Review of the National Ambient Air
Quality Standards for Lead:
Risk and Exposure Assessment
Planning Document
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EPA-452/P-11-003
June 2011
Review of the National Ambient Air
Quality Standards for Lead:
Risk and Exposure Assessment
Planning Document
U. S. Environmental Protection Agency
Office of Air Quality Planning and Standards
Office of Air and Radiation
Research Triangle Park, North Carolina 27711
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DISCLAIMER
This document has been reviewed by the Office of Air Quality Planning and Standards,
U.S. Environmental Protection Agency (EPA), and approved for publication. This document has
been prepared by staff from the Office of Air Quality Planning and Standards, U.S.
Environmental Protection Agency. Any opinions, findings, conclusions, or recommendations are
those of the authors and do not necessarily reflect the views of the EPA. Mention of trade names
or commercial products is not intended to constitute endorsement or recommendation for use.
Any questions or comments concerning human health-related portions of this document should
be addressed to Dr. Zachary Pekar, U.S. Environmental Protection Agency, Office of Air Quality
Planning and Standards, C539-07, Research Triangle Park, North Carolina 27711 (email:
pekar.zachary@epa.gov). Questions or comments concerning ecological-related portions of this
document should be addressed to Dr. J. Travis Smith, U.S. Environmental Protection Agency,
Office of Air Quality Planning and Standards, C539-07, Research Triangle Park, North Carolina
27711 (email: smith.jtravis@epa.gov).
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Table of Contents
1 Introduction 1-1
2 Human Exposure and Health Risk Assessment 2-1
2.1 Overview of the Previous Assessment 2-2
2.1.1 Conceptual Model for Risk Associated with Air-related Lead 2-2
2.1.2 Case Studies and Air Quality Scenarios 2-6
2.1.3 Analysis Approach and Modeling Elements 2-8
2.1.4 Challenges in Characterizing Air-related Exposure and Risk 2-14
2.1.5 Key Uncertainties and Limitations 2-15
2.2 Consideration of Newly Available Evidence 2-18
2.3 Key Observations and Conclusions 2-30
3 Ecological Risk Assessment 3-1
3.1 Overview of the Previous Assessment 3-3
3.1.1 Conceptual Model 3-3
3.1.2 Overview of Analytical Approach 3-7
3.1.3 Key Limitations and Uncertainties 3-10
3.2 Consideration of Newly Available Evidence 3-11
3.2.1 Factors Affecting Lead Bioavailability 3-11
3.2.2 Transport of Lead between Ecosystem Compartments 3-12
3.2.3 Relative Roles of Atmospheric Deposition and Other Pb Sources to
Ecosystems 3-13
3.2.4 Critical Loads (CL) Models 3-13
3.3 Key Observations and Conclusions 3-15
4 References 4-1
List of Figures
Figure 2-1 Conceptual Model for Previous Exposure and Risk Assessment 2-5
Figure 2-2. Overview of Analysis Approach for Exposure and Risk Assessment 2-9
Figure 2-3. Comparison of Four Concentration-response Functions Used in the Previous Risk
Assessment 2-13
Figure 3-1. Conceptual Model for Ecological Risk Assessment During the Last Review 3-6
Figure 3-2. Analytical Approach for Screening-level Assessment in the Last Review 3-8
List of Tables
Table 2-1 Air Quality Scenarios Assessed in the Risk Assessment for Previous Review 2-7
Table 2-2. Comparison of Total and Incremental IQ Loss Estimates Below 10 |ig/dL for the Four
Concentration-response Functions 2-13
Table 2-3. Assessment of Information (including methods, models, etc.) Newly Available in this
Review 2-19
in
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1 INTRODUCTION
The U.S. Environmental Protection Agency (EPA) is conducting a review of the air
quality criteria and the national ambient air quality standards (NAAQS) for lead (Pb). The
purpose of this planning document is to describe the consideration of the extent to which newly
available scientific evidence and tools or methodologies warrant the conduct of quantitative risk
and exposure assessments (REAs) that might inform this review. Also considered is the extent to
which newly available evidence may refine our characterization of exposure and risk estimates
provided by the assessments conducted for the last review.
The previous Pb NAAQS review, completed in fall of 2008, resulted in substantial
revision to the standards (73 FR 66964). In consideration of the much-expanded health effects
evidence on neurocognitive effects of Pb in children, EPA substantially revised the primary
standard from a level of 1.5 micrograms per cubic meter (|ig/m3) to a level of 0.15 |ig/m3.
EPA's decision on the level for the standard was based on the weight of the scientific evidence
and guided by an evidence-based framework that integrates evidence for relationships between
Pb in air and Pb in children's blood and between Pb in children's blood and IQ loss. The level of
0.15 ug/m3 was estimated to protect against air Pb-related IQ loss in the most highly exposed
children, those exposed at the level of the standard. Results of the quantitative risk assessment
were judged supportive of the evidence-based framework estimates. The averaging time was
revised to a rolling 3-month period with a maximum (not-to-be-exceeded) form, evaluated over a
3-year period.1 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 standards.2
As part of the previous Pb NAAQS review, EPA completed a quantitative assessment
which estimated air-related Pb exposure and the associated risk of IQ loss in children for a series
of study areas. Risks were estimated for then-current air quality conditions and for air quality
conditions associated with just meeting the then-current standard and a series of alternative
(lower) standards. Risk estimates generated as part of that analysis informed the EPA's decision
to lower the level of the standard in the last review.
1 As compared to the previous averaging time of calendar quarter, this revision was considered to be more
scientifically appropriate and more health protective. 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. 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.
2 The current NAAQS for Pb are specified at 40 CFR 50.16.
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To estimate the potential ecological risks associated with exposures to Pb emitted into
ambient air in the last review, a screening level risk assessment was performed. Hazard
quotients were developed for three case studies for which media concentrations had also been
estimated for the health risk assessment as well as for a national scale surface water and sediment
assessment. While these analyses indicated the potential for air-related Pb to pose ecological
risks of concern, limitations in available information and tools precluded our ability to parse out
estimates of air-related ecological risk associated with the then-current or alternative Pb
NAAQS.
This document (titled Risk and Exposure Assessment Planning Document - hereafter
referred to as REA Planning Document} presents a critical evaluation of information related to Pb
human and ecological exposure and risk (e.g., data, modeling approaches) newly available in this
review as identified in the first draft Integrated Science Assessment for Lead (draft ISA; USEPA,
201 la). The focus of this evaluation is consideration of the extent to which new or substantially
revised REAs for health and ecological risk are warranted by the newly available evidence.
This document is intended to facilitate consultation with the Clean Air Scientific
Advisory Committee (CASAC), as well as public review, for the purpose of obtaining advice on
EPA's consideration of the recently available evidence (information, methods, etc) with regard to
its potential impact on quantitative exposure and risk analyses, both with regard to consideration
of the extent to which new assessments are warranted in this review and with regard to our
consideration of the last assessment in evaluating risk and exposure-related considerations in our
Policy Assessment for this review. The discussion in this document is intended to build upon the
exposure and risk assessment approaches employed for the last review, and on Agency
experience with Pb exposure and risk assessment since that time, while also drawing from
information presented in the May 2011 draft of the ISA for the current review.
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Background
Sections 108 and 109 of the Clean Air Act (Act) govern the establishment and periodic
review of the NAAQS. These standards are established for pollutants that may reasonably be
anticipated to endanger public health and welfare, and whose presence in the ambient air
results from numerous or diverse mobile or stationary sources. The NAAQS are to be based
on air quality criteria, which are to accurately reflect the latest scientific knowledge useful in
indicating the kind and extent of identifiable effects on public health or welfare which may be
expected from the presence of the pollutant in ambient air. The EPA Administrator is to
promulgate and periodically review, at five-year intervals, "primary" (health-based) and
"secondary" (welfare-based)1 NAAQS for such pollutants.2 Based on periodic reviews of the
air quality criteria and standards, the Administrator is to make revisions in the criteria and
standards, and promulgate any new standards, as may be appropriate. The Act also requires
that an independent scientific review committee advise the Administrator as part of this
NAAQS review process, a function now performed by the CASAC.
EPA's overall draft plan and schedule for this Pb NAAQS review is presented in the draft
Integrated Review Plan for the National Ambient Air Quality Standards for Lead3 That plan
discusses the preparation of key documents in the NAAQS review process including an
Integrated Science Assessment (ISA) and a Policy Assessment. The ISA provides a critical
assessment of the latest available scientific information upon which the NAAQS are to be
based, and the Policy Assessment evaluates the policy implications of the information
contained in the ISA and of any policy-relevant quantitative analyses, such as quantitative
human and/or ecological risk and exposure assessments, that were performed for the review
or for past reviews. Based on this evaluation, the Policy Assessment presents staff
conclusions regarding standard-setting options for the Administrator to consider in reaching
decisions on the NAAQS.4
1 Welfare effects, as defined in section 302(h) of the Act 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.
2Section 109(b)(l) [42 U.S.C. 7409] of the Act 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." Section 109(b)(2) of the Act directs that a secondary
standard is to Aspecify 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.
^Integrated Review Plan for the National Ambient Air Quality Standards for Lead, March, 2011, available at:
http://www.epa.gov/ttn/naaqs/standards/pb/data/2011033 lpbirpdraftcasac.pdf.
4NAAQS decisions involve consideration of the four basic elements of a standard: indicator, averaging time,
form, and level. The indicator defines the pollutant to be measured in the ambient air for the purpose of
determining compliance with the standard. The averaging time defines the time period over which air quality
measurements are to be obtained and averaged, considering evidence of effects associated with various time
periods of exposure. 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.
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2 HUMAN EXPOSURE AND HEALTH RISK
ASSESSMENT
This evaluation of newly available information is structured around consideration of two
key questions: (a) is there newly available information relevant to critical uncertainties or
limitations associated with the human exposure and health risk assessments completed for the
last review; and, (b) to what extent would an updated risk model generate risk estimates that are
substantially different from estimates generated in the previous review (i.e., enhanced precision
and/or confidence, coverage for additional sensitive subpopulations and/or health endpoints)?
In designing and implementing an assessment of exposure and risk associated with Pb in
ambient air, we are faced with significant limitations and complexity that go far beyond the
situation for similar assessments typically performed for other criteria pollutants. For example,
unlike other criteria pollutants, risk associated with exposure to Pb originally released to ambient
air is multi-pathway in nature (i.e., not only an inhalation hazard), with exposure occurring
through a range of ingestion pathways associated with deposition of ambient air Pb onto surfaces
in indoor and outdoor environments, as well as inhalation of ambient air outdoors and of ambient
(outdoor) air that has infiltrated indoors. The ingestion pathways include incidental ingestion
through hand-to-mouth contact as well as dietary and drinking water ingestion. In addition,
given the persistent nature of Pb, exposure to ambient air Pb can result from Pb originally
emitted into the environment recently or at some point in the past (e.g., Pb from current or
historic sources). Furthermore, uses of Pb in house paint and solder used in water distribution
systems can also contribute to Pb exposures.
The multiple and potentially intertwined exposure pathways add substantial complexity
to designing and implementing risk and exposure assessments for Pb. For example, because of
nonlinearity in the relationship between Pb exposure and the level of Pb in blood (i.e., blood
lead, or PbB - the commonly used Pb dose metric) as well as nonlinearity that has been identified
in the concentration-response relationship for IQ loss, it is necessary to consider total Pb
exposure in modeling risk for a child scenario and not only exposure related to Pb released into
ambient air. In addition, modeling some of the key pathways involved in Pb exposure (e.g., Pb
loading of indoor residential dust by ambient air Pb that penetrates indoors and settles onto
surface), can be complicated. These are some of the factors that make modeling exposure and
risk to Pb released into ambient air a technically challenging task that often requires the use of
simplifying assumptions and that is subject to a range of technical limitations and considerable
uncertainty. This chapter first describes salient aspects and details of the previous assessment
(section 2.1) and then considers information newly available in this review and the extent to
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which it might appreciably impact a revised or updated assessment (section 2.2). Key
observations and conclusions drawn from this evaluation are presented in section 2.3.
