
all three-month periods, and the new calculation method gives equal weight to each month
within each three-month period (73 FR 77996). Further, the rolling average yields 12 three-
month averages each year to be compared to the NAAQS versus four averages in each year for
the block calendar quarters pertaining to the previous standard (73 FR 77996).
Lastly, based on the body of scientific evidence and information available, as well as
CASAC recommendations and public comment, the Administrator decided on a standard level
that, in combination with the specified choice of indicator, averaging time, and form, he judged
requisite to protect public health, including the health of sensitive groups, with an adequate
margin of safety (73 FR 67006). In reaching the decision on level for the revised standard, the
Administrator considered as a useful guide the evidence-based framework developed in that
review. As described in section 4.1.1.1 above, that framework integrates evidence for the
relationship between Pb in air and Pb in children's blood and the relationship between Pb in
4-7
-------
children's blood and IQ loss. Application of the air-related IQ loss evidence-based framework
was recognized, however, to provide "no evidence- or risk-based bright line that indicates a
single appropriate level" for the standard (73 FR 67006). Rather, the framework was seen as a
useful guide for consideration of health risks from exposure to ambient levels of Pb in the air, in
the context of a specified averaging time and form, with regard to the Administrator's decision
on a level for a revised NAAQS that provides public health protection that is sufficient but not
more than necessary under the Act (73 FR 67004).
As noted above, use of the evidence-based air-related IQ loss framework to inform
selection of a standard level involved consideration of the evidence with regard to two input
parameters. The two input parameters are an air-to-blood ratio and a C-R function for population
IQ response associated with blood Pb level (73 FR 67004). The evidence at the time of the last
review indicated a broad range of air-to-blood ratio estimates, each with limitations and
associated uncertainties. Based on the then-available evidence, the Administrator concluded that
1:5 to 1:10 represented a reasonable range to consider and identified 1:7 as a generally central
value on which to focus (73 FR 67004). With regard to C-R functions, in light of the evidence of
nonlinearity and of steeper slopes at lower blood Pb levels, the Administrator concluded it was
appropriate to focus on C-R analyses based on blood Pb levels that most closely reflected the
then-current population of children in the U.S.,3 recognizing EPA's identification of four such
analyses and giving weight to the central estimate or median of the resultant C-R functions (73
FR 67003, Table 3; 73 FR 67004). The four study groups from which C-R functions were drawn
in 2008, and the associated C-R slopes, are summarized in Table 3-3 above.4 The median
estimate of-1.75 IQ points decrement per |ig/dL was selected for use with the framework. With
the framework, as summarized in section 4.1.1.1 above, potential alternative standard levels
(|ig/m3) are multiplied by estimates of air-to-blood ratio (|ig/dL blood Pb per jig/m3 air Pb) and
the median slope for the C-R function (points IQ decrement per |ig/dL blood Pb), yielding
estimates of a mean air-related IQ decrement for a specific subset of young children (i.e., those
children exposed to air-related Pb in areas with elevated air Pb concentrations equal to specified
alternative levels). As such, the application of the framework yields estimates for the mean air-
related IQ decrements of the subset of children expected to experience air-related Pb exposures
3 The geometric mean blood Pb level for U.S. children aged five years and below, reported for NHANES in
2003-04 (the most recent years for which such an estimate was available at the time of the 2008 decision) was 1.8
ug/dL and the 5th and 95th percentiles were 0.7 ug/dL and 5.1 ug/dL, respectively (73 FR 67002).
4 One of these four is from the analysis of the lowest blood Pb subset of the pooled international study by
Lanphear et al., (2005). The nonlinear model developed from the full pooled dataset is the basis of the C-R
functions used in the 2007 REA (see section 3.4.3.3 above), in which risk was estimated over a large range of blood
Pb levels. Given the narrower focus of the evidence-based framework on IQ response at the end of studied blood Pb
levels (closer to U.S. mean level), the C-R functions in Table 3-3 are from linear analyses (each from separate
publications) for the study group subsets with blood Pb levels closest to mean for children in the U.S. today.
4-8
-------
at the high end of the distribution of such exposures. The associated mean IQ loss estimate is the
average for this highly exposed subset and is not the average air-related IQ loss projected for the
entire U.S. population of children. Uncertainties and limitations were recognized in the use of
the framework and in the resultant estimates (73 FR 67000).
In considering the use of the evidence-based air-related IQ loss framework to inform his
judgment as to the appropriate degree of public health protection that should be afforded by the
NAAQS to provide requisite protection against risk of neurocognitive effects in sensitive
populations, such as IQ loss in children, the Administrator recognized in the 2008 review that
there were no commonly accepted guidelines or criteria within the public health community that
would provide a clear basis for such a judgment. During the 2008 review, CAS AC commented
regarding the significance from a public health perspective of a 1-2 point IQ loss in the entire
population of children and, along with some commenters, emphasized that the NAAQS should
prevent air-related IQ loss of a significant magnitude, such as on the order of 1-2 IQ points, in all
but a small percentile of the population. Similarly, the Administrator stated that "ideally air-
related (as well as other) exposures to environmental Pb would be reduced to the point that no IQ
impact in children would occur" (73 FR 66998). The Administrator further recognized that, in
the case of setting a NAAQS, he was required to make a judgment as to what degree of
protection is requisite to protect public health with an adequate margin of safety (73 FR66998).
The NAAQS must be sufficient but not more stringent than necessary to achieve that result, and
the Act does not require a zero-risk standard (73 FR 66998). The Administrator additionally
recognized that the evidence-based air-related IQ loss framework did not provide estimates
pertaining to the U.S. population of children as a whole. Rather, the framework provides
estimates (with associated uncertainties and limitations) for the mean of a subset of that
population, the subset of children assumed to be exposed to the level of the standard. As
described in the final decision "[t]he framework in effect focuses on the sensitive subpopulation
that is the group of children living near sources and more likely to be exposed at the level of the
standard" (73 FR 67000). As further noted in the final decision (73 FR 67000):
EPA is unable to quantify the percentile of the U.S. population of children that
corresponds to the mean of this sensitive subpopulation. Nor is EPA confident in
its ability to develop quantified estimates of air-related IQ loss for higher
percentiles than the mean of this subpopulation. EPA expects that the mean of
this subpopulation represents a high, but not quantifiable, percentile of the U.S.
population of children. As a result, EPA expects that a standard based on
consideration of this framework would provide the same or greater protection
from estimated air-related IQ loss for a high, albeit unquantifiable, percentage of
the entire population of U.S. children.
In reaching a judgment as to the appropriate degree of protection, the Administrator
considered advice and recommendations from CASAC and public comments and recognized the
4-9
-------
uncertainties in the health effects evidence and related information as well as the role of, and
context for, a selected air-related IQ loss in the application of the framework, as described above.
Based on these considerations, the Administrator identified an air-related IQ loss of 2 points for
use with the framework, as a tool for considering the evidence with regard to the level for the
standard (73 FR 67005). In so doing, the Administrator was not determining that such an IQ
decrement value was appropriate in other contexts (73 FR 67005). Given the various
uncertainties associated with the framework and the scientific evidence base, and the focus of the
framework on the sensitive subpopulation of children that are more highly exposed to air-related
Pb, a standard level selected in this way, in combination with the selected averaging time and
form, was expected to significantly reduce and limit for a high percentage of U.S. children the
risk of experiencing an air-related IQ loss of that magnitude (73 FR 67005). At the standard
level of 0.15 |ig/m3, with the combination of the generally central estimate of air-to-blood ratio
of 1:7 and the median of the four C-R functions (-1.75 IQ point decrement per |ig/dL blood Pb),
the framework estimates of air-related IQ loss were below 2 IQ points (73 FR 67005, Table 4).
In reaching the decision in 2008 on level for the revised standard, the Administrator also
considered the results of the quantitative risk assessment to provide a useful perspective on risk
from air-related Pb. In light of important uncertainties and limitations for purposes of evaluating
potential standard levels, however, the Administrator placed less weight on the risk estimates
than on the evidence-based assessment. Nevertheless, in recognition of the general
comparability of quantitative risk estimates for the case studies considered most conceptually
similar to the scenario represented by the evidence-based framework, he judged the quantitative
risk estimates to be "roughly consistent with and generally supportive" of the evidence-based
framework estimates (73 FR 67006).
Based on consideration of the entire body of evidence and information available in the
review, as well as the recommendations of CASAC and public comments, the Administrator
decided that a level for the primary Pb standard of 0.15 |ig/m3, in combination with the specified
choice of indicator, averaging time and form was requisite to protect public health, including the
health of sensitive groups, with an adequate margin of safety (73 FR 67006). In reaching
decisions on level as well as the other elements of the revised standard, the Administrator took
note of the complexity associated with consideration of health effects caused by different
ambient air concentrations of Pb and with uncertainties with regard to the relationships between
air concentrations, exposures, and health effects For example, selection of a maximum, not to
be exceeded, form in conjunction with a rolling 3-month averaging time over a 3-year span was
expected to have the effect that the at-risk population of children would be exposed below the
standard most of the time (73 FR 67005). The Administrator additionally considered the
provision of an adequate margin of safety in making decisions on each of the elements of the
4-10
-------
standard, including, for example "selection of TSP as the indicator and the rejection of the use of
PMio scaling factors; selection of a maximum, not to be exceeded form, in conjunction with a 3-
month averaging time that employs a rolling average, with the requirement that each month in
the 3-month period be weighted equally (rather than being averaged by individual data) and that
a 3-year span be used for comparison to the standard; and the use of a range of inputs for the
evidence-based framework, that includes a focus on higher air-to-blood ratios than the lowest
ratio considered to be supportable, and steeper rather than shallower C-R functions, and the
consideration of these inputs in selection of 0.15 ug/m3 as the level of the standard" (73 FR
67007).
He additionally noted that a standard with this level would reduce the risk of a variety of
health effects associated with exposure to Pb, including effects indicated in the epidemiological
studies at lower blood Pb levels, particularly including neurological effects in children, and the
potential for cardiovascular and renal effects in adults (73 FR 67006). The Administrator
additionally considered higher and lower levels for the standard, concluding that a level of 0.15
|ig/m3 provides for a standard that is neither more or less stringent than necessary for this
purpose, recognizing that the Clean Air Act does not require that primary standards be set at a
zero-risk level, but rather at a level that reduces risk sufficiently so as to protect public health
with an adequate margin of safety (73 FR 67007). For example, the Administrator additionally
considered potential public health protection provided by standard levels above 0.15 |ig/m3,
which he concluded were insufficient to protect public health with an adequate margin of safety.
The Administrator also noted that in light of all of the evidence, including the evidence-based
framework, the degree of public health protection likely afforded by standard levels below 0.15
|ig/m3 would be greater than what is necessary to protect public safety with an adequate margin
of safety.
The Administrator concluded, based on review of all of the evidence (including the
evidence-based framework), that when taken as a whole the selected standard, including the
indicator, averaging time, form, and level, would be "sufficient but not more than necessary to
protect public health, including the health of sensitive subpopulations, with an adequate margin
of safety" (73 FR 67007).
4.1.2 Approach for the Current Review
To evaluate whether it is appropriate to consider retaining the current primary Pb
standard, or whether consideration of revision is appropriate, we have adopted an approach in
this review that builds upon the general approach used in the last review and reflects the broader
body of evidence and information now available. As summarized above, the Administrator's
decisions in the prior review were based on an integration of information on health effects
4-11
-------
associated with exposure to Pb, relationships between ambient air Pb and blood Pb; expert
judgments on the adversity and public health significance of key health effects; and policy
judgments as to when the standard is requisite to protect public health with an adequate margin
of safety. These considerations were informed by air quality and related analyses, quantitative
exposure and risk assessments, and qualitative assessment of impacts that could not be
quantified.
In conducting this assessment, we draw on the current evidence and quantitative
assessments of exposure pertaining to the public health risk of Pb in ambient air. In considering
the scientific and technical information, we consider both the information available at the time of
the last review and information newly available since the last review, including the current ISA
(USEPA, 2012), as well as the quantitative exposure/risk assessments from the last review that
estimated Pb-related IQ decrements associated with different air quality conditions in simulated
at-risk populations in multiple case studies (USEPA, 2007a). Figure 4-1 illustrates the basic
construct of our two part approach in developing conclusions regarding options appropriate for
the Administrator to consider in this review with regard to the adequacy of the current standard
and, as appropriate, potential alternate standards. In the boxes of Figure 4-1, the range of
questions considered in chapter 3 above and section 4.2 below is represented by a summary of
policy-relevant questions that frame our consideration of the scientific evidence and
exposure/risk information.
4-12
-------
Adequacy of Current Standard
Evidence-based Considerations
> Does currently available evidence and related
uncertainties strengthen or call into question prior
conclusions?
• Evidence of health effects not previously identified
or at lower exposures?
• Newly identified at-risk populations?
•Changed understanding of air-to-blood
relationships?
•Effects at lower air-related exposures then
previously understood or in conditions that would
have likely met current standards?
>Does newly available information call into question any
of the basic elements of standard?
Risk-based Considerations
> Nature, magnitude and importance of
estimated exposures and risks associated with
just meeting the current standard?
>Uncertainties in the exposure and risk
estimates?
Consider
Retaining
N0\ Current Standard
Does information call into question the
adequacy of current standard?
Consideration of Potential Alternative Standards
Elements of Potential Alternate Standards
indicator
> Averaging Time
>Form
Hevel
C
Potential Alternative Standards for Consideration
Figure 4-1. Overview of approach for review of current primary standard.
4-13
-------
4.2 ADEQUACY OF THE CURRENT STANDARD
In considering the adequacy of the current Pb standard, the overarching question we
consider is:
• Does the currently available scientific evidence- and exposure/risk-based
information, as reflected in the ISA and REA, support or call into question the
adequacy of the protection afforded by the current Pb standard?
In considering the scientific and technical information, we give our attention to both the
information available at the time of the last review and information newly available since the last
review, including most particularly that which has been critically analyzed and characterized in
the ISA. In chapter 3 above, attention was given to addressing specific questions on key aspects
of this information. To assist us in interpreting the currently available scientific evidence and
results of quantitative exposure/risk analyses to address the overarching question here, we draw
on discussions in chapter 3 above in our consideration of broader or more policy-related
questions, posed within sections 4.2.1 and 4.2.2 below.
For the purposes of this PA, staff has drawn from EPA's assessment and integrated
synthesis of the scientific evidence presented in the ISA and on the quantitative exposure and
risk information, based on the 2007 REA (USEPA, 2007a), described in section 3.4 above. The
evidence-based discussions presented in this chapter draw upon evidence from epidemiological
studies and experimental animal studies evaluating health effects related to exposures to Pb, as
discussed in the ISA. The exposure/risk-based discussions have drawn from the quantitative
health risk analyses for Pb performed in the last Pb NAAQS review in light of the currently
available evidence (2007 REA, REA Planning Document). Together the evidence-based and
risk-based considerations inform our conclusions related to the adequacy of the current primary
standard for Pb.
4.2.1 Evidence-based Considerations
In considering the evidence with regard to the issue of adequacy of the current standard,
we address several questions that build on the information summarized in chapter 3 to more
broadly address the extent to which the current evidence base supports the adequacy of the
public health protection afforded by the current primary standard. The first question addresses
our integrated consideration of the health effects evidence, in light of aspects described in
chapter 3. The second question focuses on our consideration of associated areas of uncertainty.
The third question then integrates our consideration of the prior two questions with a focus on
the standard, including each of the four elements.
4-14
-------
• To what extent has new information altered the scientific support for the
occurrence of health effects as a result of multimedia exposure associated with
levels of Pb occurring in the ambient air?
The current evidence continues to support our conclusions from the previous review
regarding key aspects of the health effects evidence for Pb and the health effects of multimedia
exposure associated with levels of Pb occurring in ambient air in the U.S. Our conclusions in
this regard are based on consideration of the assessment of the currently available evidence in the
ISA, particularly with regard to key aspects summarized in chapter 3 of this PA, in light of the
assessment of the evidence in the last review as described in the 2006 CD and summarized in the
notice of final rulemaking (73 FR 66964). Key aspects of these conclusions are summarized
below.
As at the time of the last review, blood Pb continues to be the predominant biomarker
employed to assess exposure and health risk of Pb (ISA, chapters 3 and 4), as discussed in
section 3.1 above. This widely accepted role of blood Pb in assessing exposure and risk is
illustrated by its established use in programs to prevent both occupational Pb poisoning and
childhood Pb poisoning, with the latter program, implemented by the CDC, recently issuing
updated guidance on blood Pb measurement interpretation (CDC, 2012). As in the past, the
current evidence continues to indicate the close linkage of blood Pb levels in young children to
their body burden; this linkage is associated with the ongoing bone remodeling during that
lifestage (ISA, section 3.3.5). This tight linkage plays a role in the somewhat rapid response of
children's blood Pb to changes in exposure (particularly to exposure increases), which
contributes to its usefulness as an exposure biomarker (ISA, sections 3.2.2, 3.3.5, and 3.3.5.1).
Additionally, the weight of evidence documenting relationships between children's blood Pb and
health effects, most particularly those on the nervous and hematological systems (e.g., ISA,
sections 4.3 and 4.7), speaks to its usefulness in assessing health risk.
As in the last review, the evidence on air-to-blood relationships available today continues
to be comprised of studies based on an array of circumstances and population groups (of
different age ranges), analyzed by a variety of techniques, which together contribute to
appreciable variability in the associated quantitative estimates and uncertainty with regard to the
relationships existing in the U.S. today. Accordingly, our interpretation of this evidence base, as
discussed in section 3.1 above, also includes consideration of factors that may be influencing
various study estimates, both with regard to their usefulness for our general purpose of
quantitatively characterizing relationships between Pb in ambient air and air-related Pb in
children's blood and with regard to their pertinence more specifically to conditions and
populations in the U.S. today. In so doing, we note that the current evidence, while including
two additional studies not available at the time of the last review, is not much changed from that
4-15
-------
available in the last review. The range of estimates that can be derived from the full dataset is
broad and not changed by the inclusion of the newly available estimates. Further, we recognize
significant uncertainties regarding the air Pb to air-related blood Pb relationship for the current
conditions where concentrations of Pb in both ambient air and children's blood are substantially
lower than they have been in the past. In considering the strengths, limitations and uncertainties
associated with the full dataset, the currently available evidence appears to continue to support a
range of estimates for our purposes that is generally consistent with the range given weight in the
last review, 1:5 to 1:10 (ISA, section 3.7.4 and Table 3-12; 73 FR 67001-2, 67004). We
additionally note that the generally central estimate of 1:7 identified for this range in the last
review is consistent with the study involving blood Pb for pre-school children and air Pb
conditions near a large source of Pb to ambient air with concentrations near (and/or previously
above) the level of the current Pb standard (ISA, section 3.5.1; Hilts, 2003).5 In so noting, we
also recognize the general overlap of such circumstances with those represented by the evidence-
based, air-related IQ loss framework,6 for which air-to-blood ratio is a key input. In
characterizing the range of air-to-blood ratio estimates, we recognize uncertainty inherent in such
estimates as well as the variation in currently available estimates resulting from a variety of
factors, including differences in the populations examined, as well as in the Pb sources or
exposure pathways addressed in those study analyses (ISA, section 3.7.4).
The scientific evidence continues to recognize a broad array of health effects on multiple
organ systems or biological processes related to blood Pb, including Pb in blood prenatally (ISA,
section 1.6). The currently available evidence continues to support identification of
neurocognitive effects in young children as the most sensitive endpoint associated with blood Pb
concentrations (ISA, section 1.6.1), which as an integrated index of exposure reflects the
aggregate exposure to all sources of Pb through multiple pathways (inhalation and ingestion).
Evidence continues to indicate that neurocognitive effects in young children may not be
reversible and may have effects that persist into adulthood (ISA, section 1.9.6). Thus, as
discussed in section 3.2 above, we continue to consider the evidence of Pb effects at the low end
of the studied blood Pb levels (closest to those common in the U.S. today) to be strongest and of
greatest concern for effects on the nervous system, most particularly those on cognitive function
in children.
As in the last review, evidence on risk factors continues to support the identification of
young children as an important at-risk population for Pb health effects (ISA, section 5.4). The
5 The older study by Hayes et al (1994) during time of leaded gasoline indicated a generally similar ratio of
1:8, although the blood Pb levels in that study were much higher than those in the study by Hilts (2003). Among the
studies focused on this age group, the latter study includes blood Pb levels closest to those in U.S. today.
6 Concentrations near air sources are higher than those at more distant sites (as described in section 2.2.2);
it is near-source locations where there is the potential for concentrations at or near the current standard.
4-16
-------
current evidence also continues to indicate important roles as factors that increase risk of lead-
related health effects for the following: nutritional factors, such as iron and calcium intake;
elevated blood Pb levels; and proximity to sources of Pb exposure, such as industrial releases or
buildings with old, deteriorating, leaded paint. Further, some races or ethnic groups continue to
demonstrate increased blood Pb levels relative to others, which may be related to these and other
factors (ISA, sections 5.1, 5.2 and 5.4).
With regard to our understanding of the relationship between exposure or blood Pb levels
in young children and neurocognitive effects, the evidence in this review, as in the last, does not
establish a threshold blood Pb level for neurocognitive effects in young children (ISA, sections
1.9.4 and 4.3.12). The lowest blood Pb levels at which associations with neurocognitive impacts
have been observed in pre-school and school age children continue to range down below 5
|ig/dL, with the lowest group levels that have been associated with such effects ranging down to
2 |ig/dL (ISA, sections 1.6.1 and 4.3.15.1). Additionally, as in the last review, there is evidence
that the relationship of young children's blood Pb with neurocognitive impacts, such as IQ, is
nonlinear across a wide range of blood Pb, with greater incremental impacts at lower vs. higher
blood Pb levels (ISA, sections 1.9.4 and 4.3.12). Accordingly, as in the last review, we continue
to focus our interest on C-R relationships from study groups with blood Pb levels closest to those
in children in the U.S. today, which are generally lower than epidemiological study groups. The
currently available evidence does not identify additional C-R slopes for study groups of young
children (e.g., < 7 years) with mean blood Pb levels below that of groups identified in the last
review, 2.9 - 3.8 |ig/dL, as discussed in section 3.2 above (ISA, section 4.3.12). Thus, the blood
Pb concentration - IQ response functions or slopes identified in this review for epidemiological
study groups of young children with mean blood Pb levels closest to that of children in the U.S.
today include the same set recognized at the time of the last review (see Table 3-3 above), the
median of which is 1.75 points decrement per |ig/dL blood Pb (73 FR, 67003).
• To what extent have important uncertainties identified in the last review been
reduced and/or have new uncertainties emerged?
In our consideration of the evidence, as summarized in discussing the previous question
and in chapter 3 above, we have not identified any new uncertainties as emerging since the last
review. However, we continue to recognize important uncertainties identified in the last review
that remain today. Importantly, given our focus in this review, as in the last review, on
neurocognitive impacts associated with Pb exposure in early childhood, we recognize remaining
uncertainties in our understanding of the C-R relationship of neurocognitive impacts, such as IQ
decrements, with blood Pb level in young children, particularly across the range of blood Pb
levels common in the U.S. today. With regard to C-R relationships for IQ, the evidence
available in this review does not include studies that appreciably extend the range of blood Pb
4-17
-------
levels studied beyond those available in the last review. As in the last review, the early
childhood (e.g., 2 to 6 or 7 years of age) blood Pb levels for which associations with IQ response
have been reported continue to extend at the low end of the range to study group mean blood Pb
levels of 2.9 to 3.8 |ig/dL (e.g., 73 FR 67003, Table 3). The lack of studies considering
concentration-response relationships for Pb effects on IQ at lower blood Pb levels contributes to
uncertainty regarding the quantitative relationship between blood Pb and IQ response in
populations with mean blood Pb levels closer to the most recently available mean for children
aged one to five years of age (e.g., 1.17 ng/dL in 2009-2010 [ISA, p. 3-85]). The studies at the
blood Pb levels studied, as summarized in section 3.2 above, continue to indicate higher C-R
slopes in these groups with lower blood Pb levels than in study groups with higher blood Pb
levels (ISA, section 4.3.12).
Further, we recognize important uncertainties in our understanding of the relationship
between ambient air Pb concentrations and air-related Pb in children's blood. The evidence
newly available in this review has not reduced such key uncertainties. As in the last review, air-
to-blood ratios based on the available evidence continue to vary, with our conclusions based on
the current evidence generally consistent with the range of 1:5 to 1:10 given emphasis in the last
review (73 FR 67002; ISA, section 3.7.4). There continues to be uncertainty regarding the extent
to which this range represents the relationship between ambient air Pb and Pb in children's blood
(derived from the full set of air-related exposure pathways) and with regard to its reflection of
exposures associated with ambient air Pb levels common in the U.S. today and to circumstances
reflecting just meeting the current Pb standard (ISA, section 3.7.4). We note additionally the
significant uncertainty remaining with regard to the temporal relationships of ambient Pb levels
and associated exposure with occurrence of a health effect (73 FR 67005).
• To what extent does newly available information support or call into question any
of the basic elements of the current Pb standard?
We address this question for each of the elements of the standard in light of the health
effects evidence and other relevant information available in this review. As an initial matter,
however, we recognize the weight of the scientific evidence available in this review that
continues to support our focus on effects on the nervous system of young children, specifically
neurocognitive decrements, as the most sensitive endpoint. Consistent with the evidence
available in the last review, the currently available evidence continues to indicate that a standard
that provides requisite public health protection against the occurrence of such effects in at-risk
populations would also provide the requisite public health protection against the full array of
health effects of Pb. Accordingly, the discussion of the elements below is framed by that
background.
4-18
-------
Indicator
The indicator for the current Pb standard is Pb-TSP. Key considerations in retaining this
indicator in the last review are summarized in section 4.1.1.2 above. Exposure to Pb in all sizes
of particles passing through ambient air can contribute to Pb in blood and associated health
effects by a wide array of exposure pathways (ISA, section 3.1). These pathways include the
ingestion route, as well as inhalation (ISA, section 3.1), and a wide array of particle sizes play a
role in these pathways (ISA, section 3.1.1.1). As at the time of the last review, we continue to
recognize the variability of the Pb-TSP FRM in its capture of airborne Pb particles (see section
2.2.1.3.1 above). As in the last review, we also note that an alternative approach for collection of
a conceptually comparable range of particle sizes, including ultra-coarse particles, is not yet
available, although we take note of activities underway that may remedy that situation in the
future, as referenced in section 2.2.1.3.1 above. Additionally, the limited available information
regarding relationships between Pb-TSP and Pb in other size fractions indicates appreciable
variation in this relationship, particularly near sources of Pb emissions where concentrations and
potential exposures are greatest. Thus, the information available in this review does not address
previously identified limitations and uncertainties for the current indicator. Nor does the newly
available information identify additional limitations or uncertainties.
The evidence available in this review continues to indicate the role of a range of air Pb
particle sizes in contributing to Pb exposure (e.g., ISA, section 3.1.1.1) that contributes to Pb in
blood and associated health effects. For example, the evidence indicates larger particle sizes for
Pb that occurs in soil and house dust and may be ingested as compared to Pb particles commonly
occurring in the atmosphere and the size fraction of the latter that may be inhaled (ISA, section
3.1.1.1). Taken together the evidence currently available reinforces the appropriateness of an
indicator for the Pb standard that reflects a wide range of airborne Pb particles.
Averaging time and form
The averaging time and form of the standard were revised in the last Pb NAAQS review,
based on considerations summarized in section 4.1.1.2 above. The current standard is a not-to-
be-exceeded rolling three-month average (CFR 50.16), derived from three monthly averages
calculated in accordance with the current data handling procedures (CFR, Appendix R to Part
50). The form is a maximum, evaluated within a three-year period (CFR 50.16). As at the time
of the last review, evidence continues to support the importance of periods on the order of three
months and the prominent role of deposition-related exposure pathways, with uncertainty
associated with characterization of precise time periods associating ambient air Pb with air-
related health effects. Relevant factors continue to be those pertaining to the human
physiological response to changes in Pb exposures and those pertaining to the response of air-
related Pb exposure pathways to changes in airborne Pb. The newly available evidence in this
4-19
-------
review does not appreciably improve our understanding of the period of time in which air Pb
concentrations would lead to the health effects most at issue in this review. Thus, there continue
to be limitations in the evidence to inform our consideration of these elements of the standard
and associated uncertainty. However, there is no newly available information that calls into
question this element of the current Pb standard.
Level
The level of the current standard is 0.15 |ig/m3 (CFR 50.16). As described in section
4.1.1 above, this level was selected in 2008 with consideration of, among other factors, an
evidence-based air-related IQ loss framework, for which there are two primary inputs: air-to-
blood ratios and C-R functions for blood Pb - IQ response in young children. Additionally taken
into consideration were the uncertainties inherent in these inputs. Application of the framework
also entailed consideration of a magnitude of air-related IQ loss, which as further described in
section 4.1.1.2 above, is used in conjunction with this specific framework in light of the
framework context, limitations and uncertainties. Additionally, selection of a level for the
standard in 2008 was made in conjunction with decisions on indicator, averaging time and form.
As an initial matter, we consider the extent to which the evidence-based, air-related IQ
loss framework which informed the Administrator's decision in the last review is supported by
the currently available evidence and information. In so doing, we recognize the support provided
by the currently available evidence for the key conclusions drawn in the last review with regard
to health effects of greatest concern, at-risk populations, the influence of Pb in ambient air on Pb
in children's blood and the association between children's blood Pb and decrements in
neurocognitive function (e.g., IQ). We additionally note the complexity associated with
interpreting the scientific evidence with regard to specific levels of Pb in ambient air, given the
focus of the evidence on blood Pb as the key biomarker of children's aggregate exposure. The
need to make such interpretations in the face of the associated complexity supported use of the
evidence-based framework in the last review. In considering the currently available evidence for
the same purposes in this review, we conclude that the evidence-based framework continues to
provide a useful tool for consideration of the evidence with regard to the level of the standard.
We next turn to consideration of the primary inputs to the framework: air-to-blood ratios
and C-R functions for blood Pb - IQ response in young children. With regard to the former, the
limited newly available information assessed in the ISA and discussed in section 3.1 above, is
generally consistent with the information in this area that was available at the time of the last
review. We additionally recognize the variability and uncertainty associated with quantitative
air-to-blood ratios based on this information, as also existed in the last review. As in the last
review, we recognize that factors contributing to the variability and uncertainty of these
estimates are varied and include aspects of the study populations (e.g., age and Pb exposure
4-20
-------
pathways) and the study circumstances (e.g., length of study period and variations in sources of
Pb exposure during the study period). We note that the full range of estimates associated with
the available evidence is wide and consider it appropriate to give emphasis to estimates
pertaining to circumstances closest to those in the U.S. today with regard to ambient air Pb and
children's blood Pb concentrations, while recognizing the limitations associated with the
available information with regard to this emphasis. With that in mind, we consider the currently
available evidence to continue to support the range of estimates concluded in the last review to
be most appropriate for the current population of young children in the U.S., in light of the
multiple air-related exposure pathways by which children are exposed, in addition to inhalation
of ambient air, and of the levels of air and blood Pb common today. Identification of this range
also included consideration of the limitations associated with the available information and
inherent uncertainties. This range of air-to-blood ratios included 1:10 at the upper end and 1:5 at
the lower end. We further recognize that the limited evidence for air Pb and children's blood Pb
concentrations closest to those in U.S. today continues to provide support for the Administrator's
emphasis in the 2008 decision on the relatively central estimate of 1:7.
With regard to the second input to the evidence-based framework, C-R functions for the
relationship of young children's blood Pb with neurocognitive impacts (e.g., IQ decrements), we
consider several aspects of the evidence. First, as discussed in section 3.2 above, the currently
available information continues to provide evidence that this C-R relationship is nonlinear across
the range of blood Pb levels from the higher concentrations more prevalent in the past to lower
concentrations more common today. Thus, we continue to consider it particularly appropriate to
focus on the evidence from studies with blood Pb levels closest to those of today's population,
which in the last review included studies with study group mean blood Pb levels ranging roughly
from 3 to 4 |ig/dL in children aged 24 months to 7 years (Table 3-3 above). As discussed in
sections 3.2 above, this is also consistent with the evidence currently available for this age group
of young children, and the currently available evidence does not include additional C-R slopes
for incremental neurocognitive decrement with blood Pb levels at or below this range. In
considering whether this set of functions continues to be well supported by the evidence, as
assessed in the ISA (ISA, section 4.3.2), we note the somewhat wide range in slopes
encompassed by these study groups, while also noting the stability of the median. For example,
omission of any of the four slopes considered in the last review does not appreciably change the
median (e.g., the median would change from -1.75 IQ points per |ig/dL blood Pb to -1.71 or -
1.79). Thus, we conclude that while differing judgments might be made with regard to inclusion
of each of the four study groups, these estimates are generally supported by the current review of
the evidence in the ISA. Further, the stability of the median to modifications to this limited
dataset lead us to conclude that the currently available evidence continues to support
4-21
-------
consideration of-1.75 IQ points per |ig/dL blood Pb as a well-founded and stable estimate for
purposes of describing the neurocognitive impact quantitatively on this age group of U.S.
children.
In summary, in considering the evidence and information available in this review
pertaining to the level of the current Pb standard, we note that the evidence available in this
review, as summarized in the ISA, continues to support the air-related IQ loss evidence-based
framework, with the inputs that were used in the last review. These include estimates of air-to-
blood ratios ranging from 1:5 to 1:10, with a generally central estimate of 1:7. Additionally, the
C-R functions most relevant to blood Pb levels in U.S. children today continue to be provided by
the set of four analyses considered in the last review for which the median estimate is -1.75 IQ
points per |ig/dL Pb in young children's blood. Thus, we observe that the evidence available in
this review has changed little if at all with regard to the aspects given weight in the conclusion on
level for the new standard in the last review and would not appear to call into question any of the
basic elements of the standard. In so doing, we additionally recognize that the overall decision
on adequacy of the current standard is a public health policy judgment by the Administrator; we
discuss considerations that inform such judgments in section 4.3 below.
4.2.2 Exposure/Risk-based Considerations
Our consideration of the issue of adequacy of public health protection provided by the
current standard is also informed by the quantitative exposure/risk assessment completed in the
last review, augmented as described in section 3.4 above. We have organized the discussion that
follows around two questions to assist us in interpreting the results of the assessment of case
studies simulated to meet several different air quality conditions, including those just meeting the
current standard.
• What is the level of confidence associated with estimates of air-related risk
generated for simulations just meeting the current Pb standard?
As an initial matter, we recognize the significant limitations and complexity associated
with the risk/exposure assessment for Pb that are far beyond those associated with similar
assessments typically performed for other criteria pollutants. In completing the assessment we
were constrained by significant limitations with regard to data and tools particular to the problem
at hand. Further, the multimedia and persistent nature of Pb and the role of multiple exposure
pathways contribute significant additional complexity to the assessment as compared to other
assessments that focus only on the inhalation pathway. As a result, our estimates of air-related
exposure and risk are approximate, presented as upper and lower bounds within which we
consider air-related risk likely to fall. We base our description of overall confidence in this
characterization of air-related risk on our consideration of the overall design of the analysis (as
4-22
-------
described in section 3.4 above), the degree to which key sources of variability are reflected in the
design of the analysis, and our characterization of key sources of uncertainty.
In considering the degree to which key sources of variability (discussed in section 3.4.6
above) are reflected in the design of the analysis, we note the following aspects addressed by the
risk assessment.
• Variation in distributions of potential urban residential exposure and risk across U.S.
urban residential areas. This is addressed by the inclusion of three different (location-
specific) urban study areas that reflect a diverse set of urban areas in the U.S.
• Representation of a more highly exposed subset of urban residents potentially exposed at
the level of the standard. This is addressed by the inclusion of the generalized (local)
urban study area.
• Variation in residential exposure to ambient air Pb within an urban area. This is
addressed through the partitioning of the location-specific study areas into exposure
zones to provide some representation of spatial gradients in ambient air Pb and their
interaction with population distribution and demographics. This was done in a somewhat
more precise manner in the primary Pb smelter case study, which relied on dispersion
modeling to describe gradients, as compared with the manual assignment of gradients
related to air concentration differences among monitors in an area.
• Inter-individual variability in blood Pb levels. This is addressed though the use of
empirically-derived GSDs to develop blood Pb distribution for the child population in
each exposure zone, with GSDs selected particular to each case study population.
• Inter-individual variability in IQ response to blood Pb. This is addressed through the use
of C-R functions for IQ loss based on a pooled analysis reflecting studies of diverse
populations.
We also considered key sources of uncertainty (discussed in section 3.4.7 above), in
particular those affecting the precision of the air-related risk estimates, as mentioned above.
Associated sources of uncertainty include our inability to simulate changes in air-related Pb as a
function of changes in ambient air Pb in exposure pathways other than those involving inhalation
of ambient air and ingestion of indoor dust. This contributes to the positive bias of the upper
bound for the air-related risk estimates. We additionally recognize the significant uncertainty
associated with estimating upper percentiles of the distribution of air-related blood Pb
concentration estimates (and associated IQ loss estimates) due to limitations in available
information. Lastly, we recognize the uncertainty associated with application of the C-R
function at the lower blood Pb levels in the distribution; this relates to the limited representation
of blood Pb levels of this magnitude in the dataset from which the C-R function is derived.
In the quantitative risk information available in this review, we have air-related risk
estimates for simulations just meeting the current standard from one of the location-specific
urban case studies (Chicago) and from the generalized (local) urban case study. With regard to
4-23
-------
the latter, we note its simplified design that does not include multiple exposure zones, thus
reducing the dimensions simulated. We have a reasonable degree of confidence in aspects of the
generalized (local) urban case study for the specific situation we consider it to represent (i.e., a
temporal pattern of air Pb concentrations that just meets the level of the standard), and when the
associated estimates are characterized as approximate, within upper and lower bounds (as
described in section 3.4.4 above), while also recognizing considerable associated uncertainty.