2.1 OVERVIEW OF THE PREVIOUS ASSESSMENT
This section provides an overview of the human exposure and health risk assessments
completed as part of the previous Pb NAAQS review (USEPA 2007a,b). The risk assessment
completed for the previous review focused on estimating IQ loss in children due to exposure to
Pb over the first seven years of life from a variety of sources, including, most importantly for
purposes of this review, Pb released into ambient air. The risk assessment focused on a set of
case studies. Due to limited data and models for characterizing all of the various complexities
associated with Pb exposures, our efforts to focus on and characterize risk associated with
ambient air-related sources and exposures in the last assessment included a number of
simplifying assumptions in a number of areas. Moreover, while Pb in diet and some sources of
drinking water may derive at least in part from Pb emitted into ambient air, the contribution of
these air-related exposure pathways was not explicitly separated from that of nonair pathways
due to limitations in the tools and data (as summarized in section 2.1.4 below).
This section begins with an overview of the conceptual model for our assessment of air-
related Pb exposure and risk in the last Pb NAAQS review (section 2.1.1), followed by a
discussion of the study areas on which the last assessment focused (section 2.1.2). Section 2.1.3
describes the risk model used, including key modeling elements (e.g., monitor data, air quality
models, indoor dust models, input datasets, concentration-response functions), and section 2.1.4
describes particular challenges associated with differentiating air-related exposure and risk from
those associated with nonair pathways (section 2.1.4). Lastly in section 2.1.5, we describe key
uncertainties and limitations associated with the risk model.
2.1.1 Conceptual Model for Risk Associated with Air-related Lead
This section describes the conceptual model developed for the last review for assessment
of public health risks associated with Pb from ambient air. The model identifies sources,
pathways, routes, exposed populations, and health endpoints, with specific attention to those that
were explicitly addressed in the risk assessment completed for the previous review. This is
summarized in Figure 2-1, with boxes outlined in bold indicating items included in the
quantitative risk assessment and sources and pathways for which ambient air has played a role
("air-related") identified in bold text. In this conceptualization, these are exposures with the
potential to be affected (over some time frame) by an adjustment to the Pb NAAQS. Those
pathways not associated with Pb originally emitted to the ambient air are considered policy-
relevant background since an adjustment to the Pb NAAQS is not likely to have an impact on
these exposures; these pathways are not bolded in Figure 2-1.
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Sources of Pb exposure include current and historical air emissions sources, as well as
miscellaneous nonair sources (e.g., land disposal of wastes). Such sources can contribute to Pb
in outdoor dust and soil, which may play a substantial role in human exposures, particularly for
children. Additionally, Pb in house dust, which may be derived from Pb in outdoor dust and soil,
as well as from ambient air Pb is another source of children's exposure.
In addition to airborne emissions (recent or those in the past), sources of Pb exposure also
included old leaded paint, including Pb mobilized indoors during renovation/repair activities, Pb
in drinking water and Pb in the diet (Figure 2-1).3 Pb in diet and drinking water may have air
pathway related contributions as well as contributions from background 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 these contributions in the risk assessment
performed for the last review.4 Other pathways shown in Figure 2-1 as air-related include
inhalation of newly or previously emitted Pb, ingestion of outdoor soil/dust containing
previously deposited Pb, and ingestion of indoor dust containing newly or previously emitted Pb.
Regarding exposed populations and health effects endpoints, the previous risk assessment
focused on IQ loss in children up to age 7 years. This reflected consideration of the evidence
which indicated that children received elevated Pb exposure due to hand-to-mouth activity (i.e.,
incidental soil and indoor dust ingestion) and that ambient air-related Pb has been shown to
contribute to Pb in outdoor soil and indoor residential dust. In addition, selection of this
population (or lifestage) reflected consideration of the evidence that the developing nervous
system in children is among, if not, the most sensitive of the endpoints associated with Pb
exposure. Further, the blood Pb model available for the review (summarized in section 2.1.3
below) focused on simulating PbB concentrations through the first 7 years of childhood.
In terms of internal disposition and the biometrics used to assess Pb exposure, PbB levels
continue to be extensively used as an index or biomarker of exposure by national and
international health agencies. This reflects the association of PbB with exposure, particularly
recent exposure in young children, and the relative ease of collecting PbB measurement.
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 PbB as the exposure metric. Therefore, we focused on modeling PbB in young
3 We did not explicitly consider Pb exposure related to consumer products (e.g., toys, cosmetics, dishes).
4 The assessment grouped the exposure and risk estimates for Pb in diet and drinking water together in a
"background" category which was combined with the other pathways in estimates presented for "total Pb exposure".
Characterization of the risk assessment results in the rulemaking recognized the contribution, albeit unqualified,
from air-related pathways within this category.
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children, developing estimates for two PbB metrics: "concurrent" and "lifetime average". For
the former we estimated PbB at age 7 years, while lifetime average was estimated as the average
of PbB levels across the 7 year period.
At the time of the last review, we noted that limitations precluded prediction of changes
in adult PbB 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 PbB 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 presented in the 2006 AQCD (USEPA, 2006a), the assessment
focused on risk to the central nervous system in childhood as the most sensitive effect that could
be quantitatively assessed, with decrement in Intelligence Quotient (IQ) used as the risk metric.
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Figure 2-1. Conceptual Model for Previous Exposure and Risk Assessment
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Note: Boxes outlined in bold and shaded are included in the quantitative risk assessment.
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2.1.2 Case Studies and Air Quality Scenarios
The risk assessment estimated risk for five case studies5'6that generally represent two
types of residential population exposures: (1) more highly air-pathway exposed young children
(as described below) residing in small neighborhoods or localized residential areas with air
concentrations somewhat near the standard being evaluated, and (2) location-specific urban
populations with a broader range of air-related exposures.
The case studies representing the children most highly exposed via air-related pathways
were the general urban case study and the primary Pb smelter case study. The general urban case
study was not based on a specific geographic location and reflected several simplifying
assumptions in representing exposure including uniform ambient air Pb levels associated with
the standard of interest across the hypothetical study area and a uniform study population.
Additionally, the method for simulating temporal variability in air Pb concentrations in this case
study relied on national average estimates of the relationships between air concentrations in
terms of the statistics considered for different forms of the standard being assessed and the
annual ambient air concentrations required for input to the PbB model.7 Thus, while this case
study provided characterization of risk to children that are relatively more highly air pathway
exposed (as compared to the location-specific case studies), it was not considered to represent a
high-end scenario with regard to the characterization of ambient air Pb levels and associated risk.
The primary Pb smelter case study provides risk estimates for children living in a specific area
that is currently not in attainment with the current NAAQS. We focused particularly on a
subarea within 1.5 km of the facility, where airborne Pb concentrations were closest to the
current standard and where children's air-related exposures are most impacted by emissions
associated with the Pb smelter from which air Pb concentrations were estimated.
5 A sixth case study (the secondary Pb smelter case study) is also described in the Risk Assessment Report.
However, as discussed in Section 4.3.1 of that document (USEPA, 2007a), significant limitations associated with
predicting ambient air Pb levels in the vicinity of the facility using dispersion modeling contributed to large
uncertainties in the corresponding risk estimates.
6 In addition to the six case studies included in the Risk Assessment Report, the pilot phase of the risk
assessment from the last review also included a near-roadway case study (ICF International, 2006). Based on the
pilot results and advice from CASAC, this case study was not carried into the full-scale analysis. Rather, we
substituted the general urban case study for the near-roadway case study since the near-roadway case study focused
on a small subset of the urban area (populations exposed immediately near roadways), while for purposes of the risk
assessment, we wanted a case study that provided broader coverage for residents potentially exposed at the standard
level being assessed, which was better provided by the general urban case study (USEPA, 2007a).
7 As the PbB model used in the risk assessment was limited in that it did not accept inputs of a temporal
time step shorter than annual average, ratios of relationships in the available air monitoring data between different
statistical forms being considered for the standard and an annual average were employed for the urban case studies
(that did not rely on dispersion modeling) as a method of simulating the temporal variability in air Pb concentrations
that occurs as a result of meteorology, source and emissions characteristics.
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The three location-specific urban case studies focused on specific residential areas within
Cleveland, Chicago, and Los Angeles to provide representations of urban populations with a
broader range of air-related exposures due to spatial gradients in both ambient air Pb levels and
population density. For example, the highest air concentrations in these case studies (i.e., those
closest to the standard being assessed) 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.
Based on the nature of the population exposures represented by the two categories of case
study, the first category (the general urban and primary Pb smelter case studies) includes
populations that are relatively more highly exposed by way of air pathways to air Pb
concentrations somewhat near the standard level evaluated, compared with the populations in the
three cities.
The air concentrations in the different air quality scenarios included those representing
current conditions for the different case studies, conditions meeting the then-current (at the time
of the last review) NAAQS of 1.5 ug/m3, maximum calendar quarter average, and conditions
meeting several alternate, lower standards. The set of air quality scenarios assessed in the risk
assessment is listed in Table 2-1.
Table 2-1 Air Quality Scenarios Assessed in the Risk Assessment for Previous Review.
Air Quality Scenario
Then-current Standard
Current Conditions
Alternate Standard
Alternate Standards
Averaging Time
(Form)
Calendar Quarter
(maximum)
Month
(maximum)
Level (ug/m3)
1.5
0.87 (95th percentile)
0.14 (mean)
0.14
0.36
0.09
0.2
0.5
0.2
0.05
0.02
Case Study
All
General Urban
Chicago
Cleveland
Los Angeles
General Urban
Primary Smelter
General Urban
Primary Smelter
Cleveland
All
except Los Angeles
All
All
The concentrations of Pb used for these scenarios for other media and exposure pathways
varied depending on the type of case study (as summarized below in section 2.1.3) and, in some
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cases (as summarized below in section 2.1.4), limitations in the available data and modeling
tools precluded the assessment from varying concentrations of some nonair media across the air
quality scenarios. For example, dietary and drinking water Pb concentrations, as well as soil Pb
concentrations, were not varied in any case studies across the air quality scenarios. The
modeling simulations for all cases studies did, however, include changes in indoor dust Pb
concentrations, for different air quality scenarios, although as summarized in section 2.1.3, the
methods used differed among the different types of case studies.
2.1.3 Analysis Approach and Modeling Elements
This section describes the risk assessment approach (including discussion of key analysis
steps), used in assessing risk for the two categories of case studies. As illustrated in Figure 2-2,
the risk assessment completed for the primary Pb smelter case study included four analytical
steps: (a) fate and transport of Pb released into outdoor air, including the dispersion of Pb away
from the point of release, (b) prediction of the resulting concentration of Pb in media of concern
including outdoor air and indoor dust, (c) use of these Pb concentrations together with estimates
of Pb in background exposure pathways, including diet, to estimate associated PbB levels in
children using biokinetic modeling, and (d) use of concentration-response functions derived from
epidemiology studies to estimate IQ loss associated with the estimated PbB levels. The
modeling approach for the general urban case study and location-specific urban case studies is
somewhat simpler, since it does not involve fate and transport modeling for air concentration
estimates and, instead, uses ambient monitor levels to characterize air Pb levels across the study
area. Subsequent steps in the general urban case study analysis are fairly similar to what is
described above for the point source case study, with the generation of population PbB levels
being somewhat simplified for the general urban case study. Figure 2-2 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, while the fourth is the risk
assessment step (exposure assessment and risk assessment steps are discussed separately below).
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Figure 2-2. Overview of Analysis Approach for Exposure and Risk Assessment.
RISK CHARACTERIZATION EXPOSURE ASSESSMENT
Characterizing ambient air levels and
deposition to soil
Ambient monitoring data
(general urban and location-specific urban)
\
Ambient air
concentration
for study ara
Characterizing soil and indoor
dust concentrations
4
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(all case studies)
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diet
indoor paint (actually reflected in
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(primary Pb smelter and location- ^
specific urban)
^
Characterizing risk (IQ loss)
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from that study
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Exposure Assessment
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 background 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). Both of
these uncertainties are discussed below in Section 2.1.5. Specific approaches used at the three
case study locations are briefly described below.
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 general 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 in exposure for three urban areas in the U.S. By contrast, the
general urban study area 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
(see Section 5.2.2 of US EPA, 2007a for additional detail).
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 the available empirical data was used to predict soil
levels for portions of the study area beyond this zone.