• To what extent are the air-related risks remaining upon just meeting the current
Pb standard important from a public health perspective?
In considering public health importance of estimated air-related risks, we consider here
the nature and magnitude of such estimated risks (and attendant uncertainties), including such
impacts on the affected population, and we additionally consider the size of the affected
population. Based on the evidence available in the last review and consistent with that available
today, the quantitative risk estimates developed in the 2007 REA and augmented slightly in this
review are for decrements in IQ, an established indicator of neurocognitive function. In
considering these estimates, we recognize that although some neurocognitive effects may be
transient, some effects may persist into adulthood, affecting success later in life (ISA, sections
1.9.5 and 4.3.14). We additionally recognize the potential population impacts of small changes
in population mean values of metrics such as IQ, presuming a uniform manifestation of lead-
related decrement across the range of population IQ (ISA, section 1.9.1), as noted in section 3.3
above.
Exposures and risks associated with air-related Pb under several different air quality
conditions were estimated in the 2007 REA. As summarized in section 3.4 above, limitations in
our modeling tools and data affected our ability to develop precise estimates for air-related
exposure pathways and contributed uncertainties. The results are approximate estimates which
we describe through the use of rough upper and lower bounds within which we estimate air-
related risk to fall. We have recognized a number of uncertainties in the underlying risk
estimates from the 2007 REA and in the interpolation approach employed in the new analyses
for this review. We have characterized the magnitude of air-related risk associated with the
current standard with a focus on median estimates, for which we have appreciably greater
confidence than estimates for outer ends of risk distribution (see section 3.4.7) and on risks
derived using the C-R function in which we have greatest confidence (see sections 3.4.3.3.1 and
3.4.7). These risk estimates include estimates from the last review for one of the location-
specific urban study area populations as well as estimates newly derived in this review based on
interpolation from 2007 REA results for the generalized (local) urban case study, which is
recognized to reflect a generalized high end of air-related exposure for localized populations.
Taken together, these results for just meeting the current standard include a high-end localized
4-24
-------
risk estimate for air-related Pb of a magnitude generally bounded by roughly 1 and 3 points IQ
loss, with attendant uncertainties, and with appreciably lower risks with increasing distance from
the highest exposure locations
In considering the importance of such risk from a public health perspective, we also
consider the size of at-risk populations represented by the REA case studies. As discussed in
section 3.4 above, the generalized (local) urban case study is considered to represent a localized
urban population exposed near the level of the standard, such as a very small, compact
neighborhood near a source contributing to air Pb concentrations just meeting the standard. This
case study provides representation in the risk assessment for such small populations at the upper
end of the gradient in ambient air concentrations expected to occur near sources; thus estimates
for this case study reflect exposures nearest the standard being evaluated. While we do not have
precise estimates of the number of young children living in such areas of the U.S. today, we have
information that informs our understanding of their magnitude. For example, as discussed in
section 3.3 above (Table 3-4), we estimate there to be approximately 2,400 children, aged 5
years and younger, residing within 0.5 km of a monitor with air Pb concentrations above the
current standard. We further observe several additional monitors with maximum 3-month Pb
concentrations that fall below but within 10% of the current standard level (as noted in section
3.3 above); an estimated 265 young children reside near these monitors. Thus, together we
estimate some 2700 children, aged 5 years and younger, living in localized areas with elevated
air Pb concentrations that are above or near the current standard. Based on the 2010 census
estimates of approximately 24.3 million children in the U.S. aged five years or younger, this
represents approximately one hundredth of one percent of this age group in the U.S.7 This
indicates the size of the population of young children of this age living in areas in close
proximity to areas where air Pb concentrations may be above or near the current standard
approximately a hundredth of one percent of the full population of correspondingly aged
children.8
7 While these estimates pertain to the age group of children aged 5 years and younger, we additionally note
that a focus on an alternative age range, such as inclusive of slightly older children (e.g., through age 7), while
increasing the number for children living in such locations, would not be expected to appreciably change the
percentage of the full U.S. age group that the subset represents. Further, to the extent some of the source-oriented
monitors required by the 2010 monitoring regulation summarized in section 2.2.1.1 above were not yet represented
in the analysis of monitoring data summarized in Table 3-4 above and might report such elevated concentrations,
consideration of the analysis summarized in Table 3-5 indicates the potential for only small changes in the
percentage of the full age group represented by the subset (e.g., potential for less than an additional 0.01%).
8 This estimate includes children in areas where recent information indicates the standard is exceeded
because areas not in attainment with the standard are required to attain the standard as expeditiously as practicable,
but no later than five years after designation. Accordingly, these areas are for present purposes treated as areas with
air Pb concentrations just meeting the current standard and are included for purposes of identifying the size of the at-
risk population residing in areas likely to have air Pb concentrations near the current standard.
4-25
-------
In summary, we recognize substantial uncertainty inherent in the REA estimates of air-
related risk associated with localized conditions just meeting the current standard, which we have
characterized as approximate and falling near or somewhat above the rough lower bound of 1
and below the rough upper bound of 3 IQ points.9 This approximate estimate of risk for children
living in such areas is generally overlapping with and consistent with the evidence-based air-
related IQ loss estimates summarized in section 4.2.1 above. With regard to the importance of
the estimated risks from a public health perspective, we note, based on the currently available
monitoring and census data, the estimated size of the population at risk in such areas to be
approximately 2700 young children, representing slightly more than one one hundredth of a
percent of the full population of similarly aged children. In considering the exposure/risk
estimates during the last review, the Administrator took note of the important uncertainties and
limitations associated with these assessments and, while placing less weight on the assessment
estimates, he recognized the quantitative risk estimates to be "roughly consistent with and
generally supportive" of those estimated by the evidence-based framework. In our consideration
of the risk estimates considered in the last review, as well as the estimates for the current
standard that have been newly developed in this review for the generalized (local) urban case
study (see section 3.4.3.3.2), we agree with the previous characterization. As would be expected
by the use of interpolation, the newly derived estimates are consistent with the estimates for
similar air quality scenarios that were available in the last review.
4.2.3 CASAC Advice
In our consideration of the adequacy of the current standard, in addition to the evidence-
and risk/exposure-based information discussed above, we have also considered the advice and
recommendations of CASAC, based on their review of the ISA, the REA Planning Document,
and the earlier draft of this document, as well as comments from the public on the earlier draft of
this document.
A limited number of public comments have been received on this review to date,
including comments focused on the draft IRP, the draft REA Planning Document or the draft PA.
Of the three commenters that addressed adequacy of the current primary Pb standard, two are in
agreement with staff conclusions in the draft PA. A third expressed the view that the standard
9 We note that the value of the upper bound is influenced by risk associated with exposure pathways that
were not varied with alternative standard levels, a modeling limitation with the potential to contribute to
overestimation of the upper bound with air quality scenarios involving air Pb levels below current conditions for the
study area (see sections 3.4.4 and 3.4.7 above).
4-26
-------
should be revised to be more restrictive given the evidence of Pb effects in populations with
mean blood Pb levels below 10 jig/dL.10
In their comments on the draft PA, the CAS AC Pb Panel concurred with staffs overall
preliminary conclusions that it is appropriate to consider retaining the current primary standard
without revision, stating that "the current scientific literature does not support a revision to the
Primary Lead (Pb) National Ambient Air Quality Standard (NAAQS)" (Frey, 2013). They
further noted that "[although the current review incorporates a substantial body of new scientific
literature, the new literature does not justify a revision to the standards because it does not
significantly reduce substantial data gaps and uncertainties (e.g., air-blood Pb relationship at low
levels; sources contributing to current population blood Pb levels, especially in children; the
relationship between Pb and childhood neurocognitive function at current population exposure
levels; the relationship between ambient air Pb and outdoor dust and surface soil Pb
concentrations)". In recognition of these limitations in the available information, the CAS AC
provided recommendations on research to address these data gaps and uncertainties so as to
inform future Pb NAAQS reviews (Frey, 2013).
The CAS AC comments indicated agreements with key aspects of staff s consideration of
the exposure/risk information and currently available evidence in this review (Frey, 2013,
Consensus Response to Charge Questions, p. 7).
The use of exposure/risk information from the previous Pb NAAQS review
appears appropriate given the absence of significant new information that could
fundamentally change the interpretation of the exposure/risk information. This
interpretation is reasonable given that information supporting the current
standard is largely unchanged since the current standard was issued.
The CASAC agrees that the adverse impact of low levels ofPb exposure on
neurocognitive function and development in children remains the most sensitive
health endpoint, and that a primary Pb NAAQS designed to protect against that
effect will offer satisfactory protection against the many other health impacts
associated with Pb exposure.
The CASAC concurs with the draft PA that the scientific findings pertaining to
air-to-blood Pb ratios and the C-R relationships between blood Pb and childhood
1Q decrements that formed the basis of the current Pb NAAQS remain valid and
are consistent with current data.
The CASAC concurred with the appropriateness of the application of the evidence-based
framework from the last Pb NAAQS review. With regard to the key inputs to that framework,
CASAC concluded that "[t]he new literature published since the previous review provides
10 All written comments submitted to the Agency will be available in the docket for this rulemaking, as will
be transcripts of the public meetings held in conjunction with CASAC's review of the earlier draft of this document,
of the REA Planning Document and of drafts of the ISA.
4-27
-------
further support for the health effect conclusions presented in that review" and that the studies
newly available in this review "do not fundamentally alter the uncertainties for air-to-blood
ratios or C-R functions for IQ decrements in young children (Frey, 2013, Consensus Response to
Charge Questions, p. 6).
The comments from CASAC took note of the uncertainties that remain in this review,
which contribute to the uncertainties associated with drawing conclusions regarding air-related
exposures and associated health risk at or below the level of the current standard (Frey, 2013,
Consensus Response to Charge Questions, p. 6).
This draft PA is constrained by the absence of new observational and
experimental data that address, at least in part, limitations and uncertainties in
the evidence that was present at the time of the last update of the Pb NAAQS.
Until evidence is available to assess Pb exposure and health risks related to air
Pb levels reflecting the current standard, a substantive refinement and update of
the PA will not be possible. The obvious uncertainty underlying evaluation of this
PA is whether lowering the standard would (or would not) impact exposure and
thus risk. The CASAC agrees with the EPA conclusion that "there is appreciable
uncertainty associated with drawing conclusions regarding whether there would
be reductions in blood Pb levels from alternative lower levels as compared to the
level of the current standard. "
4.3 STAFF CONCLUSIONS ON THE PRIMARY STANDARD
This section describes staff conclusions regarding adequacy of the current primary Pb
standard. These conclusions are based on considerations described above and in the discussion
below regarding the currently available scientific evidence summarized in the ISA and prior CDs
and the risk and exposure information drawn from the 2007 REA. Further, these staff
conclusions have taken into account advice from CASAC and public comment on the draft PA
and preliminary staff conclusions.
Taking into consideration the discussions responding to specific questions above in this
and the prior chapter, this section addresses the following overarching policy question.
• Does the currently available scientific evidence- and exposure/risk-based
information, as reflected in the ISA and REA, support or call into question the
adequacy of the protection afforded by the current Pb standard?
Our response to this question takes into consideration the discussions responding to the
specific policy-relevant questions in prior sections of this document (see sections 3.1-3.4, 4.2.1,
and 4.2.2). In so doing, we focus first on consideration of the evidence, including that newly
available in this review, and the extent to which it alters key conclusions supporting the current
standard. We then turn to consideration of the quantitative risk estimates drawn from the 2007
REA and associated limitations and uncertainties. We additionally consider the public health
policy judgments and judgments about the uncertainties inherent in the scientific evidence and
4-28
-------
quantitative analyses that are inherent in decisions on the adequacy of the current primary Pb
standard.
We first recognize the complexity involved in considering the adequacy of protection in
the case of the primary Pb standard, which differs substantially from that involved in
consideration of the NAAQS for other pollutants. Unlike the case for Pb, the other pollutants for
which NAAQS are set involve only inhalation exposure pathways, a relatively simpler context.11
In addition, generally an important component of the scientific evidence base considered in
reviewing the adequacy of NAAQS for other pollutants is the availability of studies that have
investigated associations between current concentrations of the pollutant in ambient air
(including in circumstances where the current standard is met) and the occurrence of health
effects judged plausibly related to ambient air exposure to the NAAQS pollutant. While such
studies, targeting locations near air Pb sources such as smelters, were available at the time the Pb
NAAQS was initially set in 1978, and to a much more limited degree at the time of the last
review, such studies of health effects under air quality conditions near those reflecting the
current standard are not available in this review. Rather, the evidence base that supports our
conclusions in this review includes most prominently epidemiological studies reporting
associations of blood Pb levels in U.S. populations, including the particularly at-risk population
of young children with health effects judged plausibly related to Pb exposures. Support for our
conclusions regarding the plausibility for ambient air Pb to play a role in such findings derives,
in part, from studies linking Pb in ambient air with the occurrence of health effects. However,
such studies (dating from the past or from other countries) involve ambient air Pb concentrations
many times greater than those that would meet the current standard. Thus, in considering the
adequacy of the current Pb standard, rather than considering studies that have investigated
current concentrations of Pb in ambient air (including in locations where the current standard is
met) and the occurrence of health effects, we primarily consider the evidence for, and risk
estimated from, models based upon key relationships, such as those between ambient air Pb, Pb
exposure, blood Pb and health effects. This evidence, with its associated limitations and
uncertainties, contributes to our conclusions regarding a relationship between ambient air Pb
conditions under the current standard and health effects.
In considering the currently available evidence, staff gives great weight to the long-
standing body of evidence on the health effects of Pb, augmented in some aspects since the last
review, which continues to support identification of neurocognitive effects in young children as
11 As described in sections 1.3 and 3.1 above, exposure to Pb from ambient air, unlike exposures for other
NAAQS pollutants, involves both ingestion and inhalation exposure pathways. As an additional complication, other
(nonair) sources of Pb also contribute to these pathways, particularly to ingestion exposure pathways. In the case of
Pb, the internal biomarker, blood Pb, is an indicator of exposure across different pathways and routes (as discussed
in section 3.1 above).
4-29
-------
the most sensitive endpoint associated with Pb exposure, as discussed in sections 3.2 and 3.3
above. The evidence continues to indicate that a standard that provides protection from
neurocognitive effects in young children additionally provides protection for other health effects
of Pb, such as cardiovascular effects later in life. Application of the evidence-based, air-related
IQ loss framework, developed in the last review, continues to provide a useful approach for
considering and integrating the evidence on relationships between Pb in ambient air and Pb in
children's blood and risks of neurocognitive effects (IQ loss). The currently available evidence
base, while somewhat expanded since the last review, is not appreciably expanded or supportive
of appreciably different conclusions with regard to air-to-blood ratios (section 3.1 above) or C-R
functions for neurocognitive decrements (section 3.2 above) in young children.
As in the last review, uncertainties remain in our understanding of important aspects of
ambient air Pb exposure and associated health effects. For example, important uncertainties
remain, both with regard to air-to-blood ratios that reflect the relationship between
concentrations of Pb in ambient air and air-related Pb in children's blood, and with regard to
estimates of the slope of the C-R function for neurocognitive impacts (IQ loss) at lower blood Pb
levels. With regard to the former, we note particularly the limitations associated with the
available studies and gaps in the evidence base with regard to studies that have investigated such
quantitative relationships under conditions pertaining to the current standard (e.g., in localized
areas near air Pb sources where the standard is met in the U.S. today). Further, in considering
our reliance on the evidence in performing quantitative modeling of exposure and risk we
additionally note important uncertainties associated with relationships between ambient air Pb
and outdoor soil/dust Pb and indoor dust Pb that particularly affect our quantitative estimates of
air-related risk under conditions of lower ambient air Pb concentrations and lower blood Pb
levels (73 FR 66981). These critical exposure pathways are also inherent in the evidence-based
air-related IQ loss framework, encompassed within the estimates of air-to-blood ratios. Thus, we
recognize uncertainties related to our understanding of these and other processes that also
contribute uncertainty to our application of the evidence-based framework. We consider this
uncertainty to be greater with application of the framework for levels below the current standard
given the weaker linkage with existing evidence, as noted below.
We additionally take note of the role of public health policy judgments in considering the
evidence-based framework and the exposure/risk information to inform the Administrator's
decision in 2008 to set the current standard, as summarized in section 4.1.1.2 above. We
recognize that public health policy judgments always play an important role in each NAAQS
review for each pollutant. One type of public health policy judgment focuses on how to consider
the nature and magnitude of the array of uncertainties that are inherent in the scientific evidence
and analyses. These judgments are traditionally made with a recognition that our understanding
4-30
-------
of the relationships between the presence of a pollutant in ambient air and associated health
effects is based on a broad body of information encompassing not only more established aspects
of the evidence but also aspects in which there may be substantial uncertainty. In the case of the
Pb NAAQS review, we recognize increased uncertainty in characterizing the relationship of
effects on IQ with blood Pb levels below those represented in the evidence base. We also
recognize increased uncertainty in projecting the magnitude of blood Pb response to ambient air
Pb concentrations at and below the level of the current standard. We recognize this increased
uncertainty particularly in light of the multiple factors that play a role in such a projection (e.g.,
meteorology, atmospheric dispersion and deposition, human physiology and behavior), for each
of which we recognize attendant uncertainties. Collectively, these aspects of the evidence and
associated uncertainties contribute to a recognition that for Pb, as for other pollutants, the
available health effects evidence generally reflects a continuum, consisting of levels at which
scientists generally agree that health effects are likely to occur, through lower levels at which the
likelihood and magnitude of the response become increasingly uncertain.
Reviews may also require judgments as to the point at which health effects become
important from a public health perspective. In the case of Pb, such a judgment includes
consideration of the public health significance of one to two points IQ loss in at-risk populations,
such as young children, in light of associated uncertainties. This type of judgment also includes
consideration of the IQ loss estimates yielded by the air-related IQ loss evidence-based
framework for specific combinations of standard level, air-to-blood ratio and C-R function.
With regard to public health significance of one to two points IQ loss in young children, staff
gives weight to the comments of CASAC and some public commenters in the last review which
recognized such a magnitude of IQ loss to be of public health significance and recommended
that a very high percentage of the population be protected from such a magnitude of IQ loss (73
FR 67000).12 With this objective in mind, we consider the extent to which the air-related IQ loss
evidence-based framework informs consideration of standards that might be concluded to
provide such a level of protection. In so doing, we first recognize that the IQ loss estimates
produced with the evidence-based framework do not correspond to a specific quantitative public
health policy goal for air-related IQ loss that would be acceptable or unacceptable for the entire
population of children in the U.S. Rather, the conceptual context for the evidence-based
framework is that it provides estimates for the mean air-related IQ loss of a subset of the
population of U.S. children (i.e., the subset living in close proximity to air Pb sources that
12 Our focus on IQ, as noted in section 3.3 above, reflects recognition of IQ being a well established, widely
recognized and rigorously standardized measure of neurocognitive function, as well as a global measure reflecting
the integration of numerous processes (ISA, section 4.3.2; 2006 CD, sections 6.2.2 and 8.4.2). Use of IQ in this
framework is thus considered to appropriately also reflect neurocognitive effects more generally.
4-31
-------
contributed to elevated air Pb concentrations that equal the current level of the standard). This is
the subset expected to experience air-related Pb exposures at the high end of the national
distribution of such exposures. The associated mean IQ loss estimate is the average for this
highly exposed subset and is not the average air-related IQ loss projected for the entire U.S.
population of children. Further, we recognize uncertainties associated with those estimates,
which increase with estimates associated with successively lower standard levels.
For the current standard level of 0.15 |ig/m3, an air-to-blood ratio estimate of 7 |ig/dL per
|ig/m3 (which we note as reasonably representative of the range supported by the evidence) and a
C-R slope of-1.75 IQ points per |ig/dL, the IQ loss estimate using the evidence-based
framework is 1.8 points.13 As noted above, this value is considered to be an estimate, with
attendant uncertainties, of mean air-related IQ loss of a subset of the population of U.S. children
in the high end of the exposure distribution for air-related Pb.14 As noted in section 4.2.2 above,
our current information on numbers of young children living near monitors above or within 10%
of the current Pb standard indicates the size of this population subset to be on the order of 2700
children aged 5 years or younger, which would correspond to approximately one hundredth of
one percent of the U.S. population of children of this age (estimated at approximately 24 million
in 2010 census). A primary objective of the monitoring network for Pb is to identify and monitor
sites of maximum concentration in areas anticipated to be at risk of exceeding the NAAQS.
While we acknowledge the possibility that the monitoring data thus far available may not
identify every occurrence of elevated Pb concentrations, the size of such a population subset can
still be concluded to fall well below one tenth of one percent of the full population of children
aged 5 years or younger in the U.S. today. Thus, we conclude that the current evidence, as
considered within the conceptual and quantitative context of the evidence-based framework, and
current air monitoring information indicates that the current standard would be expected to
achieve the public health policy goal recommended by CASAC in the last Pb NAAQS review
that IQ loss on the order of one to two IQ points be "prevented in all but a small percentile of the
population" (73 FR 67000).
In drawing conclusions from application of the evidence-based framework with regard to
adequacy of the current standard, we further recognize the degree to which IQ loss estimates
13 Using an air-to-blood ratio estimate of 8 ug/dL per ug/m3 yields a similar, but just slightly higher IQ loss
estimate (of approximately 2 IQ points).
14 In giving weight to consideration of the evidence within the context of the air-related IQ loss evidence-
based framework, we note that the air-related IQ loss estimated by the framework is for the mean of the population
subset described above. Given the lack of data on the distribution of the air-related portion of blood Pb and on the
extent to which distributions of air-related blood Pb levels might differ or correlate with total blood Pb that may be
more greatly influenced by other (nonair) Pb exposure pathways, estimates are not available that would correspond
to upper percentiles of the IQ loss distribution for this population subset. Any such estimates would have
substantial associated uncertainty.
4-32
-------
drawn from the air-related IQ loss evidence-based framework reflect mean blood Pb levels
below those represented in the currently available evidence for young children. For example, in
the case of the current standard level of 0.15 |ig/m3, multiplication by the air-to-blood ratio of 7
yields a mean air-related blood Pb level of 1.05 |ig/dL, which is half the level of the lowest blood
Pb subgroup of pre-school children in which neurocognitive effects have been observed (Table
3-2 above; Miranda et al., 2009) and well below the means of subgroups for which continuous C-
R functions have been estimated (Table 3-3 above).15 Such an extension below the lowest
studied levels may be viewed as appropriate given the lack of identified blood Pb level threshold
in the current evidence base for neurocognitive effects and the need for the NAAQS to provide a
margin of safety.16 We note, however, that the framework IQ loss estimates for still lower
potential standard levels represent still greater extrapolations from the current evidence base with
corresponding increased uncertainty.
In recognition of the role of public health policy judgments in drawing conclusions as to
adequacy of the Pb NAAQS, we consider the availability of new information or new commonly
accepted guidelines or criteria within the public health community with regard to the public
health significance of specific IQ decrements in exposed, at-risk populations that might inform
public health policy judgments on the appropriate degree of public health protection that should
be afforded to protect against risk of such neurocognitive effects in at-risk populations,17 such as
children living near air Pb sources. As an initial matter, we note that no such new information,
guidelines or criteria are described in the ISA. In further considering the occurrence of any new
actions by public health agencies that might indicate the availability of new information,
15 We recognize that children also have Pb in their blood derived from other (nonair) sources. The
evidence-based air-related IQ loss framework is used, however, to estimate IQ loss attributable to air-related Pb
because the NAAQS is intended to protect against risks from ambient air-related Pb. While children also have Pb in
their blood derived from other (nonair) sources, the evidence indicates that the neurocognitive risk per increment of
blood Pb is greater for children with the lowest blood Pb levels, as noted in section 3.2 above. Since the evidence
indicates Pb exposure to pose the greatest risk on an incremental basis at lower blood Pb levels, the focus on
estimating IQ loss attributable solely to air-related lead (i.e., assuming the presence of no other blood Pb) is a
conservative approach, the use of which contributes to the margin of safety provided by the standard.
16 As noted in section 1.2.1 above, the requirement that primary standards include an adequate margin of
safety was intended to address uncertainties associated with inconclusive scientific and technical information
available at the time of standard setting. It was also intended to provide a reasonable degree of protection against
hazards that research has not yet identified. Both kinds of uncertainties are components of the risk associated with
pollution at levels below those at which human health effects can be said to occur with reasonable scientific
certainty. Thus, in selecting primary standards that includes an adequate margin of safety, the Administrator is
seeking not only to prevent pollutant levels that have been demonstrated to be harmful but also to prevent lower
pollutant levels that may pose an unacceptable risk of harm, even if the risk is not precisely identified as to nature or
degree. The CAA does not require that primary standards be set at a zero-risk level or at background concentration
levels, but rather at a level that reduces risk sufficiently so as to protect public health with an adequate margin of
safety.
17The term at-risk populations is used here, rather then the phrase "sensitive populations" used in the last
review. In using the term at-risk, we intend the same meaning as has traditionally been intended for the term
"sensitive" consistent with discussion in section 1.2.1 above.
4-33
-------
guidelines or criteria for interpreting public health significance of such effects, we note that the
CDC has revised the blood Pb level used to prioritize young children for whom they recommend
particular follow-up health-protective actions, as summarized in section 3.1 above.18 The CDC
decision, while emphasizing the critical importance of primary prevention of Pb exposure,
provides no new guidelines or criteria with regard to the significance of specific IQ decrements
or judgments on appropriate public health protection from risk of neurocognitive effects, and
their consideration of the evidence base at the time of their decision does not substantively differ
from that presented in the ISA (CDC, 2012). Thus, we are aware of no new information or new
commonly accepted guidelines or criteria within the public health community for interpreting
public health significance of neurocognitive effects in the context of a decision on adequacy of
the current Pb standard.
With respect to exposure/risk-based considerations, we recognize the complexity of the
REA modeling analyses and the associated limitations and uncertainties. We additionally note
the differences among the case studies included in the REA and the extent to which they inform
our understanding of different aspects of the risk associated with air-related Pb in the U.S. For
example, the location-specific case studies indicate the distribution of population risk in urban
areas with differing types of Pb sources and gradients in air Pb concentrations as well as in
population density, while the generalized urban (local) case study indicates the magnitude of air-
related risk associated with those specific localized circumstances where air concentrations just
meet the Pb standard (regardless of source type). We agree with conclusions drawn in the 2008
review that the quantitative risk estimates, with a focus on those for the generalized (local) urban
case study, are "roughly consistent with and generally supportive" of estimates from the
evidence-based air-related IQ loss framework (73 FR 67006). We further take note of the
increasing uncertainty recognized for air quality scenarios involving air Pb concentrations
increasingly below the current conditions for each case study, recognizing that such uncertainty
is due in part to modeling limitations deriving from uncertainty regarding relationships between
ambient air Pb and outdoor soil/dust Pb and indoor dust Pb (as noted in section 3.4 above).
Based on the above considerations and with consideration of advice from CASAC, we
reach the conclusion that the current body of evidence, in combination with the exposure/risk
information, supports a primary standard as protective as the current standard. Further
consideration of the evidence and exposure/risk information available in this review and its
attendant uncertainties and limitations, advice from CAS AC and consideration of the availability
of other information that might also inform public health policy judgments by the Administrator,
leads us to reach the additional conclusion that it is appropriate to consider retaining the current
18 Uses identified for the CDC reference level include is the identification of " high-risk childhood
populations and geographic areas most in need of primary prevention" (CDC, 2012).
4-34
-------
standard without revision. We base these conclusions on consideration of the health effects
evidence, including consideration of this evidence in the context of the evidence-based, air-
related IQ loss framework, and in combination with the exposure/risk information (chapter 3 and
sections 4.2.1 and 4.2.2 above) and the uncertainties attendant with both. In so doing, we
recognize the complexities and limitations in the evidence base in reaching conclusions
regarding the magnitude of risk associated with the current standard, as well as the increasing
uncertainty of risk estimates for lower air Pb concentrations. Based on these considerations,
these conclusions also recognize what may be considered reasonable judgments on the public
health implications of the blood Pb levels and risk estimated for air-related Pb under the current
standard, including the public health significance of the Pb effects being considered, as well as
aspects of the use of the evidence-based framework that may be considered to contribute to the
margin of safety.
In reaching these conclusions, we additionally note that different public health policy
judgments could lead to different conclusions regarding the extent to which the current standard
provides protection of public health with an adequate margin of safety. Such public health
policy judgments include those related to the appropriate degree of public health protection that
should be afforded to protect against risk of neurocognitive effects in at-risk populations, such as
IQ loss in young children, as well as with regard to the appropriate weight to be given to
differing aspects of the evidence and exposure/risk information, and how to consider their
associated uncertainties. For example, different judgments might give greater weight to more
uncertain aspects of the evidence or reflect a differing view with regard to margin of safety. As
noted in section 4.1 above, in establishing primary standards under the Act that, in the
Administrator's judgment, are requisite to protect public health with an adequate margin of
safely, the Administrator seeks to establish standards that are neither more nor less stringent than
necessary for this purpose. The Act does not require that primary standards be set at a zero-risk
level, but rather at a level that avoids unacceptable risks to public health, even if the risk is not
precisely identified as to nature or degree. The requirement that primary standards provide an
adequate margin of safety was intended to address uncertainties associated with inconclusive
scientific and technical information available at the time of standard setting. It was also intended
to provide a reasonable degree of protection from hazards that research has not yet identified.
In this context, we recognize that the uncertainties and limitations associated with the
many aspects of the estimated relationships between air Pb concentrations and blood Pb levels
and associated health effects are amplified with consideration of increasingly lower air
concentrations. We believe the current evidence supports the conclusion that the current
standard is requisite to protect public health with an adequate margin of safety. In staffs view,
with which CASAC has agreed (Frey, 2013, p. 6) based on the current evidence, there is
4-35
-------
appreciable uncertainty associated with drawing conclusions regarding whether there would be
reductions in blood Pb levels and risk to public health from alternative lower levels of the
standard as compared to the level of the current standard. Thus, we conclude that the basis for
any consideration of alternative lower standard levels would reflect different public health policy
judgments as to the appropriate approach for weighing uncertainties in the evidence and for
providing requisite protection of public health with an adequate margin of safety.
In summary, the newly available health effects evidence, critically assessed in the ISA as
part of the full body of evidence, reaffirms conclusions on the broad array of effects recognized
for Pb in the last review. Further, we observe the general consistency of the current evidence
with the evidence available in the last review with regard to key aspects on which the current
standard is based, including those particular to the evidence-based framework developed in the
last review. We additionally observe that quantitative risk estimates associated with the current
standard, based on the risk assessment performed in the last review, indicate a level of risk
generally consistent with conclusions drawn from the evidence using the evidence-based
framework. In so doing, we also recognize the limitations and uncertainties associated with the
currently available information. These considerations and the advice from CASAC provide the
basis for the staff conclusion that consideration should be given to retaining the current standard,
without revision. In light of this conclusion, we have not identified any potential alternative
standards for consideration in this review.
4.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND DATA
COLLECTION
In this section, we highlight key uncertainties associated with reviewing and establishing
NAAQS for Pb. Such key uncertainties and areas for future health-related research, model
development, and data gathering are outlined below. In some cases, research in these areas can
go beyond aiding standard setting to aiding in the development of more efficient and effective
control strategies. We note, however, that a full set of research recommendations to meet
standards implementation and strategy development needs is beyond the scope of this discussion.
Rather, listed below are key uncertainties and research questions and data gaps that have been
thus far highlighted in this review of the health-based primary standard.
• A critical aspect of our consideration of the evidence and the quantitative risk assessment
in this review is our understanding of the C-R relationship between blood Pb levels in
young children and neurodevelopmental effects, specifically IQ decrement. An important
area of uncertainty in the Pb NAAQS review concerns interpretation of neurocognitive
impact risks and the shape of the C-R relationship at blood Pb levels similar to and below
those common in today's U.S. young child population. Accordingly, additional
epidemiological research involving substantially sized populations with mean blood Pb
levels closer to those common in today's population of young children, particularly those
4-36
-------
less affected by higher Pb exposures earlier in childhood, would help to reduce
uncertainty in our estimates of IQ decrement associated with these lower blood Pb levels
and, accordingly, in characterizing Pb health effects.
Key uncertainties with regard to other aspects of the health effects evidence include the
following.
- There remains uncertainty in the evidence base with regard to the exposure
circumstances (pre- and postnatal timing, duration, magnitude and frequency)
eliciting effects in older children and adults. Effects of particular focus include
effects on the nervous system later in life, cardiovascular function, and delayed
onset of puberty.
- Alzheimer's-like pathology has been reported in aged laboratory animals (non-
human primates and rodents) exposed to Pb early in life. Uncertainty remains,
however, regarding the relationships of such pathology with altered function or
behavior.
- Epidemiological studies indicate detrimental effects of Pb on sperm production
and quality, often in occupational cohorts. Uncertainty remains regarding these
effects in otherwise healthy cohorts without occupational Pb exposure or other
underlying medical conditions.
- An additional area of uncertainty is that related to the inverse association
observed in some studies between low blood Pb and renal function.
A key consideration in the Pb NAAQS review concerns the relationship between air Pb
concentrations and blood Pb levels, most particularly those in young children. Our
quantitative estimation of blood Pb levels in response to various exposure circumstances,
including air-related exposure pathways associated with current ambient air Pb
concentrations, would benefit from research into this relationship.
- Information is limited with regard to the temporal aspects of the relationship
between ambient air Pb and levels of air-related Pb in blood in young children,
and our understanding of the factors influencing this relationship is incomplete,
particularly in the Pb exposure circumstances common in the U.S. today.
- Important aspects of (or influence on) the air-to-blood relationship include the
relationships (1) between ambient air Pb and outdoor dust and surface soil Pb
concentrations and (2) between ambient air Pb and indoor dust Pb. Additional
information would help to reduce uncertainty in our understanding of these
relationships and in models and methods used to characterize these pathways in
future reviews. Specific mechanistic aspects for indoor dust modeling include air
exchange rates, home cleaning frequency and efficiency, among other factors.
The impact of changes in ambient air Pb on Pb in indoor dust, outdoor dust and
soil, including the temporal dynamics of these relationships, and variations for
different environments, are important aspects of the Pb NAAQS review, yet
current information on multiple aspects of these pathways is limited.
- There is appreciable uncertainty regarding the magnitude of the contribution of
air-related Pb to diet. Additional information is needed regarding sources of Pb to
4-37
-------
the diet of different age groups of the U.S. population, including particularly those
sources that relate to current ambient air Pb, as well as those related to the legacy
of historic ambient air Pb emissions.
- Information is lacking on toxicokinetics of Pb during adolescence which could
inform interpretation of epidemiological studies of relationships between blood
Pb and health effects in this lifestage.
• Future quantitative blood Pb modeling would benefit from additional research into
several aspects of population blood Pb levels, including contributing exposure pathways.
Examples include:
- Interindividual variability in blood Pb levels and methods for characterizing
interindividual variability, including consideration of both empirical and
mechanistic methods;
- Apportionment of blood Pb levels with regard to exposure pathway contributions,
with particular focus on understanding exposure pathways and sources that cause
the more elevated blood Pb levels among children today, as well as those related
to ambient air Pb; and
- Blood Pb model performance evaluations, with emphasis on applications
pertaining to blood Pb response to ambient air-related pathways and responses to
changes in exposures for those pathways.
• An understanding of the spatial gradient of ambient air Pb concentrations and associated
particle sizes in urban residential areas, as well as near Pb sources, is an important aspect
to our implementation of the NAAQS for Pb and a key element in assessing exposure and
risk. Additional research in this area is needed. Current limitations in this area
additionally contribute uncertainty to characterization of ambient air Pb levels in the risk
assessment and the resulting exposure and risk estimates. Research in the
characterization of spatial variation in ambient air Pb concentrations in different
environments and related to different air sources would help to reduce this uncertainty.
The potential for systematic trends in the relationship between ambient air Pb
concentrations and distribution of urban residential populations is of interest. Example
locations of interest include neighborhoods downwind of airports with substantial leaded
aviation gasoline usage, as well as those in the vicinity of older roads with a substantial
historical use of leaded gasoline, including inner city neighborhoods (with and without
substantial reconstruction).
• Another area of uncertainty relates to our understanding of concentrations of relatively
larger airborne particles carrying Pb that occur in areas near sources and where exposure
may occur.
4-38
-------
4.5 REFERENCES
Bellinger, D. C. and Needleman, H. L. (2003) Intellectual impairment and blood lead levels [letter]. N. Engl. J. Med.
349: 500.
Canfield, R. L.; Henderson, C. R., Jr.; Cory-Slechta, D. A.; Cox, C.; Jusko, T. A.; Lanphear, B. P. (2003)
Intellectual impairment in children with blood lead concentrations below 10 ug per deciliter. N. Engl. J.
Med. 348: 1517-1526.
Centers for Disease Control and Prevention (2012) CDC Response to Advisory Committee on Childhood Lead
Poisoning Prevention Recommendations in "Low Level Lead Exposure Harms Children: A Renewed Call
of Primary Prevention". Atlanta, GA: U.S. Department of Health and Human Services, Public Health
Service. June 7.
Frey, H.C. (2013) Letter from Dr. H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee and Clean
Air Scientific Advisory Committee Lead Review Panel, to Acting Administrator Bob Perciasepe. Re:
CASAC Review of the EPA's Policy Assessment for Lead (External Review Draft - January 2013). June 4,
2013.