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
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outdoor air indoors, deposition rates of Pb from indoor air to indoor surfaces, house cleaning
rates). For the point source case study, a combination of regression-based models obtained from
the literature and developed based on site-specific data were used, and a customized hybrid
empirical-mechanistic model was developed 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 general urban case study. Additional detail on
methods used to characterize media Pb concentrations for each case study can be found in
Sections 3.1 and 5.2.3 of US EPA, 2007a). Blood Pb levels were predicted from estimates of Pb
contained in various media (e.g., ambient air, diet, water, indoor dust) using the Integrated
Exposure and Uptake Biokinetic (IEUBK) model (Sections 3.2.1.1 and 5.2.4 of US EPA,
2007a).8 However, rather than completing a fully-probabilistic simulation of PbB levels for a set
of simulated children (where we would first simulate variability in Pb intake and then estimate
PbB levels for each child separately in IEUBK), we used IEUBK to generate a central-tendency
estimate of PbB levels for a group of children within a given study area. We then combined this
central-tendency estimate with a geometric standard deviation (GSD) reflecting variability in
PbB levels for groups of children to generate a distribution of PbB levels for a study area.9 Note,
that for all of the study areas, we assumed that pathway apportionment of PbB levels based on
the modeling of the central-tendency PbB level (using IEUBK) holds for all percentiles of PbB
levels derived by combining that central-tendency with the GSD. PbB modeling completed for
all case studies included estimates of both concurrent and lifetime-average PbB metrics, although
ultimately, we focused on the concurrent PbB metric in estimating risk.10
8 In predicting PbB levels, we assumed that Pb concentrations in exposure media remained constant
throughout the 7 year simulation period.
9 The procedure for combining the lEUBK-based central tendency blood Pb estimate with the GSD to
generate a population distribution of PbB 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 central-tendency estimate of
PbB levels and this is in turn, combined with the GSD to produce an population-distribution of PbB levels.
However, for both the primary Pb smelter and the location-specific urban study areas, smaller polygons within the
larger study area (e.g., US Census blocks for the location specific urban study areas) are used as the basis for
generating distributions of PbB levels and these are then population weighted prior to aggregation to form an overall
PbB distribution for each study area (see sections 3.2.2 and 5.2.2.3 of US EPA, 2007a).
10 As discussed in section 2.1.5 of the risk assessment report (US EPA, 2007a), 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-associated intellectual
deficits than was the maximal measured (peak) or early childhood blood lead concentrations" with the concurrent
PbB level exhibiting the strongest relationship (CD, p. 6-29).
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Risk Characterization
The risk characterization step involves generating a distribution of IQ loss estimates for
the set of children simulated in the exposure assessment. Specifically, estimated PbB levels (for
the concurrent PbB metric)11 were combined with four PbB concentration-response functions for
IQ loss (see Section 5.3.1.1 of US EPA 2007a). Four different concentration-response 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 PbB levels for which there is limited representation in the Lanphear et al
(2005) pooled dataset. For example, the 5th percentile for the concurrent PbB measurements in
that dataset was 2.5 |ig/dL (73 FR 66978). The four different functions are either based directly
on the lognormal concentration-response function described in the Lanphear et al, (2005) pooled
analysis of epidemiology studies focusing on IQ loss in children, or they are derived from data
presented in that study. The four functions are presented in Figure 2-3 and compared in Table 2-
2 with regard to total IQ loss and incremental IQ loss (IQ loss per |ig/dL) across a range of
concurrent PbB levels. A brief description of each of the functions is also provided below:
Log-linear with cutpoint: log-linear function derived from the pooled analysis applied
down to 1 |ig/dL (concurrent PbB 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 PbB 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 jUg/dL: developed by fitting a two-piece linear function
stratified at 10 |ig/dL (peak PbB metric) to the log-linear function developed from the
pooled analysis.
Dual linear-stratified at 7.5 jug/dL: as above, but based on stratification of the two-piece
function at 7.5 |ig/dL (peak PbB metric).
11 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 were given primary emphasis, however, due to the slightly more significant association found
for concurrent PbB with IQ by Lanphear et al (2005) in addition to advice from CAS AC.
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Figure 2-3. Comparison of Four Concentration-response Functions Used in the Previous
Risk Assessment.
14 -,
12
10
2 6
log-linear w ith outpoint
dual linear - stratified at
10 ug/dL, peak
dual linear - stratified at
7.5 ug/dL, peak
log-linear w ith low-
exposure linearization
34567
Concurrent blood Pb (ug/dL)
10
Table 2-2. Comparison of Total and Incremental IQ Loss Estimates Below 10 ug/dL for the
Four Concentration-response Functions.
Performance Metric
Total IQ loss
Incremental IQ
loss
(average # points
per |jg/dl_)
at2ug/dL
at 5 ug/dL
at 7.5 ug/dL
at 10 ug/dL
<2 ug/dL
<5 ug/dL
<7.5 ug/dL
<10ug/dL
Concentration-Response Function
Log-linear
with outpoint
Log-linear
with low-
exposure
linearization
Dual linear -
stratified at
10ug/dL
peak
Dual linear -
stratified at
7.5 ug/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
Two categories of risk metrics were generated for each of the 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).
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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 general urban case study, only the first type of risk metric, population risk
percentiles, was developed because this case study is not location-specific. Child frequency
counts are not applicable, since a specific location with associated demographic data was not
modeled.
2.1.4 Challenges in Characterizing Air-related Exposure and Risk
In the risk assessment, we attempted to separate estimates of total (all-pathway) PbB and
IQ loss into a policy-relevant background category and two air-related (policy relevant)
categories, referred to as "recent air" and "past air". However, significant limitations in our
modeling tools and data resulted in an inability to parse specific risk estimates into specific
pathways, such that we had approximated estimates for the air-related and background
categories.
Those Pb exposure pathways tied most directly to ambient air, which consequently have
the potential to respond relatively more quickly to changes in air Pb (i.e., inhalation and
ingestion of indoor dust Pb derived from the infiltration of ambient air Pb indoors), were placed
into the "recent air" category. The other air-related Pb exposure pathways, all of which are
associated with atmospheric deposition, were placed into the "past air" category. These include
ingestion of Pb in outdoor dust/soil and ingestion of the portion of Pb in indoor dust that after
deposition from ambient air outdoors is carried indoors with humans.
Among the limitations affecting our estimates for the air-related and background
categories is the apportionment of background (nonair) pathways. For example, while
conceptually indoor Pb paint contributions to indoor dust Pb would be considered background
and included in the "background" category for this assessment, due to technical limitations
related to indoor dust Pb modeling, dust from Pb paint was included as part of "other" indoor
dust Pb (i.e., as part of past air exposure). The inclusion of indoor paint Pb as a component of
"other" indoor dust Pb (and consequently as a component of the "past air" category) represents a
source of potential high bias in our prediction of exposure and risk associated with the "past air"
category because, conceptually, exposure to indoor paint Pb is considered part of background
exposure. At the same time, Pb in ambient air does contribute to the exposure pathways included
in the "background" category (drinking water and diet), and is likely a substantial contribution to
diet. We could not separate the air contribution from the nonair contributions, and the total
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contribution from both the drinking water and diet pathways is categorized as "background" in
this assessment. As a result, our "background" risk estimate includes some air-related risk
representing a source of potential low bias in our predictions of air-related risk.
Further, we note that in simulating reductions in exposure associated with reducing
ambient air Pb levels through alternative NAAQS (and increases in exposure if the current
NAAQS was reached in certain case studies) only the exposure pathways categorized as "recent
air" (inhalation and ingestion of that portion of indoor dust associated with outdoor ambient air)
were varied with changes in air concentration. The assessment did not simulate decreases in
"past air" exposure pathways (e.g., reductions in outdoor soil Pb levels following reduction in
ambient air Pb levels and a subsequent decrease in exposure through incidental soil ingestion and
the contribution of outdoor soil to indoor dust). These exposures were held constant across all
air quality scenarios.
In summary, because of limitations in the assessment design, data and modeling tools,
our risk estimates for the "past air" category include both risks that are truly air-related and
potentially, some background risk. Because we could not sharply separate Pb linked to ambient
air from Pb that is background, some of the three categories of risk are underestimated and others
overestimated. On balance, we believe this limitation leads to a slight overestimate of the risks
in the "past air" category. At the same time, as discussed above, the "recent air" category does
not fully represent the risk associated with all air-related pathways. Thus, we 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.
2.1.5 Key Uncertainties and Limitations
Although the risk assessment completed for the last review utilized a number of
innovative modeling elements in order to generate representative estimates of risk for our study
populations, like all risk models there was uncertainty associated with the model and its output.
For example, because of the evidence for a nonlinear response of PbB to exposure and also the
nonlinearity reflected in the C-R functions for estimation of IQ loss, the assessment first
estimated total PbB levels and associated risk (i.e., for air- and nonair-related exposure
pathways), and then separated out those estimates of PbB and associated risk for pathways of
interest in this review. We separated out the estimates of total (all-pathway) PbB and IQ loss into
a background category and two air-related categories ("past" and "recent"). However,
significant limitations in our modeling tools and data resulted in an inability to parse specific risk
estimates into specific pathways, such that we approximated estimates for the air-related and
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background categories. As discussed 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 past-air and recent-air
categories.
Additional limitations, assumptions and uncertainties, which were recognized in various
ways in the assessment and presentation of results, are listed below, beginning with those related
to design of the assessment or case studies, followed by those related to estimation of Pb
concentrations in ambient air, indoor dust, outdoor soil/dust, and blood, and estimation of Pb-
related IQ loss.
Temporal Aspects: During the 7-year exposure period, media concentrations remain
fixed and the simulated child remains at the same residence (while exposure factors and
physiological parameters are adjusted to match the age of the child).
General Urban Case Study: The design for this case study employs assumptions
regarding uniformity that are reasonable in the context of a small neighborhood
population, but would contribute significant uncertainty to extrapolation of these
estimates to a specific urban location, particularly a relatively large one. Thus, the risk
estimates for this general urban case study, while generally representative of an urban
residential population exposed to the specified ambient air Pb levels, cannot be readily
related to a specific large urban population.
Location-specific Urban Case Studies: Limitations in the ambient air monitoring network
limit our characterization of spatial gradients of ambient air Pb levels in these case
studies.
Air Quality Simulation: The proportional roll-up and roll-down procedures used in some
case studies to simulate the then-current NAAQS and alternate NAAQS levels,
respectively, assume proportional changes in air concentrations across the study area in
those scenarios for those case studies. EPA recognizes the uncertainty with our
simulation of higher air Pb concentrations that just meet the then-current 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.
Outdoor Soil/Dust Pb Concentrations: Uncertainty regarding soil/dust Pb levels and the
inability to simulate the influence of changing air Pb levels related to lowering the
NAAQS contributes uncertainty to air-related risk estimates.
Indoor Dust Pb Concentrations: Limitations and uncertainty in modeling of indoor dust
Pb levels, including the impact of reductions in ambient air Pb levels, contributes
uncertainty to air-related risk estimates.
Interindividual Variability in PbB Levels: Uncertainty related to population variability in
PbB levels and limitations in modeling of this introduces significant uncertainty into PbB
and IQ loss estimates for the 95th percentile of the population.
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Pathway Apportionment for Higher Percentile PbB andlQ Loss: Limitations primarily in
data prevented us from characterizing the degree of correlation between high-end Pb
exposures across pathways (e.g., the degree to which an individual experiencing high
drinking water Pb exposure would also potentially 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 PbB level and IQ loss is subject to greater uncertainty at lower PbB levels (e.g.,
particularly below 2.5 |ig/dL concurrent PbB).
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2.2 CONSIDERATION OF NEWLY AVAILABLE EVIDENCE
This section evaluates the information, methods and models newly available since the last
review (as summarized in the first draft Pb ISA) to assess the extent to which it has the potential
to address these limitations and uncertainties. Table 2-3 (a) identifies limitations and sources of
uncertainty in the risk assessment model developed in the last Pb NAAQS review, (b) identifies
the evidence newly available since the last review that may address these uncertainties or
limitations (in those instances where new information is available) and (c) assesses the degree to
which the information (e.g., technical insights, data, modeling approaches etc.) resulting from
that research may address the source of uncertainty or limitation. Based on the information
provided in Table 2-3, EPA staff conclusions regarding the potential role of the risk assessment
model and associated risk estimates generated in the last review in the current Pb NAAQS
review are presented below in section 2.3.
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Table 2-3. Assessment of Information (including methods, models, etc.) Newly Available in this Review.