Henderson, R. (2007a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to
Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee's (CASAC) Review of
the 1st Draft Lead Staff Paper and Draft Lead Exposure and Risk Assessments. March 27, 2007.
Henderson, R. (2007b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to
Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee's (CASAC) Review of
the 2nd Draft Lead Human Exposure and Health Risk Assessments. September 27, 2007.
Henderson, R. (2008a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to
Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee's (CASAC) Review of
the Advance Notice of Proposed Rulemaking (ANPR) for the NAAQS for lead. January 22, 2008.
Henderson, R. (2008b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to
Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee's (CASAC) Review of
the Notice of Proposed Rulemaking for the NAAQS for lead. July 18, 2008.
Hilts, S. R. (2003) Effect of smelter emission reductions on children's blood lead levels. Sci. Total Environ. 303: 51-
58.
Lanphear, B. P.; Hornung, R.; Khoury, J.; Yolton, K.; Baghurst, P.; Bellinger, D. C.; Canfield, R. L.; Dietrich, K.
N.; Bornschein, R.; Greene, T.; Rothenberg, S. J.; Needleman, H. L.; Schnaas, L.; Wasserman, G.;
Graziano, J.; Roberts, R. (2005) Low-level environmental lead exposure and children's intellectual
function: an international pooled analysis. Environ. Health Perspect. 113: 894-899.
Tellez-Rojo, M. M.; Bellinger, D. C.; Arroyo-Quiroz, C.; Lamadrid-Figueroa, H.; Mercado-Garcia, A.; Schnaas-
Arrieta, L.; Wright, R. O.; Hernandez-Avila, M.; Hu, H. (2006) Longitudinal associations between blood
lead concentrations < 10 ug/dL and neurobehavioral development in environmentally-exposed children in
Mexico City. Pediatrics 118: e323-e330.
U.S. Environmental Protection Agency. (2006) Air Quality Criteria for Lead. Washington, DC, EPA/600/R-
5/144aF. Available online at: www.epa. gov/ncea/
U.S. Environmental Protection Agency. (2007a) Lead: Human Exposure and Health Risk Assessments for Selected
Case Studies, Volume I. Human Exposure and Health Risk Assessments - Full-Scale and Volume II.
Appendices. Office of Air Quality Planning and Standards, Research Triangle Park, NC. EPA-452/R-07-
014a and EPA-452/R-07-014b.
4-39
-------
U.S. Environmental Protection Agency. (2007b) 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.
U.S. Environmental Protection Agency. (2013) Integrated Science Assessment for Lead. Washington, DC,
EPA/600/R-10/075F. Available online at: http://www.epa.gOv/ttn/naaqs/standards/pb/s pb 2010 isa.html
4-40
-------
5 WELFARE EFFECTS AND EXPOSURE/RISK INFORMATION
This chapter presents key aspects of the current evidence of Pb-related welfare effects
and presents exposure and risk information from the last review in the context of the currently
available information. Staff has drawn from the EPA's synthesis of the scientific evidence
presented in the Integrated Science Assessment for Lead (USEPA, 2013; henceforth referred to
as the ISA) and the 2006 Air Quality Criteria Document for Lead (USEPA, 2006a; henceforth
referred to as the 2006 CD) and from the screening level risk assessment performed in the last
review and described in Lead Human Exposure and Health Risk Assessments and Ecological
Risk Assessment for Selected Areas. Pilot Phase (documented in ICF International, 2006;
henceforth referred to as the 2006 REA). This chapter is organized into two sections regarding
the currently available welfare effects evidence (section 5.1) and the exposure and risk
information (section 5.2) interpreted in light of currently available evidence. Presentation within
these sections is organized to address key policy-relevant questions for this review concerning
the evidence and exposure/risk information, building upon the questions included in the
Integrated Review Plan (IRP, section 3.2).
5.1 WELFARE EFFECTS INFORMATION
Lead has been demonstrated to have harmful effects on reproduction and development,
growth, and survival in many species as described in the assessment of the evidence available in
this review and consistent with the conclusions drawn in the last review (ISA, section 1.7; 2006
CD). A number of studies on ecological effects of Pb are newly available in this review and are
critically assessed in the ISA as part of the full body of evidence. The full body of currently
available evidence reaffirms conclusions on the array of effects recognized for Pb in the last
review (ISA, section 1.7). In so doing, in the context of pollutant exposures considered
relevant,1 the ISA determines2 that causal3 or likely causal4 relationships exist in both freshwater
1 With regard to consideration of pollutant exposures for studies included in the ISA, the ISA states the
following (ISA, pp. Ix-lxi).
In drawing judgments regarding causality for the criteria air pollutants, the ISA focuses on evidence of
effects in the range of relevant pollutant exposures or doses, and not on determination of causality at
any dose. Emphasis is placed on evidence of effects at doses (e.g., blood Pb concentration) or
exposures (e.g., air concentrations) that are relevant to, or somewhat above, those currently
experienced by the population. The extent to which studies of higher concentrations are considered
varies by pollutant and major outcome category, but generally includes those with doses or exposures
in the range of one to two orders of magnitude above current or ambient conditions. Studies that use
higher doses or exposures may also be considered to the extent that they provide useful information to
inform understanding of mode of action, interspecies differences, or factors that may increase risk of
effects for a population. Thus, a causality determination is based on weight of evidence evaluation for
health, ecological or welfare effects, focusing on the evidence from exposures or doses generally
ranging from current levels to one or two orders of magnitude above current levels.
5-1
-------
and terrestrial ecosystems for Pb with effects on reproduction and development in vertebrates
and invertebrates; growth in plants and invertebrates; and survival in vertebrates and
invertebrates (ISA, table 1-3). Although considerable uncertainties are recognized in
generalizing effects observed under particular, small-scale conditions, up to the ecosystem level
of biological organization, the ISA determines that the cumulative evidence reported for Pb
effects at higher levels of biological organization and for the above described population-level
endpoints is sufficient to conclude that a causal relationship is likely to exist between Pb
exposures and community and ecosystem-level effects in freshwater and terrestrial systems (ISA,
section 1.7.3.7). The ISA also presents evidence for saltwater ecosystems, concluding that
current evidence is inadequate to make causality determinations for most population-level
responses, as well as community and ecosystem effects, while finding the evidence to be
suggestive linking Pb and effects on reproduction and development in marine invertebrates (ISA,
Table 1-3, section 6.3.12 and section 6.4.21).
Based on the extensive assessment of the full body of evidence available in this review,
the major conclusions drawn by the ISA regarding ecological effects of Pb include the following
(ISA, Executive Summary, p. xcvi).
With regard to the ecological effects ofPb, uptake ofPb into fauna and
subsequent effects on reproduction, growth and survival are established and are
further supported by more recent evidence. These may lead to effects at the
population, community, and ecosystem level of biological organization. In both
terrestrial and aquatic organisms, gradients in response are observed with
increasing concentration ofPb and some studies report effects within the range of
Pb detected in environmental media over the last several decades. Specifically,
observations from controlled studies on reproduction, growth, and survival in
sensitive freshwater invertebrates are well-characterized at concentrations at or
near Pb concentrations occasionally encountered in U.S. fresh surface waters....
However, in natural environments, modifying factors affect Pb bioavailability and
toxicity and there are considerable uncertainties associated with generalizing
effects observed in controlled studies to effects at higher levels of biological
organization. Furthermore, available studies on community and ecosystem-level
2 Since the last Pb NAAQS review, the ISAs which have replaced CDs in documenting each review of the
scientific evidence (or air quality criteria) employ a systematic framework for weighing the evidence and describing
associated conclusions with regard to causality, using established descriptors ("causal" relationship with relevant
exposure, "likely" to be causal, evidence is "suggestive" of causality, "inadequate" evidence to infer causality, "not
likely") (ISA, Preamble).
3 In determining that a causal relationship exists for Pb with specific ecological effects, EPA has concluded
that "[e]vidence is sufficient to conclude that there is a causal relationship with relevant pollutant exposures (i.e.,
doses or exposures generally within one to two orders of magnitude of current levels)" (ISA, p. Ixii)
4 In determining a likely causal relationship exists for Pb with specific ecological effects, EPA has
concluded that "[e]vidence is sufficient to conclude that there is a likely causal relationship with relevant pollutant
exposures ... important uncertainties remain" (ISA, p. Ixii).
5-2
-------
effects are usually from contaminated areas where Pb concentrations are much
higher than typically encountered in the environment. The contribution of
atmospheric Pb to specific sites is not clear and the connection between air
concentration ofPb and ecosystem exposure continues to be poorly
characterized. Furthermore, the level at which Pb elicits a specific effect is
difficult to establish in terrestrial and aquatic systems, due to the influence of
other environmental variables (e.g., pH, organic matter) on both Pb
bioavailability and toxicity, and also to substantial species differences in Pb
sensitivity.
As in prior reviews of the Pb NAAQS, this review is focused on those effects most
pertinent to ambient air Pb exposures. Given the reductions in ambient air Pb concentrations
over the past decades, these effects are generally those associated with the lowest levels of Pb
exposure that have been evaluated. Additionally, we recognize the limitations on our ability to
draw conclusions about environmental exposures from ecological studies of organism-level
effects, as most studies were conducted in laboratory settings which may not accurately represent
field conditions or the multiple variables that govern exposure.
Our consideration of welfare effects evidence in this review is framed by key policy-
relevant questions drawn from those included in the IRP. In the following sections, we discuss
the pathways by which Pb exposure occurs in ecosystems, the mechanisms that distribute Pb in
the environment and the bioavailability of Pb in different ecosystems. Understanding the
movement of Pb in the environment is important to understanding exposure and bioavailability
and, thus, informs the subsequent discussion of the effects of Pb on terrestrial and aquatic
ecosystems. Finally, we discuss the association of ambient air Pb with effects and the important
role a "critical loads" approach5 might play in assessing the overall ability of ecosystems to
recover from past Pb exposures and the degree to which newly deposited Pb may affect
ecosystem function and recovery.
• To what extent has the newly available evidence altered our understanding of the
movement and accumulation of air-deposited Pb through ecosystems over time?
The extensive history of Pb uses in developed countries coupled with atmospheric
transport processes has left a legacy of Pb in ecosystems globally (e.g., 1977 CD, section 6.3.1).
Records of U.S. atmospheric emissions of Pb in the twentieth and late nineteenth centuries have
been documented in sediment cores, as noted in section 2.3 above (ISA, section 2.6.2; Landers et
5 As discussed further in subsequent text of this section, the phrase "critical loads" is generally used to
describe loading (i.e. addition of a pollutant) to a system that can occur without causing a critical impact, e.g.,
deposition rates of air pollutants that current knowledge indicates will not cause long-term adverse effects to
ecosystem structure and function. A critical loads analysis approach takes into account what is known about the
release of a specific chemical into the environment, its distribution and cycling within and across ecosystems and
each ecosystem's sensitivity to the chemical (ISA, section 6.1.3).
5-3
-------
al., 2010). Once deposited, Pb can be transported by stormwater runoff or resuspension to
catchments and nearby waterbodies or stored in soil layers in forested areas, its further
movement influenced by soil or sediment composition and chemistry and physical processes.
Some new studies are available that provide additional information, briefly summarized below,
on Pb cycling, flux and retention within terrestrial and aquatic systems. This new information
does not fundamentally change our understanding from the last review of Pb movement through
or accumulation in ecosystems over time but rather improves our understanding of some of the
underlying processes and mechanisms in soil, water and sediment. There is little new
information, however, on fate and transport in ecosystems specifically related to air-derived Pb
(ISA, section 2.3). There is limited newly available information with regard to the timing of
ecosystem recovery from historic atmospheric deposition of Pb.
Overall, recent studies in terrestrial ecosystems provide deposition data consistent with
deposition fluxes reported in the 2006 CD, and demonstrate consistently that atmospheric
deposition of Pb has decreased since the phase-out of leaded on-road gasoline, as described in
section 2.3.2.2 above (ISA, section 2.3.3). Follow-up studies in several locations at high
elevation sites indicate little change in soil Pb concentrations since the phase-out of leaded on-
road gasoline in surface soils, consistent with the high retention reportedly associated with
reduced microbial activity at lower temperatures associated with high elevation sites. However,
amounts of Pb in the surface soils at some lower altitude sites were reduced over the same time
period in the same study (ISA, section 2.3.3). New studies in the ISA also enhance our
understanding of Pb sequestration in forest soils by providing additional information on the role
of leaf litter as a Pb reservoir in some situations and the effect of litter decomposition on Pb
distribution (ISA, section 2.3.3).
Recent research on Pb transport in aquatic systems has provided a large body of
observations confirming that such transport is dominated by colloids rich in iron and organic
material (ISA, section 2.3.2). Recent research on Pb flux in sediments provides greater detail on
resuspension processes than was available in the 2006 CD, including research on resuspended Pb
largely associated with organic material or iron and manganese particles and research on the
important role played by anoxic or depleted oxygen environments in Pb cycling in aquatic
systems. This newer research is consistent with prior evidence in indicating that appreciable
resuspension and release from sediments largely occurs during discrete events related to storms.
It has also confirmed that resuspension is an important process that strongly influences the
lifetime of Pb in bodies of water. Finally, there have been advances in understanding and
modeling of Pb partitioning between organic material and sediment in aquatic environments
(ISA, section 2.7.2).
5-4
-------
In summary, the newly available evidence builds on our understanding of some specific
aspects of processes involved in the movement and accumulation of Pb through ecosystems over
time. The new information, however, does not substantially alter our overall understanding of
the fate and transport of Pb in ecosystems or provide a broad quantitative understanding of U.S.
ecosystem responses to atmospheric Pb deposition.
• Does the newly available evidence further inform our understanding of the
bioavailability of Pb in different types of ecosystems and organisms?
As discussed in the ISA, bioavailability of Pb is an important component of
understanding the effects Pb is likely to have on organisms and ecosystems (ISA, section 6.3.3).
It is the amount of Pb that can interact within the organism that leads to toxicity, and there are
many factors which govern this interaction (ISA, sections 6.2.1 and 6.3.3; USEPA, 2007a). The
bioavailability of metals varies widely depending on the physical, chemical, and biological
conditions under which an organism is exposed (USEPA, 2007a). In both aquatic and terrestrial
systems, a primary factor influencing the bioavailability of Pb, as well as its fate and tranport is
solubility (ISA, p. 6-63). Additionally important characteristics that affect bioavailability are
(1) chemical form or species, (2) particle size, (3) lability, and (4) source. The bioavailability of a
metal is also dependent upon the fraction of metal that is bioaccessible. The bioaccessible
fraction of a metal is the portion (fraction or percentage) of environmentally available metal that
actually interacts at the organism's contact surface and is potentially available for absorption or
adsorption by the organism (USEPA, 2007a; ISA, section 6.3.3).
Studies newly available since the last Pb NAAQS review provide additional insight into
factors that influence the bioavailability of Pb to specific organisms (ISA, section 6.3.3). In
general, this evidence, briefly summarized below, is supportive of previous conclusions and does
not identify significant new variables from those identified previously. Section 6.3.3 of the ISA
provides a detailed discussion of bioavailability in terrestrial systems. With regard to aquatic
systems, a detailed discussion of bioavailability in freshwater systems is provided in sections
6.4.3 and 6.4.4 of the ISA, and section 6.4.14 of the ISA discusses bioavailability in saltwater
systems.
In terrestrial systems, the amount of bioavailable Pb present determines the impact of soil
Pb to a much greater extent than does the total amount present (ISA, section 6.3.11). In such
ecosystems, Pb is deposited either directly onto plant surfaces or onto soil where it can bind with
organic matter or dissolve in pore water.6 The Pb dissolved in pore water is particularly
bioavailable to organisms in the soil and thereby influences the impact of soil Pb on terrestrial
ecosystems to a much greater extent than the total amount of Pb present (ISA, section 6.3.11).
6 The term "pore water" refers to the water occupying the spaces among the grains of sediment or soil.
5-5
-------
Several soil characteristics control the amount of Pb that is dissolved in pore water, and the ISA
presents evidence that has advanced scientific understanding of some of these variables (ISA,
section 6.4.21). Studies have shown that the two most important determinants of both Pb
solubility and toxicity in soils are pH and cation exchange capacity (ISA, section 2.6.1). Also,
evidence newly available in this review has confirmed the important influence of organic matter
on Pb sequestration, leading to relatively longer retention in soils with higher organic matter
content (ISA, section 2.6.1). When soils are amended with soluble metals, aging, both under
natural conditions and simulated through leaching, reduces the bioavailability of Pb to plants and
soil organisms (ISA, sections 6.3.2, 6.3.9 and 6.3.11; USEPA, 2007a). In general, soils with
higher organic matter content have the capacity for greater retention of Pb in the soil matrix and
lesser availability of Pb for release into pore water. Reduction in soil organic material, such as
through decomposition, can contribute to subsequent increased availability of Pb (ISA, section
6.3.9; 2006 CD, section 6.1.5).
In aquatic systems as in terrestrial systems, the amount of Pb bioavailable to organisms is
a better predictor of effect on organisms than the overall amount of Pb in the system. Once
atmospherically derived Pb enters surface water bodies through deposition or runoff, its fate and
bioavailability are influenced by many water quality characteristics, such as pH, suspended
solids levels and organic content (ISA, section 6.4.2). In sediments, bioavailability of Pb to
sediment-dwelling organisms may be influenced by the presence of other metals, sulfides, iron
oxides and manganese oxides and also by physical disturbance (ISA, section 2.6.2). For many
aquatic organisms Pb dissolved in the water column can be the primary exposure route, while for
others sediment ingestion is significant (ISA, section 2.6.2). As recognized in the 2006 CD and
further supported in the ISA, there is a body of evidence showing that uptake and elimination of
Pb vary widely among aquatic species.
Although in freshwater systems the presence of humic acid in dissolved organic material
(DOM) is considered to reduce the bioavailable fraction of metals in the water column, there is
evidence presented in the ISA that DOM does not have the same effect on free Pb ion
concentration and toxicity in seawater (ISA, section 6.4.2). For example, the ISA discusses two
new studies, performed in artificial seawater systems, that suggest that in saltwater, the presence
of DOM increases (rather than decreases) uptake of Pb by mussel gill structures, potentially
through the alteration of membrane permeability (ISA, section 6.4.2.4). These studies also
investigated the individual roles of some DOM components. This recent evidence supports the
conclusion from the last review that factors that modify bioavailability of Pb in saltwater
environments are not identical to those in freshwater systems (ISA, section 6.4.14).
The newly available evidence about bioavailability from experimental systems, briefly
summarized above, builds on our fundamental understanding of Pb bioavailability in aquatic and
5-6
-------
terrestrial systems and species from the last review. Bioavailability remains an important
consideration in Pb toxicity and a significant source of uncertainty in relating ambient Pb and
adverse effects.
• Does the current evidence alter our conclusions from the previous review
regarding the ecological effects associated with exposure to Pb? Does the newly
available evidence indicate new exposure levels at which ecological systems or
receptors are expected to experience effects?
There is a substantial amount of new evidence in this review regarding the ecological
effects of Pb on individual terrestrial and aquatic species. On the whole, this evidence supports
previous conclusions that Pb has effects on growth, reproduction and survival, and that under
some conditions these effects can be adverse to organisms and ecosystems. The ISA provides
evidence of effects in additional species, and in a few cases, at lower exposures than reported in
the previous review, but does not substantially alter our understanding of the ecological
endpoints affected by Pb from the previous review. Looking beyond organism-level evidence,
the evidence of adversity in natural systems remains sparse due to the difficulty in determining
the effects of confounding factors such as co-occurring metals or system characteristics that
influence bioavailability of Pb in field studies. The following is a brief comparison of the newly
available evidence to evidence considered in the 2006 review.
Terrestrial Ecosystems
The evidence available in the last review indicated a range of biological effects of Pb on
terrestrial organisms that varied with type of organism and life stage, duration of exposure, form
of Pb, and soil characteristics. New research since the 2006 CD has broadened our
understanding of the evidence of damage to photosynthetic ability in plants exposed to Pb and
provided additional evidence of oxidative stress in response to Pb exposure (ISA, section 6.3.4).
For example, reactive oxygen species have been found to increase in plant tissue grown in Pb-
contaminated soil, and, with increasing Pb exposure, the plant tissue responded with increased
antioxidant activity (ISA, section 6.3.4). In addition, recent studies have reported reduced
growth of plants with increased Pb concentration in soil in some experiments, as well as
evidence of genotoxicity, decreased germination, and pollen sterility (ISA, section 6.3.4).
In terrestrial invertebrates, previous CDs have reported adverse effects of Pb on
neurological and reproductive endpoints. Recently published studies have further explored the
potential for neurotoxic action of Pb, albeit under artificial liquid media conditions (ISA,
section 6.3.4.2). Increased mortality was found in recent studies of earthworms at
concentrations similar to those in studies reviewed previously, with additional evidence
indicating the strong dependence of effects on soil characteristics including pH, cation exchange
capacity, and aging (ISA, section 6.3.4.2). There is also newly available evidence for adverse
5-7
-------
effects in terrestrial snails and arthropods exposed through soil or diet (ISA, section 6.3.4.2).
The effects vary with species and exposure conditions, and they include diminished growth and
fecundity, endocrine and reproductive anomalies, and body deformities. Increasing
concentration of Pb in the exposure medium generally resulted in increased effects within each
study, but the relationship between concentration and effects is highly variable between studies,
even when the same medium, e.g. soil, was used. Current evidence suggests that soil aging and
pH are important modifiers of Pb toxicity in these studies (ISA, section 6.3.11).
In terrestrial vertebrates, some new evidence is available for effects of Pb on amphibians
and reptiles as well as birds.7 Effects reported in reptiles and amphibians include decreased white
blood cell counts, decreased testis weight, and behavioral anomalies (ISA, section 6.3.4.3).
However, depending on various factors, studies report large differences in effects in different
species at the same concentration of Pb in soil, and effects were generally smaller when field-
collected soils were used. In some birds, recent studies have found maternal elevated blood Pb
level to be associated with decreased hatching success, smaller clutch size, high corticosteroid
level, and abnormal behavior in offspring. Studies on some species show little or no effect of
elevated blood Pb level. Effects of dietary exposure have been studied in several mammalian
species, with cognitive, endocrine, immunological, and growth effects observed (ISA, section
6.3.11) in some studies.
Experimental evidence of organism-level effects presented in the ISA demonstrates that
increased exposure to Pb is generally associated with increases in observed effects in terrestrial
species (ISA, section 6.3.11). It also demonstrates that many factors, including the form of Pb
and various soil physiochemical properties, influence the Pb concentration-response relationship
(ISA, section 6.3.11). Further, results from amended soil exposures generally do not reflect the
important effect of environmental aging on bioavailability and associated toxicity of such soil
Pb amendments and therefore make interpretation of the results in an ecosystem context
difficult. Given that in natural settings, these modifying factors are highly variable, the ISA
notes that without quantitatively accounting for these factors, laboratory-derived
"characterizations of exposure-response relationships would likely not be transferable outside of
experimental settings" (ISA, section 1.7.1). Newly available soil invertebrate studies of
multiple Pb concentrations in different soil systems also provide inconsistent results with
respect to exposure-response relationships (ISA, sections 1.7.1 and 6.3.5). In consideration of
these results, the ISA notes that "laboratory-amended artificial soils provide a poor model for
predicting the toxicity of Pb-contaminated field soils, because aging and leaching processes,
7 Elevated blood and tissue concentrations of Pb reported in avian species in some areas have been
indicated to be a result of nonair pathways, including ingestion of lead-containing materials such as paint chips in
urban areas and Pb ammunition fragments in other areas (ISA, sections 6.3.3.3 and 6.3.4.3).
5-8
-------
along with variations in physiochemical proterties ... influence metal bioavailability" (ISA,
section 6.3.5)
As reported in both the ISA and the 2006 CD, direct evidence for community- and
ecosystem-level effects comes from locations near sources of Pb to the environment, where Pb
concentrations are much higher than typically observed environmental concentrations and often
derive from multiple sources to multiple media (e.g. soil, water, air). Impacts of Pb on terrestrial
ecosystems near smelters, mines, and other industrial sources have been studied for several
decades (ISA, section 6.3.12.7). Atmospheric emissions of Pb from smelting and other
industrial activities are commonly accompanied by other trace metals (e.g., Zn, Cu, Cd) and
SO2 that may cause toxic effects independently or in concert with Pb. Those impacts have been
shown to include decreases in species diversity and changes in floral and faunal community
composition in locations with histories of substantial Pb emissions affecting air concentrations
that were likely well in exceedance of the current NAAQS, (e.g., 1977 CD, section 8.8; 1986
CD, section 8.1.1.3; 2006 CD, p. 7-15). Interpretation of ecosystem-level field studies with
regard to ambient Pb levels associated with ecosystem and community effects is complicated by
these confounding factors and the inherent variability in natural systems (ISA, section 6.3.12.7).
Limited new evidence of effects of Pb at the community scale has been reported. This
evidence includes several studies of the ameliorative effects of mycorrhizal fungi on plant
growth with Pb exposure as well as recently published research on soil microbial communities,
which have been shown to be impacted by Pb in both composition and activity (ISA, sections
1.7.1 and 6.3.6). Many recent studies have been conducted using mixtures of metals, which
have attempted to separate the effects of individual metals when possible. In studies that
included only Pb, or where effects of Pb could be separated, soil microbial activity was
generally diminished with increased Pb concentration and was shown in some of those cases to
recover with time (ISA, section 6.3.6). In studies involving heavily contaminated soils from
historic smelters, mining sites, or natural Pb deposits, microbial species and genotype
composition were consistently altered after Pb exposure, and findings indicate that those
alterations were long-lasting or permanent (ISA, section 6.3.6, pg 6-120).
A recent review has examined differences in species sensitivity, using blood Pb level in
birds and mammals as an exposure index rather than external dose (ISA, section 6.3.9.1;
Buekers et al., 2009). In this analysis, variation across organisms was lower with the blood Pb
index compared to use of media concentration, and variation of Pb absorption from the diet of
the organism largely accounted for the variation seen in the blood Pb. The analysis also suggests
a larger variation in sensitivity across avian species tested compared to mammalian species with
regard to the association between blood Pb concentration and toxicity (ISA, section 6.3.9.1).
5-9
-------
Overall, recent studies cited in this review support previous conclusions about the effects
of Pb on terrestrial ecosystems, namely that increasing soil Pb concentrations in areas of Pb
contamination (e.g. mining sites and industrial sites) can cause decreases in microorganism
abundance, diversity, and function. Previous reviews have also reported on effects on bird and
plant communities (2006 CD, section AX7.1.3). The shifts in bacterial species and fungal
diversity have been observed near long-established sources of Pb contamination (ISA, section
6.3.12.7). Most recent evidence for Pb toxicity to terrestrial plants, invertebrates and vertebrates
is from single-species assays in laboratory studies which do not capture the complexity of
bioavailability and other modifiers of effect in natural systems (ISA, section 6.3.12.7). Further,
models that might account for modifiers of bioavailability have proven difficult to develop
(ISA, p. 6-16).
Freshwater Ecosystems
Studies newly available in this review address trophic transfer of Pb in freshwater
ecosystems (ISA, section 6.4.4.4). Evidence summarized in the 2006 CD indicated that
measured concentrations of Pb in the tissues of aquatic organisms were generally higher in
algae and benthic organisms than in higher trophic-level consumers, indicating that Pb was
bioconcentrated but not biomagnified (ISA, section 1.7.2). Some recent studies indicate transfer
of Pb in aquatic food webs; while other recent studies that have traced Pb in freshwater aquatic
food webs have found, similar to the 2006 CD findings, that Pb concentration decreases with
increasing trophic level (biodilution) (ISA, sections 1.7.2 and 6.4.4.4).
Evidence presented in the ISA further supports the findings of past CDs that Pb in
freshwater can be highly toxic to aquatic organisms, with toxicity varying with species and life
stage, duration of exposure, form of Pb, and water quality characteristics. The 2006 CD
identified evidence of adverse growth effects on several species of freshwater algae from Pb
exposure (2006 CD, Section 7.2.4). The ISA describes several new studies which expand the
list of algal species for which these adverse effects have been identified (ISA, section 6.4.5.1).
For vascular plants, the ISA describes additional evidence that oxidative damage, decreased
photosynthesis and reduced growth occur with elevated Pb exposure (ISA, section 6.4.5.2).
Since the 2006 CD, there is some additional evidence for Pb effects on cellular processes
in aquatic invertebrates. Recent studies of reproductive and developmental effects of Pb
augment similar findings in the 2006 CD and add additional species information on
reproductive endpoints for rotifers and freshwater snails as well as multigenerational effects of
Pb in mosquito larvae (ISA, section 6.4.5.2). In the 2006 CD, study concentrations cited at
which effects were observed in various aquatic invertebrates reflected an expansive range from
5ug/L (for acute toxicity to Pb nitrate in a test system at a hardness of 18 mg/L calcium
carbonate) to greater than 8000 |ig/L (for acute toxicity to Pb chloride at a hardness of 280-300
5-10
-------
mg/L calcium carbonate) (ISA, p. 1-45; 2006 CD, Table AX7-2.4.1). Recent studies cited in the
ISA provide additional evidence of effects from chronic exposures. These findings are
generally consistent with those of the previous review and reflect the variability of Pb toxicity
under different environmental conditions and in species with varying sensitivity.
Evidence of effects in aquatic vertebrates presented in the ISA reiterates the findings of
reproductive, behavioral, and growth effects stated in previous CDs. Some additional
mechanisms of Pb toxicity in the gill and the renal system offish have been elucidated since the
2006 CD as well as the identification of potential new molecular targets for Pb neurotoxicity
(ISA, section 1.7.2).
As in terrestrial organisms, evidence presented in the ISA and prior CDs demonstrates the
toxicity of Pb in aquatic ecosystems and the role of many factors, including Pb speciation and
various water chemistry properties, in modifying toxicity (ISA, section 1.7.2). Since the 2006
CD, additional evidence for community and ecosystem level effects of Pb is available, primarily
in microcosm studies or field studies with other metals present (ISA, section 6.4.11). Such
evidence described in previous CDs includes alteration of predator-prey dynamics, species
richness, species composition, and biodiversity. New studies available in this review provide
evidence in additional habitats for these community and ecological-scale effects, specifically in
aquatic plant communities and sediment-associated communities at both acute and chronic
exposures involving concentrations similar to those previously reported (ISA, section 6.4.7). In
many cases it is difficult to characterize the nature and magnitude of effects and to quantify
relationships between ambient concentrations of Pb and ecosystem response due to existence of
multiple ecosystem-level stressors, variability in field conditions, and differences in Pb
bioavailability (ISA, sections 1.7.3.7 and 6.4.7). Additionally, the degree to which air
concentrations have contributed to such effects in freshwater ecosystems is largely unknown.
Saltwater Ecosystems
As assessed in the ISA, the evidence for saltwater species and ecosystems is generally
inadequate to draw conclusions regarding the effect of Pb (ISA, Tables 1-3 and II). The extent
of newly available evidence in the context of prior available evidence is summarized here.
With regard to evidence in marine plants, recently available evidence on the toxicity of
Pb to marine algae augments the 2006 CD findings of variation in sensitivity across marine
species. Recent studies on Pb exposure include reports of growth inhibition and oxidative stress
in a few additional species of marine algae (ISA, section 6.4.15).
Recent literature provides little new evidence of endpoints or effects in marine
invertebrates beyond those reported in the 2006 CD. For example, some recent studies
strengthen the evidence of Pb effects on enzymes and antioxidant activity in marine
invertebrates and have identified an additional behavioral endpoint (i.e., valve closing speed in
5-11
-------
juveniles of a marine scallop affected by 20 days exposure to 40-400 jig/L Pb nitrate) from
those discussed previously (ISA, section 6.4.15.2). Also, as noted in the 2006 CD and supported
by new studies reviewed in the ISA, Pb exposure negatively affects the growth of marine
invertebrates (ISA, section 6.4.15.2). Recent studies also identify several species exhibiting
particularly low sensitivity to high acute exposures (ISA, section 6.4.15.2).
Little new evidence is available of Pb effects on marine fish and mammals for
reproductive, growth and survival endpoints that are particularly relevant to the population level
of biological organization and higher (ISA, section 6.4.15). Evidence for effects at higher levels
of biological organization in saltwater habitats is primarily supported by observations in a small
number of microcosm and field studies where shifts in nematode community structure are the
most commonly observed effects of Pb in experimentally contaminated sediments (ISA,
sections 6.4.17 and Table 6-6). These types of studies were presented in the 2006 CD, and
while there are new studies presented in the ISA, they primarily expand the types of
communities (seagrass and amphipods) for which data exist but reach similar conclusions about
community structure as the 2006 CD. However, there is no evidence of adverse effects in
saltwater environments associated with current ambient air Pb concentrations, and linkages
between any level of ambient air deposition and effects are unknown in all but a few organisms.
New studies on organism-level effects from Pb in saltwater ecosystems (ISA, section
6.4.15) provide little evidence to inform our understanding of linkages between atmospheric
concentrations, ambient exposures in saltwater systems and such effects or our conclusions
regarding the likelihood of adverse effects under conditions associated with the current NAAQS
for Pb. Nor does the currently available evidence indicate significantly different exposure
levels from the previous review at which ecological systems or receptors are expected to
experience effects.
• To what extent is there new information that informs our understanding of
critical loads of Pb, including critical loads in sensitive ecosystems?
Critical loads analyses are a method that facilitates the assessment of ecosystem impacts
as a result of pollutant loading which may arise from multiple pathways. A critical loads
analysis approach can take into account what is known about the release of a specific chemical
into the environment, its distribution and cycling within (and, as appropriate, across) ecosystems
and each ecosystem's sensitivity to the chemical (ISA, section 6.1.3). Thus, this approach
provides a conceptual framework for linking atmospheric deposition to environmental media
concentration target values related to ecological endpoints associated with impairment (termed
"critical limits"). Given the potential relevance to consideration of the secondary NAAQS for
Pb, research in this area has been assessed in the current ISA and the 2006 CD.
5-12
-------
The following generally accepted definition for a critical load of atmospheric pollutant
deposition was developed from a pair of international workshops in the late 1980s (USEPA,
2008).
A quantitative estimate of an exposure to one or more pollutants below which
significant harmful effects on specified sensitive elements of the environment do
not occur according to present knowledge.
As critical loads estimates reflect the current state of knowledge and policy priorities, as
well as scientific and science policy judgments pertaining to the context for their use, there is no
single "definitive" critical load for a natural resource. The state of scientific knowledge in this
area can change in reflection of new information in various areas including, for example, new
information about dose-response relationships; more comprehensive and detailed
characterization of ecosystem resources (e.g., improved maps, inventories and survey datasets);
more detailed information on pollutant concentrations (e.g., continuing time-series monitoring);
and improved numerical models of pollutant fate and transport and ecosystem response. Science
policy judgments reflect their context (e.g., goal for protection) as well as the state of scientific
knowledge and consideration of its attendant strengths, limitations and uncertainties.
Additionally inherent in critical loads analyses, due to their predictive nature, are a variety of
assumptions, which may be relatively more or less numerous depending on the extent of
knowledge on environmental processes for a particular application.
Some of the earliest uses of critical loads analyses date to consideration of the evidence
for air pollutant deposition impacts on acidification of sensitive lake systems (2006 CD, section
7.3.2). Accordingly, the integrated science assessment of the evidence for the air pollutants
nitrogen oxides (NOx) and sulfur oxides (SOx) described in detail the critical loads concept and
the substantial evidence base pertaining to its application in consideration of acidification and
eutrophication of aquatic ecosystems (USEPA, 2008). In this case, the substantial evidence of
these ecosystem effects and the role of NOx/SOx atmospheric deposition was assessed (USEPA,
2008), and multiple alternative biological indicators, critical biological responses, chemical
indicators, and critical chemical limits were presented that could be used to determine
appropriate critical loads for aquatic and terrestrial ecosystems with regard to acidification and
eutrophi cation (e.g., USEPA, 2008, Table 3-1, sections 3.2 and 3.3 and Annexes B, C and D).
A comparable evidence base does not exist with regard to impacts of air deposition of Pb
on ecosystems. Nonetheless, the potential exists for critical loads to be an especially powerful
tool allowing us to assess Pb atmospheric input into an ecosystem (e.g., deposition) and the
potential ecological impairment resulting from that input. Critical load analyses are dependent on
data relating pollutant release into an ecosystem (or multiple connected systems) from various
sources with an understanding of the ecosystem concentrations likely to result in significant
5-13
-------
harmful effects. In the context of Pb, a persistent, naturally occurring material, the
bioavailability and mobility are influenced by multiple ecosystem characteristics; the data types
for such analysis are numerous and may include information in the following areas:
• Pathways and rates by which Pb is released into ecosystems;
• Current Pb presence within and among ecosystems,8 including spatial distribution,
bioavailability and mobility;
• Fate and transport processes, within and among ecosystem components, as well as
associated rates and factors influencing them;
• Forms and concentrations of Pb in ecosystem exposure media that likely result in
critical ecosystem effects (e.g., concentrations that might relate to critical limits).
Additional information pertaining to the consideration of critical loads analyses in the
context of ambient air standard setting for Pb includes factors that influence the transport and
spatial pattern of deposition of airborne Pb, such as particle size (ISA, section 2.3.1).
During the last review, the 2006 CD assessed the available information on critical loads
for Pb (2006 CD, section 7.3). This information included publications on methods and example
applications, primarily in Europe, specific to the bedrock geology, soil types, vegetation, and
historical deposition trends in each European country (2006 CD, p. E-24), with no analyses
available for U.S. locations (2006 CD, sections 7.3.4-7.3.6).9 As a result, the 2006 CD
concluded that "[Considerable research is necessary before critical load estimates can be
formulated for ecosystems extant in the United States" (2006 CD, p. E-24). More generally, the
2006 CD identified the largest sources of uncertainty to include: derivation of the critical limit,
Pb speciation, and soil runoff as an input to aquatic ecosystems (2006 CD, p. 7-45). Overarching
conclusions reached included the following (2006 CD, p. 7-46).
... At this time, the methods and models commonly used for the calculation of
critical loads have not been validated for Pb. Many of the methods neglect the
speciation ofPb when estimating critical limits, the uptake ofPb into plants, and
out flux ofPb in drainage water, limiting the utility of current models. Future
efforts should focus on fully incorporating the role ofPb speciation into critical
load models, and validating the assumptions used by the models.
8 In the case of Pb, in addition to the role of current air-related pathways, its presence in the ecosystem
results from larger historical air emissions as well as contributions from nonair pathways which may be appreciable
in some areas (e.g., industrial discharges to surface waters, contaminated waste disposal, drainage from metals
mining sites, Pb ammunition near outdoor shooting areas).
9 The work in Europe is largely responsive to developments, beginning in the late 1980s, associated with
the consideration of the critical-load concept for a range of air pollutants in future international agreements limiting
air pollutant emissions (2006 CD, section 7.3.2). A key impetus for such international cooperation efforts was
research in the 1960s and 1970s indicating the role of long-range trans-boundary transport on ecosystems (e.g.,
sulfur emissions on the European continent contributing to acidification of Scandinavian lakes). Since about 1990,
research has been exploring the use of critical loads in Europe for other air pollutants, including metals (2006 CD,
section 7.3.2).
5-14
-------
Accordingly, the quantitative assessment for the last Pb NAAQS review (ICF, 2006) did not
involve critical load analyses.
Newly available evidence pertaining to critical loads analysis in this review includes
limited recent research on consideration of bioavailability in characterizing Pb effect
concentrations or indices and on modeling approaches to incorporate chemistry effects on Pb
speciation and bioavailability (ISA, sections 6.3.7 and 6.4.8). With consideration of this
information and the four critical load analysis studies newly available in this review (none of
which are for U.S. ecosystems), the ISA does not modify the conclusions noted above from the
2006 CD (ISA, sections 6.1.3, 6.3.7 and 6.4.8). In summary, the new information in this review
does not appreciably change our evidence base or further inform our understanding of critical
loads of Pb, including critical loads in sensitive ecosystems.
• To what extent is there information that improves our understanding of the
portion of environmental Pb derived from ambient air and the associated effects
on sensitive ecosystems?
There is no new evidence since the last review that substantially improves our
understanding of the relationship between ambient air Pb and measurable ecological effects. As
stated in the last review, the role of ambient air Pb in contributing to ecosystem Pb has been
declining over the past several decades. It remains difficult to apportion exposure between air
and other sources to better inform our understanding of the potential for ecosystem effects that
might be associated with air emissions. As noted in the ISA, "[t]he amount of Pb in ecosystems
is a result of a number of inputs and it is not currently possible to determine the contribution of
atmospherically-derived Pb from total Pb in terrestrial, freshwater or saltwater systems" (ISA,
section 6.5). Further, considerable uncertainties also remain in drawing conclusions from
evidence of effects observed under laboratory conditions with regard to effects expected at the
ecosystem level in the environment. In many cases it is difficult to characterize the nature and
magnitude of effects and to quantify relationships between ambient concentrations of Pb and
ecosystem response due to the existence of multiple stressors, variability in field conditions, and
differences in Pb bioavailability at that level of organization (ISA, section 6.5). In summary, the
ISA concludes that "[rjecent information available since the 2006 Pb AQCD, includes additional
field studies in both terrestrial and aquatic ecosystems, but the connection between air
concentration and ecosystem exposure continues to be poorly characterized for Pb and the
contribution of atmospheric Pb to specific sites is not clear" (ISA, section 6.5).
5-15
-------
5.2 EXPOSURE AND RISK INFORMATION
The risk information available for this review and described here is based primarily on
the pilot ecological risk assessment developed in the last review of the Pb NAAQS (henceforth
referred to as the 2006 REA [ICF, 2006]). This information is described within the context of
the evidence presented in the ISA that is newly available for this review. As described in the
IRP, careful consideration of newly available information in this review led us to conclude that
developing a new REA for this review was not warranted. In light of critical limitations and
uncertainties that are still unresolved in the current evidence, staff concluded that currently
available information does not provide the basis for developing a new quantitative risk and
exposure assessment with substantially improved utility for informing the Agency's
consideration of welfare effects and evaluation of the adequacy of the current secondary standard
or alternatives (REA Planning Document, section 3.3). More specificallly, we also indicated our
conclusion that the information newly available in this review did not provide the means by
which to develop an updated or enhanced risk model that would substantially improve the utility
of risk estimates in informing the current Pb NAAQS review (REA Planning Document, section
3.3). Based on their consideration of the REA Planning Document, the CASAC Pb Review
Panel generally concurred with the conclusion that a new REA was not warranted in this review
(Frey, 2011; Frey, 2013). Accordingly, the information described here is drawn primarily from
the 2006 REA.
The focus for the risk assessment and associated estimates presented here is on Pb
derived from sources emitting Pb to ambient air. While there is some new evidence that
improves our understanding of some of the environmental variability affecting the disposition
and toxicity of Pb in the environment, the information and methods to support a quantitative
assessment of the role of atmospheric Pb in the U.S are limited. Specific constraints include the
limited availability of location-specific data describing a range of U.S. ecosystems and their
pertinent environmental characteristics as well as a more complete understanding of
bioavailability and its modifiers and data and methods to inform the apportionment of Pb
allowed by the current standard and of lead-related effects between air and non air sources.
These data gaps and areas of uncertainty in the current evidence restrict our ability to assess
quantitatively the relationship between concentrations of Pb in ambient air and terrestrial and/or
aquatic systems, and their effect on welfare.
As discussed in section 1.3 above, the multimedia and persistent nature of Pb, the role of
multiple exposure pathways (illustrated in Figure 1-1 above), and the contributions of nonair
sources of Pb to exposure media all present challenges and contribute significant additional
complexity to the ecological risk assessment that goes far beyond the situation for similar
assessments typically performed for other NAAQS pollutants (e.g., that focus only on a single
5-16
-------
media pathway or for which air is the only significant source). Limitations in the available data
and models affected our characterization of the various complexities associated with exposure to
ambient air Pb. As a result, the 2006 assessment was conducted as a pilot study with a number
of simplifying assumptions with regard to the representativeness of the case studies for
ecological exposures and our ability to isolate case studies where air-derived Pb was the only or
most significant source. Therefore, this section presents a brief summary of the screening-level
ecological risk assessment conducted in 2006 for the Pb NAAQS review completed in 2008 and
addresses several questions relating to the current evidence and understanding that may inform
our view of the results of that assessment. The discussion here also takes into consideration
CAS AC recommendations in the last review with regard to interpretation of the screening-level
assessment (Henderson, 2007a, b), as well as comments received from the CASAC Pb Panel in
the current review, as part of the consultation on the REA Planning Document (Frey, 2011).
5.2.1 Screening Assessment from Last Review
The screening-level risk assessment performed for the last review was focused on
estimating the potential for ecological risks associated with ecosystem exposures to Pb emitted
into ambient air (2006 REA, section 7). A national-scale screen was used to evaluate surface
water and sediment monitoring locations across the United States for the potential for ecological
impacts that might be associated with atmospheric deposition of Pb (described in detail in 2006
REA, section 7.1.2). In addition to the national-scale screen (2006 REA, section 3.6), the
assessment involved a case study approach, with case studies for areas surrounding a primary Pb
smelter (2006 REA, section 3.1) and a secondary Pb smelter (2006 REA, section 3.2), as well as
a location near a non-urban roadway (2006 REA, section 3.4). An additional case study, focused
on consideration of atmospherically derived Pb effects on an ecologically vulnerable ecosystem
(Hubbard Brook Experimental Forest), was identified (2006 REA, section 3.5). The Hubbard
Brook Experimental Forest (FffiEF), in the White Mountain National Forest, near North
Woodstock, New Hampshire, was selected as a fourth case study because of its location and its
long record of available data on concentration trends of Pb in three media (air or deposition from
air, soil, and surface water). While no quantitative analyses were performed, summary review of
the literature search was included in the assessment report (2006 REA, Appendix E). For the
other three case studies, exposure concentrations of Pb in soil, surface water, and/or sediment
concentrations were estimated from available monitoring data or modeling analysis and then
compared to ecological screening benchmarks (2006 REA, section 7.1).
All three case studies and the national-scale assessment generally considered then-current
or recent environmental conditions. In all cases but the primary Pb smelter case study, current
air quality conditions were below the then-current NAAQS. Air Pb concentrations in the
5-17
-------
primary Pb smelter case study exceeded the then-current NAAQS. A complete discussion of air
quality in each of the case studies can be found in section 4 of the 2006 REA.
An overview of the approach developed to implement the selected elements of the
conceptual model for the ecological risk assessment is provided in Figure 5-1. This figure shows
the key types of information and models involved in each part of the assessment and how they
are related to each other and to the other parts of the analysis. Appendix 5 A gives the locations
and spatial resolution for each of the case studies and the national scale screen while
summarizing the source of the screening values used or each location and media type. As
indicated in Figure 5-1 and Appendix 5A, the specific approach for each case study differed
based on the nature of the case study (e.g., type of source, locations of populations) and the site-
specific measurements available.
5-18
-------
Exposure Assessment: Estimating Media Concentrations
National-Scale
Secondary Pb Surface Water &
Smelter Case Study Sediment Screening
Assessment
Primary Pb
Smelter
Case Study
Near Roadway
N on-urban
Case Study
Ecological
Effects
Assessment
Site-specific soil,
surface water, and
sediment
monitoring data
Stack and fugitive
emissions
estimates
Air dispersion
model
Pb deposition rates
across study area
Soil
mixing
model
Outdoor soil
concentrations
Water column
concentrations
Sediment
concentrations
Risk
Chara cter izatio n
Media-specific Hazard Quotients
Figure 5-1. Analytical approach for screening-level ecological risk assessment in the last
review (2006 REA, Exhibit 2-6).
5-19
-------
To estimate the potential for ecological risk, modified ecological soil screening levels
(Eco-SSLs) derived from those developed by EPA's Superfund program (USEPA, 2005a,b),
EPA's recommended ambient water quality criteria (2006 REA, section 7.1) and sediment
screening values developed by MacDonald and others (2000, 2003) were used, as described in
detail in section 7.1.3 of the 2006 REA. A hazard quotient (HQ) was calculated for adverse
effects on the survival, growth, and reproduction of exposed ecological receptors to determine
the potential for risk to that receptor. Ecological receptors used in the pilot are discussed in detail
in section 7.1 of the 2006 REA. The HQ was calculated as the ratio of the media concentration to
the ecotoxicity screening value. In each case study, HQ values were calculated for each location
where either modeled or measured media concentrations were available. Separate soil HQ
values were calculated for each ecological receptor group for which an ecotoxicity screening
value has been developed (i.e., birds, mammals, soil invertebrates, and plants), as described in
detail in section 7.1.2 of the 2006 REA. HQ values less than or equal to 1.0 were concluded to
suggest that Pb concentrations in a specific medium were unlikely to pose significant risks to
ecological receptors, while HQ values greater than 1.0 indicated a potential for adverse effects.
5.2.2 Screening Assessment Results and Interpretation
The results for the ecological screening assessment for the three case studies and the
national-scale screen for surface water and for sediment indicated a potential for adverse effect
from ambient Pb to multiple ecological receptor groups in terrestrial and aquatic locations.10
Below are descriptions of the location-specific case studies and the national screening
assessment, key findings of the risk assessment for each, and an interpretation of the results with
regard to past air conditions as well as the current standard (USEPA, 2007b).
• What do the key findings of the 2006 screening-level assessment indicate
regarding the likelihood that adverse welfare effects would result from levels of
air-related Pb that would meet the current standard?
In addressing this question, the findings of the 2006 REA are summarized below.
Primary Pb Smelter Case Study
• The primary Pb smelter case study location is at one of the largest and longest-
operating primary Pb smelters in the world (since 1892), the only one currently
operating in the U. S. (ICF, 2006).u
• Concentrations of total Pb in several of the soil and sediment locations within the case
study were measured in 2000 and exceeded screening values, indicating a potential for
adverse effects to terrestrial and sediment-dwelling organisms.
10 It is important to note that the screening values available and used in the assessment lacked adjustment
for some critical measures of bioavailability. See uncertainty discussion below.
11 As noted in section 2.1.2 above, this smelter ceased smelting operations at this facility at the end of 2013.
5-20
-------
• While the contribution to these Pb concentrations from air as compared to nonair
sources is not quantified, air emissions from this facility are substantial (ICF, 2006). In
addition, this facility that has been emitting Pb for many decades, including some
seven decades prior to establishment of any Pb NAAQS, such that it is likely air
concentrations associated with the facility were substantial relative to the 1978
NAAQS, which it exceeded at the time of the last review. At the time of the previous
review (2006) and also since the adoption of the current standard, concentrations
monitored near this facility exceeded the level of the applicable NAAQS (USEPA
2007b, Appendix 5 A and Appendix 2D of this document). Accordingly, this case
study is not informative for considering the likelihood of adverse welfare effects
related to Pb from air sources under air quality conditions associated with meeting the
current Pb standard.
Secondary Pb Smelter Case Study
• The secondary Pb smelter location falls within the Alabama Coastal Plain in Pike
County, Alabama, in an area of disturbed forests. The industrial facility in this case
study is much younger than the primary Pb smelter, becoming active less than ten years
prior to the establishment of the 1978 Pb standard.
• Estimates of total Pb concentration in soils (based on fate and transport modeling using
1997-2000 emissions data and data for similar locations measured in a 1995 study)
exceeded screening values for plants, birds and mammals, indicating the potential for
adverse effects to these groups.
• While the contributions from air-related Pb to the total Pb concentrations modeled in
soils at this location are unclear, the facility continues to emit Pb, and the county where
this facility is located does not meet the current Pb standard (Appendix 2D and 5A).
Given the exceedances of the current standard, which likely extend back over 4 to 5
decades, this case study also is not informative for considering the likelihood of
adverse welfare effects related to Pb from air sources under air quality conditions
associated with meeting the current Pb standard.
Near-Roadway Non-urban Case Study
• This case study comprises two non-urban sites adjacent to established highways for
which soil Pb data were available: (1) in Corpus Christi, Texas (ICF, 2006), and (2) in
Atlee, Virginia (ICF, 2006). Measured soil concentration data were used to develop
estimates of Pb in soils for each location.
• Estimates of total Pb concentrations taken in 1994 and 1998 in soils in this case study
exceeded screening values for plants, birds and mammals, indicating the potential for
adverse effect to these groups.
These case study locations are highly impacted by past deposition of gasoline Pb. It is
unknown whether current conditions at these sites exceed the current Pb standard, but
given evidence from the past of Pb concentrations near highways that ranged above the
previous (1978) Pb standard (1986 CD, section 7.2.1), conditions at these locations
during the time of leaded gasoline very likely exceeded the current standard. Similarly,
those conditions likely resulted in Pb deposition associated with leaded gasoline that
exceeds that being deposited under air quality conditions that would meet the current
5-21
-------
Pb standard. Given this legacy, consideration of the potential for environmental risks
from levels of air-related Pb associated with meeting the current Pb standard in these
locations is highly uncertain.
Vulnerable Ecosystem Case Study
• This case study was focused on consideration of information available for the Hubbard
Brook Experimental Forest (HBEF) in the White Mountain National Forest near North
Woodstock, New Hampshire, which included a long record (from 1976 through 2000)
of available data on concentration trends of Pb in three media (air or deposition from
air, soil, and surface water).
• While no quantitative analyses were performed, a summary review of literature
published on FffiEF was developed. This literature indicated: (1) atmospheric Pb
inputs do not directly affect stream Pb levels at HBEF because deposited Pb is almost
entirely retained in the soil profile; and (2) soil horizon analysis results showed Pb to
have become more concentrated at lower soil depths over time, with the soil serving as
a Pb sink, appreciably reducing Pb in pore water as it moves through the soil layers to
streams (dissolved Pb concentrations were reduced from 5 |ig/L to about 5 ng/L from
surface soil to streams). Further, the available studies concluded insignificant
contribution of dissolved Pb from soils to streams (ICF, 2006, Appendix E). It is
unlikely that conditions have changed from the previous conclusions made based on
soil data through 2000, and, therefore, current ambient air concentrations likely do not
directly impact stream Pb levels under air quality conditions associated with meeting
the current standard.
National-scale Surface Water and Sediment Screen
• The national-scale screen was performed using a national database of surface water and
sediment monitoring data (see Appendix 5A; ICF, 2006).
- The screen identified 15 non-mining sites at which at least one surface water
dissolved Pb concentration taken between 1994 and 2004 exceeded the chronic
screening value, indicating a potential for adverse effect if concentrations were
persistent over long time periods. The acute screening value was not exceeded
at any of these locations.
- Analysis of the sediment concentrations for the 15 sites taken from 1991 to
2000 analyzed in the surface water screen identified a subset for which
concentrations exceeded the screening value, indicating a potential for adverse
effects to sediment dwelling organisms.
• The extent to which past air emissions of Pb have contributed to surface water or
sediment Pb concentrations at the locations identified in the screen is unclear. For
some of the surface water locations, nonair sources likely contributed significantly to
the surface water Pb concentrations. For other locations, a lack of nearby nonair
sources indicated a potential role for air sources to contribute to observed surface water
Pb concentrations. Additionally, these concentrations may have been influenced by Pb
in resuspended sediments and may reflect contribution of Pb from erosion of soils with
Pb derived from historic as well as current air emissions.
5-22
-------
There are multiple sources of uncertainty associated with different aspects of this
assessment (discussed in detail in 2006 REA, section 7.4). For example, there are significant
limitations and uncertainties associated with conclusions that can be drawn from the primary Pb
smelter case study regarding the impact of atmospheric deposition under conditions associated
with meeting the Pb NAAQS (past or present). Additionally, while case study locations were
chosen with the objective of including locations for which recent Pb data were available and for
which Pb exposures might be influenced by air-related Pb and not be dominated by nonair
sources, there is significant uncertainty regarding the extent to which nonair sources and
conditions associated with historic emissions (e.g., prior to establishment of past or present Pb
NAAQS) have likely contributed to the Pb exposure estimates in some locations. The screening
values available and used in the assessment (e.g., ambient water quality criteria, Eco-SSLs,
sediment criteria) lacked adjustment for some critical measures of bioavailability and were
sources of uncertainty with regard to potential for ecological risk. There is also uncertainty
regarding the extent to which the screening values could identify potential hazards of Pb for
some threatened or endangered species or unusually sensitive aquatic ecosystems (ICF 2006).
Thus, while the assessment results are generally consistent with evidence-based observations of
the potential influence of Pb on ecological systems, they are limited with regard to quantitative
conclusions and potential hazard or risk associated with the Pb NAAQS, most particularly with
regard to the current standard. The Hubbard Brook case study represents the most applicable
case study for current conditions, and based on the previous analysis undertaken in the last
review, current ambient air concentrations likely do not directly impact stream Pb levels under
air quality conditions associated with meeting the current standard. With data limitations and the
difficulties in apportioning Pb in ecosystems, there are no additional known locations in the U.S.
that would likely provide additional insight into the effects of ambient Pb under the current
standard, therefore no additional case study analyses were undertaken in this review.
• What are the important uncertainties associated with interpreting the prior
assessment in light of newly available evidence in this review?
In interpreting the results from the 2006 REA, we consider newly available evidence that
may inform our interpretation of risk under the current standard. Factors necessary to alter our
interpretation of risk would include new evidence of harm at lower concentrations of Pb, new
linkages that enable us to draw more explicit conclusions as to the air contribution of
environmental exposures, and/or new methods of interpreting confounding factors that were
largely uncontrolled in the previous risk assessment. In general, however, the key uncertainties
identified in the last review remain today, as described below.
With regard to new evidence of harm at lower concentrations, it is necessary to consider
that the evidence of adversity due specifically to Pb in natural systems is limited, in no small part
5-23
-------
because of the difficulty in determining the effects of confounding factors such as multiple
metals and modifying factors influencing bioavailability in field studies. Modeling of Pb-related
exposure and risk to ecological receptors is subject to a wide array of sources of both variability
and uncertainty. Variability is associated with geographic location, habitat types, physical and
chemical characteristics of soils and water that influence Pb bioavailability, terrestrial and
aquatic community composition. Furthermore Pb uptake rates by invertebrates, fish, and plants
may vary by species and season. For wildlife, variability also is associated with food ingestion
rates by species and season, prey selection, and locations of home ranges for foraging relative to
the Pb contamination levels (USEPA, 2005b).
There are significant difficulties in quantifying the role of air emissions under the current
standard, which is significantly lower than the previous standard. As recognized in section 1.3.2
above, Pb deposited before the standard was enacted remains in soils and sediments,
complicating interpretations regarding the impact of the current standard; historic Pb emitted
from leaded gasoline usage continues to move slowly through systems along with more recently
deposited Pb and Pb derived from non air sources. The results from the location-specific case
studies and the surface and sediment screen performed in the last review are difficult to interpret
in light of the current standard and are not largely useful in informing our judgments of the
potential for adverse effects at levels of deposition meeting the current standard. Under such
constraints it is difficult to assess the merit of the risk findings from the previous review.
5-24
-------
5.3 REFERENCES
Buekers, J; Redeker, ES; Smolders, E. (2009). Lead toxicity to wildlife: Derivation of a critical blood concentration
for wildlife monitoring based on literature data [Review]. Sci Total Environ 407: 3431-3438.
http://dx.doi.0rg/10.1016/j.scitotenv.2009.01.044
Frey, H.C. (2011) Letter from Dr. H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee Lead
Review Panel, to Administrator Lisa P. Jackson. Re: Consultation on EPA's Review of the National
Ambient Air Quality Standards for Lead: Risk and Exposure Assessment Planning Document. October 14,
2011.
Frey, H.C. (2013) Letter from Dr. H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee Lead
Review Panel, to Acting Administrator Bob Perciasepe. Re: Review of EPA's Policy Assessment for the
Review of the National Ambient Air Quality Standards for Lead. June 4, 2013.
Henderson, R. (2007a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to
Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee's (CASAC) Review of
the 1st Draft Lead Staff Paper and Draft Lead Exposure and Risk Assessments. March 27, 2007.
Henderson, R. (2007b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to
Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee's (CASAC) Review of
the 2nd Draft Lead Human Exposure and Health Risk Assessments. September 27, 2007.
ICF International. (2006) Lead Human Exposure and Health Risk Assessments and Ecological Risk Assessment for
Selected Areas. Pilot Phase. Draft Technical Report. Prepared for the U.S. EPA's Office of Air Quality
Planning and Standards, Research Triangle Park, NC. December.
Landers, DH; Simonich, SM; Jaffe, D; Geiser, L; Campbell, DH; Schwindt, A; Schreck, C; Kent, M; Hafner, W;
Taylor, HE; Hageman, K; Usenko, S; Ackerman, L; Schrlau, J; Rose, N; Blett, T; Erway, MM. (2010). The
Western Airborne Contaminant Assessment Project (WACAP): An interdisciplinary evaluation of the
impacts of airborne contaminants in western U.S. National Parks. Environ Sci Technol 44: 855-859.
MacDonald, D.D., Ingersoll, C.G., and Berger, T.A. (2000) Development and evaluation of consensus-based
sediment quality guidelines for freshwater ecosystems. Archives of Environmental Contamination and
Toxicology. 39:20-31.
MacDonald, D.D., Ingersoll, C.G., Smorong, D.E., Lindskoog, R.A., Sloane, G., and Biernacki, T. (2003)
Development and Evaluation of Numerical Sediment Quality Assessment Guidelines for Florida Inland
Waters. British Columbia: MacDonald Environmental Sciences, Lt. Columbia, MO: U.S. Geological
Survey. Prepared for: Florida Department of Environmental Protection, Tallahassee, FL. January.
U.S. Environmental Protection Agency. (2005a) Guidance for Developing Ecological Soil Screening Levels.
Washington, DC: Office of Solid Waste and Emergency Response.OSWER Directive 9285.7-55.
November 2003; revised (chapter 4) February 2005.
U.S. Environmental Protection Agency. (2005b) Ecological Soil Screening Levels forLead, Interim Final.
Washington, DC: Office of Solid Waste and Emergency Response. OSWER Directive 9285.7-70.
Available at http://www.epa.gov/ecotox/ecossl/pdf/eco-ssl lead.pdf.
U.S. Environmental Protection Agency. (2006a) Air Quality Criteria for Lead. Washington, DC, EPA/600/R-
5/144aF. Available online at: http://www.epa. gov/ttn/naaqs/standards/pb/s_pb cr.html
U.S. Environmental Protection Agency. (2006b) Analysis Plan for Human Health and Ecological Risk Assessment
for the Review of the Lead National Ambient Air Quality Standards. Office of Air Quality Planning and
Standards, Research Triangle Park, NC. Available at:
http://www.epa.gov/ttn/naaqs/standards/pb/s_pb cr_pd.html
5-25
-------
U.S. Environmental Protection Agency. (2007a). Framework for metals risk assessment [EPA Report]. (EPA 120/R-
07/001). Washington, D.C. Available online at: http://www.epa.gov/raf/metalsframework/index.htm
U.S. Environmental Protection Agency. (2007b). Review of the National Ambient Air Quality Standards for Lead:
Policy Assessment of Scientific and Technical Information OAQPS Staff Paper. Washington, DC, EPA-
452/R-07-013. Available online at: http://www.epa. gov/ttn/naaqs/standards/pb/s_pb cr.html
U.S. EPA (Environmental Protection Agency). 2008. Integrated Science Assessment (ISA) for Oxides of Nitrogen
and Sulfur-Ecological Criteria (Final Report). EPA/600/R-08/082F. U.S. Environmental Protection
Agency, National Center for Environmental Assessment-RTF Division, Office of Research and
Development, Research Triangle Park, NC. Available at
http://cfpub.epa.gov/ncea/cfm/recordisplav.cfm?deid=201485.
U.S. Environmental Protection Agency. (2013) Integrated Science Assessment for Lead. Washington, DC,
EPA/600/R-10/075F. Available online at: http://www.epa.gOv/ttn/naaqs/standards/pb/s pb index.html
5-26
-------
6 REVIEW OF THE SECONDARY STANDARD FOR LEAD
This chapter presents staff conclusions regarding the secondary Pb standard. These staff
conclusions are guided by consideration of key policy-relevant questions and based on the
assessment and integrative synthesis of information presented in the ISA and by staff analyses
and evaluations presented in chapters 2 and 5 herein. These evaluations and staff conclusions
have also taken into consideration CASAC advice and public comment on the draft PA and will
inform the Administrator's decisions on whether to retain or revise the existing secondary
standard for Pb.
Following an introductory section on the general approach for reviewing the secondary
standard (section 6.1), including a summary of considerations in the last review, the discussion in
this chapter focuses on whether the information available in this review supports or calls into
question the adequacy of the current secondary standard. Building on the responses to specific
policy-relevant questions on the scientific evidence and exposure-risk information in chapter 5,
presentation in section 6.2 is also organized into consideration of key policy-relevant questions
framing evidence-based and exposure/risk-based considerations. The policy-relevant questions
in this document are based on those included in the IRP (IRP, section 3.2). Staff conclusions are
reported in Section 6.3. Section 6.4 presents a brief overview of key uncertainties and areas for
future research.
6.1 APPROACH
Staffs approach for reviewing the current secondary standard takes into consideration the
approaches used in the last Pb NAAQS review and involves addressing key policy-relevant
questions in light of currently available scientific and technical information. The past and
current approaches described below are all based most fundamentally on using EPA's
assessment of the current scientific evidence and previous quantitative analyses to inform the
Administrator's judgment with regard to the secondary standard for Pb. In drawing conclusions
for the Administrator's consideration with regard to the secondary standard, we note that the
final decision on the adequacy of the current secondary Pb standard is largely a public welfare
policy judgment to be made by the Administrator. The Administrator's final decision must draw
upon scientific information and analyses about welfare effects, exposure and risks, as well as
judgments about the appropriate response to the range of uncertainties that are inherent in the
scientific evidence and analyses. This approach is consistent with the requirements of the
NAAQS provisions of the Clean Air Act. These provisions require the Administrator to
establish a secondary standard that, in the judgment of the Administrator, is "requisite to protect
the public welfare from any known or anticipated adverse effects associated with the presence of
6-1
-------
the pollutant in the ambient air". In so doing, the Administrator seeks to establish standards that
are neither more nor less stringent than necessary for this purpose.
6.1.1 Approach Used in the Last Review
In the last review, completed in 2008, the current secondary standard for Pb was set equal
to the primary standard (73 FR 66964). As summarized in section 1.2.2 and described in more
detail in section 4.1.1, the primary standard was substantially revised in the last review based on
the much-expanded health effects evidence of neurocognitive effects of Pb in children. The level
of the revised NAAQS is 0.15 |ig/m3. The averaging time was also revised to a rolling three-
month period with a maximum (not-to-be-exceeded) form, evaluated over a three-year period.
Compared to the previous averaging time of one calendar quarter, this revision was considered to
be more scientifically appropriate and more protective for human health. The indicator of Pb-
TSP was retained, reflecting the evidence that Pb particles of all sizes pose health risks (73 FR
67007). The 2008 decision considered the body of evidence as assessed in the 2006 CD
(USEPA, 2006) as well as the 2007 Staff Paper assessment of the policy-relevant information
contained in the 2006 CD and the screening-level ecological risk assessment (ICF, 2006;
USEPA, 2007), the advice and recommendations of CASAC (Henderson 2007a, 2007b, 2008a,
2008b), and public comment.
In the 2008 review, the Staff Paper concluded, based on laboratory studies and current
media concentrations in a wide range of locations, that it seemed likely that adverse effects were
occurring, particularly near point sources, under the then-current standard (73 FR 67010). Given
the limited data on Pb effects in ecosystems, and associated uncertainties, such as those with
regard to factors such as the presence of multiple metals and historic environmental burdens, it
was at the time, as it is now, necessary to look at evidence of Pb effects on organisms and
extrapolate to ecosystem effects. Taking into account the available evidence and current media
concentrations in a wide range of locations, the Administrator concluded that there was potential
for adverse effects occurring under the then-current standard; however there were insufficient
data to provide a quantitative basis for setting a secondary standard different than the primary
(73 FR 67011). Therefore, citing a general lack of data that would indicate the appropriate level
of Pb in environmental media that may be associated with adverse effects, as well as the
comments of the CASAC Pb panel that a significant change to current air concentrations (e.g.,
via a significant change to the standard) was likely to have significant beneficial effects on the
magnitude of Pb exposures in the environment, the secondary standard was revised to be
consistent with the revised primary standard (73 FR 67011).
6-2
-------
6.1.2 Approach for the Current Review
In evaluating whether it is appropriate to consider retaining the current secondary Pb
standard, or whether consideration of revision is appropriate, we have adopted an approach in
this review that builds on the general approach from the last review and reflects the body of
evidence and information now available. As summarized above, the Administrator's decisions in
the previous review were based on the conclusion that there was the potential for adverse
ecological effects under the previous standard. In our approach here, we intend to focus on
consideration of the extent to which a broader body of scientific evidence is now available that
would inform decisions on either the potential for adverse effects to ecosystems under the current
standard or the ability to set a more ecologically relevant secondary standard than was feasible in
the previous review. In conducting this assessment, we draw on the ecological effects evidence
presented in detail in the ISA and aspects summarized above in chapter 5, along with the
information associated with the screening-level risk assessment also summarized above. Figure
6-1 illustrates the basic construct of our approach in developing conclusions regarding options
appropriate for the Administrator to consider in this review with regard to the adequacy of the
current secondary NAAQS standard and, as appropriate, potential alternate standards.
In developing conclusions in this review, we have taken into account both evidence-
based and risk-based considerations framed by a series of policy-relevant questions. These
questions are outlined in the sections below and generally discuss the extent to which we are able
to better characterize effects and the likelihood of adverse effects in the environment under the
current standard. Our approach to considering these questions recognizes that the available
welfare effects evidence generally reflects laboratory-based evidence of toxicological effects on
specific organisms exposed to concentrations of Pb. It is widely recognized, however, that
environmental exposures from atmospherically derived Pb are likely to be lower and/or
accompanied by significant confounding and modifying factors (e.g., other metals, acidification),
which increases our uncertainty about the likelihood and magnitude of organism and ecosystem
responses.
6-3
-------
Adequacy of Current Standard
Evidence-based Considerations
> Does currently available evidence and related
uncertainties strengthen or call into question prior
conclusions?
• Evidence of welfare effects not previously identified
or at lower exposures?
• Newly identified at-risk ecosystems?
•Changed understanding of lead bioavailability and
movement of through ecosystems?
•Effects at lower air-related exposures than
previously understood or in conditions that would
have likely met current standard?
Risk-based Considerations
> Nature, magnitude and importance of
screening level risk information?
> Uncertainties in the screening level risk
assessment?
Does information call into
question the adequacy of
current standard?
Consider
Retaining
Current Standard
Consideration of Potential Alternative Standards
Elements of Potential Alternative Standards
>Indicator
> Averaging Time
>Form
> Level
c
Potential Alternative Standards for Consideration
Figure 6-1. Overview of approach for review of current secondary standard.
6-4
-------
6.2 ADEQUACY OF THE CURRENT STANDARD
In considering the adequacy of the current Pb standard, the overarching question we
consider is:
• Does the currently available scientific evidence- and exposure/risk-based
information, as reflected in the ISA and REA, support or call into question the
adequacy of the protection afforded by the current Pb standard?
To assist us in interpreting the currently available scientific evidence and screening-level
risk information to address this question, we have focused on a series of more specific questions,
posed within sections 6.2.1 and 6.2.2 below. In so doing, we consider both the information
available at the time of the last review and information newly available since the last review
which has been critically analyzed and characterized in the ISA.
6.2.1 Evidence-based Considerations
In considering the welfare effects evidence with respect to the adequacy of the current
standard, we consider the array of evidence newly assessed in the ISA with regard to the degree
to which this evidence supports conclusions about the effects of Pb in the environment that were
drawn in the last review and the extent to which it reduces previously recognized areas of
uncertainty. Further, we consider the current evidence and associated conclusions about the
potential for effects to occur as a result of the much lower ambient Pb concentrations allowed by
the current secondary standard (set in 2008) than those allowed by the prior standard, which was
the focus of the last review. These considerations, discussed in the context of the specific
questions below, inform our conclusions regarding the extent to which the evidence supports or
calls into question the adequacy of protection afforded by the current standard.
• To what extent does the available information indicate that Pb-related effects are
occurring as a result of multimedia pathways associated with ambient air
conditions that would meet the current standard?
The current evidence continues to support our conclusions from the previous review
regarding key aspects of the ecological effects evidence for Pb and the effects of exposure
associated with levels of Pb occurring in ecological media in the U.S. Our conclusions in this
regard are based on consideration of the assessment of the currently available evidence in the
ISA, particularly with regard to key aspects summarized in chapter 5 of this PA, in light of the
assessment of the evidence in the last review as described in the 2006 CD and summarized in the
notice of final rulemaking (73 FR 67008). Key aspects of conclusions drawn in the last review
(73 FR 67010) are summarized below.
• There are several difficulties to quantifying the role of recent air emissions of Pb in the
environment:
6-5
-------
- While the removal of Pb from on-road gasoline and reductions in industrial
emissions have resulted in dramatic reductions in overall deposition rates (2006
CD, pp. AX7-34 and AX7-103), Pb deposited before the 1978 standard, and the
relatively lesser amount deposited since, is still present in soils and sediments.
- Historic Pb from gasoline-derived and other air emissions as well as nonair sources
has produced a legacy of Pb in forest soils that continues to move slowly through
these systems (2006 CD, section AX7.1.4.3).
• The evidence of adversity in natural systems is very sparse due in no small part to the
difficulty in determining the effects of confounding factors such as multiple metals or
factors influencing bioavailability of Pb in field studies (2006 CD, E-19).
• For areas influenced by stationary sources of air Pb that met the standard considered in
the last review at the time of the last review (although they likely did not throughout
their active period), concentrations of Pb in soil may exceed by many orders of
magnitude the concentrations which are considered harmful to laboratory organisms
(2006 CD, sections 3.2 and AX7.1.2.3).
• Environmental conditions exist in which Pb-associated adverse effects to aquatic
organisms and thereby ecosystems may be anticipated given experimental results.
While the evidence does not indicate that dissolved Pb in surface water constitutes a
threat to those ecosystems that are not directly influenced by point sources, the
evidence regarding Pb in sediment is less clear. Some areas with long term historical
deposition of Pb to sediment from a variety of sources as well as areas influenced by
point sources have the potential for adverse effects to aquatic communities (2006 CD,
sections AX7.2.2.2 and AX7.2.4).
The range of effects that Pb can exert on terrestrial and aquatic organisms indicated by
information available in the current review is summarized in the ISA (ISA, sections 1.7, 6.3 and
6.4) and largely mirror the findings of from the previous review (summarized above). The
integrated synthesis contained in the ISA conveys how effects of Pb can vary with species and
life stage, duration of exposure, form of Pb, and media characteristics such as soil and water
chemistry. A wide range of organism effects are recognized, including effects on growth,
development (particularly of the neurological system) and reproductive success (ISA, section 6.3
and 6.4). Lead is recognized to distribute from the air into multiple environmental media, as
summarized in section 1.3 above, contributing to multiple exposure pathways for ecological
receptors. As discussed in section 5.1 above, many factors affect the bioavailability of Pb to
receptors in terrestrial and aquatic ecosystems, contributing to differences between laboratory -
6-6
-------
assessed toxicity and Pb toxicity in these ecosystems, challenging our consideration of
environmental impacts of Pb emitted to ambient air.