Limitation/Uncertainty in Risk
Model
Information Newly Available in this
Review
Consideration of Potential Utility and Impact on
Quantitative Exposure/Risk Assessment
Characterizing Exposure Pathways
A) Characterizing spatial gradients
in ambient air Pb levels in the urban
context. Limitations in our monitoring
network and in studies of smaller scale
spatial gradients in ambient Pb levels
in the urban setting introduced
uncertainty into our characterization of
exposure levels and risk for residential
populations modeled for the location-
specific urban study areas. Similarly,
limitations in our characterization of
ambient air Pb levels prevented us
from characterizing areas across the
U.S. with the attributes associated with
the general urban study area.
Section 3.5.1.2 (Intra-urban Variability) of the
draft ISA observes that evidence from a
number of studies suggests that there is
substantial intra-urban variability in ambient
air Pb levels with elevated levels being
associated with proximity to specific sources
(and often captured by source-oriented
monitors), while lower levels are often
associated with more generalized urban areas.
However, the monitoring network in place is
generally not refined enough to provide
comprehensive coverage for an urban area
such that the nature of the spatial gradient can
be well-characterized on a more localized
(neighborhood) level. The draft ISA also
highlights the fact that monitors from
different networks can capture different size
gradients for particles containing Pb, which
can make it hard to compare monitored levels
across monitors (i.e., if they are from different
networks).
In the last risk assessment, we used monitoring data to
try and identify the fraction of monitor locations with
ambient air Pb levels near the current standard level (or
alternative lower standard levels) which, therefore,
could have potential risks at or near those estimated for
the general urban study area. However, without having
more information on the gradient in air Pb levels near
those higher source-oriented monitors, any assessment
of the size of populations experiencing those elevated
air Pb levels is highly uncertain. The newly available
information does not appear to provide substantially
improved data for characterizing gradients at this more
refined spatial scale. We also note, that even if we did
have highly-refined information on ambient air Pb
gradients in urban areas, in order to complete more
detailed residential Pb-risk modeling, we would also
need more detailed information on other aspects of Pb
exposure specific to those residential areas (e.g., indoor
dust Pb concentrations, soil concentrations, and
drinking water Pb concentrations). Availability of this
level of refined exposure information for the urban
areas that might be of interest is likely limited or
lacking. In addition, we would still be hampered by
limitations in our ability to apportion total risk between
air and nonair pathways especially for individuals
exposed to higher pathway-specific Pb levels, as would
be associated with this type of specific residential
location (i.e., we do not have information on the degree
of correlation among Pb exposure pathways).
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Limitation/Uncertainty in Risk
Model
Information Newly Available in this
Review
Consideration of Potential Utility and Impact on
Quantitative Exposure/Risk Assessment
B) Limitations in our ability to
simulate alternative (lower)
standard levels (implementing
rollback). Significant uncertainty is
associated with the prediction of
reductions in ambient air Pb levels,
reflecting potential actions by urban
areas to attain alternative (lower)
standards.
Section 2.1.1 (Sources, Fate and Transport of
Ambient Lead) and section 3.3 (Fate and
Transport of Lead) of the draft ISA note that
Pb associated with coarse PM will tend to
deposit near sources, while Pb associated with
finer PM will tend to be transported further.
The draft ISA also notes that the cycle of
deposition and resuspension for even coarse-
phase Pb can be substantial leading to
diffusion in the urban context. This more
generalized information on the relationship
between Pb particle size and deposition helps
us to better understand and frame
conceptually the issue of spatial gradients in
reduction around sources. However, there
does not appear to be new research or
information on how ambient air Pb levels
might decrease given reductions in Pb
emissions from specific sources, or categories
of sources.
It does not appear that we have substantially improved
information to support design of our rollback strategies
for specific case studies. However, it is also important
to note that the general urban study area does not
require this type of representative characterization of
simulated reduction in ambient air Pb levels, since that
case study assumes that ambient air Pb levels are at the
standard level being assessed (i.e., it provides an
estimate of risk for children living in an area at or near
the standard level). While it is difficult to characterize
areas across the U.S. that reflect key aspects of the
general urban study area (e.g., to estimates how many
children it may represent), this case study provides an
important assessment of risk for children living in areas
that just meet the standard assessed (i.e., a reasonable
higher-end risk associated with a particular standard).
C) Characterizing Pb levels in other
exposure media, including soil,
drinking water and dietary items
(indoor dust is discussed separately
below - see entry "D"). Limitations in
our ability to characterize Pb levels in
other media (besides ambient air) and
differentiate those levels for different
subsets of urban populations in the
location-specific urban study areas
evaluated, introduces uncertainty into
the analysis.
Section 3.6.1 (Soils) of the draft ISA provides
a table (3-9) identifying soil Pb levels in
urban areas from the literature, including a
number of values from studies published
since the previous review yet conducted
across a broad range of years back to 1976.
Therefore, depending on the availability of
information to clarify the context for these
measurements particularly with regard to air-
related and other sources, these may include
new data to inform the characterization of
urban soil Pb levels for the risk assessment.
Section 4.1.1.3 of the draft ISA describes
It is important to note that while improved soil Pb data
(and data for Pb in other exposure media including
drinking water and dietary items) would provide us
with refined central-tendency estimates of Pb exposure
and risk for the study areas, the key factor that would
need to be addressed to substantially improve our
estimates of exposure and risk is the degree of
correlation between Pb exposure pathways, particularly
for individuals experiencing elevated exposure (e.g., to
what extent is higher drinking water Pb exposure
correlated with higher soil Pb exposure and with areas
of elevated ambient air Pb exposure). This type of
correlational information for more highly Pb exposed
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Limitation/Uncertainty in Risk
Model
Information Newly Available in this
Review
Consideration of Potential Utility and Impact on
Quantitative Exposure/Risk Assessment
information on Pb in drinking water
(including studies on the role of different
drinking water systems in releasing Pb from
pipes) and Pb in dietary items (Pb in crops,
fish and game).
children will only be available if we have matched sets
of measured Pb levels in exposure media for a
moderate to larger set of children (as noted below,
ideally, this would include PbB measurements so we
can look in detail at the air-blood ratios). In the
absence of this improved information on the nature of
correlations between Pb exposure pathways, we are not
in a position to substantially improve our estimates of
exposure and risk (including the ambient air-related
fraction of risk), particularly for higher PbB children,
including those with elevated ambient air-sourced Pb
exposures.
D) Modeling the relationship
between ambient air Pb (outdoors)
and indoor dust Pb (focusing on
uncertainties related to application
of the hybrid indoor dust model).
Elements of the hybrid (mechanistic-
empirical) indoor dust model are
subject to uncertainty including: (a) the
simulation of the interplay between air
exchange rates (ambient outdoor and
indoor), loading to indoor surfaces
from indoor air and removal through
cleaning, (b) estimating the fraction of
indoor dust Pb that originates from old
paint versus the fraction originating
from ambient outdoor air Pb (combines
mechanistic modeling for ambient air-
related indoor dust with empirical data
on total dust Pb, including the fraction
from indoor paint), and (c) converting
estimates of indoor dust Pb loading to
Section 4.1.1.2. (Exposure to Lead in Soil
and Dust) of the draft ISA discusses research
published since the last review focused on
assessing risk reductions associated with
vacuuming of surfaces with Pb dust (Hunt et
al., 2008). This study suggests that, while
vacuuming may clean much of the soil mass
deposited onto hard surface flooring, Pb dust
in a relatively fine form (1-3 urn particles,
which may be more accessible through
incidental hand-to-mouth activity by children)
remains. While this study provides
information on cleaning efficiency, it is
important to note that the soil Pb used in the
analysis was sourced from the Herculaneum
location and the study focused exclusively on
hard-surface flooring, providing no new
information regarding cleaning efficiencies
for indoor environments with additional types
of surfaces (e.g., fabrics).
While the Hunt et al. (2008) study provides some
information on cleaning efficiency and highlights the
potential for vacuuming to leave fine-particle Pb on
floors, the utility of the study in providing inputs to the
hybrid dust model (e.g. additional data on cleaning
efficiency) is limited by the fact that the study used soil
Pb samples from Herculaneum and the fact that it
focused on hard floors (and did not evaluate carpeted
flooring or any other textiles common in indoor
environments). Given the site-specific nature of this
material (i.e., associated with primary Pb smelting
activity that includes a significant historical signal
combined with repeated remediation activity), data
originating from the study, while potentially useful in
guiding remediation efforts and house cleaning
strategies for residences near Herculaneum, cannot be
readily extrapolated to other urban scenarios involving
Pb exposure. Note, however, that information obtained
from the study may be used qualitatively to further help
interpret risk estimates generated in the previous
review. Specifically, the Hunt et al., 2008 study
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Limitation/Uncertainty in Risk
Model
Information Newly Available in this
Review
Consideration of Potential Utility and Impact on
Quantitative Exposure/Risk Assessment
dust Pb concentrations, which are
needed for PbB simulation in IEUBK.
identifies the potential for low-bias in our risk
estimates, if dust containing Pb that is not cleaned is
ultimately in a finer form that is more accessible to
incidental ingestion by children. Conversely, the Hunt
study also identifies the potential for high-bias in
residences that lack carpets and other fabrics, if their
relative cleaning efficiency rates hold in a more
generalized urban setting (their rates are generally
higher than ours). Note, however that the Hunt et al,
(2008) study exclusively focused on hard floor surfaces
and not carpeting, and we would expect carpeting to
have substantially lower cleaning efficiency.
E) Modeling the relationship
between ambient air Pb (outdoors)
and indoor dust Pb and then relating
these to PbB levels (focusing here
more broadly on the relationship
between ambient air Pb and PbB,
with indoor dust Pb as the primary
linkage). There is uncertainty in
relating changes in ambient air Pb to
changes in indoor dust Pb and PbB.
Any data characterizing this
relationship between ambient air Pb
and PbB (including matched data sets
for a group of children) could be used
in performance assessing and possibly
calibrating, the exposure component of
the risk assessment.
Section 4.5.2. (Environmental Lead-Blood
Lead Relationships) discusses studies based
on the CDC's National Health and Nutrition
Examination Survey (NHANES) data from
1999-2004. These studies assess the
relationship between residential dust Pb and
PbB levels in children (e.g., Gaitens et al.,
2009 and Dixon et al., 2009). However, these
studies do not account for ambient air Pb (and
its potential relationship with indoor dust Pb
and consequently, total Pb exposure).
While NHANES-based studies and other studies of
specific locations provide insights into which factors
drive indoor dust Pb levels and PbB levels, an
important limitation of these studies is that they do
include measurements of ambient air Pb. Because
these studies do not provide explicit coverage for urban
areas with elevated ambient air Pb levels (where this Pb
source can be of greater importance), their utility in
performance assessing elements of the risk assessment
is limited. Had these studies included consideration for
ambient air Pb (including areas with elevated air Pb
levels), then the utility of the studies in the context of
the risk assessment would be greater.
Note, that as part of the risk assessment completed for
the last review, we considered studies based on the
EPA-sponsored National Human Exposure Assessment
Survey (NHEXAS) in performance evaluating
simulation of indoor dust Pb levels (see Appendix G,
Exhibit G-6 of the Pb HEHR, USEPA, 2007a).
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Information Newly Available in this
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Estimating Exposure andPbBfor Young Children
F) Uncertainty in modeling multiple-
pathway exposure to Pb in young
children, with consideration for the
degree of correlation between
pathways. If we had detailed survey
data on pathway exposures for a set of
children (including ambient air Pb,
indoor dust, soil Pb and dietary Pb
levels for each child), we could then
use those data to enhance our
simulation of total Pb exposure for the
urban case studies. This kind of
matched pathway-specific data for a
set of children would allow us, in
particular, to define potential
correlations between Pb exposure
pathways (e.g., the extent to which
children with high drinking water Pb
are also exposed to high indoor dust Pb
and ambient air Pb). This, in turn,
would potentially improve our ability
to simulate risk for children with
elevated Pb exposures and parse out
the fraction associated with ambient air
Pb.
G) Modeling PbB levels in young
children given pathway-specific
intake estimates (use of IEUBK).
There is uncertainty both in the
Section 4.1.1 (Pathways for Lead Exposure)
in the draft ISA discusses research based on
the EPA-sponsored National Human
Exposure Assessment Survey (NHEXAS)
dataset. For example, Egeghy et al., 2005,
used a dataset for Maryland location to
examine determinants of variability in PbB
levels (including ambient air Pb, dust Pb and
dietary Pb levels). While this analysis did use
a matched dataset for a group of 80
individuals, an important attribute of the study
is that all individuals are >6 yrs of age (i.e.,
ranging older than the age group modeled in
our risk assessment). Additionally, the air Pb
measurements were restricted to particles
smaller than 10 microns potentially affecting
conclusions regarding pathways involving
deposition of larger particles. The short
sampling period (8 days) also may preclude a
representative sample.
Section 4.6 (Biokinetic Models of Lead
Exposure-Blood Lead Relationships) of the
draft ISA observes, that while modeling of
human Pb exposures and biokinetics has
Consideration of Potential Utility and Impact on
Quantitative Exposure/Risk Assessment
While the NHEXAS-Maryland dataset used in the
Egeghy et al., (2005) study includes data for a variety
of exposure pathways (including ambient air Pb,
dietary pathways, soil and drinking water), because the
analysis includes predominantly individuals outside of
our child age range of interest, it is of reduced utility in
informing our consideration of pathways of exposure
and potential correlation between those pathways. In
addition, the relatively small sample size (80
individuals), could potentially limit any more detailed
assessment of the degree of correlation between
pathways for different percentiles of the study
population with regard to PbB level. It is interesting to
note, that in the Egeghy et al., 2005 study, outdoor air
Pb, while statistically associated with indoor air Pb,
was not associated directly with indoor dust Pb levels,
although this may reflect the fact that their dataset
reflected residential areas with relatively low ambient
air Pb, such that other factors (e.g., home age,
condition of indoor paint and construction material)
drove loadings of indoor dust Pb.
It does not appear that there have been significant
developments in the modeling of PbB levels in children
since the last review. While there are data that could be
used to update the GSDs used in the risk assessment to
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prediction of central-tendency PbB
levels as well as the application of
geometric standard deviations (GSDs)
for characterizing population
variability in PbB levels around those
central-tendency estimates. As noted
in the risk assessment, we did not
complete a probabilistic simulation of
PbB variability based on modeling
PbB levels for each simulated
individual using IEUBK and, instead,
relied on GSDs to characterize
variability around the lEUBK-modeled
central tendency PbB level for a
particular study population.
advanced considerably during the past several
decades, there have been relatively few
developments since the 2006 Pb AQCD
(USEPA, 2006a) was published in the last
review (draft ISA, p. 4-93).
Regarding newer data characterizing
population variability in PbB levels (i.e.,
sources for updating the GSDs used to
characterize population variability in PbB
levels in the risk assessment), there are
updated characterizations of PbB variability
in children for the U.S. based on the 2005-
2008 NHANES data (see section 4.4.1 - Lead
in Blood - in the draft ISA). In addition,
recent studies of Pb effects in children could
provide characterization of variability in PbB
levels for smaller (more localized) groups of
children (for example, see section 5.3.3.1.
Epidemiologic Studies of Behavioral Effects
in Children - in the draft ISA).
characterize population variability in PbB levels (for
children), without improved characterization of the
potential correlations between pathways, updated
estimates of higher percentile PbB levels (and IQ loss),
will still be subject to substantial uncertainty due to an
inability to reliably apportion total risk between the
contributing pathways (at those higher-end total Pb
exposure levels).
Estimating Exposure for Other Populations/Lifestages
H) Estimating exposure for other
populations/lifestages. Limitations in
our ability to relate changes in recent
air Pb-related exposure to PbB levels
in adults was one of the reasons that
adult health endpoints were not part of
the assessment for the last review. A
As noted above, section 4.6 (Biokinetic
Models of Lead Exposure-Blood Lead
Relationships) of the draft ISA does not
identify substantial improvements in PbB
prediction models, including models for
simulating changes in PbB (or other
biometrics) for adults and for children older
It does not appear that there have been significant
improvements in our ability to model exposure
(including PbB levels) for adult or older child
populations. Furthermore, predicting changes in PbB
levels for older children and adults resulting from
recent changes in ambient air Pb-related exposures is
complicated significantly by the presence of
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critical source of uncertainty in
modeling adult PbB is the complex
role played by the storage of Pb in
various compartments (mainly in bone)
over a person's lifetime, as well as the
mobilization of this Pb during certain
physiological conditions. This
accumulated Pb in adults derives from
earlier exposures when both Pb intake
and environmental concentrations, may
have been substantially higher.
The models available for children older
than 7 yrs (the age limit of IEUBK)
and into adulthood (e.g., Leggett,
1993) have not been routinely used by
the EPA in supporting regulatory risk
assessment or subjected to the
extensive and rigorous performance
evaluation which has been so
thoroughly reported for IEUBK
(AQCD, section 4.4.10). In addition,
some of the same uncertainties
identified above for adults also pertain
to some extent in modeling older
children/teenagers .
Information Newly Available in this
Review
than 7 years (the IEUBK limit), including
teenagers.12
Regarding the potential for empirical air-to-
PbB models, section 4.5.1.2 of the Pb ISA,
which addresses the availability of recent
studies in this area, describes an occupational
exposure study. The study size was relatively
small with occupational exposure
concentrations well above those common in
ambient air (the geometric mean Pb
concentration over the two week period was
58 ng/m3).
Estimating Risk for Young Children
I) Modeling IQ loss in young
children. Uncertainty associated with
The ISA (Section 2.8.2) summarizes the
current evidence that informs characterization
Consideration of Potential Utility and Impact on
Quantitative Exposure/Risk Assessment
accumulated Pb in bone which can contribute to PbB
levels and can itself reflect Pb exposure earlier in life.
The varied studies on associations between IQ and PbB
now available do not provide a strong foundation for
: As noted in the draft ISA, EPA's All Ages Lead Model is still in development,
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the magnitude of IQ loss predicted for
simulated children, particularly at
lower total PbB levels (e.g., < 2.5
(ig/dL) reflects the appreciably less
extensive information available on
which to base our characterization of
the concentration-response function at
lower PbB levels levels.
of concentration-response relationships for
those health endpoints for which such
evidence is most well established. These
relationships are for PbB levels in children
with cognitive deficits and PbB levels in
adults with increased blood pressure,
mortality, and indicators of nephrotoxicity.
With regard to studies published since the last
review that might inform our understanding
of the concentration-response relationship for
Pb associated IQ loss, three studies (Chiodo et
al., 2007; Jusko et al., 2008; Kim et al., 2009)
report effect estimates for IQ loss in study
populations with mean PbB levels at or below
5 (ig/dL.13 However, there is limited
representation of PbB levels below 3 (ig/dL in
Chiodo et al. (2007) and Jusko et al. (2008).
In comparison to these two studies, Kim et al.
(2008), which involved South Korean
children aged 8-11 years of age, includes a
lower distribution of PbB levels.
development of a new or adjusted concentration-
response function. As noted in section 2.1.3 above, the
risk assessment for the last review included four
different quantitative functions (based on or extending
from the nonlinear function from Lanphear et al 2005)
for the concentration-response relationship in the
lowest PbB level region (see table 2-2 and figure 2-3).
The new studies do not provide support for
development of a quantitative function for this PbB
level region that falls outside of the range of C-R
functions represented by these approaches.
Of the three studies (Chiodo et al., 2007; Jusko et al.,
2008; Kim et al., 2009) identified since the last review,
only Kim et al. (2009) provides information on the
blood-Pb IQ concentration-response relationship for
PbB levels below 3 (ig/dL. Further, Kim et al. (2009)
utilizes a Korean population and an age group older
than the group modeled in the last risk assessment.
With this older population, there is greater uncertainty
regarding the exposure conditions associated with the
observed response. Further, the Agency's well
established PbB model, the IEUBK model, which was
used in the last assessment, does not provide estimates
for ages beyond 7 years.
J) Modeling other endpoints in
young children. The assessment for
the last review did not quantitatively
assess risk of health endpoints other
than IQ loss primarily due to
The ISA (Section 2.8.2) describes the current
evidence that informs characterization of
concentration-response relationships for those
health endpoints for which such evidence is
most well established. These relationships are
The extent to which the evidence provides strong
support for a quantitative characterization of the
concentration -response relationship for non-IQ
behavioral endpoints is unclear. Further,
concentration-response functions utilized in
1 Chiodo et al.(2007) and Jusko et al. (2008) will be included in the second draft ISA.
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Consideration of Potential Utility and Impact on
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limitations in the available information
or an absence of relevant information
for developing informative
concentration-response functions.
for PbB levels in children with cognitive
deficits and PbB levels in adults with
increased blood pressure, mortality, and
indicators of nephrotoxicity.
With regard to the evidence for concentration-
response relationships of neurobehavioral
outcomes (other than IQ), a number of recent
studies have investigated impacts on cognitive
domains at lower PbB levels including those
less than 5 (ig/dL (e.g., Chiodo et al., 2008;
Jedrychowski et al., 2008; Krieg et al., 2010;
Miranda et al., 2009) and behavior (e.g.,
Braun et al. 2006, 2008; Nigg et al., 2008;
Wang et al., 2008; Nicolescu et al,, 2010) in
children. Among these studies, some involve
child populations ranging in age up to 15 or
16 years of age. Additionally they variously
provide continuous and/or noncontinuous
effect estimates and some analyze
associations of prenatal exposure (based on
cord blood measurements).14
The ISA also recognizes evidence for
associations of renal, immune system,
hematological, and reproductive effects with
PbB levels below 5 (ig/dL in child
populations (draft ISA, Tables 2-2 and 2-3).
However, the evidence for these effects has
limited applicability for a quantitative
assessment of the risk of specific health
quantitative risk assessment are typically developed
from epidemiological analyses that report continuous
functions and not typically developed from non-
continuous epidemiological analyses (e.g., quartile
regression analyses). There is reduced resolution
associated with the information from the latter which
contributes additional uncertainty to concentration-
response functions developed from these analyses.
Since most of the recent studies of non-IQ
neurobehavioral endpoints do not include continuous
effect estimates (e.g., quartile regression analysis), they
do not provide strong support for a concentration-
response function for use in quantitative risk
assessment. Additionally, some of these studies focus
on older (teenage) children, and as noted in the
discussion (see prior row) of the Kim et al. (2009)
study, EPA's established childhood PbB model, the
IEUBK model, does not provide estimates for older
children.
Regarding the other non-neurological endpoints, we
recognize that the evidence is unclear regarding the
role of lead-induced changes in individual immune
system, red blood cell function indicators and delayed
onset to puberty in eliciting or contributing to
immunological, hematological or reproductive health
outcomes. An improved understanding of these
linkages is needed to support quantitative risk
assessment for the impact of ambient air Pb exposure
in contributing to risk of outcomes related to these
endpoints.
1 Jedrychowski et al. (2008), Nigg et al. (2008), and Wang et al. (2008) will be included in the second draft ISA.
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Information Newly Available in this
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Consideration of Potential Utility and Impact on
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outcomes. The recent studies include: an
NHANES analysis (Fadrowski et al, 2010),
which reports associations between PbB and a
kidney function indicator in adolescents aged
12-20 years; some studies reporting Pb-
associated changes in specific immune system
indicators in child populations ranging in age
from 6 months through mid teenage years
(e.g, Sarasua et al., 2000, Karmaus et al.,
2005) or associations of prenatal exposure
(based on cord blood measurements) with
allergic sensitization in young children
(Jedrychowski et al., 2011); a study reporting
an association of low cord PbB levels with
decreased calcium-magnesium ATPase
activity in newborn red blood cells (Huel et
al., 2008); and, two studies reporting an
association of childhood PbB with delayed
onset of puberty (e.g., Hauser et al., 2008;
Williams etal., 2010).
More detailed limitations associated with applicability
of recent non-neurological endpoint studies for
quantitative risk assessment variously include: focus on
older children, for which there is increased uncertainty
associated with interpretations regarding the exposure
conditions contributing to the measured PbB levels and
to the associated effects; focus on associations with
measures of prenatal exposures (e.g., cord blood) for
which we are lacking in established PbB modeling
tools; and, focus on non-U.S. populations for which
characteristics influencing Pb uptake (e.g., diet) may
differ from U.S. populations. Additionally,
quantitative risk assessment for some of the identified
effects (e.g., kidney function) would require baseline
incidence data the availability of which may be limited
for the age groups studied.