In studies in a variety of ecosystems, adverse ecosystem-level effects (including
decreases in species diversity, loss of vegetation, changes to community composition, primarily
in soil microbes and plants, decreased growth of vegetation, and increased number of invasive
species) have been demonstrated near smelters, mines and other industries that have released
substantial amounts of Pb, among other materials, to the environment (ISA, sections 6.3.12 and
6.4.12). As noted in section 5.1 above, however, our ability to characterize the role of air
emissions of Pb in contributing to these effects is complicated because of coincident releases to
other media and of other pollutants. Co-released pollutants include a variety of other heavy
metals, in addition to sulfur dioxide, which may cause toxic effects in themselves and may
interact with Pb in the environment, contributing uncertainty to characterization of the role of Pb
from ambient air with regard to the reported effects. These uncertainties limit our ability to draw
conclusions regarding the extent to which Pb-related effects may be associated with ambient air
conditions that would meet the current standard.
The role of historically emitted Pb, as discussed in section 1.3.2 above, poses additional
complications in addressing this question. The vast majority of Pb in the U.S. environment
today, particularly in terrestrial ecosystems, was deposited in the past during the use of Pb
additives in gasoline (2006 CD, pp. 2-82, AX7-36 to AX7-38, AX7-98; Johnson et al., 2004),
although contributions from industrial activities, including metals industries have also been
documented (ISA, section 2.2.2.3, Jackson et al., 2004). The gasoline-derived Pb was emitted in
very large quantities (2006 CD, p. AX7-98 and ISA, Figure 2-8) and predominantly in small
sized particles which were widely dispersed and transported across large distances, within and
beyond the U.S. (ISA, section 2.2). As recognized in sections 2.3.1 and 2.3.3.2 above, historical
records provided by sediment cores in various environments document the substantially reduced
Pb deposition (associated with reduced Pb emissions) in many locations (ISA, section 2.2.1). As
Pb is persistent in the environment, these substantial past environmental releases are expected to
generally dominate current nonair media concentrations. There is limited evidence to relate
specific ecosystem effects with current ambient air concentrations of Pb through deposition to
terrestrial and aquatic ecosystems and subsequent movement of deposited Pb through the
environment (e.g., soil, sediment, water, organisms). The potential for ecosystem effects of Pb
from atmospheric sources under conditions meeting the current standard is difficult to assess due
to limitations on the availability of information to fully characterize the distribution of Pb from
the atmosphere into ecosystems over the long term, as well as limitations on information on the
bioavailability of atmospherically deposited Pb (as affected by the specific characteristics of the
receiving ecosystem). Therefore, while information available since the 2006 CD includes
6-7
-------
additional terrestrial and aquatic field studies, "the connection between air concentration and
ecosystem exposure and associated potential for welfare effects continues to be poorly
characterized for Pb" (ISA, section 6.5). Such a connection is even harder to characterize with
respect to the current standard than it was in the last review with respect to the previous, much
higher, standard.
• To what extent have important uncertainties identified in the last review been
reduced and/or have new uncertainties emerged?
In the characterization of effects associated with Pb in ambient air for the last review, the
areas of largest uncertainty were identified to be associated with our abilities to determine the
extent of lead-related effects in the natural environment and to apportion effects between air and
nonair sources, and with the relationship between effects and environmental conditions
associated with the standard. While we have some new evidence with regard to bioavailability
and its role in influencing the potential for effects in the environment, overall these remain the
major sources of uncertainty in our evaluation of effects and exposure evidence for Pb in
ecosystems. Moreover, the impact of these uncertainties is larger in this review given our
current focus on a secondary standard much lower than that which was the focus of the last
review.
With regard to the extent of lead-related effects in the natural environment, it remains
difficult to assess the concentrations at which Pb elicits specific effects in terrestrial and aquatic
systems, due to the influence of other environmental variables on both Pb bioavailability and
toxicity and also due to substantial species differences in Pb susceptibility (ISA, sections 6.3.2-
6.3.4 and 6.4.2 -6.4.5). There is little new information that would facilitate extrapolation of
evidence on individual species, generally from controlled laboratory studies, to conclusions
regarding adversity to populations or ecosystems within the natural environment. For example, in
terrestrial systems, evidence reviewed in the ISA (ISA, sections 6.2.3 and 6.2.4) demonstrates
that exposure to Pb is generally associated with negative effects on growth, reproduction and
survival in terrestrial ecosystems. Many factors, including species composition and various soil
physiochemical properties, interact strongly with Pb concentration to modify effects. Also, the
changes associated with environmental aging of lead-contaminated material is a particularly
important factor in terrestrial systems, where soil is the main route of exposure, however, aging
of lead-contaminated soil is difficult to reproduce experimentally (ISA, sections 6.3.9.3 and
6.3.11). Without quantitatively accounting for these factors, laboratory-derived
"characterizations of exposure-response relationships would likely not be transferable outside of
experimental settings" (ISA, p. 1-42).
With regard to the role of air-related Pb, as discussed above and noted in the ISA, "the
connection between air concentration and ecosystem exposures continues to be poorly
6-8
-------
characterized for Pb and the contribution of atmospheric Pb to specific sites is not clear" (ISA, p.
6-264). Thus, the limited evidence and associated uncertainties connecting air concentrations to
ecosystem exposures and possible effects, in combination with those that influence Pb
bioavailability and ecosystem mobility, are areas particularly limiting the extent to which critical
loads analyses might otherwise be useful to our assessment in this review, as discussed in section
5.1. Thus, the evidence is lacking in quantitative relationships between Pb in ambient air and
welfare effects, including identification of a specific exposure metric or index (e.g.,
mathematical formulation of averaging time and concentration) by which to consider ambient air
Pb concentrations with regard to the potential for adverse effects to public welfare. In the
decision in the last review to set the secondary standard equal to the primary standard, EPA
similarly recognized a lack of evidence that related welfare effects to Pb in ambient air and from
which differing standard elements (e.g., averaging time and concentration) might be derived for
the secondary standard.1 These limitations in the evidence base remain in the current review.
As in the last review, consideration of the environmental risks and potential welfare
effects associated with the current standard is complicated by the environmental burden
associated with air Pb concentrations, predominantly in the past, that exceeded both the
previously existing standard and the current standard (USEPA, 2007, section 6.4.4.2). For
example, a large portion of Pb deposited before the current standard was enacted is likely still
present in soils and sediments, and historic Pb from gasoline (and other historic sources)
continues to move slowly through systems as does Pb derived from current air and nonair
sources. As a general matter, the currently available evidence, as assessed in the ISA, does not
significantly reduce any of the areas of uncertainty described here which, given the standard
considered in the present review (with its much lower level than the previous standard), weigh
heavily in our consideration of the adequacy of the current standard.
6.2.2 Exposure/Risk-based Considerations
• To what extent does risk or exposure information indicate that air-related
ecosystem exposures important from a public welfare perspective are likely to
occur with air Pb levels that just meet the current standard?
The current evidence continues to support our conclusions with regard to interpreting the
risk and exposure results from the previous review. Our conclusions in this regard are based on
1 As described in section 6.1.1 above, the EPA concluded in the last review that the then-current secondary
standard did not provide requisite protection from effects adverse to public welfare. In considering the appropriate
revision, EPA recognized that the Agency lacked the relevant data to provide a clear quantitative basis for setting a
secondary Pb NAAQS that differs from the primary standard, yet recognized that significant beneficial effects were
likely to result in terms of reduced magnitude of Pb exposures in the environment and associated toxicity impacts on
ecosystems from a significant change to the level for the secondary standard, such as the order-of-magnitude change
which was achieved by setting the secondary standard identical to the revised primary standard (73 FR 67012).
6-9
-------
consideration of the screening-level ecological risk assessment results from the previous review
as described in the 2006 REA and summarized in the notice of final rulemaking (73 FR 67009)
and in light of the currently available evidence in the ISA. Key aspects of these results in the
context of the current standard are summarized below, drawing from the discussion of the 2006
REA results in section 5.2.2 above, which is based on the information in the 2006 REA (ICF,
2006).
Primary Pb Smelter Case Study
• While the contribution to Pb concentrations from air as compared to nonair sources is
not quantified, air emissions from this facility are substantial (ICF, 2006). Currently,
the county where this facility is located exceeds the now-current Pb NAAQS.
Secondary Pb Smelter Case Study
• While the contribution from air deposited Pb to the overall Pb concentrations modeled
in soils at this location is unclear, the facility continues to emit Pb and the county
where this facility is located exceeds the now-current Pb NAAQS (Appendices 2D and
5A).
Near Roadway Non-urban Case Study
• These case study locations are highly impacted by past deposition of gasoline Pb. It is
unknown whether current conditions at these sites exceed the now-current Pb standard,
but given evidence from the past of Pb concentrations near highways that ranged above
the previous (1978) Pb standard (1986 CD, section 7.2.1), conditions at these locations
during the time of leaded gasoline very likely exceeded the 1978 standard.
Vulnerable Ecosystem Case Study
• The previous review concluded that atmospheric Pb inputs do not directly affect stream
Pb levels at Hubbard Brook Experimental Forest because deposited Pb is almost
entirely retained in the soil profile and that there was "little evidence that sites affected
primarily by long-range Pb transport [such as this one] have experienced significant
effects on ecosystem structure or function" (2006 CD, p. AX-98). Further, it is
unlikely that conditions have changed from the data through 2000 on which the
previous conclusions were based, and, therefore, current ambient air concentrations
likely do not directly impact stream Pb levels under air quality conditions associated
with meeting the now-current standard.
National-scale Surface Water and Sediment Screen
• The extent to which past air emissions of Pb have contributed to surface water or
sediment Pb concentrations at the locations identified in the screen is unclear. For
some of the surface water locations, nonair sources likely contributed significantly to
the surface water Pb concentrations. For other locations, a lack of nearby nonair
sources indicated a potential role for air sources to contribute to observed surface water
Pb concentrations. Additionally, these concentrations may have been influenced by Pb
6-10
-------
in resuspended sediments and/or reflect contribution of Pb from erosion of soils with
Pb derived from historic as well as current air emissions.
Although the available risk and exposure information continues to be sufficient to
conclude that the 1978 standard was not providing adequate protection to ecosystems, that
information, when considered with regard to air-related ecosystem exposures likely to occur with
air Pb levels that just meet the now-current standard, does not provide evidence that the current
secondary standard (set in 2008) is inadequate.
6.2.3 CASAC Advice
In our consideration of the adequacy of the current standards, in addition to the evidence-
and risk/exposure-based information discussed above, we have also considered the advice and
recommendations of CASAC, based on their review of the ISA and the earlier draft of this
document. Comments from the public on earlier drafts of this document did not address the
adequacy of the current secondary standard.2
In their advice and comments conveyed in the context of their review of the draft PA, the
CASAC agreed with staffs preliminary conclusions that the available information since the last
review is not sufficient to warrant revision to the secondary standard (Frey, 2013). On this
subject, the CASAC letter said the following.
Overall, the CASAC concurs with the EPA that the current scientific literature
does not support a revision to the Primary Lead (Pb) National Ambient Air
quality Standard (NAAQS) nor the Secondary Pb NAAQS.
The CASAC also recognized the many uncertainties and data gaps in the new scientific literature
and recommended that research be performed in the future to address these limitations.
Given the existing scientific data, the CASAC concurs with retaining the current
secondary standard without revision. However, the CASAC also notes that
important research gaps remain. For example questions remain regarding the
relevance of the primary standard's indicator, level, averaging time, and form for
the secondary standard. Other areas for additional research to address data gaps
and uncertainty include developing a critical loads approach for U.S. conditions
and a multi-media approach to account for legacy Pb and contributions from
different sources. Addressing these gaps may require reconsideration of the
secondary standard in future assessments.
2 All written comments submitted to the Agency will be available in the docket for this rulemaking, as will
be transcripts of the public meetings held in conjunction with CASAC's review of the earlier draft of this document,
of the REA Planning Document and of drafts of the ISA.
6-11
-------
6.3 STAFF CONCLUSIONS ON THE SECONDARY STANDARD
This section describes staff conclusions regarding adequacy of the current secondary Pb
standard. These conclusions are based on considerations described above and in the discussion
below regarding the currently available scientific evidence summarized in the ISA and prior CDs
and the risk and exposure information drawn from the 2006 REA. These conclusions also take
into account advice from CASAC and public comment on the draft PA and preliminary
conclusions.
Taking into consideration the discussions responding to specific questions above in this
and the prior chapter, this section addresses the following overarching policy question:
• Does the currently available scientific evidence- and exposure/risk-based
information, as reflected in the ISA and REA, support or call into question the
adequacy of the protection afforded by the current secondary Pb standard?
With respect to evidence-based considerations, the body of evidence on the ecological
effects of Pb, expanded in some aspects since the last review, continues to support identification
of ecological effects in organisms relating to growth, reproduction, and survival as the most
relevant endpoints associated with Pb exposure. In consideration of the appreciable influence of
site-specific environmental characteristics on the bioavailability and toxicity of environmental Pb
in our assessment here, we give greater weight to studies conducted under conditions most
closely reflecting the natural environment as compared to laboratory-based exposures. The
currently available evidence, while somewhat expanded since the last review, does not include
evidence of significant effects at lower concentrations or evidence of higher level ecosystem
effects beyond those reported in the last review. There continue to be significant difficulties in
interpreting effects evidence from laboratory studies to the natural environment and linking those
effects to ambient air Pb concentrations. Further, we are aware of no new critical loads
information that would inform our interpretation of the public welfare significance of the effects
of Pb in various ecosystems (as discussed in section 5.1). In summary, while new research has
added to the understanding of Pb biogeochemistry and expanded the list of organisms for which
Pb effects have been described, there remains a significant lack of knowledge about the potential
for adverse effects on public welfare from ambient air Pb in the environment and the exposures
that occur from such air-derived Pb, particularly under the current standard.
With respect to exposure/risk-based considerations, we recognize the complexity of
interpreting the previous risk assessment with regard to the ecological risk of ambient air Pb
associated with conditions meeting the current standard and the associated limitations and
uncertainties of such assessments. For example, the location-specific case studies as well as the
national screen conducted in the last review reflect both current air Pb deposition as well as past
air and nonair source contributions. We conclude that while the previous assessment is
6-12
-------
consistent with and generally supportive of the evidence-based conclusions about Pb in the
environment, the limitations of apportioning Pb between past and present air contributions and
between air and nonair sources remain significant.
In now considering the adequacy of the current standard in this review, we have
considered the ecological and welfare effects evidence assessed in the ISA and discussed in
sections 5.1, 2.3 and 6.2.1 above, as well screening-level exposure;/risk information gained from
the 2006 REA discussed in sections 5.2 and 6.2.2 above, and staff judgments on associated
implications with regard to public welfare. As summarized, in section 6.2.1 above, the scientific
evidence presented in detail in the ISA, inclusive of that newly available in this review, is not
substantively changed, most particularly with regard to our needs in reviewing the current
standard, from the information that was available in the last review. The evidence base does not
indicate that the current standard is inadequate. Further, our updated consideration of the
screening-level risk information from the 2006 REA, as summarized in section 6.2.2 above,
additionally does not provide evidence that the current secondary standard is inadequate. Thus,
we conclude that the currently available evidence and exposure/risk information do not call into
question the adequacy of the current standard to provide the requisite protection for public
welfare. Accordingly, we reach the conclusion that it is appropriate to consider retaining the
current secondary standard without revision.
6.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND DATA
COLLECTION
In this section, we highlight key uncertainties associated with reviewing the secondary
NAAQS for Pb. Such key uncertainties and recommendations for ecosystem-related research,
model development, and data gathering are outlined below. In some cases, research in these
areas can go beyond supporting standard setting to aiding in the development of more efficient
and effective control strategies. We note, however, that a full set of research recommendations
to meet standards implementation and strategy development needs is beyond the scope of this
discussion. Rather, listed below are key uncertainties and research questions and data gaps that
have been thus far highlighted in this review of the welfare-based secondary standard for Pb.
• Our understanding of the extent and degree of adverse impact occurring in the
environment due to Pb (from atmospheric and other sources) is incomplete and leads to
uncertainty in characterizing environmental effects of Pb, which is necessary to assess
potential associated effects on public welfare.
- The available studies on community and ecosystem-level effects are sparse and
usually from contaminated areas where Pb concentrations are much higher than
typically encountered in the environment as a result of atmospheric input and are
usually co-occurring with elevated concentrations of other pollutants.
6-13
-------
- Many ecosystem-specific characteristics affect bioavailability and associated
toxicity, contributing uncertainty to our interpretation of study results from
laboratory test-systems. For example, the role of modifying factors such as soil and
water chemistry on Pb toxicity continues to be a source of uncertainty when
determining the degree of adverse impact from Pb.3
- Evidence regarding relationships between organism-level effects of Pb (e.g.,
reproduction, growth, and survival) and effects at the population level and higher is
lacking especially in natural systems.
- A better understanding of the potential for adverse effects from Pb in estuarine and
marine systems is needed.
• There is appreciable uncertainty in our understanding of the current dynamics of Pb in
U.S. ecosystems.
- In general, the connection between air concentration of Pb and ecosystem exposure
continues to be poorly characterized and is complicated by the legacy of historical
inputs both from air and, in some systems, also from other sources.
- There is uncertainty in characterizing the fate and transport of Pb in the
environment through air, water, and soil media. This limits our ability to account
for the role of past Pb releases in current media concentrations and to link effects to
current air contributions.
- An important source of uncertainty in characterizing the effects of air-related Pb in
some U.S. ecosystems is that associated with distinguishing air-related Pb from
other sources of Pb. It is difficult to determine the portion of Pb occurring in some
ecosystems that derives from the atmosphere as compared to that from other
sources.
• Development of critical loads information for U.S. ecosystems would allow for a
much improved understanding of the significance of air contributions to ecosystems
and ecological receptor exposures, as well as that of contributions from other sources.
Development of a critical loads approach, with sensitivity analysis, would inform
identification of processes critical to ecological receptor exposures and toxicity.
- Such critical loads analyses could inform characterization of the variability of
response across ecosystems to determine which ecosystems are most sensitive.
- Additional research is needed to provide inputs for development of critical loads,
particularly for a broader range of ecosystem-level endpoints.
• Information is currently lacking to inform identification of standard elements, such as
averaging time and form, specifically reflecting a ecological and public welfare
context for ambient air Pb.
3 Further uncertainty accompanies the interpretation of toxicity data from test systems involving artificial
media such as hydroponic systems, agar or culture media.
6-14
-------
6.5 REFERENCES
Frey, H.C. (2013) Letter from Dr. H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee and Clean
Air Scientific Advisory Committee Lead Review Panel, to Acting Administrator Bob Perciasepe. Re:
CASAC Review of the EPA's Policy Assessment for Lead (External Review Draft - January 2013). June 4,
2013.
Henderson, R. (2007a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to
Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee's (CASAC) Review of
the 1st Draft Lead Staff Paper and Draft Lead Exposure and Risk Assessments. March 27, 2007.
Henderson, R. (2007b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to
Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee's (CASAC) Review of
the 2nd Draft Lead Human Exposure and Health Risk Assessments. September 27, 2007.
Henderson, R. (2008a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to
Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee's (CASAC) Review of
the Advance Notice of Proposed Rulemaking (ANPR) for the NAAQS for lead. January 22, 2008.
Henderson, R. (2008b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to
Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee's (CASAC) Review of
the Notice of Proposed Rulemaking for the NAAQS for lead. July 18, 2008.
ICF International. (2006) Lead Human Exposure and Health Risk Assessments and Ecological Risk Assessment for
Selected Areas. Pilot Phase. Draft Technical Report. Prepared for the U.S. EPA's Office of Air Quality
Planning and Standards, Research Triangle Park, NC. December.
Jackson, B. P.; Winger, P. V.; Lasier, P. J. (2004) Atmospheric lead deposition to Okefenokee Swamp, Georgia,
USA. Environ. Pollut. 130: 445-451.
Johnson, C. E.; Petras, R. J.; April, R. H.; Siccama, T. G. (2004) Post-glacial lead dynamics in a forest soil. Water
Air Soil Pollut. 4:579-590.
U.S. Environmental Protection Agency. (2006) Air Quality Criteria for Lead. Referred to as 2006 CD. Washington,
DC, EPA/600/R-5/144aF. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr.html
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. Washington, DC, EPA-
452/R-07-013. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr.html
U.S. Environmental Protection Agency. (2013) Integrated Science Assessment for Lead. Referred to as ISA.
Washington, DC,. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb index.html
6-15
-------
This page is intentionally blank
-------
APPENDICES
Appendix 2 A. Recent Regulatory Actions on Stationary Sources of Lead 2 A-1
Appendix 2B. The 2008 NEI: Data Sources, Limitations and Confidence 2B-1
Appendix 2C. Criteria for Air Quality Data Analysis 2C-1
Appendix 2D. Air Quality Data Analysis Summary 2D-1
Appendix 3 A. Interpolated Risk Estimates for the Generalized (Local) Urban Case Study.. 3A-1
Appendix 5 A. Additional Detail on 2006 Ecological Screening Assessment 5 A-1
-------
APPENDIX 2A
RECENT REGULATORY ACTIONS ON STATIONARY SOURCES OF LEAD
The table below identifies recent actions projected to result in reductions in Pb emissions
from stationary sources.
Action
NESHAP
NESHAP
NESHAP
NESHAP
NESHAP
NESHAP
NESHAP,
NSPS
EGES,
NSPS
EGES,
NSPS
NESHAP
EGES,
NSPS
Source Categories Affected
Secondary Lead Smelting
Primary Lead Smelting
Area Sources: Clay Ceramics Manufacturing, Glass
Manufacturing, and Secondary Nonferrous Metals
Processing
Area Sources: Electric Arc Furnace Steelmaking Facilities
Iron and Steel Foundries Area Sources
Area Source Standards for Aluminum, Copper, and Other
Nonferrous Foundries
Portland Cement Manufacturing Industry
Commercial and Industrial Solid Waste Incineration Units
Standards of Performance for New Stationary Sources and
Emission Guidelines for Existing Sources: Sewage Sludge
Incineration Units
Major Sources: Industrial, Commercial, and Institutional
Boilers, and Process Heaters
Standards of Performance for New Stationary Sources and
Emissions Guidelines for Existing Sources:
Hospital/Medical/lnfectious Waste Incinerators
Citation
77FR555
(1/5/2012)
76 FR 70834
(11/15/2011)
72 FR 731 79
(12/26/2007)
72 FR 74088
(12/28/2007)
73FR225
(1/2/2008)
74 FR 30366
(6/25/2009)
78 FR 10006
(2/12/2013)
76 FR 91 12
(02/07/2013)
76 FR 15372
(3/21/2011)
78 FR 7138
(1/31/2013)
74 FR 51 367
(10/6/2009)
Estimated Pb
Emissions
Reduction
(tons per
year)
13.6
10
Unquantified*
Unquantified*
Unquantified*
Unquantified*
6.72
2.51
1.2-1.5
Unquantified*
0.16
Year of
Compliance
(year in which
reductions
estimated to
begin)
2014
2013
2007, 2009,
2007
2008 or 20 10
2010
2011
2015
2018
2016
2016
2014
EGES = Emissions Guidelines for Existing Sources
NESHAP = National Emission Standards for Hazardous Air Pollutants
NSPS = New Source Performance Standards
"Unqualified = Reductions in Pb emissions expected from controls in response to regulatory action have not been quantified.
2A-1
-------
APPENDIX 2B
THE 2008 NEI: DATA SOURCES, LIMITATIONS AND
CONFIDENCE
The process of identifying sources that emit Pb into the air has been ongoing since before
the Clean Air Act of 1970. The comprehensiveness of emission inventories generally, and the
NEI, specifically, depends upon knowledge of source types emit Pb, their locations and their
operating characteristics, as well as the reporting of this information to the inventory. As noted
above, the NEI relies on information that is available from a variety of sources for this
information. There are numerous steps, each with its own uncertainties, associated with the
development of this information for use in the emissions inventory. First, the categories emitting
Pb must be identified. Second, the sources' processes and control devices must be known.
Third, the activity throughputs and operating schedules of these sources must be known. Finally,
we must have emission factors to relate emissions to the operating throughputs, process
conditions and control devices. The process, control device, throughputs and operating
schedules are generally available for each source. However, the emission factors represent
average emissions for a source type and average emissions may differ significantly from source
to source. In some cases, emissions testing provides source-specific information. In others,
emissions factors must be estimated from similar sources or source categories, or from other
information. More information on emission factors and the estimation of emissions is found in
the introduction to EPA's Compilation of Air Pollutant Emissions Factors.1
The Pb emissions information presented in chapter 2 is drawn largely from EPA's NEI
for 2008. The NEI is based on information submitted from State, Tribal and local air pollution
agencies and data obtained during the preparation of technical support information for EPA's
hazardous air pollutant regulatory programs. Data in the 2008 NEI for Pb emissions from the
use of leaded aviation gasoline were developed by EPA using the Federal Aviation
Administration's operations activity data, where available.2 The data were then reviewed by
State, Tribal, and local air pollution agencies. With some additions, the information presented in
this document is primarily based on version 3 of the NEI for 2008, available on the EPA's
CHIEF website at (http://www.epa.gov/ttn/chief/net/2008inventory.html). The NEI is limited
1 U.S. Environmental Protection Agency. (1996-2011). AP-42, Compilation of Air Pollutant Emission
Factors, 5th Edition. Volume 1: Stationary Point and Area Sources, Chapter 13: Miscellaneous Sources. Available
at: http://www.epa.gov/ttn/chief/ap42/chl3/index.html. Further information on emission factors is available at:
http://www.epa.gov/ttn/chief/ap42/
2 Eastern Research Group (ERG), 201 la. Project report: Documentation for Aircraft Component of the
National Emissions Inventory Methodology, ERG No. 0245.03.402.011, January 27, 2011.
2B-1
-------
with regard to Pb emissions estimates for some sources. For example, we have not yet
developed estimates for the NEI of Pb emissions for the miscellaneous categories of on-road
emissions (e.g., combustion of fuel with Pb traces, lubricating oil, mechanical wear of vehicle
components, etc.) and Pb that may be emitted from wildfires, or for emissions associated with
resuspension of Pb residing in roadway dust and nearby surface soil in areas not otherwise
associated with industrial facilities (see section 2.1.2).
The 2008 NEI underwent extensive external review, including a review of the process for
developing the inventory which includes extensive quality assurance and quality control steps
(QA/QC). We provided feedback reports to point source data providers and we posted several
versions of the inventory on our website. We also conducted additional QA targeted at facilities
with appreciable Pb emissions in previous years to ensure that 2008 Pb emissions were reported,
and we augmented with TRI where facilities with annual emissions greater than 0.5 tpy in 2005
were not reported to NEI in 2008 due to Pb emissions reporting thresholds
(ftp://ftp.epa.gov/EmisInventory/20008v2/doc/2008neiv2_issues.xlsx). Further, there was
additional QA/QC conducted for emission inventory information for facilities that are included
in Risk and Technology Review source categories.3 As a result we have strong confidence in the
quality of the data for these facilities. In summary, generic limitations to the 2008 NEI include
the following.
• Consistency: The 2008 NEI for Pb is a composite of emissions estimates generated by
state and local regulatory agencies, industry, and EPA. Because the estimates
originated from a variety of sources, as well as for differing purposes, they will in turn
vary in quality, whether Pb is reported for particular source types, method of reporting
compound classes, level of detail, and geographic coverage.
• Variability in Quality and Accuracy of Emission Estimation Methods: The accuracy of
emission estimation techniques varies with pollutants and source categories. In some
cases, an estimate may be based on a few or only one emission measurement at a
similar source. The techniques used and quality of the estimates will vary between
source categories and between area, major, and mobile source sectors. Generally, the
more review and scrutiny given to emissions data by states and other agencies, the
more certainty and accuracy there is in those estimates.
3 The Risk and Technology Review is a combined effort to evaluate both risk and technology as required
by the Clean Air Act (CAA) after the application of maximum achievable control technology (MACT) standards.
Section 112(f)(2) of the CAA directs EPA to conduct risk assessments on each source category subject to MACT
standards, and to determine if additional standards are needed to reduce residual risks. Section 112(d)(6) of the CAA
requires EPA to review and revise the MACT standards, as necessary, taking into account developments in
practices, processes and control technologies. For more information: http://www.epa.gov/ttn/atw/rrisk/rtrpg.html.
2B-2
-------
APPENDIX 2C
CRITERIA FOR AIR QUALITY DATA ANALYSIS
Criteria for the 2010-2012 data analysis presented in Figures 2-10 through 2-13 are as
listed below, with abbreviations defined following this list.
• Years utilized were 2010-2012. November and December 2009 data were also used for
the rolling 3-month average analysis.
• Data were extracted from EPA's Air Quality System in June of 2013.
• Data for parameter 14129 (Pb-TSP FRM/FEM LC) were used for Pb-TSP analysis;
data for parameters 84128 (Pb-PM2.5 STP) and 88128 (Pb-PM2.5 LC) were used for Pb-
PM2.5 analysis; and data for parameters 82128 (Pb-PMio STP), 85128 (Pb-PMio LC),
and 85129 (Pb-PMio FRM/FEM LC) were used for Pb-PMlO analysis. No adjustment
was made to the STP or LC data to make them more comparable to each other; based
on previous analysis, the LC and STP versions of same-site-day samples are extremely
similar. Collocated data - for same size cut- were combined to a site basis by using the
following hierarchy, evaluated each site-day: LC FRM/FEM parameter data takes
precedence over LC (non-FRM/FEM) parameter data, and those data take precedence
overSTP parameter data; also, within those categories, lower POC numbers take
precedence over higher POC numbers.
• For maximum rolling 3-month average analysis, the 2010-2012 databases also
encompassed the prior 2 months (i.e., November and December 2009 data): 3 or more
observations were needed to make a valid monthly; 3 valid consecutive months were
required to make a valid rolling 3-month period; 6 valid rolling 3-month periods were
required to make a valid year; and 1, 2, or 3 valid years were required to make a valid
3-year metric. Thus, the shortest duration that could potentially meet these criteria for
the maximum 3-month average analysis is 8 months. The 3-year maximum rolling 3-
month average metric (by size cut for 2010-2012) was identified as the highest valid 3-
month average across the valid (1, 2, or 3) years.
• For maximum monthly analysis: 3 or more observations were needed to make a valid
monthly; 6 valid months were required to make a valid year; and 1, 2, or 3 valid years
were required to make a valid 3-year metric. Thus, the shortest duration that could
potentially meet these criteria for the maximum monthly analysis is 6 months. The 3-
year maximum monthly metric (by size cut for 2010-2012) was identified as the
highest valid monthly average across the valid (1, 2, or 3) years.
• For annual average analysis: monthly averages were used to construct annual
averages,3 or more observations were required to make a valid; 6 valid months were
required to make a valid year (i.e., annual average) and 1, 2, or 3 valid years were
required to make a valid annual metric. Thus, the shortest duration that could
potentially meet these criteria for the annual average analysis is 6 months. The 3-year
annual mean metric (by size cut for 2010-2012) was identified as the average of the 1,
2, or 3 (2010, 2011, and/or 2012) valid annual means.
2C-1
-------
Definitions for Abbreviations
FEM - Federal equivalent method
FRM - Federal reference method
LC - Local conditions
POC - Parameter occurrence code
STP - Standard temperature and pressure
The process for classifying monitors as "source oriented" or "non-source-oriented" began
with the application of these criteria: (a) a minimum of 0.5 cumulative tons per year of Pb
emissions within 1 mile of the monitoring site based on 2008 NEI and/or (b) monitors identified
as "source-oriented" within AQS based on the same-name Monitoring Objective tag. Next, the
Regional monitoring leads reviewed the listings and provided local, and often monitor-specific
information and lastly Google Earth and more focused queries were applied.
The 14 monitors sited for the airport monitoring study, along with the 3 monitors sited at
airports estimated to emit at least 1 tpy were classified as source-oriented (airport) sites and the
remaining source-oriented sites were classified as source-oriented (non-airport) sites.
Among the remaining sites that were not classified as "source-oriented", previous source-
oriented sites were those that had previously been active source sites but for which current
information indicated the impacting facility had closed. The particular circumstances related to
the emission sources associated with these nine monitoring sites vary considerably. In some
instances the emission sources have been closed for more than a decade and the facility locations
have undergone remediation. For other sources, production and clean-up status was not fully
ascertained.
Non-source sites were what was left after making the airport source-oriented, non-airport
source-oriented, and previous source-oriented designations.
2C-2
-------
APPENDIX 2D
Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2010-2012.
State
Alabama
Alabama
Alaska
Arizona
Arizona
Arizona
Arizona
California
California
California
California
California
California
California
California
California
California
California
California
California
California
California
California
California
California
California
California
California
California
California
Colorado
County
Limestone
Pike
Anchorage Municipal
Gila
Gila
Maricopa
Pima
Fresno
Imperial
Los Angeles
Los Angeles
Los Angeles
Los Angeles
Los Angeles
Los Angeles
Los Angeles
Los Angeles
Los Angeles
Los Angeles
Los Angeles
Riverside
Riverside
San Bernardino
San Bernardino
San Diego
San Diego
San Diego
San Mateo
Santa Clara
Santa Clara
Arapahoe
Site
010830005
011090003
020200051
040071002
040078000
040134018
040191028
060190011
060250005
060371103
060371302
060371402
060371403
060371404
060371405
060371406
060371602
060374002
060374004
060375005
060651003
060658001
060711004
060719004
060730003
060731020
060731021
060812002
060852010
060852011
080050007
Maximum 3
month
mean
(M9/m3)
0.009
1.296
0.067
0.267
0.061
0.038
0.002
0.005
0.026
0.013
0.015
0.061
0.110
0.108
0.450
0.072
0.013
0.009
0.010
0.006
0.008
0.008
0.010
0.011
0.006
0.331
0.119
0.093
0.023
Annual
average
(M9/m3)
0.007
0.613
0.054
0.131
0.030
0.031
0.002
0.004
0.017
0.009
0.007
0.033
0.055
0.042
0.241
0.035
0.008
0.005
0.006
0.003
0.005
0.006
0.006
0.007
0.005
0.127
0.058
0.255
0.090
0.070
0.014
Maximum
monthly
mean
(M9/m3)
0.012
2.262
0.073
0.306
0.077
0.049
0.003
0.005
0.031
0.014
0.014
0.092
0.124
0.140
0.523
0.085
0.017
0.010
0.010
0.008
0.010
0.010
0.012
0.013
0.007
0.234
0.074
0.401
0.151
0.102
0.035
Non-airport
source-
oriented
(during
2010-
2012)
0
1
0
1
1
0
0
0
0
0
0
0
1
1
1
1
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
Airport
source-
oriented
1
0
1
0
0
1
0
0
0
0
0
1
0
0
0
0
0
0
0
0
0
0
0
0
0
1
1
1
1
1
1
Previous
source-
oriented
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
2D- 1
-------
APPENDIX 2D
Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2010-2012.
State
Colorado
District of Columt
Florida
Florida
Florida
Georgia
Georgia
Georgia
Georgia
Georgia
Hawaii
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Indiana
County
Denver
District of Columbia
Hillsborough
Hillsborough
Hillsborough
Bartow
DeKalb
Muscogee
Muscogee
Muscogee
Honolulu
Cook
Cook
Cook
Cook
Cook
Cook
Cook
Cook
Cook
Cook
Macon
Madison
Madison
Peoria
Peoria
Peoria
St. Glair
Whiteside
Winnebago
Delaware
Site
080310025
110010043
120570100
120571066
120571073
130150003
130890003
132150009
132150010
132150011
150030010
170310001
170310022
170310026
170310052
170310110
170310210
170313103
170313301
170314201
170316003
171150110
171190010
171193007
171430037
171430110
171430210
171630010
171950110
172010110
180350009
Maximum 3
month
mean
(M9/m3)
0.010
0.004
0.044
0.984
0.423
0.027
0.004
0.230
0.170
0.071
0.001
0.024
0.047
0.034
0.024
0.294
0.053
0.041
0.027
0.011
0.042
0.199
0.416
0.036
0.011
0.016
0.015
0.029
0.028
0.063
0.338
Annual
average
(M9/m3)
0.006
0.003
0.025
0.374
0.151
0.015
0.003
0.128
0.114
0.023
0.001
0.018
0.034
0.023
0.017
0.077
0.032
0.014
0.019
0.010
0.024
0.073
0.140
0.020
0.010
0.012
0.011
0.020
0.020
0.028
0.159
Maximum
monthly
mean
(M9/m3)
0.013
0.005
0.100
1.959
0.977
0.039
0.006
0.424
0.234
0.140
0.001
0.028
0.064
0.038
0.032
0.580
0.092
0.103
0.028
0.012
0.080
0.386
0.848
0.053
0.013
0.024
0.026
0.038
0.040
0.118
0.476
Non-airport
source-
oriented
(during
2010-
2012)
0
0
1
1
1
1
0
1
1
0
0
0
0
0
0
1
1
0
0
0
0
1
1
0
0
1
1
0
1
1
1
Airport
source-
oriented
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
Previous
source-
oriented
0
0
0
0
0
0
0
0
0
1
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
1
0
0
0
2D-2
-------
APPENDIX 2D
Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2010-2012.