Estimating Risk for Other Populations/Lifestages
K) Modeling endpoints for adult
cohorts. The assessment for the last
review did not quantitatively assess the
risk of health endpoints that have been
associated with PbB levels in adults in
epidemiological studies primarily due
to uncertainties regarding the role of
The draft ISA (Section 2.8.2) describes the
current evidence that informs characterization
of concentration-response relationships for
those health endpoints for which such
evidence is most well established. Among
adults, these relationships with blood lead
levels are increased blood pressure, mortality,
Lack of information regarding the specific Pb
exposures during a lifetime (time periods and
magnitudes) which contribute to the observed health
outcomes continues to introduce substantial uncertainty
to the simulation of adult health outcomes resulting
from changes in air Pb. This prevents us from
developing concentration-response functions for
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historical exposures in eliciting these
health outcomes.
Additionally, we are limited in our
capabilities for simulating the impact
of changes in ambient air Pb levels on
adult PbB levels (or bone Pb) (see
entry "H" above).
and indicators of nephrotoxicity.
With regard to the evidence for concentration-
response relationships, a number of studies
have investigated impacts at lower blood lead
levels including those less than 5 (ig/dL with
neurobehavioral outcomes, (e.g., Krieg et al.,
2009), cardiovascular effects (e.g., Sun et al.,
2008), renal effects (e.g., Akesson et al.,
2005), and immune system indicators (e.g.,
Kim et al., 2007).
However, substantial uncertainty continues to
be associated with the interpretation of adult
epidemiology studies as to the role of
historical exposures in eliciting the health
outcomes observed and with regard to the role
of endogenous Pb in influencing concurrent
blood or bone Pb measurements.
Furthermore, ongoing research has not
substantially reduced uncertainty related to
predicting changes in PbB or bone Pb
associated with reductions in ambient air Pb-
related exposures.
modeling potential adult health endpoints.
The absence of biokinetic models specifically covering
adults also limits our ability to model adult health
endpoints as a component in a risk assessment
evaluating ambient air Pb. Our consideration of any
effect estimates for adult health endpoints occurring at
non-occupational levels of Pb exposure is limited by
our lack of a reliable means for estimating relationships
between air-Pb levels (e.g., associated with alternate
potential standards) and PbB levels in adulthood.
Further, the contribution to blood lead from
endogenous Pb (e.g., stored in bone) that can reflect
historical Pb exposures complicates the utilization of
blood lead as a biomarker of current exposures in
adults, and consequently contributes uncertainty in
interpreting epidemiological studies with regard to the
Pb exposures eliciting observed health outcomes.
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2.3 KEY OBSERVATIONS AND CONCLUSIONS
Information presented in Table 2-3 reflects EPA staff assessment of the degree to which
research published since the last Pb NAAQS review (as summarized in the draft ISA) can
address specific uncertainties associated with the Pb NAAQS risk assessment. In those instances
where there is new information in the areas of an identified source of uncertainty in the previous
assessment, the critical consideration by EPA staff is with regard to the extent to which use of
that new information in a quantitative assessment would provide risk estimates for exposure to
air-related Pb that are appreciably different or with which the uncertainty is appreciably lower
than the estimates generated for the previous review. In considering this point, staff recognizes
that this and all newly available evidence will be considered in the Policy Assessment in terms of
both evidence-based considerations and risk/exposure-based considerations. With regard to the
latter, to the extent to which a decision is made not to develop a new version of the risk model to
generate new exposure and risk estimates, staff intends to consider any newly available
information to help to qualitatively interpret the risk estimates generated for the last review.
The decision whether to develop a comprehensive new assessment of exposure and risk
associated with air-related Pb for this review focuses on consideration of the extent to which the
newly available information, if used to update the risk model, has the potential to result in new
exposure and risk estimates that are substantially different from estimates generated for the
previous review. In this context, "substantially different" would 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. As noted above, in the event that a new exposure and
risk assessment is not warrant, newly available evidence may still be used to qualitatively or
semi-quantitatively interpret exposure and risk estimates generated for the last review, in order to
enhance their potential utility in informing the current review.
Key observations regarding the potential impact of newly available information in a
revised risk model are presented below, in the general order in which sources of uncertainty are
considered in Table 2-3.
Ambient air Pb levels (focus on urban study areas): We are not in a position to
substantially improve our characterization of ambient air Pb levels in the context of the
urban study areas, including our simulation of current and alternative standard levels
using proportional adjustment. Furthermore, we do not have additional information that
would help us further interpret risk estimates generated for the urban study areas in the
last review with regard to this element of the analysis.
Urban soil Pb and drinking water Pb levels: While there is updated information on
Pb levels in urban soil (and likely drinking water), we do not have updated data for
improving our characterization of the degree of correlation between pathways in
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modeling total Pb exposure and risk. This means that, even if we were to incorporate
improved data on urban soil Pb and drinking water Pb, estimates of higher-end
exposures (which are of particular interest in the risk assessment) would still be subject
to uncertainty reflecting our inability to representatively characterize the degree to
which pathway exposures are correlated (particularly at higher-percentiles of
exposure).
Simulation of urban dust Pb levels using the hybrid model: New information
characterizing the cleaning efficiency of vacuuming on hard surface floors (and
associated information on the size of Pb particles left behind) may be informative to
our interpretation of the dust modeling and associated urban residential risk estimates
developed in the last review. However, the new data are not directly applicable in the
context of updating or even quantitatively performance-evaluating the hybrid indoor
dust model.
Assessing the pathway-specific nature of child Pb exposure (including ambient
air-sourced Pb) in the urban residential context: New studies based on analysis of
NHANES and NHEXAS datasets and other studies in specific locations provide
insights on factors related to PbB levels in children, including detailed assessment of
housing characteristics linked to indoor dust Pb levels and ultimately PbB and/or
consideration for dietary and drinking-water exposure in addition to indoor dust Pb.
However, a number of factors preclude the direct use of these studies to either update
elements of the risk assessment, or quantitatively evaluate the performance of models
(e.g., the studies exclude consideration of ambient air-sourced Pb, while focusing on
other sources such as indoor paint Pb, or the studies may focus on an older study
population that is not directly comparable to the child population reflected in the risk
assessment). For these reasons, while information from these studies is not conducive
to updating the risk model, in some instances, the information may be useful in further
interpreting risk estimates generated in the previous analysis.
Predicting PbB levels for residential child populations: There have not been
significant refinements to the IEUBK model (or further development of alternative
models) for simulating child PbB levels. By contrast, there are newer data available for
characterizing the variability in child PbB levels (i.e., the GSDs used in defining
population variability in PbB levels in the risk assessment). However, our ability to
refine estimates of higher-end PbB levels through the use of enhanced GSDs is
compromised significantly by ongoing uncertainty (referenced above) in characterizing
pathway contributions to total exposure and risk for these higher percentiles of the
simulated population. Therefore, while the newer data on PbB variability could be
useful in further interpreting risk estimates generated for the previous review, we
believe there is little utility in using these updated GSDs to generate new risk
estimates.
Modeling IQ loss in young children: Studies published since the last review continue
to support the conclusions from the last review regarding the role of environmental
levels of Pb exposure in contributing to IQ loss and the evidence continues to support
the association of this endpoint with the lowest blood levels studied. These findings
reaffirm our emphasis on this endpoint as risk metric for quantifying the impact of Pb
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exposure on neurocognitive function in young children (up to 7yrs of age) in the last
review. The newly available studies of PbB associations with IQ loss do not provide
strong support for development of a new or revised concentration-response function for
blood lead-IQ loss.
Modeling other endpoints in children or other populations/lifestages: The newly
available studies for additional endpoints in children that are recognized in the draft
ISA (e.g., Table 2-2) inform our understanding of Pb-associated effects as discussed in
the draft ISA, and will be additionally considered in the subsequent Policy Assessment
for this review. However, these studies do not appear to provide support for
quantitative risk assessment for these endpoints. For example, as noted in Table 2-3
above, there is uncertainty in interpreting the relationship of some of the immune
system and red blood cell function indicators with health outcomes. Additionally, our
capability for quantitatively assessing endpoints for older cohorts (e.g., older than 7
years of age) is limited by the fact that EPA's well established IEUBK model that we
used in the last risk assessment does not cover these older cohorts. Our ability to
model risk of lead-induced health outcomes in older children and adults in
epidemiological studies is limited by uncertainties regarding the role of past exposures
in eliciting the health outcomes associated with current PbB levels (as well as
influencing current PbB levels). In the case of adult studies, the role of past exposures,
which are likely higher, contributes particular uncertainty regarding the specific Pb
exposures eliciting the observed outcomes. There is also uncertainty associated with
simulation of changes in adult PbB levels (or bone Pb) resulting from reductions in
exposure to Pb originally sourced from ambient air. These uncertainties affect our
ability to disentangle the effects of past exposures from exposures to the lower air
concentrations associated with the current standards.
In conclusion, we note the availability of new information on Pb exposure and risk
published since the last review that may be useful in further interpreting risk estimates generated
for the previous review, thereby enhancing their utility in informing the current review.
However, we do not believe that the information newly available in this review provides 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. Specifically, we do not
believe that any of the primary sources of uncertainty identified to have the greatest impact on
risk estimates would be substantially reduced by using this new information to update the risk
model, including inputs to that model. Notwithstanding our consideration here of the use of
newly available information in a new or updated risk assessment, we note the need to carefully
consider the newly available information (as characterized in the final ISA) with regard to any
appropriate further interpretation of the risk assessment findings from the last review in our risk
and exposure based considerations in the Policy Assessment for this review.
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3 ECOLOGICAL RISK ASSESSMENT
The evaluation of information newly available in this review is structured around
consideration of two key questions:
Is there newly available information relevant to critical uncertainties or limitations
associated with ecological risk assessment in the last review?
To what extent does the currently available information support the development
of an updated or new quantitative risk assessment that would generate results
providing more specific or more certain estimates of ecological risk associated
with the current Pb secondary standard?
Overall, we consider the extent to which the available information supports a new
quantitative risk assessment likely to contribute to substantive new conclusions regarding the risk
to welfare associated with Pb under current air quality conditions that will better inform the
Administrator's judgment of the adequacy of protection against adverse environmental effects
afforded by the current NAAQS.
As noted in chapter 1 above, the CAA ง 302(h) defines "Effects on welfare" to include a
wide range of effects including effects on soil, water, crops, vegetation, and manmade materials,
"whether caused by transformation, conversion, or combination with other pollutants." Because
of the broad range of effects that must be considered in the design and implementation of an
assessment of exposure and risk associated with Pb, we are faced with a level of complexity that
is substantially greater than for similar assessments typically performed for other criteria
pollutants. For example, unlike most other criteria pollutants, risk associated with exposure to
Pb originally released to ambient air is multimedia in nature, with exposure and risk associated
with a range of pathways associated with deposition of ambient air Pb. Additionally, the
persistent nature of Pb means that exposure and risk can be associated with Pb originally emitted
into the ambient air recently or at some point in the past, from current or historic sources, under
conditions associated with previous Pb NAAQS or under those prior to the existence of any Pb
NAAQS. Furthermore, ecological exposures and risk also result from uses of Pb that contribute
Pb to the environment without passing through ambient air, such as land and water disposal of
wastes, leaching of solder used in water distribution systems into water that flows through
wastewater treatment facilities and land uses such as mining.
The screening-level ecological risk assessment for aquatic and terrestrial case studies
completed for the last review, while limited and accompanied by various uncertainties, suggested
occurrences of environmental Pb concentrations with the potential for adverse environmental
effects to exist under the then-current standards. These findings supported similar, largely
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qualitative, conclusions drawn from consideration of the evidence. Given the limited
quantitative understanding at that time of the impacts of air-related Pb in ecosystems under
conditions meeting the NAAQS, evidence of Pb effects on organisms was generally extrapolated
to ecosystem effects. Taken together, the Agency concluded that the available data and
evidence, primarily qualitative, suggested the potential for adverse environmental impacts under
the then-current standard. While lacking data to provide a quantitative basis for setting a
secondary standard different from the primary, the Administrator concurred with CASAC's
conclusion that the level of the secondary standard should be reduced to at least as low as the
level of the revised primary standard. Accordingly, the secondary standard was revised to be
identical to the revised primary standard (USEPA, 2007c; 73 FR 66964).
In the previous review, the scientific evidence of direct effects of Pb from ambient air
under conditions meeting the then-current standard was limited or lacking for specific
ecosystems, ecosystem services, or organisms. In considering the extent to which the now
available information warrants development of a quantitative ecological risk assessment in this
review, we consider the availability of evidence to support a more refined understanding of the
direct and indirect effects of deposited ambient Pb on ecosystems and organisms and of the long-
term behavior of deposited Pb. We focus most specifically on the ability of current data sets to
characterize exposure of ecosystems in the U.S. to ambient Pb being deposited under the current
standard. Critical to this focus is consideration of the extent to which the available information
improves our understanding of ecological effects attributable to Pb deposited from ambient air
under conditions associated with the current standard in light of other sources of current and
historic Pb in the environment. We also look to any new scientific evidence that might be
available to provide additional insight into the responsiveness of ecosystems to changes in Pb
deposition. As part of this evaluation we consider the adequacy of any new scientific evidence
on critical loads that might be used in assessing ecosystems potentially vulnerable to Pb on a
scale that is large enough to provide information which could inform the Administrator regarding
the adequacy of the current standard.
While focusing here on evaluation of the newly available evidence with regard to a role
in quantitative risk assessment, we will be further and more comprehensively evaluating the
evidence, as well as past quantitative analyses in the context of the Policy Assessment to be
developed for this review. As described in the integrated review plan, the Policy Assessment, a
draft of which will be completed subsequent to completion of the ISA, will consider conclusions
that can be drawn from the currently available evidence as well as any available quantitative
analysis, including that from the previous review, in light of that evidence, as to the adequacy of
the current standard (USEPA, 201 Ib).
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This chapter first provides an overview of the quantitative exposure and welfare risk
assessment performed in the last review (section 3.1) and then considers the extent to which
information and conclusions presented in the ISA provide support for the development of a new
quantitative assessment of welfare effects (section 3.2), particularly with regard to the extent
which such an assessment could be expected to inform our consideration of the adequacy of the
current standard. Key observations and conclusions drawn from this evaluation are presented in
section 3.3.
3.1 OVERVIEW OF THE PREVIOUS ASSESSMENT
3.1.1 Conceptual Model
In planning for the quantitative ecological risk assessment in the last review, we
developed and considered a conceptual model of environmental pathways of Pb distribution,
associated exposures and associated endpoints and risk metrics (Figure 3-1). This model
provided a framework in which to consider the evidence for Pb in designing the approach for the
assessment. Central to this model is the assessment of terrestrial and aquatic exposures and,
specifically within the context of the NAAQS review process, the portion of these exposures that
are associated with ambient air concentrations allowed under the current standard.
The focus in the review of the Pb NAAQS, and consequently for an informative
assessment, is on Pb emitted to ambient air. As recognized in Figure 3-1, however, other
(nonair) sources of environmental Pb (including mining activities, contaminated landfills, etc.)
also contribute to Pb concentrations in environmental media. Of most interest in the quantitative
analysis for the review were present and past emissions to air and the associated deposition to
sensitive ecosystems.
Ecologically significant pathways of exposure to air-related Pb are predominantly those
involving deposition of Pb from air to other media (soils, surface waters, and sediments).
Exposure to Pb in air has been considered a relatively less significant ecological exposure/risk
pathway. Accordingly, the analysis developed for the last review focused primarily on
deposition and resulting concentrations in environmental media.
Those organisms in contact with Pb-contaminated media, whether directly or by ingestion
of prey species that have accumulated Pb due to direct contact with contaminated media, are
likely to be the most highly exposed organisms in the environment. There is limited evidence for
biomagnification of Pb in food chains, but sensitivities to Pb vary widely within and among
groups of organisms with similar exposures.
As recognized in the 2006 AQCD and the Staff Paper developed for the review,
sufficiently elevated environmental exposure to Pb can cause a range of effects at the species and
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population levels thereby altering ecosystem processes. Known effects of elevated Pb exposure
include changes in growth, development and reproduction, hematological effects,
neurobehavioral effects, and increased mortality rates among some organisms. These effects, in
turn, can adversely impact community structure, biodiversity and ecosystem functions. In a
general sense, changes in the functioning of ecosystems can impact services provided by an
ecosystem to human populations.15
In planning the quantitative analysis for the last review, staff considered the potential for
developing risk metrics descriptive of individual, population, and ecosystem effects estimated to
result from Pb exposures. Given data and other limitations, the focus was on organism and
population-level metrics. Individual-level toxicity data considered informative to thresholds for
population-level effects in sensitive species were used to develop the screening levels used in the
assessment performed during the previous review.
On an ecosystem scale, an approach for integrating the consideration of exposure
pathways and risk for multimedia pollutants such as Pb is represented by critical loads
analyses.16 Application of this type of approach requires a wide array of data to support the
quantitative characterization of the disposition and impact of the pollutant in specific
ecosystems.17 During the last review, the 2006 AQCD assessed the available information on
critical loads for Pb which was drawn primarily from then somewhat recent work in Europe.
Analyses were not available for U.S. locations, and the European critical load values for Pb that
had been developed were highly specific to the bedrock geology, soil types, vegetation, and
historical deposition trends in each European country (AQCD, p. E-24). As a result, the 2006
AQCD concluded that "[a]t this time, the methods and models commonly used for the
calculation of critical loads have not been validated for Pb" and that "[m]any of the methods
neglect the speciation of Pb when estimating critical limits, the uptake of Pb into plants, and
15 In the current review of the secondary standards for nitrogen and sulfur oxides, for which there was
sufficient evidence to provide for such a consideration, ecological services has been recognized as a useful tool for
assessing adverse impacts to public welfare (USEPA, 2011).
16 In the 2006 AQCD, critical loads were defined as threshold deposition rates of air pollutants that current
knowledge indicates will not cause long-term adverse effects to ecosystem structure and function (AQCD, p. 7-33).
Conceptually, the critical load approach provides a means of gauging whether a particular ecosystem in a given area
receives deposition that results in a level of biological harm that is defined by a critical limit in the sentinel
parameter for the targeted pollutant and type of ecosystem harm. The critical load estimate for an ecosystem is
analogous to a quantitative estimate of that ecosystem's "susceptibility" to the type of ecosystem harm being
assessed. The greater the critical load value, the greater the ability of the ecosystem to accommodate the pollutant
loading without harm.
17 The critical load concept was recently used in the quantitative assessment developed for consideration in
the currently ongoing review of the secondary NAAQS for oxides of nitrogen and sulfur (USEPA, 2009). That
assessment was based on the well-established state-of-knowledge and location-specific data, developed over the past
four decades, on nitrogen and sulfur deposition and their role on ecosystem acidification in the U.S., with resulting
impacts to various ecosystem services.
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outflux of Pb in drainage water, limiting the utility of current models" (AQCD, p. 7-46).
Further, the AQCD noted that future efforts were needed that fully incorporated the role of Pb
speciation into critical load models, and include validations of the assumptions used by the
models (AQCD, p. 7-46). Accordingly, the quantitative assessment for the last Pb NAAQS
review did not involve critical load analyses.
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Figure 3-1. Conceptual Model for Ecological Risk Assessment During the Last Review.
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3-6
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3.1.2 Overview of Analytical Approach
The screening-level assessment in the lastNAAQS review involved several case studies
and a national-scale screening assessment (Figure 3-2). Three quantitative case studies were
designed to estimate the potential for ecological risks associated with exposures to Pb emitted
into ambient air in three situations: areas surrounding a primary Pb smelter, areas surrounding a
secondary Pb smelter, and a near-roadway, nonurban location. Activities for a fourth case study
(ecologically vulnerable locations) focused on identification and description of the location as
well as consideration of literature findings regarding the role of atmospheric Pb and the
movement of Pb within this ecosystem, although new quantitative analyses were not
performed.18
Exposure concentrations in soil, surface water, and/or sediment were estimated for the
three case studies from available monitoring data or modeling analysis and then compared to
ecological screening benchmarks (e.g. Ecological Soil Screening Levels (Eco-SSLs) and
Ambient Water Quality Criteria (AWQC)) to assess the potential for ecological impacts from Pb
that was emitted into the air. A national-scale screening assessment was also used to evaluate
surface water and sediment monitoring locations across the United States for the potential for
ecological impacts associated with atmospheric deposition of Pb.
18 The Hubbard Brook Experimental Forest (HBEF), in the White Mountain National Forest, near North
Woodstock, New Hampshire, was selected as a fourth case study because: (1) it is in an acidified watershed and
therefore was expected to have higher bioavailability of Pb, (2) there were no identified point sources of Pb in the
surrounding area, which might allow for an evaluation of impacts of regional background Pb concentrations; (3) it is
in an elevated area subject to comparatively higher deposition of Pb due to wind speed and precipitation; and (4)
there are available data on concentration trends 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 (USEPA, 2006, Appendix E). Studies of the three media variously reported the following: (1)
atmospheric Pb inputs do not directly affect Pb levels in streams at HBEF because deposited Pb is almost entirely
retained in the soil profile; (2) results of the soil horizon analysis show that Pb has become more concentrated at
lower depths over time and that the soil profile serves as a Pb sink, drastically reducing dissolved Pb levels 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, leading authors to conclude that the contribution of dissolved Pb from soils
to streams is insignificant (less than 0.2 g'ha~1-yr~1).
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Figure 3-2. Analytical Approach for Screening-level Assessment in the Last Review.
Exposure Assessment: Estimating Media Concentrations
Primary Pb
Smelter
Case Study
Near Roadway
Non-urban
Case Study
Secondary Pb
Smelter Case Study
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National-Scale
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The measures of exposure in the screening assessment for the last review were total Pb
concentrations in soil, dissolved Pb concentrations in fresh surface waters (water column), and
total Pb concentrations in freshwater sediments. Exposure concentrations were estimated for the
three case studies and the national-scale screening assessment as described below.
For the primary Pb smelter case study, which involved a smelter that had been operation
for more than 100 years, measured concentrations of total Pb in soil, dissolved Pb in
surface waters, and total Pb in sediment were used to develop point estimates for
locations with Pb thought to be associated with atmospheric Pb deposition, rather than
with nonair sources, such as runoff from waste storage piles.
For the secondary Pb smelter case study, soil concentrations of Pb were estimated using
fate and transport modeling based on EPA's Multiple Pathways of Exposure (MPE)
methodology (USEPA 1998).
For the near-roadway non-urban case study, soil concentration measurements collected for
two locations adjacent to interstate highways, one in an area of fairly high-density
development (Corpus Christi, Texas) and another in an area of medium-density
development (Atlee, Virginia), were used to develop point estimates of Pb associated
with historical deposition.
In the national-scale surface water and sediment screening assessment, measurements of
dissolved Pb concentrations in surface water and total Pb concentrations in sediments for
locations across the United States were used. Air emissions, water discharge, and land
use data for the areas surrounding these locations were assessed to identify locations
where atmospheric Pb deposition may be expected to contribute to potential ecological
impacts. The exposure assessment focused on these locations.
The tools used for assessing the potential for effects included ecological screening values,
derived from the Ecological Soil Screening Levels (Eco-SSLs) developed by the EPA's
Superfund program (USEPA 2003, 2005c), EPA's recommended ambient water quality criteria
(AWQC), and sediment screening values developed by MacDonald and others (2000, 2003). A
hazard quotient (HQ) was calculated for various receptors to determine the potential for risk to
that receptor. The HQ was calculated as:
HQ = (estimated media concentration) / (ecotoxicity screening value)
For each case study, HQ values were calculated for each location where either modeled
or measured media concentrations were available. Separate soil HQ values were calculated for
each ecological receptor group for which an ecotoxicity screening value has been developed (i.e.,
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birds, mammals, soil invertebrates, and plants). HQ values less than 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.
3.1.3 Key Limitations and Uncertainties
While the screening-level analyses performed in the previous review provided examples
of the distribution of atmospheric Pb into other media where it can contribute to ecological risks,
they were severely limited in the extent to which they could inform an understanding of the role
of atmospheric deposition under conditions associated with the NAAQS.19
The ecological risk screen was limited to specific case study locations and other locations
for which Pb data were available. The limited availability of U.S. locations for which
recent measurements of Pb concentrations were available even with the reliance of
national databases to identify ecosystems and datasets constrained our ability to
characterize what we knew nationally regarding current conditions, including the
influence of current atmospheric Pb conditions, or those associated with the then-current
standard.
Further, while efforts were made to identify situations in which the Pb exposures would
have primary contributions from airborne Pb and not be dominated by nonair sources,
there was uncertainty as to whether other sources might have actually contributed to the
Pb exposure estimates, and the extent to which air-attributable contributions represented
conditions when the then-current standard was not met.