State
Indiana
Indiana
Indiana
Indiana
Indiana
Indiana
Indiana
Indiana
Indiana
Indiana
Iowa
Iowa
Kansas
Kansas
Kentucky
Kentucky
Kentucky
Kentucky
Louisiana
Louisiana
Louisiana
Massachusetts
Michigan
Michigan
Michigan
Michigan
Michigan
Michigan
Michigan
Michigan
Minnesota
County
Lake
Lake
Lake
Lake
Marion
Marion
Marion
Porter
Porter
Vanderburgh
Pottawattamie
Scott
Saline
Wyandotte
Boyd
Madison
Madison
Russell
East Baton Rouge Pi
East Baton Rouge Pi
St. John the Baptist F
Nantucket County
Charlevoix
Ionia
Ionia
Kent
Oakland
Tuscola
Wayne
Wayne
Anoka
Site
180890023
180890032
180890033
180892008
180970063
180970076
180970078
181270023
181270027
181630020
191550011
191630015
201690004
202090021
210190016
211510003
211510005
212070001
220330009
220330014
220950003
250190001
260290011
260670002
260670003
260810020
261250013
261570001
261630001
261630033
270031002
Maximum 3
month
mean
(M9/m3)
0.077
0.060
0.139
0.046
0.079
0.020
0.011
0.022
0.041
0.006
0.263
0.012
0.421
0.011
0.004
0.248
1.584
0.063
0.002
0.011
0.053
0.010
0.006
0.049
0.284
0.008
0.022
0.034
0.006
0.023
0.011
Annual
average
(M9/m3)
0.031
0.023
0.055
0.020
0.028
0.010
0.006
0.013
0.027
0.004
0.123
0.010
0.164
0.008
0.003
0.057
0.703
0.027
0.002
0.004
0.025
0.009
0.005
0.071
0.096
0.005
0.019
0.021
0.005
0.012
0.006
Maximum
monthly
mean
(M9/m3)
0.087
0.144
0.298
0.103
0.125
0.029
0.021
0.032
0.085
0.008
0.282
0.024
0.488
0.012
0.007
0.281
2.244
0.109
0.003
0.027
0.066
0.020
0.010
0.298
0.414
0.010
0.027
0.063
0.007
0.034
0.012
Non-airport
source-
oriented
(during
2010-
2012)
1
1
1
0
1
1
0
1
1
0
1
0
1
0
1
1
1
1
0
1
1
0
1
1
1
0
0
1
0
0
0
Airport
source-
oriented
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
1
0
0
0
0
1
0
0
0
0
Previous
source-
oriented
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
2D-
-------
APPENDIX 2D
Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2010-2012.
State
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
County
Anoka
Beltrami
Cass
Dakota
Dakota
Dakota
Hennepin
Hennepin
Hennepin
Mille Lacs
Ramsey
St. Louis
St. Louis
Stearns
Washington
Washington
Iron
Iron
Iron
Iron
Iron
Iron
Iron
Iron
Iron
Jasper
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Site
270036020
270072303
270210001
270370020
270370465
270370470
270530963
270530966
270531007
270953051
271230871
271377001
271377555
271453053
271630438
271630446
290930016
290930021
290930027
290930029
290930032
290930033
290930034
290939007
290939008
290970005
290990004
290990005
290990009
290990013
290990020
Maximum 3
month
mean
(M9/m3)
0.038
0.004
0.259
0.002
0.004
0.005
0.004
0.001
0.007
0.008
0.004
0.008
0.005
0.001
0.882
1.147
0.083
0.115
0.057
0.402
0.581
0.387
0.019
1.122
0.396
0.191
0.305
0.865
Annual
average
(M9/m3)
0.017
0.001
0.001
0.004
0.096
0.001
0.003
0.004
0.003
0.000
0.005
0.002
0.003
0.004
0.003
0.000
0.484
0.522
0.033
0.038
0.354
0.026
0.241
0.392
0.209
0.014
0.888
0.223
0.055
0.135
0.546
Maximum
monthly
mean
(M9/m3)
0.078
0.002
0.002
0.018
0.568
0.004
0.006
0.008
0.007
0.002
0.010
0.022
0.008
0.012
0.008
0.003
1.436
1.698
0.107
0.271
0.987
0.105
0.615
0.844
0.538
0.024
1.576
0.498
0.280
0.418
1.233
Non-airport
source-
oriented
(during
2010-
2012)
1
0
0
0
1
0
0
0
0
0
0
0
0
1
0
0
1
1
0
0
1
1
1
1
1
0
1
1
1
1
1
Airport
source-
oriented
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
Previous
source-
oriented
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
1
1
0
0
0
0
0
0
0
0
0
0
0
2D-4
-------
APPENDIX 2D
Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2010-2012.
State
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Nebraska
Nebraska
Nebraska
Nevada
New Mexico
New York
New York
New York
New York
Ohio
Ohio
County
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Reynolds
Reynolds
Reynolds
Reynolds
St. Francois
St. Francois
St. Louis
St. Louis city
Dodge
Douglas
Nemaha
Clark
Bernalillo
Orange
Orange
Orange
Suffolk
Butler
Columbiana
Site
290990022
290990023
290990024
290990025
290990026
290990027
290999001
290999002
290999003
290999004
290999005
290999006
291790001
291790002
291790003
291790034
291870006
291870007
291892003
295100085
310530005
310550019
311270002
320030540
350010023
360713001
360713002
360713004
361030024
390170015
390290019
Maximum 3
month
mean
(M9/m3)
0.630
0.563
0.659
0.085
0.080
0.592
1.100
0.431
0.327
0.442
1.432
0.103
0.059
0.068
0.100
0.161
0.132
0.134
0.008
0.028
0.139
0.006
0.115
0.006
0.101
1.027
0.007
0.027
0.009
0.057
Annual
average
(M9/m3)
0.469
0.386
0.340
0.042
0.036
0.454
0.812
0.228
0.175
0.156
0.913
0.049
0.031
0.034
0.027
0.078
0.043
0.053
0.007
0.026
0.055
0.005
0.034
0.003
0.003
0.025
0.123
0.005
0.017
0.006
0.020
Maximum
monthly
mean
(M9/m3)
0.861
0.700
0.862
0.134
0.138
0.857
1.558
0.593
0.551
0.545
2.185
0.136
0.087
0.172
0.268
0.297
0.302
0.364
0.009
0.045
0.197
0.008
0.206
0.004
0.012
0.134
2.821
0.011
0.031
0.013
0.136
Non-airport
source-
oriented
(during
2010-
2012)
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
0
0
0
0
1
0
1
0
0
1
1
1
0
0
0
Airport
source-
oriented
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
1
0
0
Previous
source-
oriented
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
2D-5
-------
APPENDIX 2D
Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2010-2012.
State
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Oklahoma
Oklahoma
Oklahoma
Oklahoma
Oregon
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
County
Columbiana
Columbiana
Cuyahoga
Cuyahoga
Cuyahoga
Cuyahoga
Cuyahoga
Cuyahoga
Franklin
Fulton
Logan
Marion
Marion
Montgomery
Stark
Trumbull
Washington
Washington
Ottawa
Ottawa
Pittsburg
Tulsa
Yamhill
Allegheny
Allegheny
Allegheny
Allegheny
Beaver
Beaver
Beaver
Berks
Site
390290020
390290022
390350038
390350042
390350049
390350060
390350061
390350072
390490025
390510001
390910006
391010003
391010004
391137001
391510017
391550012
391670008
391670010
401159006
401159007
401210416
401431127
410711702
420030002
420030008
420030070
420031009
420070006
420070007
420070505
420110020
Maximum 3
month
mean
(M9/m3)
0.025
0.044
0.021
0.030
0.531
0.030
0.023
0.035
0.011
0.178
0.006
0.088
0.017
0.008
0.023
0.011
0.007
0.008
0.022
0.034
0.004
0.008
0.045
0.016
0.014
0.056
0.138
0.085
0.253
0.151
0.509
Annual
average
(M9/m3)
0.015
0.019
0.013
0.013
0.136
0.020
0.015
0.014
0.009
0.070
0.004
0.041
0.013
0.007
0.015
0.007
0.005
0.005
0.012
0.018
0.003
0.006
0.021
0.014
0.008
0.018
0.035
0.051
0.166
0.089
0.158
Maximum
monthly
mean
(M9/m3)
0.035
0.065
0.026
0.044
0.719
0.035
0.030
0.054
0.016
0.210
0.008
0.155
0.028
0.012
0.032
0.017
0.010
0.010
0.049
0.056
0.006
0.009
0.078
0.024
0.020
0.110
0.149
0.198
0.393
0.291
1.064
Non-airport
source-
oriented
(during
2010-
2012)
0
0
0
0
1
0
0
1
0
1
0
1
1
0
1
1
0
0
0
0
1
0
1
0
0
1
1
1
1
1
1
Airport
source-
oriented
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
Previous
source-
oriented
0
0
0
0
0
0
1
0
0
0
1
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
2D-6
-------
APPENDIX 2D
Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2010-2012.
State
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
South Carolina
South Carolina
South Carolina
South Carolina
South Carolina
South Carolina
South Carolina
Tennessee
Tennessee
Tennessee
Tennessee
Tennessee
Tennessee
Tennessee
Tennessee
Texas
Texas
County
Berks
Berks
Berks
Carbon
Delaware
Delaware
Franklin
Indiana
Lancaster
Lawrence
Luzerne
Philadelphia
Philadelphia
Westmoreland
Charleston
Florence
Florence
Florence
Greenville
Richland
Richland
Knox
Knox
Knox
Shelby
Sullivan
Sullivan
Sullivan
Sullivan
Cameron
Collin
Site
420110021
420110022
420111717
420250214
420450002
420450004
420550002
420630005
420710009
420730011
420790036
421010449
421011002
421290009
450190003
450418001
450418002
450418003
450450015
450790007
450790019
470930023
470930027
470931017
471570075
471633001
471633002
471633003
471633004
480610006
480850003
Maximum 3
month
mean
(M9/m3)
0.139
0.118
0.217
0.047
0.047
0.046
0.049
0.068
0.023
0.137
0.029
0.051
0.046
0.007
0.044
0.015
0.011
0.006
0.005
0.024
0.165
0.042
0.037
0.005
0.076
0.044
0.053
0.080
0.008
0.371
Annual
average
(M9/m3)
0.044
0.035
0.146
0.104
0.028
0.028
0.028
0.025
0.039
0.026
0.054
0.021
0.030
0.023
0.005
0.013
0.006
0.005
0.005
0.004
0.011
0.108
0.020
0.018
0.004
0.056
0.036
0.038
0.044
0.004
0.136
Maximum
monthly
mean
(M9/m3)
0.319
0.261
0.285
0.321
0.048
0.048
0.047
0.058
0.093
0.046
0.268
0.029
0.069
0.047
0.013
0.101
0.024
0.013
0.008
0.007
0.061
0.214
0.078
0.058
0.005
0.107
0.052
0.056
0.124
0.018
0.625
Non-airport
source-
oriented
(during
2010-
2012)
1
1
1
1
0
1
1
1
1
1
1
0
0
1
0
1
1
0
0
0
0
1
1
1
0
0
0
0
0
0
1
Airport
source-
oriented
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
Previous
source-
oriented
0
0
0
0
0
0
0
0
0
0
0
1
0
0
0
0
0
0
0
0
0
0
0
0
0
1
1
1
1
0
0
2D-7
-------
APPENDIX 2D
Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2010-2012.
State
Texas
Texas
Texas
Texas
Texas
Texas
Texas
Texas
Texas
Texas
Texas
Texas
Texas
Texas
Utah
Virginia
Virginia
Virginia
Virginia
Washington
Washington
West Virginia
Wisconsin
Puerto Rico
Puerto Rico
Puerto Rico
County
Collin
Collin
Collin
Dallas
El Paso
El Paso
El Paso
El Paso
El Paso
Harris
Harris
Kaufman
Potter
Webb
Salt Lake
Amherst
Buchanan
Henrico
Roanoke city
King
Snohomish
Cabell
Sheboygan
Arecibo Municipio, Pi
Bayamon Municipio,
Salinas Municipio, PL
Site
480850007
480850009
480850029
481130069
481410002
481410033
481410037
481410055
481410058
482011034
482011039
482570020
483750024
484790016
490351001
510090007
510270006
510870014
517700011
530330029
530610013
540110006
551170008
720130001
720210010
721230002
counts — >
Maximum 3
month
mean
(Mg/m3)
0.199
0.774
0.180
0.013
0.040
0.019
0.025
0.019
0.022
0.008
0.004
0.104
0.020
0.026
0.057
0.018
0.014
0.005
0.109
0.055
0.023
0.012
0.152
0.339
0.011
0.017
236
Annual
average
(Mg/m3)
0.093
0.388
0.052
0.009
0.022
0.017
0.022
0.010
0.016
0.005
0.003
0.044
0.007
0.018
0.024
0.006
0.012
0.005
0.033
0.036
0.013
0.010
0.056
0.171
0.004
0.008
243
Maximum
monthly
mean
(Mg/m3)
0.240
1.178
0.335
0.022
0.087
0.023
0.032
0.032
0.022
0.009
0.008
0.110
0.029
0.035
0.086
0.016
0.021
0.024
0.272
0.087
0.032
0.013
0.225
0.416
0.027
0.042
243
Non-airport
source-
oriented
(during
2010-
2012)
1
1
1
0
0
0
1
0
0
0
0
1
1
0
1
1
1
0
1
0
0
0
1
1
0
0
121
Airport
source-
oriented
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
1
1
0
0
0
0
0
15
Previous
source-
oriented
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
11
2D-8
-------
APPENDIX 2D
Table 2D-2. Pb-PM10 concentrations at urban Pb-PM10 sites, 2010-2012.
State
North Carolin
Georgia
Massachusetts
New Hampshi
North Carolin
Oregon
Oregon
Oregon
Oregon
Vermont
Florida
Florida
Kentucky
Nevada
New York
Arkansas
California
Delaware
District of Co
Florida
Idaho
Massachusetts
Rhode Island
Washington
California
Florida
Kentucky
Kentucky
Michigan
New Jersey
Arizona
Ohio
Texas
Arizona
Kentucky
Massachusetts
New York
Utah
County
Wake
DeKalb
Suffolk
Rockingham
Mecklenburg
Jackson
Jackson
Lane
Lane
Chittenden
Hillsborough
Pinellas
Henderson
Clark
Monroe
Pulaski
Sacramento
New Castle
District of Colum
Orange
Ada
Suffolk
Providence
King
Santa Clara
Pinellas
Fayette
Fayette
Wayne
Essex
Maricopa
Hamilton
Harris
Maricopa
Jefferson
Hampden
Bronx
Davis
Site
371830014
130890002
250250002
330150018
371190041
410290133
410292129
410390060
410390062
500070007
120573002
121030018
211010014
320030540
360551007
051190007
060670006
100032004
110010043
120951004
160010010
250250042
440070022
530330080
060850005
121030026
210670012
210670014
261630001
340130003
040139997
390610040
482011039
040134009
211110067
250132009
360050110
490110004
Maximum
3 -month
mean
(|ig/m3)
0.002
0.002
0.002
0.003
0.002
0.002
0.002
0.003
0.003
0.003
0.003
0.004
0.003
0.004
0.004
0.002
0.005
0.003
0.004
0.006
0.004
0.004
0.005
0.006
0.005
0.006
0.005
0.004
0.006
0.006
0.006
0.006
Annual
average
(|ig/m3)
0.002
0.001
0.002
0.002
0.002
0.002
0.002
0.001
0.002
0.001
0.002
0.002
0.003
0.003
0.003
0.003
0.002
0.003
0.003
0.002
0.002
0.003
0.003
0.003
0.002
0.002
0.003
0.004
0.004
0.003
0.004
0.005
0.002
0.005
0.005
0.004
0.006
0.003
Maximum
monthly
mean
(|ig/m3)
0.002
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.004
0.004
0.004
0.004
0.004
0.005
0.005
0.005
0.005
0.005
0.005
0.005
0.005
0.005
0.006
0.006
0.006
0.006
0.006
0.006
0.007
0.007
0.007
0.008
0.008
0.008
0.008
0.009
2D-9
-------
APPENDIX 2D
Table 2D-2. Pb-PM10 concentrations at urban Pb-PM10 sites, 2010-2012.
State
Illinois
Wisconsin
New York
Oregon
Connecticut
Maryland
Texas
Virginia
California
Kentucky
California
Illinois
Missouri
Michigan
Alabama
Mississippi
County
Cook
Milwaukee
Bronx
Multnomah
New Haven
Prince George's
Harris
Henri co
Los Angeles
Boyd
Riverside
St. Clair
St. Louis city
Wayne
Jefferson
Hinds
Site
170314201
550790010
360050080
410510246
090090027
240330030
482011035
510870014
060371103
210190002
060658001
171639010
295100085
261630033
010730023
280490019
counts — »
Maximum
3 -month
mean
(|ig/m3)
0.006
0.008
0.006
0.008
0.008
0.008
0.007
0.013
0.020
0.013
0.017
0.023
0.029
45
Annual
average
(|ig/m3)
0.004
0.006
0.006
0.004
0.004
0.004
0.005
0.003
0.007
0.013
0.006
0.015
0.012
0.011
0.019
0.074
54
Maximum
monthly
mean
(|ig/m3)
0.010
0.010
0.012
0.012
0.013
0.016
0.016
0.016
0.026
0.029
0.030
0.031
0.032
0.035
0.040
0.082
54
2D- 10
-------
APPENDIX 2D
Table 2D-3. Pb-PM25 concentrations at urban CSN PM25 sites, 2010-2012.
state_name
California
Hawaii
Wyoming
California
Colorado
Florida
Idaho
North Carolina
North Carolina
Oklahoma
Rhode Island
South Carolina
South Carolina
Texas
Vermont
Wisconsin
Alabama
Arizona
California
California
California
Colorado
District of Colum
Florida
Florida
Georgia
Georgia
Iowa
Iowa
Louisiana
Minnesota
Mississippi
Missouri
Nevada
New Jersey
New York
North Carolina
county _name
Kern
Honolulu
Laramie
Butte
Adams
Broward
Ada
Buncombe
Wake
Oklahoma
Providence
Charleston
Richland
Harris
Chittenden
Brown
Madison
Pima
Butte
Fresno
Ventura
Weld
District of Columbia
Hillsborough
Pinellas
Clarke
DeKalb
Linn
Polk
East Baton Rouge Parish
Hennepin
Hinds
Clay
Washoe
Morris
Monroe
Catawba
SITE
060299001
150030010
560210100
060070008
080010006
120111002
160010010
370210034
371830014
401091037
440071010
450190049
450790007
482011039
500070012
550090005
010890014
040191028
060070002
060190008
061112002
081230008
110010043
120573002
121030026
130590001
130890002
191130037
191530030
220330009
270530963
280490019
290470005
320310016
340273001
360551007
370350004
Maximum
3 -month
mean
(|ig/m3)
0.001
0.001
0.000
0.002
0.001
0.001
0.001
0.002
0.001
0.002
0.002
0.002
0.001
0.002
0.001
0.002
0.002
0.003
0.002
0.002
0.002
0.002
0.002
0.002
0.002
0.002
0.002
0.002
0.003
0.002
0.003
0.002
0.002
0.002
0.002
0.002
Annual
average
(|ig/m3)
0.001
0.000
0.000
0.002
0.001
0.001
0.001
0.001
0.001
0.001
0.002
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.002
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.002
0.001
0.002
0.002
0.001
0.001
0.001
0.001
0.002
0.002
Maximum
monthly
mean
(|ig/m3)
0.001
0.001
0.001
0.002
0.002
0.002
0.002
0.002
0.002
0.002
0.002
0.002
0.002
0.002
0.002
0.002
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.003
2D- 11
-------
APPENDIX 2D
Table 2D-3. Pb-PM25 concentrations at urban CSN PM25 sites, 2010-2012.
state_name
North Carolina
North Carolina
Oregon
Pennsylvania
South Dakota
Tennessee
Texas
Texas
Texas
Washington
California
California
Colorado
Georgia
Illinois
Indiana
Indiana
Maryland
Massachusetts
Michigan
Nevada
New Jersey
New Jersey
New Mexico
New York
North Dakota
Ohio
Ohio
Oklahoma
Pennsylvania
Tennessee
Washington
Arizona
Arizona
California
California
California
county _name
Mecklenburg
Rowan
Lane
Centre
Minnehaha
Roane
Cameron
Jefferson
Travis
Yakima
Fresno
Santa Clara
Denver
Bibb
Madison
Elkhart
Vanderburgh
Prince George's
Hampden
Wayne
Clark
Middlesex
Union
Bernalillo
New York
Cass
Franklin
Lucas
Tulsa
Adams
Shelby
Clark
Maricopa
Maricopa
Kern
Riverside
Sacramento
SITE
371190041
371590021
410392013
420270100
460990008
471451001
480612004
482450021
484530020
530770009
060190011
060850005
080310025
130210007
171199010
180390008
181630021
240330030
250130008
261630001
320030540
340230006
340390004
350010023
360610134
380171004
390490081
390950026
401431127
420010001
471570024
530110013
040134009
040139997
060290014
060658001
060670010
Maximum
3 -month
mean
(|ig/m3)
0.002
0.006
0.002
0.002
0.002
0.002
0.002
0.002
0.002
0.002
0.002
0.003
0.002
0.003
0.003
0.003
0.002
0.003
0.003
0.003
0.003
0.004
0.002
0.003
0.002
0.003
0.003
0.003
0.002
0.003
0.003
0.004
0.003
0.004
0.003
0.003
Annual
average
(|ig/m3)
0.001
0.001
0.001
0.001
0.001
0.002
0.001
0.002
0.001
0.001
0.001
0.001
0.001
0.001
0.002
0.002
0.002
0.001
0.002
0.002
0.001
0.002
0.002
0.001
0.002
0.001
0.002
0.002
0.001
0.001
0.002
0.001
0.003
0.002
0.001
0.002
0.002
Maximum
monthly
mean
(|ig/m3)
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.003
0.004
0.004
0.004
0.004
0.004
0.004
0.004
0.004
0.004
0.004
0.004
0.004
0.004
0.004
0.004
0.004
0.004
0.004
0.004
0.004
0.004
0.004
0.005
0.005
0.005
0.005
0.005
2D- 12
-------
APPENDIX 2D
Table 2D-3. Pb-PM25 concentrations at urban CSN PM25 sites, 2010-2012.
state_name
California
California
California
Delaware
Illinois
Indiana
Minnesota
New Jersey
New York
North Carolina
Pennsylvania
Pennsylvania
Tennessee
Tennessee
Tennessee
Texas
Virginia
Washington
West Virginia
California
Delaware
Illinois
Illinois
Iowa
Michigan
Nebraska
New York
Pennsylvania
Rhode Island
Tennessee
Wisconsin
Connecticut
Indiana
Kentucky
Maryland
Michigan
Ohio
county _name
San Diego
San Diego
Tulare
New Castle
Cook
Clark
Olmsted
Essex
Bronx
Davidson
Chester
Philadelphia
Davidson
Hamilton
Montgomery
Nueces
Henrico
Snohomish
Kanawha
Alameda
Kent
Cook
St. Clair
Linn
Kent
Douglas
Albany
Westmoreland
Providence
Shelby
Milwaukee
New Haven
Marion
Boyd
Baltimore
Monroe
Summit
SITE
060730003
060731002
061072002
100032004
170314201
180190006
271095008
340130003
360050110
370570002
420290100
421010055
470370023
470654002
471251009
483550034
510870014
530611007
540390011
060010007
100010003
170310076
171630900
191130040
260810020
310550019
360010005
421290008
440070022
471570075
550790026
090090027
180970078
210190017
240053001
261150005
391530023
Maximum
3 -month
mean
(|ig/m3)
0.004
0.004
0.004
0.004
0.003
0.003
0.003
0.003
0.004
0.003
0.004
0.003
0.003
0.003
0.003
0.003
0.002
0.004
0.003
0.005
0.003
0.004
0.005
0.003
0.004
0.004
0.004
0.004
0.004
0.003
0.004
0.004
0.004
0.005
0.006
0.005
0.005
Annual
average
(|ig/m3)
0.002
0.002
0.002
0.002
0.002
0.002
0.001
0.002
0.003
0.001
0.002
0.002
0.002
0.002
0.001
0.002
0.001
0.001
0.002
0.002
0.001
0.003
0.003
0.002
0.002
0.001
0.002
0.003
0.003
0.002
0.003
0.002
0.003
0.003
0.002
0.002
0.004
Maximum
monthly
mean
(|ig/m3)
0.005
0.005
0.005
0.005
0.005
0.005
0.005
0.005
0.005
0.005
0.005
0.005
0.005
0.005
0.005
0.005
0.005
0.005
0.005
0.006
0.006
0.006
0.006
0.006
0.006
0.006
0.006
0.006
0.006
0.006
0.006
0.007
0.007
0.007
0.007
0.007
0.007
2D- 13
-------
APPENDIX 2D
Table 2D-3. Pb-PM25 concentrations at urban CSN PM25 sites, 2010-2012.
state_name
Pennsylvania
Tennessee
Texas
Utah
Washington
West Virginia
West Virginia
Alaska
California
Florida
Georgia
Georgia
Illinois
Kansas
Kansas
Oregon
Pennsylvania
South Carolina
Texas
Texas
Texas
Washington
California
California
Georgia
Louisiana
Ohio
Pennsylvania
Pennsylvania
New York
Pennsylvania
West Virginia
Kentucky
North Carolina
Ohio
Pennsylvania
Pennsylvania
county _name
Erie
Knox
Dallas
Davis
King
Kanawha
Marshall
Fairbanks North Star Boroug
Solano
Leon
Richmond
Walker
DuPage
Sedgwick
Wyandotte
Multnomah
Washington
Greenville
Ellis
El Paso
Harris
Pierce
Sacramento
Stanislaus
Floyd
Bossier Parish
Hamilton
Lancaster
York
Queens
Lackawanna
Ohio
Fayette
Forsyth
Cuyahoga
Dauphin
Philadelphia
SITE
420490003
470931020
481130050
490110004
530330080
540391005
540511002
020900010
060950004
120730012
132450091
132950002
170434002
201730010
202090021
410510080
421255001
450450015
481390016
481410044
482010024
530530029
060670006
060990005
131150003
220150008
390610040
420710007
421330008
360810124
420692006
540690010
210670012
370670022
390350060
420430401
421010004
Maximum
3 -month
mean
(|ig/m3)
0.004
0.006
0.005
0.003
0.003
0.005
0.007
0.005
0.006
0.004
0.004
0.005
0.004
0.004
0.006
0.005
0.005
0.006
0.006
0.006
0.006
0.005
0.004
0.005
0.005
0.006
0.005
0.007
0.006
0.005
0.006
0.008
0.006
0.006
0.009
0.007
0.006
Annual
average
(|ig/m3)
0.002
0.003
0.003
0.002
0.001
0.002
0.004
0.002
0.003
0.002
0.001
0.002
0.002
0.002
0.004
0.003
0.003
0.002
0.003
0.003
0.003
0.003
0.001
0.003
0.002
0.003
0.002
0.003
0.002
0.002
0.003
0.005
0.002
0.002
0.006
0.003
0.003
Maximum
monthly
mean
(|ig/m3)
0.007
0.007
0.007
0.007
0.007
0.007
0.007
0.008
0.008
0.008
0.008
0.008
0.008
0.008
0.008
0.008
0.008
0.008
0.008
0.008
0.008
0.008
0.009
0.009
0.009
0.009
0.009
0.009
0.009
0.010
0.010
0.010
0.011
0.011
0.011
0.011
0.011
2D- 14
-------
APPENDIX 2D
Table 2D-3. Pb-PM25 concentrations at urban CSN PM25 sites, 2010-2012.
state_name
Kentucky
Massachusetts
Ohio
Ohio
Ohio
Texas
Utah
Washington
Wisconsin
Alabama
Arkansas
California
Missouri
New York
Pennsylvania
Utah
Iowa
Missouri
Ohio
Texas
Indiana
Pennsylvania
Texas
Illinois
Minnesota
Ohio
Pennsylvania
California
Pennsylvania
Alabama
Ohio
Pennsylvania
California
Michigan
Alabama
Michigan
Georgia
county _name
Jefferson
Suffolk
Cuyahoga
Jefferson
Lawrence
Dallas
Utah
King
Waukesha
Montgomery
Pulaski
Los Angeles
St. Louis city
Erie
Berks
Salt Lake
Scott
Jefferson
Mahoning
Lubbock
Lake
Northampton
El Paso
St. Clair
Anoka
Stark
Philadelphia
Alameda
Allegheny
Jefferson
Lorain
Cambria
Imperial
Wayne
Russell
Wayne
Muscogee
SITE
211110067
250250042
390350038
390811001
390870012
481130069
490494001
530330057
551330027
011011002
051190007
060371103
295100085
360290005
420110011
490353006
191630015
290990019
390990014
483030325
180890022
420950025
481410053
171639010
270031002
391510017
421011002
060010011
420030008
010732003
390933002
420210011
060250005
261630015
011130001
261630033
132150011
Maximum
3 -month
mean
(|ig/m3)
0.007
0.005
0.008
0.009
0.009
0.007
0.006
0.008
0.010
0.008
0.006
0.015
0.010
0.012
0.013
0.007
0.010
0.009
0.012
0.007
0.011
0.008
0.017
0.014
0.012
0.012
0.012
0.011
0.016
0.018
0.012
0.013
0.018
0.012
0.016
0.017
0.014
Annual
average
(|ig/m3)
0.004
0.002
0.004
0.005
0.005
0.003
0.002
0.004
0.005
0.003
0.002
0.002
0.006
0.007
0.007
0.002
0.005
0.004
0.007
0.003
0.005
0.003
0.006
0.010
0.006
0.007
0.006
0.004
0.008
0.006
0.006
0.007
0.012
0.006
0.004
0.006
0.004
Maximum
monthly
mean
(|ig/m3)
0.012
0.012
0.012
0.012
0.012
0.012
0.012
0.013
0.013
0.014
0.014
0.015
0.016
0.016
0.016
0.016
0.017
0.017
0.017
0.017
0.018
0.018
0.018
0.019
0.019
0.019
0.020
0.021
0.022
0.023
0.023
0.023
0.025
0.027
0.028
0.028
0.029
2D- 15
-------
APPENDIX 2D
Table 2D-3. Pb-PM25 concentrations at urban CSN PM25 sites, 2010-2012.
state_name
Michigan
Illinois
Washington
Ohio
California
Indiana
California
Pennsylvania
Alabama
Illinois
county _name
St. Clair
Madison
Pierce
Montgomery
San Bernardino
Lake
Orange
Allegheny
Jefferson
Cook
SITE
261470005
171190024
530530031
391130032
060712002
180892004
060590007
420030064
010730023
170310057
counts — »
Maximum
3 -month
mean
(|ig/m3)
0.015
0.020
0.015
0.014
0.037
0.022
0.042
0.038
0.041
0.069
193
Annual
average
(|ig/m3)
0.004
0.010
0.004
0.003
0.017
0.010
0.013
0.018
0.020
0.011
195
Maximum
monthly
mean
(|ig/m3)
0.030
0.032
0.032
0.033
0.037
0.037
0.043
0.051
0.063
0.199
195
2D- 16
-------
APPENDIX 2D
Table 2D-4. Pb-PM25 concentrations at non-urban IMPROVE PM25 sites, 2010-2012.
state_name
Alaska
Alaska
Alaska
Alaska
Alaska
Arizona
Arizona
Arizona
Arizona
Arkansas
Arkansas
California
California
California
California
California
California
Colorado
Colorado
Colorado
Colorado
Colorado
Colorado
Colorado
Colorado
Connecticut
Georgia
Hawaii
Hawaii
Hawaii
Idaho
Idaho
Iowa
Iowa
Iowa
Kansas
Kansas
county _name
Aleutians East Borough
Denali Borough
Kenai Peninsula Borough
Northwest Arctic Borough
Yukon-Koyukuk Census Are
Apache
Gila
Gila
Navajo
Newton
Polk
Del Norte
Inyo
Mariposa
Mono
Siskiyou
Trinity
Alamosa
Garfield
Jackson
La Plata
Montezuma
Pitkin
Rio Blanco
San Juan
Litchfield
Charlton
Hawaii
Hawaii
Hawaii
Custer
Lemhi
Montgomery
Van Buren
Van Buren
Brown
Chase
SITE
020130002
020680003
021220009
021889000
022909000
040018001
040070010
040078100
040170119
051019000
051130003
060150002
060270101
060430003
060519000
060930005
061059000
080039000
080450015
080579000
080679000
080839000
080979000
081039000
081119000
090050005
130499000
150019000
150019001
150019002
160370002
160590007
191370002
191770006
191779000
200139000
200170001
Maximum
3 -month
mean
(|ig/m3)
0.002
0.001
0.001
0.001
0.001
0.005
0.001
0.001
0.002
0.002
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.002
0.002
0.005
0.001
0.002
0.003
0.003
0.002
Annual
average
(|ig/m3)
0.001
0.000
0.000
0.000
0.001
0.003
0.001
0.001
0.001
0.001
0.000
0.001
0.001
0.000
0.000
0.001
0.000
0.001
0.000
0.001
0.001
0.000
0.001
0.001
0.001
0.001
0.000
0.002
0.002
0.002
0.001
Maximum
monthly
mean
(|ig/m3)
0.002
0.001
0.002
0.001
0.002
0.008
0.002
0.002
0.003
0.003
0.001
0.002
0.002
0.001
0.001
0.001
0.002
0.002
0.001
0.001
0.001
0.001
0.001
0.002
0.002
0.010
0.001
0.003
0.004
0.003
0.003
2D- 17
-------
APPENDIX 2D
Table 2D-4. Pb-PM25 concentrations at non-urban IMPROVE PM25 sites, 2010-2012.
state_name
Kansas
Louisiana
Maine
Maine
Maine
Maryland
Massachusetts
Michigan
Michigan
Michigan
Minnesota
Minnesota
Minnesota
Missouri
Missouri
Missouri
Montana
Montana
Montana
Montana
Montana
Montana
Montana
Montana
Montana
Montana
Nebraska
Nebraska
Nebraska
Nevada
Nevada
Nevada
New Hampshire
New Mexico
New Mexico
New Mexico
New Mexico
county _name
Trego
Winn Parish
Aroostook
Hancock
Washington
Garrett
Dukes
Keweenaw
Keweenaw
Schoolcraft
Lake
Rock
Winona
Cedar
Stoddard
Taney
Fergus
Flathead
Lake
Lewis and Clark
Powell
Ravalli
Roosevelt
Rosebud
Sanders
Sheridan
Garden
Thomas
Thurston
Elko
Mineral
White Pine
Coos
Catron
Chaves
Lincoln
Los Alamos
SITE
201950001
221279000
230031020
230090103
230291004
240239000
250070001
260839000
260839001
261539000
270759000
271339000
271699000
290390001
292070001
292130003
300279000
300299001
300479000
300499000
300779000
300819000
300859000
300870762
300899000
300919000
310699000
311719000
311739000
320079000
320219000
320339000
330074002
350039000
350059000
350279000
350281002
Maximum
3 -month
mean
(|ig/m3)
0.001
0.001
0.002
0.001
0.001
0.002
0.001
0.001
0.002
0.001
0.002
0.002
0.002
0.004
0.002
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
Annual
average
(|ig/m3)
0.001
0.001
0.001
0.001
0.001
0.002
0.001
0.001
0.001
0.001
0.002
0.002
0.002
0.003
0.002
0.001
0.000
0.000
0.000
0.000
0.000
0.001
0.000
0.000
0.001
0.001
0.001
0.000
0.000
0.001
0.001
0.001
0.001
0.001
Maximum
monthly
mean
(|ig/m3)
0.001
0.002
0.004
0.002
0.002
0.003
0.002
0.002
0.002
0.002
0.003
0.002
0.003
0.005
0.003
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.001
0.002
0.001
0.001
0.001
0.002
0.002
0.002
2D- 18
-------
APPENDIX 2D
Table 2D-4. Pb-PM25 concentrations at non-urban IMPROVE PM25 sites, 2010-2012.
state_name
New Mexico
New Mexico
New Mexico
New York
North Carolina
North Carolina
North Dakota
North Dakota
Ohio
Oklahoma
Oklahoma
Oklahoma
Oregon
Oregon
Oregon
South Dakota
Texas
Texas
Utah
Utah
Utah
Vermont
Virginia
Virginia
Washington
Washington
Washington
Washington
Washington
Washington
Washington
Washington
West Virginia
Wyoming
Wyoming
Wyoming
Wyoming
county _name
Rio Arriba
Socorro
Taos
Steuben
Avery
Hyde
Billings
Burke
Noble
Adair
Ellis
Kay
Klamath
Union
Wallowa
Jackson
Brewster
Culberson
Garfield
San Juan
Wayne
Bennington
Madison
Rockbridge
Clallam
Clallam
Clallam
Kittitas
Klickitat
Klickitat
Lewis
Okanogan
Tucker
Albany
Campbell
Johnson
Park
SITE
350399000
350539000
350559000
361019000
370110002
370959000
380070002
380130004
391219000
400019009
400450890
400719010
410358001
410610010
410630002
460710001
480430101
481099000
490170101
490379000
490559000
500038001
511139000
511639000
530090013
530090014
530090020
530370004
530390010
530390011
530410007
530470012
540939000
560019000
560050123
560199000
560299002
Maximum
3 -month
mean
(|ig/m3)
0.001
0.001
0.001
0.001
0.002
0.001
0.001
0.005
0.002
0.001
0.002
0.001
0.001
0.002
0.001
0.002
0.001
0.001
0.001
0.001
0.001
0.002
0.004
0.000
0.001
0.001
0.002
0.001
0.001
0.001
0.002
0.000
0.001
0.001
Annual
average
(|ig/m3)
0.001
0.001
0.000
0.002
0.001
0.001
0.001
0.001
0.003
0.002
0.001
0.001
0.000
0.000
0.001
0.001
0.001
0.001
0.001
0.001
0.000
0.001
0.001
0.003
0.000
0.001
0.001
0.001
0.001
0.000
0.000
0.001
0.000
0.000
0.000
Maximum
monthly
mean
(|ig/m3)
0.002
0.002
0.001
0.002
0.002
0.002
0.001
0.001
0.008
0.003
0.001
0.003
0.001
0.001
0.003
0.001
0.002
0.002
0.001
0.001
0.001
0.002
0.002
0.006
0.001
0.002
0.001
0.002
0.001
0.001
0.001
0.002
0.001
0.001
0.001
2D- 19
-------
APPENDIX 2D
Table 2D-4. Pb-PM25 concentrations at non-urban IMPROVE PM25 sites, 2010-2012.
state name
Wyoming
Wyoming
Wyoming
Virgin Islands
county name
Sublette
Sublette
Teton
St John
SITE
560359000
560359001
560399000
780209000
counts — »
Maximum
3 -month
mean
(|ig/m3)
0.001
0.001
0.001
0.001
102
Annual
average
(|ig/m3)
0.000
0.000
0.000
0.001
104
Maximum
monthly
mean
(|ig/m3)
0.001
0.001
0.001
0.001
104
2D-20
-------
APPENDIX 2D
Table 2D-5. Distribution of maximum 3-month means, 2010-2012.
(units are |jg/m3)
All Pb-TSP sites
Pb-TSP non-airport source-oriented sites
Pb-TSP airport source-oriented sites
Pb-TSP previous source-oriented sites
Pb-TSP not source-oriented sites
Pb-PM10 urban sites
Pb-PM2.5 urban CSN sites
Pb-PM2.5 non-urban IMPROVE sites
n
235
119
13
11
93
45
193
102
min
0.001
0.004
0.010
0.006
0.001
0.002
0.000
0.000
Pct1
0.001
0.004
0.010
0.006
0.001
0.002
0.001
0.000
Pct5
0.004
0.011
0.010
0.006
0.002
0.002
0.002
0.001
PctIO
0.006
0.017
0.010
0.023
0.004
0.002
0.002
0.001
Pct25
0.011
0.045
0.020
0.029
0.006
0.003
0.002
0.001
mean
0.1396
0.2493
0.0677
0.0554
0.0180
0.0065
0.0064
0.0014
PctSO
0.040
0.109
0.040
0.053
0.011
0.005
0.004
0.001
Pct75
0.132
0.338
0.070
0.080
0.024
0.006
0.007
0.002
Pct90
0.416
0.659
0.120
0.083
0.041
0.013
0.013
0.002
Pct95
0.659
1.100
0.330
0.115
0.047
0.020
0.017
0.003
Pct99
1.296
1.432
0.330
0.115
0.134
0.029
0.042
0.005
max
1.584
1.584
0.330
0.115
0.134
0.029
0.069
0.005
2D-21
-------
APPENDIX 2D
Table 2D-6. Distribution of annual means, 2010-2012.
(units are |jg/m3)
All Pb-TSP sites
Pb-TSP non-airport source-oriented sites
Pb-TSP airport source-oriented sites
Pb-TSP previous source-oriented sites
Pb-TSP not source-oriented sites
Pb-PM10 urban sites
Pb-PM2.5 urban CSN sites
Pb-PM2.5 non-urban IMPROVE sites
n
242
121
15
11
96
54
195
104
min
0.000
0.003
0.004
0.004
0.000
0.001
0.000
0.000
Pct1
0.001
0.003
0.004
0.004
0.000
0.001
0.000
0.000
Pct5
0.003
0.006
0.004
0.004
0.001
0.001
0.001
0.000
PctIO
0.004
0.012
0.009
0.015
0.003
0.002
0.001
0.000
Pct25
0.007
0.024
0.014
0.020
0.004
0.002
0.001
0.000
mean
0.0718
0.1261
0.0557
0.0298
0.0101
0.0055
0.0029
0.0009
PctSO
0.021
0.044
0.033
0.033
0.006
0.003
0.002
0.001
Pct75
0.055
0.140
0.071
0.038
0.014
0.005
0.003
0.001
Pct90
0.166
0.386
0.128
0.044
0.020
0.011
0.006
0.002
Pct95
0.386
0.522
0.254
0.056
0.028
0.015
0.008
0.002
Pct99
0.812
0.888
0.254
0.056
0.053
0.074
0.018
0.003
max
0.913
0.913
0.254
0.056
0.053
0.074
0.020
0.003
2D-22
-------
APPENDIX 2D
Table 2D-7. Distribution of maximum monthly means, 2010-2012.
(units are |jg/m3)
All Pb-TSP sites
Pb-TSP non-airport source-oriented sites
Pb-TSP airport source-oriented sites
Pb-TSP previous source-oriented sites
Pb-TSP not source-oriented sites
Pb-PM10 urban sites
Pb-PM2.5 urban CSN sites
Pb-PM2.5 non-urban IMPROVE sites
n
243
121
15
11
96
54
184
104
min
0.000
0.010
0.010
0.010
0.000
0.000
0.000
0.000
Pct1
0.000
0.010
0.010
0.010
0.000
0.000
0.000
0.000
Pct5
0.010
0.020
0.010
0.010
0.000
0.000
0.000
0.000
PctIO
0.010
0.030
0.020
0.030
0.010
0.000
0.000
0.000
Pct25
0.020
0.080
0.030
0.030
0.010
0.000
0.000
0.000
mean
0.2213
0.4012
0.0933
0.0882
0.0299
0.0109
0.0098
0.0005
PctSO
0.060
0.210
0.070
0.060
0.010
0.010
0.010
0.000
Pct75
0.230
0.500
0.100
0.120
0.030
0.010
0.010
0.000
Pct90
0.580
0.990
0.230
0.140
0.060
0.030
0.020
0.000
Pct95
0.990
1.580
0.400
0.270
0.100
0.030
0.030
0.000
Pct99
2.240
2.260
0.400
0.270
0.360
0.080
0.050
0.010
max
2.820
2.820
0.400
0.270
0.360
0.080
0.200
0.010
2D-23
-------
APPENDIX 2D
Table 2D-8. Pb-TSP metric ratios, 2010-2012.
State
Alabama
Alabama
Alaska
Arizona
Arizona
Arizona
Arizona
California
California
California
California
California
California
California
California
California
California
California
California
California
California
California
California
California
California
California
California
California
California
California
Colorado
Colorado
District of Columbia
Florida
Florida
County
Limestone
Pike
Anchorage Municipality
Gila
Gila
Maricopa
Pima
Fresno
Imperial
Los Angeles
Los Angeles
Los Angeles
Los Angeles
Los Angeles
Los Angeles
Los Angeles
Los Angeles
Los Angeles
Los Angeles
Los Angeles
Riverside
Riverside
San Bernardino
San Bernardino
San Diego
San Diego
San Diego
San Mateo
Santa Clara
Santa Clara
Arapahoe
Denver
District of Columbia
Hillsborough
Hillsborough
Site
010830005
011090003
020200051
040071002
040078000
040134018
040191028
060190011
060250005
060371103
060371302
060371402
060371403
060371404
060371405
060371406
060371602
060374002
060374004
060375005
060651003
060658001
060711004
060719004
060730003
060731020
060731021
060812002
060852010
060852011
080050007
080310025
110010043
120570100
120571066
Maximum
3-month
mean
(M9/m3)
0.009
1.296
0.067
0.267
0.061
0.038
0.002
0.005
0.026
0.013
0.015
0.061
0.110
0.108
0.450
0.072
0.013
0.009
0.010
0.006
0.008
0.008
0.010
0.011
0.006
0.331
0.119
0.093
0.023
0.010
0.004
0.044
0.984
Annual
average
(M9/m3)
0.007
0.613
0.054
0.131
0.030
0.031
0.002
0.004
0.017
0.009
0.007
0.033
0.055
0.042
0.241
0.035
0.008
0.005
0.006
0.003
0.005
0.006
0.006
0.007
0.005
0.127
0.058
0.255
0.090
0.070
0.014
0.006
0.003
0.025
0.374
Ratio of max
3-month
mean to
annual mean
1.2857
2.1142
1.2407
2.0382
2.0333
1.2258
1.0000
1.2500
1.5294
1.4444
2.1429
1.8485
2.0000
2.5714
1.8672
2.0571
1.6250
1.8000
1.6667
2.0000
1.6000
1.3333
1.6667
1.5714
1.2000
1.2980
1.3222
1.3286
1.6429
1.6667
1.3333
1.7600
2.6310
Ratio of max 3-
month mean to
annual mean for
CBSAsMM
population
1.2258
1.4444
2.1429
1.8485
2.0000
2.5714
1.8672
2.0571
1.6250
1.8000
1.6667
2.0000
1.6000
1.3333
1.6667
1.5714
1.2000
1.2980
1.3222
1.3286
1.6429
1.6667
1.3333
1.7600
2.6310
2D-24
-------
APPENDIX 2D
Table 2D-8. Pb-TSP metric ratios, 2010-2012.
State
Florida
Georgia
Georgia
Georgia
Georgia
Georgia
Hawaii
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Illinois
Indiana
Indiana
Indiana
Indiana
Indiana
Indiana
Indiana
Indiana
Indiana
County
Hillsborough
Bartow
DeKalb
Muscogee
Muscogee
Muscogee
Honolulu
Cook
Cook
Cook
Cook
Cook
Cook
Cook
Cook
Cook
Cook
Macon
Madison
Madison
Peoria
Peoria
Peoria
St. Glair
Whiteside
Winnebago
Delaware
Lake
Lake
Lake
Lake
Marion
Marion
Marion
Porter
Site
120571073
130150003
130890003
132150009
132150010
132150011
150030010
170310001
170310022
170310026
170310052
170310110
170310210
170313103
170313301
170314201
170316003
171150110
171190010
171193007
171430037
171430110
171430210
171630010
171950110
172010110
180350009
180890023
180890032
180890033
180892008
180970063
180970076
180970078
181270023
Maximum
3-month
mean
(M9/m3)
0.423
0.027
0.004
0.230
0.170
0.071
0.001
0.024
0.047
0.034
0.024
0.294
0.053
0.041
0.027
0.011
0.042
0.199
0.416
0.036
0.011
0.016
0.015
0.029
0.028
0.063
0.338
0.077
0.060
0.139
0.046
0.079
0.020
0.011
0.022
Annual
average
(M9/m3)
0.151
0.015
0.003
0.128
0.114
0.023
0.001
0.018
0.034
0.023
0.017
0.077
0.032
0.014
0.019
0.010
0.024
0.073
0.140
0.020
0.010
0.012
0.011
0.020
0.020
0.028
0.159
0.031
0.023
0.055
0.020
0.028
0.010
0.006
0.013
Ratio of max
3-month
mean to
annual mean
2.8013
1.8000
1.3333
1.7969
1.4912
3.0870
1.0000
1.3333
1.3824
1.4783
1.4118
3.8182
1.6563
2.9286
1.4211
1.1000
1.7500
2.7260
2.9714
1.8000
1.1000
1.3333
1.3636
1.4500
1.4000
2.2500
2.1258
2.4839
2.6087
2.5273
2.3000
2.8214
2.0000
1.8333
1.6923
Ratio of max 3-
month mean to
annual mean for
CBSAsMM
population
2.8013
1.8000
1.3333
1.3333
1.3824
1.4783
1.4118
3.8182
1.6563
2.9286
1.4211
1.1000
1.7500
2.9714
1.8000
1.4500
2.4839
2.6087
2.5273
2.3000
2.8214
2.0000
1.8333
1.6923
2D-25
-------
APPENDIX 2D
Table 2D-8. Pb-TSP metric ratios, 2010-2012.
State
Indiana
Indiana
Iowa
Iowa
Kansas
Kansas
Kentucky
Kentucky
Kentucky
Kentucky
Louisiana
Louisiana
Louisiana
Massachusetts
Michigan
Michigan
Michigan
Michigan
Michigan
Michigan
Michigan
Michigan
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
Minnesota
County
Porter
Vanderburgh
Pottawattamie
Scott
Saline
Wyandotte
Boyd
Madison
Madison
Russell
East Baton Rouge Parish
East Baton Rouge Parish
St. John the Baptist Parish
Nantucket County
Charlevoix
Ionia
Ionia
Kent
Oakland
Tuscola
Wayne
Wayne
Anoka
Anoka
Beltrami
Cass
Dakota
Dakota
Dakota
Hennepin
Hennepin
Hennepin
Mille Lacs
Ramsey
St. Louis
Site
181270027
181630020
191550011
191630015
201690004
202090021
210190016
211510003
211510005
212070001
220330009
220330014
220950003
250190001
260290011
260670002
260670003
260810020
261250013
261570001
261630001
261630033
270031002
270036020
270072303
270210001
270370020
270370465
270370470
270530963
270530966
270531007
270953051
271230871
271377001
Maximum
3-month
mean
(M9/m3)
0.041
0.006
0.263
0.012
0.421
0.011
0.004
0.248
1.584
0.063
0.002
0.011
0.053
0.010
0.006
0.049
0.284
0.008
0.022
0.034
0.006
0.023
0.011
0.038
0.004
0.259
0.002
0.004
0.005
0.004
0.001
0.007
0.008
Annual
average
(M9/m3)
0.027
0.004
0.123
0.010
0.164
0.008
0.003
0.057
0.703
0.027
0.002
0.004
0.025
0.009
0.005
0.071
0.096
0.005
0.019
0.021
0.005
0.012
0.006
0.017
0.001
0.001
0.004
0.096
0.001
0.003
0.004
0.003
0.000
0.005
0.002
Ratio of max
3-month
mean to
annual mean
1.5185
1.5000
2.1382
1.2000
2.5671
1.3750
1.3333
4.3509
2.2532
2.3333
1.0000
2.7500
2.1200
1.1111
1.2000
0.6901
2.9583
1.6000
1.1579
1.6190
1.2000
1.9167
1.8333
2.2353
1.0000
2.6979
2.0000
1.3333
1.2500
1.3333
1.4000
4.0000
Ratio of max 3-
month mean to
annual mean for
CBSAsMM
population
1.5185
1.3750
2.1200
1.1579
1.2000
1.9167
1.8333
2.2353
1.0000
2.6979
2.0000
1.3333
1.2500
1.3333
1.4000
2D-26
-------
APPENDIX 2D
Table 2D-8. Pb-TSP metric ratios, 2010-2012.
State
Minnesota
Minnesota
Minnesota
Minnesota
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
Missouri
County
St. Louis
Stearns
Washington
Washington
Iron
Iron
Iron
Iron
Iron
Iron
Iron
Iron
Iron
Jasper
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Jefferson
Reynolds
Reynolds
Reynolds
Reynolds
Site
271377555
271453053
271630438
271630446
290930016
290930021
290930027
290930029
290930032
290930033
290930034
290939007
290939008
290970005
290990004
290990005
290990009
290990013
290990020
290990022
290990023
290990024
290990025
290990026
290990027
290999001
290999002
290999003
290999004
290999005
290999006
291790001
291790002
291790003
291790034
Maximum
3-month
mean
(M9/m3)
0.004
0.008
0.005
0.001
0.882
1.147
0.083
0.115
0.057
0.402
0.581
0.387
0.019
1.122
0.396
0.191
0.305
0.865
0.630
0.563
0.659
0.085
0.080
0.592
1.100
0.431
0.327
0.442
1.432
0.103
0.059
0.068
0.100
0.161
Annual
average
(M9/m3)
0.003
0.004
0.003
0.000
0.484
0.522
0.033
0.038
0.354
0.026
0.241
0.392
0.209
0.014
0.888
0.223
0.055
0.135
0.546
0.469
0.386
0.340
0.042
0.036
0.454
0.812
0.228
0.175
0.156
0.913
0.049
0.031
0.034
0.027
0.078
Ratio of max
3-month
mean to
annual mean
1.3333
2.0000
1.6667
1.8223
2.1973
2.5152
3.0263
2.1923
1.6680
1.4821
1.8517
1.3571
1.2635
1.7758
3.4727
2.2593
1.5842
1.3433
1.4585
1.9382
2.0238
2.2222
1.3040
1.3547
1.8904
1.8686
2.8333
1.5685
2.1020
1.9032
2.0000
3.7037
2.0641
Ratio of max 3-
month mean to
annual mean for
CBSAsMM
population
1.6667
1.2635
1.7758
3.4727
2.2593
1.5842
1.3433
1.4585
1.9382
2.0238
2.2222
1.3040
1.3547
1.8904
1.8686
2.8333
1.5685
2.1020
2D-27
-------
APPENDIX 2D
Table 2D-8. Pb-TSP metric ratios, 2010-2012.
State
Missouri
Missouri
Missouri
Missouri
Nebraska
Nebraska
Nebraska
Nevada
New Mexico
New York
New York
New York
New York
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Ohio
Oklahoma
Oklahoma
County
St. Francois
St. Francois
St. Louis
St. Louis city
Dodge
Douglas
Nemaha
Clark
Bernalillo
Orange
Orange
Orange
Suffolk
Butler
Columbiana
Columbiana
Columbiana
Cuyahoga
Cuyahoga
Cuyahoga
Cuyahoga
Cuyahoga
Cuyahoga
Franklin
Fulton
Logan
Marion
Marion
Montgomery
Stark
Trumbull
Washington
Washington
Ottawa
Ottawa
Site
291870006
291870007
291892003
295100085
310530005
310550019
311270002
320030540
350010023
360713001
360713002
360713004
361030024
390170015
390290019
390290020
390290022
390350038
390350042
390350049
390350060
390350061
390350072
390490025
390510001
390910006
391010003
391010004
391137001
391510017
391550012
391670008
391670010
401159006
401159007
Maximum
3-month
mean
(M9/m3)
0.132
0.134
0.008
0.028
0.139
0.006
0.115
0.006
0.101
1.027
0.007
0.027
0.009
0.057
0.025
0.044
0.021
0.030
0.531
0.030
0.023
0.035
0.011
0.178
0.006
0.088
0.017
0.008
0.023
0.011
0.007
0.008
0.022
0.034
Annual
average
(M9/m3)
0.043
0.053
0.007
0.026
0.055
0.005
0.034
0.003
0.003
0.025
0.123
0.005
0.017
0.006
0.020
0.015
0.019
0.013
0.013
0.136
0.020
0.015
0.014
0.009
0.070
0.004
0.041
0.013
0.007
0.015
0.007
0.005
0.005
0.012
0.018
Ratio of max
3-month
mean to
annual mean
3.0698
2.5283
1.1429
1.0769
2.5273
1.2000
3.3824
2.0000
4.0400
8.3496
1.4000
1.5882
1.5000
2.8500
1.6667
2.3158
1.6154
2.3077
3.9044
1.5000
1.5333
2.5000
1.2222
2.5429
1.5000
2.1463
1.3077
1.1429
1.5333
1.5714
1.4000
1.6000
1.8333
1.8889
Ratio of max 3-
month mean to
annual mean for
CBSAsMM
population
1.1429
1.0769
4.0400
8.3496
1.4000
1.5882
1.5000
1.6154
2.3077
3.9044
1.5000
1.5333
2.5000
1.2222
2D-28
-------
APPENDIX 2D
Table 2D-8. Pb-TSP metric ratios, 2010-2012.
State
Oklahoma
Oklahoma
Oregon
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
Pennsylvania
South Carolina
South Carolina
South Carolina
South Carolina
South Carolina
South Carolina
South Carolina
Tennessee
Tennessee
Tennessee
County
Pittsburg
Tulsa
Yamhill
Allegheny
Allegheny
Allegheny
Allegheny
Beaver
Beaver
Beaver
Berks
Berks
Berks
Berks
Carbon
Delaware
Delaware
Franklin
Indiana
Lancaster
Lawrence
Luzerne
Philadelphia
Philadelphia
Westmoreland
Charleston
Florence
Florence
Florence
Greenville
Richland
Richland
Knox
Knox
Knox
Site
401210416
401431127
410711702
420030002
420030008
420030070
420031009
420070006
420070007
420070505
420110020
420110021
420110022
420111717
420250214
420450002
420450004
420550002
420630005
420710009
420730011
420790036
421010449
421011002
421290009
450190003
450418001
450418002
450418003
450450015
450790007
450790019
470930023
470930027
470931017
Maximum
3-month
mean
(M9/m3)
0.004
0.008
0.045
0.016
0.014
0.056
0.138
0.085
0.253
0.151
0.509
0.139
0.118
0.217
0.047
0.047
0.046
0.049
0.068
0.023
0.137
0.029
0.051
0.046
0.007
0.044
0.015
0.011
0.006
0.005
0.024
0.165
0.042
0.037
Annual
average
(M9/m3)
0.003
0.006
0.021
0.014
0.008
0.018
0.035
0.051
0.166
0.089
0.158
0.044
0.035
0.146
0.104
0.028
0.028
0.028
0.025
0.039
0.026
0.054
0.021
0.030
0.023
0.005
0.013
0.006
0.005
0.005
0.004
0.011
0.108
0.020
0.018
Ratio of max
3-month
mean to
annual mean
1.3333
1.3333
2.1429
1.1429
1.7500
3.1111
3.9429
1.6667
1.5241
1.6966
3.2215
3.1591
3.3714
1.4863
1.6786
1.6786
1.6429
1.9600
1.7436
0.8846
2.5370
1.3810
1.7000
2.0000
1.4000
3.3846
2.5000
2.2000
1.2000
1.2500
2.1818
1.5278
2.1000
2.0556
Ratio of max 3-
month mean to
annual mean for
CBSAsMM
population
2.1429
1.1429
1.7500
3.1111
3.9429
1.6667
1.5241
1.6966
1.6786
1.6786
1.3810
1.7000
2.0000
2D-29
-------
APPENDIX 2D
Table 2D-8. Pb-TSP metric ratios, 2010-2012.
State
Tennessee
Tennessee
Tennessee
Tennessee
Tennessee
Texas
Texas
Texas
Texas
Texas
Texas
Texas
Texas
Texas
Texas
Texas
Texas
Texas
Texas
Texas
Texas
Utah
Virginia
Virginia
Virginia
Virginia
Washington
Washington
West Virginia
Wisconsin
Puerto Rico
Puerto Rico
Puerto Rico
County
Shelby
Sullivan
Sullivan
Sullivan
Sullivan
Cameron
Collin
Collin
Collin
Collin
Dallas
El Paso
El Paso
El Paso
El Paso
El Paso
Harris
Harris
Kaufman
Potter
Webb
Salt Lake
Amherst
Buchanan
Henrico
Roanoke city
King
Snohomish
Cabell
Sheboygan
Arecibo Municipio, Puerto Rico
Bayamon Municipio, Puerto Rico
Salinas Municipio, Puerto Rico
Site
471570075
471633001
471633002
471633003
471633004
480610006
480850003
480850007
480850009
480850029
481130069
481410002
481410033
481410037
481410055
481410058
482011034
482011039
482570020
483750024
484790016
490351001
510090007
510270006
510870014
517700011
530330029
530610013
540110006
551170008
720130001
720210010
721230002
Maximum
3-month
mean
(M9/m3)
0.005
0.076
0.044
0.053
0.080
0.008
0.371
0.199
0.774
0.180
0.013
0.040
0.019
0.025
0.019
0.022
0.008
0.004
0.104
0.020
0.026
0.057
0.018
0.014
0.005
0.109
0.055
0.023
0.012
0.152
0.339
0.011
0.017
Annual
average
(M9/m3)
0.004
0.056
0.036
0.038
0.044
0.004
0.136
0.093
0.388
0.052
0.009
0.022
0.017
0.022
0.010
0.016
0.005
0.003
0.044
0.007
0.018
0.024
0.006
0.012
0.005
0.033
0.036
0.013
0.010
0.056
0.171
0.004
0.008
Ratio of max
3-month
mean to
annual mean
1.2500
1.3571
1.2222
1.3947
1.8182
2.0000
2.7279
2.1398
1.9948
3.4615
1.4444
1.8182
1.1176
1.1364
1.9000
1.3750
1.6000
1.3333
2.3636
2.8571
1.4444
2.3750
3.0000
1.1667
1.0000
3.3030
1.5278
1.7692
1.2000
2.7143
1.9825
2.7500
2.1250
Ratio of max 3-
month mean to
annual mean for
CBSAsMM
population
1.2500
2.7279
2.1398
1.9948
3.4615
1.4444
1.6000
1.3333
2.3636
2.3750
1.0000
1.5278
1.7692
2.7500
2D-30
-------
APPENDIX 3A
INTERPOLATED RISK ESTIMATES FOR THE GENERALIZED
(LOCAL) URBAN CASE STUDY
This Appendix describes the method used to develop risk estimates for conditions just
meeting the current standard (0.15 |ig/m3, as a maximum 3-month average) for the generalized
(local) urban case study. These risk estimates were developed by interpolation from the 2007
REA results for this case study. The general approach was to identify the two alternative
standard scenarios simulated in the 2007 REA which represented air quality conditions
bracketing those for the current standard and then linearly interpolate an estimate of risk for the
current standard based on the slope created from the two bracketing estimates. In representing
air quality conditions for these purposes, we focused on the annual average air Pb concentration
estimates as that is the metric which had been the IEUBK model inputs for the various air quality
scenarios (IEUBK does not accept air quality inputs of a temporal scale shorter than a year).1 An
annual average concentration estimate to represent the current standard was identified in a
manner consistent with that employed in the 2007 REA for this case study (see section 3.4.3.2
above, use of 2003-2005 data) with the use of currently available monitoring data (2010-2012)
for relationships between air quality metrics for representation of the current standard. By this
method, the air quality scenario for the current standard (0.15 |ig/m3, as a not-to-be-exceeded 3-
month average) was found to be bracketed by the scenarios for alternative standards of 0.5 and
0.20 |ig/m3 (maximum monthly averages). A risk estimate for the current standard was then
derived using the slope relating generalized (local) urban case study IQ loss to the annual
average Pb concentration used for those two air quality scenarios. We used this interpolation
approach to develop median risk estimates for the current standard based on each of the four C-R
functions. Details on the method for the interpolation approach are provided below.
1. Identify an estimate of annual average air Pb concentration to represent each air quality
scenario. For the alternative scenarios, this was done in the 2007 REA using the 2003-
2005 Pb-TSP dataset for urban areas of population greater than one million. For analysis
1 Although many different patterns of temporally varying air concentration will just meet a given potential
alternative standard, the shortest time step accommodated by the blood Pb model is a year. Thus, the air Pb
concentration inputs to the blood Pb model for each air quality scenario are annual average air Pb concentrations.
For the generalized (local) urban case study, the national Pb-TSP monitoring dataset was analyzed to characterize
the distribution of site-specific relationships between metrics reflecting the averaging time and form for the air
quality scenarios being assessed (Table 3-8 of this document) and the annual average. The IEUBK annual average
input was then derived by multiplying the level for a given air quality scenario by the ratio for the averaging time
and form for that air quality scenario. For the location-specific case studies, however, the full temporally varying air
Pb concentration dataset for each exposure zone was used to derive the average annual concentration for the IEUBK
input.
3A-1
-------
of the current standard here, this uses the recent Pb-TSP dataset (2010-2012) for urban
areas of population greater than one million. The concentration in terms of the metric
being assessed (e.g., maximum 3-month or calendar quarter average) was derived per
monitoring site, as was the annual average concentration and also the ratio of the two
(2007 REA, Appendix A; Appendix 2D of this document). From the average of the
monitor-specific ratios we derived the annual average estimate. [In the 2007 REA, this
was the IEUBK air quality input for each AQ scenario.] With the 2010-2012 data, the
average, across monitors in urban areas greater than 1 million population, of the ratio of
maximum 3-month average to annual average is 1.92 (Appendix 2D in this document).
This ratio was used to derive an annual average air Pb-TSP concentration
estimate to represent the current standard scenario (annual value = 0.15 ug/m3
* 1/1.92 = 0.078 ug/m3). The annual average values for the scenarios
included in the 2007 REA and also for the current standard scenario
considered in this interpolation are shown in Table 3A-1 below.
Table 3A-1. Annual average air Pb-TSP concentration estimates for different air quality
scenarios.
Air Quality Scenarios
Maximum
Quarterly Average D
(ug/m3)
1.5 (previous NAAQS)
0.2
Maximum
Monthly Average
(ug/m3)
0.5
0.2
0.05
0.02
Maximum
3-month Average
(ug/m3)
0.15
Annual Average Estimate
(ug/m3)
0.60
0.130
0.08
0.078*
0.05
0.013
0.005
* Derived as described in step 1 using 2010-2012 air quality dataset.
2. Identify the two "bounding" alternative standard levels that will be used to derive a
slope for the risk interpolation for the current standard level. Based on comparison of
the annual ambient air Pb estimates for each of the 2007 REA air quality scenarios and
for the current standard we determine which scenarios "bound" the current standard (in
terms of the annual average ambient Pb estimate). As Table 3A-1 above shows, the
bounding scenarios are the scenarios for just meeting maximum monthly average
concentrations of 0.5 and 0.2 ug/m3.
3. Calculate the slopes of generalized (local) urban case study IQ loss per unit annual
average Pb estimate for each risk estimate of interest for the two bounding scenarios.
This calculation is (IQ Lossscenario x - IQ Lossscenario Y)/ (annual averagescenario x - annual
averagescenario Y). The risk estimates for the 4 different C-R functions and two exposure
pathway categories of interest {Recent Air and Recent + Past Air), with the derived
slopes, are in Table 3A-2.
3A-2
-------
Table 3A-2. Risk estimates for bounding air quality scenarios and associated slopes.
0.2 jig/m3, max
quarterly average
0.2 jig/m3 max
monthly average
Slope *
Risk Estimates
for different C-R functions and exposure pathway categories
Log-linear with
low-exposure
linearization
Recent
air
1.53
1.21
10.69
Recent +
past air
3.37
3.16
7.03
Dual linear -
stratified
atlOug/dLpeak
Recent
air
0.54
0.41
4.10
Recent +
past air
1.18
1.08
3.38
Log-linear with
cutpoint
Recent
air
0.63
0.47
5.31
Recent +
past air
1.38
1.22
5.28
Dual linear -
stratified
at 7.5 ug/dL peak
Recent
air
1.97
1.53
14.77
Recent +
past air
4.34
3.99
11.66
* In terms of points IQ loss per unit annual average air Pb in generalized (local) urban case study (see texts for explanation).
4. Derive interpolated risk estimates for the current standard scenario. Using the
slopes presented in Table 3 A-2 and the lower bounding air quality scenario risk
estimates, derive corresponding risk estimates for the current standard scenario:
Risk = lower bounding risk + (increment annual average Pb * slope)
Where:
• lower bounding risk = risk for the lower bound air quality scenario (i.e.,
for 0.2 u.g/m3 maximum monthly average)
• increment annual average Pb is the difference between the annual average
estimates for the current standard and the lower bounding scenario.
• slope is the value described in Step 4, which differs across the 8
combinations of C-R functions and exposure pathway categories.
The resulting interpolated risk estimates are presented in Table 3A-3.
Table 3A-3. Interpolated risk estimates for the current NAAQS scenario for the
generalized (local) urban case study.
Interpolated
Estimate*
Risk Estimates
for different C-R functions and exposure pathway categories
Log-linear with
low-exposure
linearization
Recent
air
1.51
Recent +
past air
3.36
Dual linear -
stratified
atlOug/dLpeak
Recent
air
0.53
Recent +
past air
1.17
Log-linear with
cutpoint
Recent
air
0.62
Recent +
past air
1.37
Dual linear -
stratified
at 7.5 ug/dL peak
Recent
air
1.94
Recent +
past air
4.32
* Points IQ loss in generalized (local) urban case study (see text for explanation).
3A-3
-------
APPENDIX 5A
ADDITIONAL DETAIL ON 2006 ECOLOGICAL SCREENING
ASSESSMENT
Primary
Smpltpr Ca«;p
\JIIIGILGI WC19G
Ctl irl\l
otuay
Seconday
Smelter Case
Study
Near Roadway
Non-Urban
Case Study
Vulnerable
Ecosystem
Case Study
National
Surface Water
Screen
Setting and spatial
extent of dataset or
modeling analysis
Herculaneum, Missouri:
soil and waterbody
samples from study
area 6 km diameter,
centered on point
source
Troy (Pike County),
Alabama: soil
concentrations in
census blocks near
facility predicted from
dispersion and soil
mixing model
\3
Twodatasets: Corpus
Christi, Texas (within 4
m from road), and
Atlee, Virginia (within 2
to 30 m from road)
Hiihh^rrl Rrnnk
1 IUUUOIU LJIVJVJiX
Experimental Forest,
New Hampshire: forest
in oblong basin about 8
km long by 5 km wide
Surface water bodies in
the 47 basin study units
from all regions of the
United States, covering
approx. 50% of U.S.
land base
Media Screened and Screening Levels Used
Soil
Soil
screening
values
developed
based on
U S EPA
\-j • vji i — i r\
Superfund
methodology
for
i \ji
developing
ecological
soil screening
levels
(USEPA,
2005a,b)
Freshwater
water column
U.S. EPA
freshwater AWQC
for aquatic life
adjusted for site-
specific water
hardness
NA
Freshwater
Sediment
Sediment screening
values based on
MacDonald et al.
(2000) sediment quality
assessment guidelines
NA
While no quant tative analyses were performed, summary
review of literature search indicated: (1) atmospheric Pb inputs
do not directly affect stream Pb levels at HBEF because
deposited Pb is almost entirely retained in the soil profile; (2)
soil horizon analysis results show Pb has become more
concentrated at lower depths over time and that the soil profile
serves as a Pb sink, appreciably reducing Pb in porewater as it
moves through the soil layers to streams, (3) dissolved Pb
concentrations were reduced (5 ppb to about 5 ppt) as Pb
moves from the Oa horizon to streams. Studies concluded
insignificant contribution of dissolved Pb from soils to streams
(less than 0.2 g 'ha~1 'yf 1). (ICF, 2006, Appendix E)
NA
U.S. EPA
freshwater AWQC
for aquatic life
adjusted for
hardness at site or
nearby water body
Sediment screening
values based on
MacDonald et al.
(2000) sediment quality
assessment
guidelines
AWQC= Ambient water quality criteria. NA = Not applicable; medium not part of case study.
NOTE: Information here is drawn from ICF, 2006 and EPA, 2007b.
5A-1
-------
ATTACHMENT
Clean Air Scientific Advisory Committee Letter (June 4, 2013)
-------
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON D.C. 20460
OFFICE OF THE ADMINISTRATOR
SCIENCE ADVISORY BOARD
June 4, 2013
EPA-CASAC-13-005
The Honorable Bob Perciasepe
Acting Administrator
U.S. Environmental Protection Agency
1200 Pennsylvania Avenue, N.W.
Washington, D.C. 20460
Subj ect: CAS AC Review of the EPA' s Policy Assessment for the Review of the Lead National
Ambient Air Quality Standards (External Review Draft - January 2013)
Dear Acting Administrator Perciasepe:
The Clean Air Scientific Advisory Committee (CAS AC) Lead Review Panel met on February 5-6,
2013, to peer review the EPA's Policy Assessment for the Review of the Lead National Ambient Air
Quality Standards (External Review Draft - January 2013), hereafter referred to as the PA. The
CAS AC's consensus responses to the agency's charge questions and the individual review comments
from the CASAC Lead Review Panel are enclosed. The CASAC's key points are highlighted below.
Overall, the CASAC concurs with the EPA that the current scientific literature does not support a
revision to the Primary Lead (Pb) National Ambient Air Quality Standard (NAAQS) nor the Secondary
Pb NAAQS. Although the current review incorporates a substantial body of new scientific literature, the
new literature does not justify a revision to the standards because it does not significantly reduce
substantial data gaps and uncertainties (e.g., air-blood Pb relationship at low levels; sources contributing
to current population blood Pb levels, especially in children; the relationship between Pb and childhood
neurocognitive function at current population exposure levels; the relationship between ambient air Pb
and outdoor dust and surface soil Pb concentrations). Further details on these and other research needs
are provided in the consensus responses. The CASAC recommends that research be performed to
address these data gaps and uncertainties to inform future Pb NAAQS reviews.
The CASAC has additional comments and recommendations on improving the document. With the
completion of the recommended revisions outlined below and in the consensus responses, the PA will
serve its intended purpose. Another CASAC review of the document is not needed.
The PA should include a discussion that Pb is a unique pollutant in many ways. Unlike other criteria air
pollutants, Pb is of concern from a multimedia perspective. Millions of tons of Pb are present in the
environment from legacy sources. The distribution of this substantial reservoir of Pb is not known. Thus,
the extent of current human exposure from this legacy cannot be reliably estimated.
The PA generally captures the key aspects of the health effects evidence presented in the Integrated
Science Assessment, but can be made more concise and clear by providing summary conclusions
-------
regarding the health effects evidence at the beginning of the sections. The risk and exposure information
from the previous Pb NAAQS review is adequately presented. The CASAC concurs that a new risk and
exposure assessment (REA) is not needed due the lack of sufficient new scientific information to
warrant revision of the prior REA data and methods.
The application of the evidence-based framework and the use of the health risk and exposure
information from the previous Pb NAAQS review seem appropriate and provide a sufficient rationale to
support retaining the current primary standard without revision. However, there should be more
description in the PA of the data and rationale behind the averaging time and form of the current primary
standard. Additionally, research is needed to address uncertainties and data gaps in the evidence-based
framework and in the health risk and exposure information for future Pb NAAQS reviews.