Additionally, the screening-level tools used for effects assessment (e.g., AWQC, Eco-
SSLs, sediment criteria) and/or the media-specific parameters available for the media
concentration estimates in the assessment did not accommodate a more rigorous or
detailed consideration of bioavailability characteristics influential to Pb toxicity in these
media (USEPA, 2007c).
The screening assessment results included several locations where concentrations of Pb
in soil, surface water and sediments exceeded screening values for these media, indicating the
potential for adverse effects associated with Pb. However, the contribution of air emissions to
19 Limitations in the assessment generally reflected those recognized by the AQCD assessment of the
evidence: In summary, due to the deposition of Pb from past practices (e.g., leaded gasoline, ore smelting) and the
long residence time ofPb in many aquatic and terrestrial ecosystems, a legacy of environmental Pb burden exists,
over which is superimposed much lower contemporary Pb loadings. The potential for ecological effects of the
combined legacy and contemporary Pb burden to occur is a function of the bioavailability or bioaccessibility of the
Pb, which, in turn, is highly dependent upon numerous site factors (e.g., soil organic carbon content, pH, water
hardness). Moreover, while the more localized ecosystem impacts observed around smelters are often striking, these
perturbations cannot be attributed solely to Pb. Many other stressors (e.g., other heavy metals, oxides of sulfur and
nitrogen) can also act singly or in concert with Pb to cause such notable environmental impacts. [AQCD, p. E-24]
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concentrations, and consequently to potential risk, in all of these cases is unknown. While it was
not possible to dissect the contributions of air Pb emissions from other sources, and it is likely
that, at least for the long-operating primary smelter, the air contribution is significant, the Pb
source at that location had been in operation well before the establishment of the Pb NAAQS.
Thus, the assessment results were consistent with evidence-based observations of the influence
of airborne Pb and changes in airborne Pb on Pb in aquatic systems, such as those drawn from
historical patterns observed in sediment cores from lakes and from other Pb measurements.
However, the quantitative analyses, as well as the available evidence, were severely limited in
their ability to inform quantitative conclusions regarding the secondary standard.
3.2 CONSIDERATION OF NEWLY AVAILABLE EVIDENCE
In considering the evidence newly available in this review, we focus here on the extent to
which it addresses information gaps or areas of uncertainty associated with the information
available in the last review. Such gaps limited the quantitative assessment that could be
developed in that review as well as conclusions that could be drawn from it. As discussed in the
sections above, key areas included limitations and gaps in the information needed to support a
critical loads analysis, or other analyses that would quantitatively inform consideration of the
adequacy of the then-current secondary standard to provide the requisite protection against
welfare effects associated with Pb in ambient air.
In the subsections below, four areas of limited information in the last review are
considered with regard to the availability of new information in this review as described in the
first draft ISA. Our focus in these sections is on the extent to which the now available
information addresses key limitations in developing quantitative analyses that would
substantively and quantitatively inform consideration of the adequacy of the current secondary
NAAQS. Further, beyond these four areas, we note that with regard to ecosystem services, the
draft ISA concludes that "[although evidence is available to support Pb impacts to supporting,
provisioning, regulating and cultural ecosystem services, there [are] insufficient data available to
adequately quantify these adverse effects" (draft ISA, p. 7-112).
3.2.1 Factors Affecting Lead Bioavailability
As recognized in the last review, a wide range of environmental factors affect the
distribution of Pb in the environment and Pb bioavailability and, accordingly, Pb-induced
toxicity and associated ecological risk (2006 AQCD, summarized in Section 8.7; draft ISA,
section 2.6.1. The first draft ISA discusses the current evidence regarding various aspects of Pb
bioavailability and toxicity. For example, the draft ISA concludes that the evidence in this
review further supports the findings of the previous Pb AQCDs that biological effects of Pb on
terrestrial organisms vary with species and life stage, duration of exposure, form of Pb, and soil
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characteristics (draft ISA, p. 2-29). The evidence reviewed in sections 7.2.3 and 7.2.4 of the
draft ISA used as the basis for the conclusion demonstrates that "many factors, including species
and various soil physiochemical properties, interact strongly with Pb concentration to modify
those effects" (ISA, p. 2-30).
Newly available evidence on Pb bioavailability from sediments and soils to aquatic and
terrestrial vegetation, respectively, indicates Pb to be relatively more bioavailable in sediment
than in soil (draft ISA, 7.3.10.2). Currently available models for predicting bioavailability in
aquatic systems focus on acute toxicity and do not consider all possible routes of uptake, making
them of limited applicability, especially when considering species-dependent differences in
uptake and bioaccumulation of Pb (draft ISA, 7.3.10.1). With regard to this area, the draft ISA
concludes "there are large differences in species sensitivity to Pb, and many environmental
variables (e.g., pH, organic matter) determine the bioavailability and toxicity of Pb" (draft ISA,
section 2.6.11).
3.2.2 Transport of Lead between Ecosystem Compartments
At the time of the last review, information supporting quantitative descriptions of Pb
transport within and among different ecosystem compartments was limited.
With regard to terrestrial systems, the currently available information supports and
expands on the evidence regarding some of the complexities associated with the movement of Pb
in those systems, particularly vertical transport across soil horizons. For example, location-
specific differences in soil horizons have been observed to affect Pb movement across those
horizons (draft ISA, section 3.3.3.1). Recent research provides insights into the details of Pb
sequestration processes (draft ISA, section 3.3.3.2) and the roles of iron, manganese and calcium
in soils (draft ISA, section 3.3.3.2).
Recent research on Pb transport in aquatic systems confirms the dominant role of iron
and organic rich colloids in Pb transport and provides additional information on Pb residence
times in some rivers and lakes (draft ISA, section 3.3.2.1). Newly available studies provide
additional detail on resuspension processes of Pb from sediments in natural waters, including the
influence of organic material, iron and manganese, as well as the role of sediment anoxic or
depleted oxygen conditions in Pb cycling (draft ISA, section 3.3.2.3). This newly available
research confirms the important influence of resuspension on the lifetime of Pb in aquatic
systems (draft ISA, section 3.3.2.3). Additionally, newly available information expands the
evidence base describing the movement of Pb in surface runoff, including greater detail on
amounts, particle size distributions and composition (draft ISA, 3.3.2.4).
In considering the available information on the movement of Pb among ecosystem
compartments, the draft ISA concludes that despite our increasing knowledge there is a lack of
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information not only on bioavailability, as affected by the specific characteristics of the receiving
ecosystem, but also on the kinetics of Pb distribution in ecosystems in long-term exposure
scenarios (draft ISA, section 2.6.11). This lack of information limits our ability to assess the
proportion of observed effects that are attributable to atmospheric sources.
3.2.3 Relative Roles of Atmospheric Deposition and Other Pb Sources to
Ecosystems
The role of current atmospheric deposition on Pb-associated risk to ecosystems was a
large source of uncertainty that limited the design of and conclusions drawn from the quantitative
assessment in the last review. As a general matter, recent studies reviewed in the draft ISA
report deposition data consistent with fluxes reported in the 2006 AQCD and consistently
demonstrate reductions in Pb deposition to soils since the phase-out of leaded on-road gasoline
(draft ISA, section 3.3.3.1).
Chapter 3 of the 1st draft ISA (201 la) reviews the sources of ambient Pb and deposition
into ecological systems. This included studies on ambient deposition, runoff and re-suspension.
Atmospheric deposition is thought to be the largest source of Pb in surface waters (AQCD, 2006;
ISA, Section 3.3.2), however runoff is also identified as a major source.
As summarized in the draft ISA, the recently completed Western Airborne Contaminants
Assessment Project (WACAP) of the U.S. National Parks Service is the most comprehensive
database, to date, on contaminant transport and depositional effects on sensitive ecosystems in
the U.S. In this study, contaminants were shown to accumulate geographically based on
proximity to individual sources or source areas, primarily agriculture and industry. A clear
decline in Pb concentrations in sediments after the discontinued use of leaded on-road gasoline
was observed in sediment cores at almost all WACAP locations. Although, Pb was measured in
snow, water, sediment, lichen and fish during the multiyear project, this metal was not quantified
in air samples (draft ISA, section 3.6.2).
In its assessment of this area of the current evidence, the draft ISA concludes that there is
"limited evidence to relate ambient air concentrations of Pb to levels of deposition onto
terrestrial and aquatic ecosystems and subsequent movement of atmospherically-deposited Pb
though environmental compartments (e.g., soil, sediment, water, biota)," and the relative
contribution from atmospheric versus other sources in studies reporting on Pb accumulation in
biota is usually not known (draft ISA, section 2.6.11).
3.2.4 Critical Loads (CL) Models
As noted in section 3.1.1. above, the critical load (CL) models for both terrestrial and
aquatic systems available at the time of the last review (AQCD, 2006) did not account for Pb
bioavailability within the system, fluxes within systems, or focused solely on atmospheric
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deposition, ignoring other contributions. This was considered a main limitation to the use of CL
models in the risk assessment. The draft ISA reviews several new studies utilizing CL models
in terrestrial systems, however, as summarized in the draft ISA, "since the 2006 Pb AQCD there
is no new significant information on critical loads of Pb in aquatic systems" (draft ISA, p. 7-
112).
Since the last review our understanding of how CL can be used in the context of the
NAAQS review process has improved. A CL model was utilized in the recently completed
review of the Secondary National Ambient Air Quality Standards for Oxides of Nitrogen and
Oxides of Sulfur (US EPA 2008, 2009, 201 Ic) and the overall approach was reviewed favorably
by the CASAC committee. As noted above, that assessment was based on the well-established
state-of-knowledge and location-specific data, developed over the past four decades, on nitrogen
and sulfur deposition and their role on ecosystem acidification in the U.S., with resulting impacts
to various ecosystem services. Thus, while since the last review we have gained experience with
critical loads modeling, and in the case of Pb our understanding of the various factors that
influence its environmental movement and toxicity is improving, we are still strongly limited
with regard to data to quantify these processes and influences adequately in CL modeling of U.S.
ecosystems.
As reviewed in the previous sections, there is new research available for the areas which
were considered limitations during the previous review; however, the data remain difficult to
incorporate into a larger-scale CL model. The CL study by De Vries and Groenenberg (2009),
reviewed in the draft ISA (Section 7.2.7), did include fluxes of Pb within a system, one area
previously considered a limitation in the model, however, application of this methodology at a
national scale, requires localized data across a wide range of ecosystems, which are currently
unavailable or inadequate. It is this lack of data regarding bioavailability, speciation, sources
and fluxes at a local scale, which could be applied in a large-scale assessment that remains the
primary limitation in using a CL model approach.
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3.3 KEY OBSERVATIONS AND CONCLUSIONS
As described in section 3.2 above, the draft ISA describes evidence that expands our
knowledge of the movement and potential adverse effects of Pb in ecosystems.
Unavailability, speciation, fluxes and sources of Pb. New research on bioavailability
and speciation of Pb continues to describe the complexity of Pb bioavailability in
ecosystems and the associated challenges to describing toxicity. The evidence currently
available does not support the development of exposure-response functions. If such
exposure-response functions were developed, for example for adverse impacts on fish
populations, they could be directly linked to ecosystem services...
Contribution of atmospheric Pb to ecosystem loading. The concept of critical loads
has been applied in the literature to assess the risk to ecosystems from atmospheric
deposition of pollutants. However, in the case of Pb, there are substantial limitations in
the data needed to incorporate the necessary components (flux, bioavailability,
speciation, and source) at ecosystem levels in a way that could support a large-scale
application of a CL model to inform the NAAQS review.
In summary, while there are a number of new studies that improve 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. 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.
The new evidence reviewed in the draft ISA generally supports conclusions drawn in the
previous review regarding the potential for Pb to impact ecosystems and also adds to our
understanding of some aspects of the effects of Pb in ecosystems. However, gaps, limitations
and uncertainties remain in the information available regarding areas that are critical to
developing quantitative estimates of ecosystem risk associated with Pb in ambient air. In light of
these critical limitations and uncertainties, staff concludes that the currently available
information does not provide the means 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.
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United States Office of Air Quality Planning and Standards Publication No. EPA-452/P-11-003
Environmental Protection Health and Environmental Impacts Division June 2011
Agency Research Triangle Park, NC
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