Given the existing scientific data, the CASAC concurs with retaining the current secondary standard
without revision. However, the CASAC also notes that important research gaps remain. For example
questions remain regarding the relevance of the primary standard's indicator, level, averaging time, and
form for the secondary standard. Other areas for additional research to address data gaps and uncertainty
include developing a critical loads approach for U.S. conditions and a multi-media approach to account
for legacy Pb and contributions from different sources. Addressing these gaps may require
reconsideration of the secondary standard in future assessments.
The CASAC also wishes to highlight the importance of a separate but related policy issue. The CASAC
notes that it has not considered this separate policy issue in providing advice on the NAAQS. The
decrease in childhood lead poisoning in the United States over the last three decades is a great public
health success story. Concurrently, there is a trend of increased relocation of Pb production, recycling,
and recovery to other nations. One example is the export of spent lead acid batteries (SLAB) to Mexico.
As detailed in a report by the Secretariat of the Commission for Environmental Cooperation (CEC),
environmental and health protections in the secondary lead industry in other countries are not
functionally equivalent to those in the United States. The CEC offers recommendations to avoid
development of pollution havens and for the United States to work with Mexico and Canada to foster
adoption of best practices throughout North America. The CASAC recognizes the role of the EPA
Administrator as a member of the CEC Council and strongly urges the EPA to carefully consider the
recommendations of the CEC report, and to support decisive action that will enable the success of the Pb
NAAQS in the United States to be a role model for development of best practices internationally that
avoid adverse public health impacts abroad. For example, the considerable effort by the EPA to develop
the ISA and the PA could be a valuable starting point for other countries to develop or revise their own
ambient standards for lead.
-------
The CAS AC appreciates the opportunity to provide advice and looks forward to receiving the EPA's
response.
Sincerely,
/signed/
Dr. H. Christopher Frey, Chair
Clean Air Scientific Advisory Committee
Enclosures
-------
NOTICE
This report has been written as part of the activities of the EPA's Clean Air Scientific Advisory
Committee (CASAC), a federal advisory committee independently chartered to provide extramural
scientific information and advice to the Administrator and other officials of the EPA. The CASAC
provides balanced, expert assessment of scientific matters related to issues and problems facing the
agency. This report has not been reviewed for approval by the agency and, hence, the contents of this
report do not necessarily represent the views and policies of the EPA, nor of other agencies within the
Executive Branch of the federal government. In addition, any mention of trade names or commercial
products does not constitute a recommendation for use. The CASAC reports are posted on the EPA
website at: http://www.epa.gov/casac.
-------
U.S. Environmental Protection Agency
Clean Air Scientific Advisory Committee
CASAC Lead Review Panel (2010-2013)
CHAIR
Dr. H. Christopher Frey, Distinguished University Professor, Department of Civil, Construction and
Environmental Engineering, College of Engineering, North Carolina State University, Raleigh, NC
OTHER CASAC MEMBER
Mr. George A. Allen, Senior Scientist, Northeast States for Coordinated Air Use Management
(NESCAUM), Boston, MA
CONSULTANTS
Dr. Herbert Allen, Professor Emeritus, Department of Civil and Environmental Engineering,
University of Delaware, Newark, DE
Dr. Richard Canfield, Senior Research Associate, Division of Nutritional Sciences, Cornell University,
Ithaca, NY
Dr. Deborah Cory-Slechta, Professor, Department of Environmental Medicine, School of Medicine
and Dentistry, University of Rochester, Rochester, NY
Dr. Cliff Davidson, Professor, Civil and Environmental Engineering, Syracuse University, Syracuse,
NY
Dr. Philip E. Goodrum, Senior Consultant, Cardno ENTRIX, Syracuse, NY
Dr. Sean Hays, President, Summit Toxicology, Allenspark, CO
Dr. Philip Hopke, Bayard D. Clarkson Distinguished Professor, Department of Chemical and
Biomolecular Engineering, Clarkson University, Potsdam, NY
Dr. Chris Johnson, Professor, Department of Civil and Environmental Engineering , Syracuse
University, Syracuse, NY
Dr. Susan Korrick, Assistant Professor of Medicine , Department of Medicine, Brigham and Women's
Hospital, Channing Laboratory, Harvard Medical School, Boston, MA
Dr. Michael Kosnett, Associate Clinical Professor, Division of Clinical Pharmacology and Toxicology,
Department of Medicine, University of Colorado School of Medicine, Denver, CO
11
-------
Dr. Roman Lanno, Associate Professor and Associate Chair, Department of Evolution, Ecology, and
Organismal Biology, Ohio State University, Columbus, OH
Mr. Richard L. Poirot, Environmental Analyst, Air Pollution Control Division, Department of
Environmental Conservation, Vermont Agency of Natural Resources, Waterbury, VT
Dr. Joel G. Pounds, Laboratory Fellow, Cell Biology & Biochemistry, Biological Sciences Division,
Pacific Northwest National Laboratory, Richland, WA
Dr. Michael Rabinowitz, Geochemist, Marine Biological Laboratory, Newport, RI
Dr. William Stubblefield, Senior Research Professor, Department of Molecular and Environmental
Toxicology, Oregon State University, Corvallis, OR
Dr. Ian von Lindern, President, TerraGraphics Environmental Engineering, Inc., Moscow, ID
Dr. Gail Wasserman, Professor of Clinical Psychology in Child Psychiatry, Division of Child and
Adolescent Psychiatry, College of Physicians and Surgeons, Columbia University, New York, NY
Dr. Michael Weitzman, Professor, Pediatrics; Psychiatry, New York University School of Medicine,
New York, NY
SCIENCE ADVISORY BOARD STAFF
Mr. Aaron Yeow, Designated Federal Officer, U.S. Environmental Protection Agency, Science
Advisory Board (1400R), 1200 Pennsylvania Avenue, NW, Washington, DC
in
-------
U.S. Environmental Protection Agency
Clean Air Scientific Advisory Committee
CASAC
CHAIR
Dr. H. Christopher Frey, Distinguished University Professor, Department of Civil, Construction and
Environmental Engineering, College of Engineering, North Carolina State University, Raleigh, NC
MEMBERS
Mr. George A. Allen, Senior Scientist, Northeast States for Coordinated Air Use Management
(NESCAUM), Boston, MA
Dr. Ana Diez-Roux, Professor of Epidemiology, School of Public Health, University of Michigan, Ann
Arbor, MI
Dr. Jack Harkema, Professor, Department of Pathobiology, College of Veterinary Medicine, Michigan
State University, East Lansing, MI
Dr. Helen Suh, Associate Professor, Bouve School of Health Sciences, Northeastern University,
Boston, MA
Dr. Kathleen Weathers, Senior Scientist, Gary Institute of Ecosystem Studies, Millbrook, NY
Dr. Ronald Wyzga, Technical Executive, Air Quality Health and Risk, Electric Power Research
Institute, Palo Alto, CA
SCIENCE ADVISORY BOARD STAFF
Dr. Holly Stallworth, Designated Federal Officer, U.S. Environmental Protection Agency, Science
Advisory Board (1400R), 1200 Pennsylvania Avenue, NW, Washington, DC
IV
-------
Consensus Responses to Charge Questions on
EPA's Policy Assessment for the Review of the Lead National Ambient Air Quality Standards
(External Review Draft - January 2013)
Chapter 1 - Introduction
This chapter provides context for the review, including the background of past reviews, as well as the
scope for the current review. This includes discussion of fate and multimedia pathways of ambient air
Pb and other nonair sources ofPb in the environment.
Does the Panel find the introductory and background material, including that pertaining to previous
reviews of the Pb standard and the scope of the current review to be appropriately characterized and
clearly communicated?
Chapter 1 of the Policy Assessment (PA) is reasonably well characterized and for the most part clearly
communicated, although there are several improvements that should be made (see below). The CASAC
concurs with the EPA that the current scientific evidence does not justify a change to the current Lead
(Pb) National Ambient Air Quality Standards (NAAQS), with the caveats stated below.
Chapter 1 should emphasize Pb as a unique pollutant in many ways. Historically, anthropogenic
emissions of Pb to the air around the globe exceeded natural emissions by a huge margin, more than any
other trace metal. Natural emissions come from unpolluted soil, seaspray, and other natural sources.
Removal of Pb from gasoline, paint, solder, and other anthropogenic sources constitutes what is
arguably the biggest environmental success story for any pollutant to-date. Unlike other criteria air
pollutants, Pb is of concern from a multimedia perspective; human exposure to Pb comes from
inhalation of air and also from ingestion of food, water, and dust. In addition, Pb may be the pollutant
with the biggest legacy problem: millions of tons of Pb are now present in the environment as a result of
discharges from years ago. The distribution of this huge reservoir of Pb is not known, and thus current
human exposure from this legacy cannot reliably be estimated. What is known, however, is that human
activities have on average substantially elevated the Pb content of soil at numerous locations around the
United States, more so than other trace metals processed in large quantities. Although air Pb levels are
much lower because of reduced emissions, soil Pb can be expected to remain elevated for many years.
These unique aspects of Pb, especially the problem of not knowing the distribution of legacy Pb, should
be clearly discussed in the PA.
This chapter concludes that there is no information published in the last five years justifying
reconsideration of the current NAAQS. Although that is true, this conclusion should be conveyed with
an assessment of the adequacy of the old information. In particular, there were significant unknowns and
uncertainties associated with a lack of information five years ago; those unknowns and uncertainties still
remain.
There are no statements in the PA that the Integrated Science Assessment (ISA) is limited only to
exposures and data sources considered currently relevant to the U.S. population, as opposed to
populations outside of the United States. Furthermore, the literature is considered only to assess how
new studies relate to conclusions drawn in the past review, and then only to studies in the peer-reviewed
literature. This has resulted in an ISA that is dedicated predominately to toxicology, health effects,
1
-------
biokinetics, and causal determinations. These are areas that were data rich in the last review, and
continue to produce volumes of new peer-reviewed information. In contrast, in areas where the least is
known and EPA relies on past findings, uncertainty is becoming greater as the existing information
becomes outdated. Additionally, the current assessment excludes consideration of impacts on
populations outside of the United States.
There is considerable discussion dedicated to the reduction of Pb in air and other media in the United
States over the last four decades. Most of the reduction was achieved through the elimination of tetra-
ethyl Pb gasoline additives. Another major component of the reduction was substantial decreases in
emissions from primary and secondary smelters, and metals processing industries. In the case of motor
vehicle gasoline-related emissions, these ceased and other non-Pb products were substituted in
commerce. This resulted in decreased Pb emissions and health and environmental effects in both the
United States and globally. Within the United States, Pb continues to be used as an octane boosting fuel
additive for very high octane fuels used in general aviation for piston engine aircraft. In the case of Pb
production and secondary recovery, however, this production and recovery were exported overseas.
There is no mention of the impact of the "avoided emissions" in their new locales.
Thus, overall, there is no reason to change the current airborne Pb standard. However, although airborne
Pb is far more limited as a problem within the United States, potential exposure to Pb in other
environmental media in the United States is likely to be more significant. Furthermore, there may be
increasing Pb exposures overseas (e.g., as described in CEC, 2013).
There are a few areas that need revision for clarity and accuracy. On page ES-1, line 25, the following
sentence should be added to the end of the paragraph: "This approach was taken to aid in the decision to
retain or revise the current standards." On page 1-13 line 35, it states: "And we recognize that past Pb
emissions in many situations were well in excess of the current Pb standard." One cannot compare
emissions to an airborne standard. This sentence can be revised to state: "We recognize that past Pb
emissions in many situations caused airborne Pb concentrations far in excess of the current Pb standard."
Chapter 2 - Ambient Air Lead
This chapter provides an overview of current information on air Pb emissions and monitoring data,
consideration of the current air Pb monitoring requirements and an overview of current information on
Pb in nonair media.
To what extent does the Panel agree that the most relevant information on emissions (section 2.1), air
quality (section 2.2.2), andPb concentrations in other media (section 2.3) is presented, and to what
extent is the information presented appropriately characterized and clearly communicated?
With a few minor exceptions (see specific individual panel member comments), the information on Pb
emissions, air quality and concentrations in other media is appropriately characterized and clearly
presented. Historical and recent (2008) emissions data are summarized quantitatively in clear charts and
tables, with additional detail on the 2008 National Emissions Inventory (NEI) data sources and
limitations provided in Appendix 2A. There are also qualitative discussions and an informative
Appendix 2B on recent regulatory actions, indicating that current emissions have declined since 2008,
with additional reductions pending. However, quantitative estimates of emissions reductions would be
-------
informative. To the extent that these or other historical controls of U.S. Pb source categories have
shifted Pb emissions to other countries, it would be informative to include discussion of those displaced
emissions.
The information on ambient air concentrations is clearly presented (for sites with 1 to 3 years of valid
data for 2009 to 2011) in maps, charts and in a detailed appendix (Appendix 2D). More recent
measurements from sites (including near airports) initiated since the previous Pb NAAQS review would
help inform the current Pb NAAQS review, as well as the separate Section 231 aviation gasoline
("avgas") review.
Given the "not to be exceeded" 3-month rolling average form of the Pb NAAQS, an exceedance could
be determined with as few as 3 months of new data. Therefore, it would be useful if more recent data are
summarized in the next Pb PA, without being limited to sites with multiple years of valid data.
The information on Pb concentrations in other media is clearly presented. The sections (2.3.2.1 and
2.3.2.2) on indoor and outdoor dust are highly relevant to exposure assessments and would benefit from
some added discussion of how dust Pb concentration, loading, and loading rates are measured. In
particular, information relating to the differences in particle sizes in dust samples and ambient air
samples would be helpful. More information on changes, if any, over time in the availability of
historically deposited soil Pb for resuspension to the air or for direct uptake through ingestion could help
clarify the significance of this potentially important source category.
With regard to information on ambient Pb monitoring (section 2.2.1), to what extent is this information
appropriately characterized and clearly communicated?
The information on ambient Pb monitoring is appropriately characterized and clearly communicated. It
is understood that the high-volume (Hi-Vol) Total Suspended Particulates (TSP) sampler is an imperfect
historical artifact, and that there is not time for this review cycle of the Pb NAAQS to develop, fully test,
and deploy alternative samplers that would consistently capture particles (less than and) greater than 10
microns with appropriate collection efficiencies and size ranges under varying wind speeds and
directions. The draft PA notes that the EPA expects a new, improved sampler to be "available for
consideration in a future review." Toward this goal, discussion is needed regarding the desirable cut size
characteristics of, and practical constraints on, an alternative sampler. Information from the ISA could
be cited here, such as material currently on page 3-67 of the 3r external draft of the ISA that may be
revised for the final ISA regarding discussion of the desirable cut size.
If an alternative low-volume sampler could be developed with an upper 50% particle cut size in the
range of 15 to 20 microns, and without the wind speed and direction biases of the Hi-Vol TSP sampler,
it seems likely that such a sampler would typically capture as much (or occasionally more) Pb as the Hi-
Vol TSP sampler. The CAS AC has previously recommended the development of a new air Pb sampler
that collects larger particle sizes, that could improve the quality of sampling in the National Air Toxics
Trends Station (NATTS) network, and that could serve as an Federal Reference Method (FRM) or
Federal Equivalent Method (FEM) for Pb. Filters collected by this sampler also would be amenable to
multi-elemental analyses by lower-cost analytical methods and could be useful for more accurate and
precise assessments of other paniculate pollutants with significant coarse mode concentrations,
including chemical contaminants (like hexavalent chromium, silica, and cadmium) and biological
components like pollen, fungi, and endotoxins.
-------
Chapter 3 - Health Effects and Exposure/Risk Information
This chapter discusses key policy relevant aspects of the health effects evidence and exposure/risk
information.
To what extent does the information in sections 3.1 (Internal Disposition andBiomarkers of Exposure
and Dose), 3.2 (Nature of Effects) and 3.3 (Public Health Implications and At-Risk Populations) capture
and appropriately characterize the key aspects of the evidence assessed and integrated in the ISA?
Chapter 3 of the draft PA generally captures the key aspects of the evidence presented in the ISA;
therefore, concerns about content stem from the content of the ISA and not its condensation in the PA.
Recognizing the degree of condensation needed to summarize the ISA in only a few pages, this format
presents a great writing challenge, and the writing in the chapter lacks clarity. Wordiness should be
reduced to directly and efficiently convey the meaning. For example, sentences such as the following
could be shortened and recast in a more active voice: "The results from the various case studies
assessed, with consideration of the context in which they were derived (e.g., the extent to which the
range of air-related pathways were simulated, and limitations associated with those simulations), and the
multiple sources of uncertainty (see section 3.4.7 below) are also informative to our understanding of
air-to-blood ratios." (Please refer to Dr. Canfield's individual comments for details on the sentences in
need of streamlining and clarification.)
In addition, there are a few places where legacy text from the previous PA remains, so extraneous words
need to be deleted and tenses updated. What needs the most attention is the length and complexity of
some sentences.
To what extent is the newly available evidence on air-to-blood ratios appropriately characterized and
considered in light of information previously available in past reviews?
The new information on air-to-blood ratios is presented in context of previous information and no
change in the estimate is justified at this time.
When revising this section (3.1) it would be helpful to first read the last (summary paragraph) on page 3-
14. Those conclusions should be included in the first paragraph of the section and then restated at the
end of the section when the reader will be in a position to understand the context.
To what extent is the newly available evidence on concentration-response functions for IQ decrements
in young children appropriately characterized and considered in light of information previously
available in past reviews?
The newly available evidence is appropriately characterized. Parametric information could be extracted
from these data to produce quantitative results for blood Pb subgroups, but the quality of the data would
not likely provide a useful basis for altering the conclusions reached from the data available prior to
2008.
There is a critical need for more information about effects of Pb at levels in the 0-5 |ig/dL range. Studies
about effects of Pb at these low levels are a future research need.
-------
With regard to the exposure and risk information, to what extent is the information drawn from the
human exposure and health risk assessment in the last review sufficiently characterized and clearly
communicated? To what extent is the information appropriately interpreted in light of the currently
available information and for the purpose of assessing the adequacy of the now current standard?
Information from the last review is well-characterized and appropriately interpreted, but the clarity of
communication should be improved. Putting the conclusion in the first paragraph of the section was very
helpful. The CAS AC concurs that a new risk and exposure assessment (RE A) is not warranted at this
time.
Are the limitations and uncertainties in the exposure/risk information appropriately characterized and
considered in our interpretation of the information in the context of this current review?
The limitations and uncertainties in the exposure/risk information are well characterized.
Epidemiological data are inherently limited; there is a lack of data on the effects of Pb exposure at the
levels that are common today and thus concentration-response (C-R) estimates require extrapolation.
Parameter choices for biokinetic models typically require restrictive assumptions. No single air quality
scenario is adequate.
There are specific areas of the chapter that should be revised for clarity:
• Page 3-2, Line 15, referring to distribution of Pb from bone to blood, includes the sentence:
"Changes in Pb exposure circumstances also can influence these exchanges, e.g., substantial
reductions in exposure levels contribute to increased release of Pb from the bone into the blood
(ISA, section 4.3.5)." This sentence should be revised, as it appears to incorrectly characterize
the information in section 4.3.5 of the ISA. A reduction in external Pb exposure does not, from a
pharmacodynamic standpoint, induce an increase in the release of Pb from bone. In the context
of the paragraph, the intended point could be expressed as follows: "When there are substantial
reductions in external Pb exposure, the relative contribution of Pb from bone to the concentration
of Pb in blood increases."
• Page 3-5, line 29 to Page 3-6, line 9: The italicized sentence in this paragraph, reproduced
below, should be revised to improve clarity:
"The response of adult blood Pb levels to appreciable changes in exposure circumstances is
generally slower than that of blood Pb levels in young children. For example, simulations using
biokinetic models indicate that blood Pb levels in adults achieve a new quasi-steady state within
75-100 days (approximately 3-4 times the blood elimination half-life) subsequent to abrupt
increases in Pb intake (ISA, section 4.3.5.2); similar models indicate a much quicker response of
blood Pb levels in children both with regard to abrupt increases and reductions in Pb exposure
(ISA, section 4.3.5.1). The response in young children may reflect their much more labile bone
pool associated with the rapid turnover of bone mineral in response to their rapid growth rates
(ISA, section 4.3.5). As a result of these physiological processes in young children, their blood
Pb levels tend to more quickly reflect changes in their total body burden (associated with their
shorter exposure history), and also can reflect changes in recent exposures (ISA, section 4.3.5)."
-------
Instead of the italicized sentence above, substitution of a sentence such as the following might
enhance clarity: "Because the skeletal compartment of Pb is relatively smaller and subject to
more rapid turnover in children compared to adults, the blood Pb concentration of children is
more reflective of their recent external exposure."
Page 3-19 lines 23-24: It might be clearer to use the phrase "qualitatively change" rather than
"appreciably change" to allow for appreciable strengthening of the previous conclusion but no
change of consequence.
Page 3-22 lines 17-23: This is a helpful discussion of the problem with unknown earlier
exposures in adults and older children. The topic comes up multiple times throughout this
document and becomes redundant. Maybe this should be covered fully (including this as a
general critique of cross-sectional studies), early in the chapter and then simply referred back to
when the context warrants.
Chapter 4 - Review of the Primary Standard for Lead
This chapter describes the basis for the current primary standard and consideration of the current
evidence and exposure/risk-based information with regard to reaching preliminary staff conclusions
about the adequacy of the current standard.
In this chapter, staff applies the same evidence-based air-related IQ loss framework as developed and
used in the last review, which has fundamentally two key inputs: an air-to-blood ratio and the slope of a
concentration-response (C-R) function for IQ decrements in young children.
This draft PA is constrained by the absence of new observational and experimental data that address, at
least in part, limitations and uncertainties in the evidence that was present at the time of the last update
of the Pb NAAQS. Until evidence is available to assess Pb exposure and health risks related to air Pb
levels reflecting the current standard, a substantive refinement and update of the PA will not be possible.
The obvious uncertainty underlying evaluation of this PA is whether lowering the standard would (or
would not) impact exposure and thus risk. The CASAC agrees with the EPA conclusion that "there is
appreciable uncertainty associated with drawing conclusions regarding whether there would be
reductions in blood Pb levels from alternative lower levels as compared to the level of the current
standard." If lowering the primary standard would lower blood Pb levels amongst the U.S. population,
then there would be potential public health benefits from a lower standard. Research priorities discussed
below are designed to help inform these uncertainties.
To what extent does the Panel agree with application of the evidence-based framework from the last
review, particularly with regard to consideration of the currently available information, and related
limitations and uncertainties, for air-to-blood ratios and C-R functions for IQ decrements in young
children?
The application of the evidence-based framework from the previous Pb NAAQS review seems
appropriate. The new literature published since the previous review provides further support for the
health effect conclusions presented in that review. Additionally, the new studies do not fundamentally
alter the uncertainties for air-to-blood ratios or C-R functions for IQ decrements in young children.
-------
As previously discussed with CASAC, staff concluded that the current information does not warrant
development of a new REA in this review. Thus, exposure/risk information was drawn from the REA
conducted in the last review.
What are the Panel's views on staff's interpretation of the exposure/risk information, and on staff's
conclusions that the information is generally supportive of conclusions drawn from the evidence-based
framework as to the adequacy of the current standard?
The use of exposure/risk information from the previous Pb NAAQS review appears appropriate given
the absence of significant new information that could fundamentally change the interpretation of the
exposure/risk information. This interpretation is reasonable given that information supporting the current
standard is largely unchanged since the current standard was issued.
The CASAC agrees that the adverse impact of low levels of Pb exposure on neurocognitive function and
development in children remains the most sensitive health endpoint, and that a primary Pb NAAQS
designed to protect against that effect will offer satisfactory protection against the many other health
impacts associated with Pb exposure.
The CASAC concurs with the draft PA that the scientific findings pertaining to air-to-blood Pb ratios
and the C-R relationships between blood Pb and childhood IQ decrements that formed the basis of the
current Pb NAAQS remain valid and are consistent with current data.
In reaching preliminary staff conclusions, staff notes that, like any NAAQS review, this Pb NAAQS
review requires public health policy judgments. The public health policy judgments for this review
include the public health significance of a given magnitude oflQ loss in a small subset of highly exposed
children (i.e., those likely to experience air-related Pb exposures at the level of the standard), as well as
how to consider the nature and magnitude of the array of uncertainties that are inherent in the evidence
and in the application of this specific framework.
What are the Panel's views on public health policy judgments that inform staff's preliminary
conclusions with regard to the adequacy of current standard and a lack of support for consideration of
potential alternative standards?
The PA states repeatedly that no threshold for Pb effects on IQ can be identified. In some respects, the
ability to define a threshold may already be a moot issue. Reductions in IQ in children are being
reported at blood Pb values as low as 2 |ig/dL. In essence, these effects are being reported at the lowest
levels of Pb in blood that can be reliably measured by most laboratories doing such analyses.
Child IQ is the Pb-sensitive health endpoint on which this PA (and the previous one) is based. Thus, the
discussion of health policy judgment needs to be carefully considered in light of the far-reaching public
health value of childhood cognitive and neurobehavioral health. For example, the 2012 Centers for
Disease Control and Prevention (CDC) update of recommendations regarding childhood Pb poisoning
acknowledges that there is no blood Pb level in childhood that has been shown to be without deleterious
effects. In this context, defining the threshold for "unacceptable risks to public health" or "sufficient
public health protection" is difficult. Indeed, such language - with its implicit use of a threshold
approach to a process that presumably has no threshold - may no longer be appropriate. Although there
is evidence that even very low Pb levels are related to measurable reductions in IQ in children, the
extent to which the blood Pb levels observed in children are linked to ambient air Pb levels below the
7
-------
current standard (as opposed to other sources of Pb in the environment) has not been established.
Therefore there is not justification for modifying the current standard based on these data at this point in
time. However additional research on air to blood Pb at low levels may require reconsideration of this
decision in the future.
In the Panel's view, does the discussion in section 4.3 provide an appropriate and sufficient rationale to
support staff's preliminary conclusion that it is appropriate to consider retaining the current standard
(including the indicator, level, averaging time, and form) without revision?
Given the evidence-based framework, the discussion in section 4.3 provides an appropriate and
sufficient rationale to support retaining the current standard without revision. For example, there is
discussion in the PA regarding the choice of indicator level. However, there should be more description
of supporting data and rationale behind the recommendation for the averaging time and form of the
current standard.
The CASAC concurs that the new science does not support lowering the Pb NAAQS from its current
level (0.15 |ig/m3). Additionally, the CASAC concurs with the caveats provided about the uncertainty in
the science behind the NAAQS for Pb. In particular it appreciates and affirms a key point on page 4-28,
lines 2-3: "We also recognize increased uncertainty in projecting the magnitude of blood Pb response to
ambient air Pb concentrations at and below the level of the current standard." Likewise, the key idea on
page 4-32, lines 32-35 is important, but a clarifying revision is recommended as follows:
Page 4-32, lines 32-35, current text: "In staffs view, based on current evidence there is
appreciable uncertainty associated with drawing conclusions regarding whether there would be
reductions in risk to public health from alternative lower levels as compared to the level of the
current standard." This should be re-written to read "In staffs view, based on current evidence
there is appreciable uncertainty associated with drawing conclusions regarding whether there
would be reductions in blood lead levels from alternative lower levels as compared to the level of
the current standard."
Does the Panel have any recommendations regarding additional interpretations and conclusions based
on the available information that would be appropriate for consideration beyond those discussed in this
chapter?
As noted above, repeated statements about a threshold do not seem warranted given that IQ reductions
now occur at the lowest blood Pb levels that can be reliably measured in most laboratories. It is for this
reason that the Advisory Committee on Childhood Lead Poisoning Prevention recommended to CDC a
complete elimination of the phrase 'level of concern' and stated that no blood Pb level in children has
been shown to be without deleterious effects.
The EPA should encourage development of research programs to address those limitations and
uncertainties in currently available evidence (and exposure/risk information) that are critical to the
identification of "sufficiently health protective" air Pb standards in the future.
-------
There are some areas that need revision for clarity:
• Page 4-34, line 13: The statement should be edited to: "Factors affecting relationships between
Pb in ambient air and Pb in blood at low exposures experienced in the general population
today"
• Page 4-34, lines 19-21: This research need is profound, but as written is too vague to be
appreciated by the average reader. This research need should be revised to: "Apportionment of
blood Pb levels with regard to exposure pathways, with particular focus on understanding
exposure pathways and sources that cause the more elevated blood Pb levels among children
today."
Research Needs
Several areas of research that could assist in further refinement of the Pb NAAQS include:
1. For the purposes of policy and decision making, key research priorities should be studies that
elucidate: (1) the air-blood Pb relationship at low levels; (2) sources (exposure pathways)
contributing to current population blood Pb levels, especially in children; (3) the relationship
between Pb and childhood neurocognitive function at current population exposure levels; and (4)
the relationship between ambient air Pb and outdoor dust and surface soil Pb concentrations,
including the temporal dynamics of that relationship. These research priorities are of particular
interest because of the prominent contribution of past (as opposed to recent) Pb emissions to Pb
in soil and dust, and the significant contribution of dust and soil matrices to the Pb exposure of
children.
2. For the typical American adult not subject to current or past point sources or occupational Pb
exposure, Pb in the diet is likely to constitute the largest fraction of daily Pb exposure. Therefore,
another research need of considerable interest is to determine the source of contemporary dietary
Pb, including the indirect contribution of historical air Pb emissions (i.e. "legacy Pb"). Further,
there remains a need to determine how much of dietary Pb is from legacy and how much can be
amenable to interventions.
3. The shape of the C-R curve for IQ reductions at extremely low levels requires further
clarification. In addition, studies on more sensitive endpoints in the domain of emotion and
behavior regulation are warranted, given that they may yield specific and sensitive measures and
thereby assist in defining appropriate intervention strategies for children.
4. There has been a long-term reliance on the Integrated Exposure Uptake Biokinetic (IEUBK)
model. However, greater understanding of inter-individual variability, as quantified in the
Geometric Standard Deviation (GSD) input parameter, is needed. Information about
toxicokinetics during adolescence remains limited. The All Ages Lead Model could be utilized to
improve this understanding. There is also the need to know more about gene-environment
interactions, particularly in driving inter-individual susceptibility and vulnerability.
5. Characterization and better understanding of Pb exposure hotspots/sources will give better
representation of significant exposure risks.
-------
6. Understanding of the impacts of Pb exposures during critical developmental windows and their
contribution to adverse outcomes; e.g., little is known about the specific effects of prenatal
exposure.
7. The effect of contemporary Pb exposure (i.e., that resulting in blood Pb concentrations on the
order of 5 |ig/dL or lower) on the future risk of hypertension and cardiovascular morbidity and
mortality, and on age-related neurodegeneration, as these could lead to additional information
related to most sensitive health outcomes.
8. A further understanding of the role of "reverse causation" in the inverse association observed in
some studies between low blood Pb concentration and renal function (e.g., glomerular filtration
rate).
9. The extent to which product substitution, i.e., replacement of Pb with less hazardous alternative
substances in contemporary commerce, may result in reduction of human Pb exposure. The EPA
might consider supporting studies on Pb potentially undertaken by programs such as the Toxic
Use Reduction Program in Massachusetts, and the Green Chemistry Initiative in California.
10. As yet, the extent to which global warming will influence exposure to Pb (e.g., through soil
erosion, resuspension) has not been evaluated.
Chapter 5 - Welfare Effects and Exposure/Risk Information
This chapter discusses key policy relevant aspects of the environmental evidence and exposure/risk
information.
Chapter 5 of the PA is a well-written synthesis of the findings related to ecological effects in the ISA.
The ISA supports the conclusion that recent research has not changed our fundamental understanding of
Pb fate, transport and toxicity in the environment.
To what extent does the information in section 5.1 (Welfare Effects Information) capture and
appropriately characterize the key aspects of the evidence assessed and integrated in the ISA?
Section 5.1 does a good job of summarizing the evidence for ecological effects from the ISA. The
general conclusion is that recent research has added depth and nuance to the understanding of the fate
and transport of Pb in ecological systems, and to the understanding of effects on organisms in terrestrial
and aquatic ecosystems, but has not changed the understanding in a way that merits reconsideration of
the relationships used to assess risk.
A persistent theme in the ecological effects sections of the ISA and this PA document is that it is
difficult to isolate the effects of air Pb on ecosystems from other Pb sources, including "legacy" Pb
accumulated in soils and sediments. The threat of release of legacy Pb in soils and sediments, whatever
the original source, may necessitate a lower secondary air quality standard than would be warranted in
the absence of the legacy Pb. With respect to critical loads, it is recommended that Chapter 5
acknowledge the impact on raptors and water fowl of Pb in spent ammunition; these are the ecological
10
-------
receptors most heavily exposed to Pb, and thus potentially the most susceptible to the incremental
contribution of Pb in air.
With regard to the exposure and risk information in section 5.2 (Exposure and Risk Information), to
what extent is the information drawn from the screening-level risk assessment in the last review
sufficiently characterized and clearly communicated? To what extent is the information appropriately
interpreted in light of the currently available information and for the purpose of assessing the adequacy
of the current standard?
The results of the 2006 REA are summarized in section 5.2. The summary is concise and clear, both in
the explanation of the model employed and in the descriptions of the case studies used in the assessment.
The interpretation of the results from the 2006 REA is appropriate insofar as it re-states the conclusions
from that document, and there have been no fundamental changes to our understanding of key thresholds
or ecological receptors in the intervening years. Of four terrestrial case studies employed, the results
from two (the primary and secondary smelter cases) are judged to be "not informative." The relevance
of a third case study (non-urban near-roadway conditions) is deemed "highly uncertain" due to the
presence of legacy Pb in roadside soils. The only terrestrial case study that is deemed relevant is the
Hubbard Brook case, where ambient Pb concentrations are far below the current (and proposed)
standard. Results from analysis of surface water and sediment data are judged to be inconclusive
because of possible non-air sources to waters and legacy Pb in sediments. Therefore, overall, four of the
five major efforts in the 2006 REA are judged to be of limited or no value for the purposes of this PA.
Given that there is little field research underway on Pb in U.S. ecosystems that are not impacted by point
sources, it would appear to be unlikely that data for new REA case studies is forthcoming. A robust
critical loads approach, which is a research priority to support a future review, is needed to fill this gap.
Are the limitations and uncertainties in the exposure/risk information appropriately characterized and
considered in our interpretation of the information in the context of this current review?
The discussion of limitations and uncertainties is generally good. Issues such as legacy Pb, multi-
stressor effects, and lab-to-field applicability create considerable uncertainty. The use of conservative
screening levels in the calculation of hazard quotients is particularly useful because the calculated risks
are overstated.
Chapter 6 - Review of the Secondary Standard for Lead
This chapter describes the basis for the current secondary standard and consideration of the current
evidence and exposure/risk-based information with regard to reaching preliminary staff conclusions
about the adequacy of the current standard.
Does the Panel agree with preliminary staff conclusions about the evidence and previous risk
assessment in light of current standards as presented in section 6.2 (Adequacy of the Current
Standard)?
11
-------
The preliminary staff conclusions provide a good assessment of the available evidence and the previous
risk assessment in light of the current secondary standard. The CAS AC notes, however, the concerns
raised in the response to the chapter 5 charge questions regarding the previous risk assessment.
In the Panel's view, does the discussion in this chapter provide an appropriate and sufficient rationale
to support preliminary staff conclusions that it is appropriate to consider retaining the current standard
(including the indicator, level, averaging time, and form) without revision?
The discussion provides appropriate and sufficient rationale to support retaining the current secondary
standard without revision. A general lack of new data that would indicate the appropriate level of Pb in
environmental media that may be associated with adverse effects suggests that the secondary standard
should be retained. Questions remain regarding the relevance of the indicator, level, averaging time and
form to the secondary standard (ecological context). A multi-media approach may be necessary to
account for legacy Pb and contributions from different sources for a secondary standard.
Does the Panel have any recommendations regarding additional interpretations and conclusions based
on the available information that would be appropriate for consideration beyond those discussed in this
chapter?
The CASAC does not have any recommendations regarding additional interpretations and conclusions
beyond what is contained in the chapter. Developing a critical loads approach for U.S. conditions would
be an important area for additional research. The discussion of uncertainties at the end of the chapter is
excellent. It should include mention of the use and/or relevance of toxicity data that are generated in test
systems that deploy exposures to media other than soil or water for appropriate organisms (e.g., plants in
hydroponic systems, soil nematodes in agar or culture medium).
Research Needs
Application of a critical loads approach with sensitivity analysis will help to determine which processes
are most important in determining Pb exposure to ecological receptors. This would be an integrated,
holistic, multi-media approach that could be used to examine the contributions of current aerial Pb
deposition to historical aerial deposition as well as Pb from other sources. Current critical loads models
are largely qualitative and empirical. Mechanistic sub-models need to be incorporated into the critical
loads model to provide an adequate means to predict Pb bioavailability, exposure, and toxicity. This
critical loads approach could be integrated to include other aerial pollutants such as oxides of nitrogen
and oxides of sulfur.
12
-------
Reference
Secretariat of the Commission for Environmental Cooperation (CEC), (2013), Hazardous Trade? An
Examination of US-generated Spent Lead-acid Battery Exports and Secondary Lead Recycling in
Mexico, the United States and Canada, Final Report, 15 April.
13
-------
OQ
3
3
o
c±.
o
a o
%&
^ ' L^
ft rn '-i
o <. c
tr* H^ ca
H § 5=
s-lt
B ^ n2
fffl ^ f\1
3
OQ
fa
2£
< 3
s: g-
B a
a;
o'
O
p
W
to
I?
o o
h^ O
------- |