Review of the National Ambient Air 

Quality Standards for Lead: 

Risk and Exposure Assessment 

Planning Document 

 
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
 ii 

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). 
 iii 

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 μg/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
 1-1 

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 (μg/m3

) to a level of 0.15 μg/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 μg/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. 
 1-2 

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, 

2011a). 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. 

 
 1-3 

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 Lead.

3

 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. 

2

Section 109(b)(1) [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. 

3

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/20110331pbirpdraftcasac.pdf. 

4

NAAQS 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. 
 2-1 

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 
 2-2 

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 airrelated 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 policyrelevant 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. 
 2-3 

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 doseresponse 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 unquantified, 

from air-related pathways within this category. 
 2-4 

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. 

 
 2-5 

Figure 2-1. Conceptual Model for Previous Exposure and Risk Assessment 

 

Note: Boxes outlined in bold and shaded are included in the quantitative risk assessment. 

 
 2-6 

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. 
 2-7 

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 μg/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 Averaging Time 

(Form) Level (μg/m3

) Case Study 

Then-current Standard 

Calendar Quarter 

(maximum)

1.5 All 

Current Conditions 

0.87 (95th percentile) 

0.14 (mean) General Urban 

0.14 Chicago 

0.36 Cleveland 

0.09 Los Angeles 

Alternate Standard 0.2 General Urban 

Primary Smelter 

Alternate Standards Month 

(maximum) 

0.5 

General Urban 

Primary Smelter 

Cleveland 

0.2 All 

except Los Angeles

0.05 All 

0.02 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 
 2-8 

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). 

 
 2-9 

Figure 2-2. Overview of Analysis Approach for Exposure and Risk Assessment. 

Characterizing ambient air levels and 

deposition to soil

Air dispersion modeling

(primary Pb smelter)

Ambient monitoring data 

(general urban and location-specific urban)

Stack and 

fugitive 

emissions data

Ambient air 

concentrations 

for study areas

Characterizing soil and indoor 

dust concentrations

Outdoor residential 

soil concentrations

Site-specific soil 

monitoring data 

combined with 

statistical 

extrapolation 

(primary Pb 

smelter)

Nationally-representative 

residential soil Pb value selected 

from literature

(general urban and locationspecific urban) Combination of (a) statistical 

(regression) and/or (b) mechanistic 

(compartmental) indoor dust prediction 

models 

(all case studies)

Indoor residential dust 

concentrations

Biokinetic blood Pb

modeling 

(all ase studies)

Background Pb exposure levels

• diet

• drinking water

• indoor paint (actually reflected in 

dust modeling)

Probabilistic modeling of blood Pb

levels for children within each case 

study location

(all case studies)

GSD reflecting interindividual variability 

in behavior related to 

Pb exposure and 

biokinetics

Characterizing blood Pb levels

Concentration-response functions 

based on log-normal functios

(Lanphear pooled analysis), or on data 

from that study

Demographics (distribution of 

children within study areas)

(primary Pb smelter and locationspecific urban)

Distribution of IQ loss for 

study populations 

(partitioned between policyrelevant exposures and 

policy-relevant background)

Characterizing risk (IQ loss)

Ambient air 

concentrations 

(see above)

Risk estimation - IQ 

change estimation

(all case studies)

EXPOSURE ASSESSMENT RISK CHARACTERIZATION
 2-10 

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 
 2-11 

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 IEUBK-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 IEUBK-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). 
 2-12 

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 μg/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 μg/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 μg/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 μg/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 μg/dL: developed by fitting a two-piece linear function 

stratified at 10 μg/dL (peak PbB metric) to the log-linear function developed from the 

pooled analysis. 

 Dual linear-stratified at 7.5 μg/dL: as above, but based on stratification of the two-piece 

function at 7.5 μg/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 CASAC. 
 2-13 

Figure 2-3. Comparison of Four Concentration-response Functions Used in the Previous 

Risk Assessment. 

Table 2-2. Comparison of Total and Incremental IQ Loss Estimates Below 10 μg/dL for the 

Four Concentration-response Functions. 

Performance Metric 

Concentration-Response Function 

Log-linear 

with cutpoint 

Log-linear 

with lowexposure 

linearization

Dual linear - 

stratified at 

10 μg/dL 

peak 

Dual linear - 

stratified at 

7.5 μg/dL 

peak 

Points, IQ loss 

Total IQ loss 

at 2 μg/dL 1.9 4.6 1.6 5.9 

at 5 μg/dL 4.3 7.0 3.9 11.1 

at 7.5 μg/dL 5.4 8.1 4.3 11.5 

at 10 μg/dL 6.2 8.9 4.6 11.9 

Incremental IQ 

loss 

(average # points 

 per μg/dL) 

<2 μg/dL 0.94 2.29 0.80 2.94 

<5 μg/dL 0.87 1.41 0.80 2.24 

<7.5 μg/dL 0.73 1.09 0.58 1.55 

<10 μg/dL 0.62 0.89 0.47 1.20 

Two categories of risk metrics were generated for each of the case studies: 

 Population risk percentiles: 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). 

0

2

4

6

8

10

12

14

0 1 2 3 4 5 6 7 8 9 10

Concurrent blood Pb (ug/dL)

IQ loss

log-linear w ith cutpoint

dual linear - stratified at

10 ug/dL, peak

dual linear - stratified at

7.5 ug/dL, peak

log-linear w ith low -

exposure linearization
 2-14 

 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 
 2-15 

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 
 2-16 

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 Pbrelated 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. 
 2-17 

 Pathway Apportionment for Higher Percentile PbB and IQ 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 μg/dL concurrent PbB). 
 2-18 

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. 
 2-19 

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 U

Quantitative Exposure/

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 locationspecific 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 utry and identify the fraction of mambient air Pb levels near the cualternative lower standard levelcould have potential risks at or nthe general urban study area. Hmore information on the gradienthose higher source-oriented moof the size of populations experair Pb levels is highly uncertaininformation does not appear to pimproved data for characterizinrefined spatial scale. We also nhave highly-refined information gradients in urban areas, in ordedetailed residential Pb-risk modneed more detailed information exposure specific to those residdust Pb concentrations, soil condrinking water Pb concentrationlevel of refined exposure informareas that might be of interest is lacking. In addition, we would slimitations in our ability to appoair and nonair pathways especiaexposed to higher pathway-specbe associated with this type of slocation (i.e., we do not have inof correlation among Pb exposu
 2-20 

Limitation/Uncertainty in Risk 

Model 

Information Newly Available in this 

Review 

Consideration of Potential U

Quantitative Exposure/

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 coarsephase 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 information to support design ofor specific case studies. Howevto note that the general urban strequire this type of representativsimulated reduction in ambient case study assumes that ambienstandard level being assessed (iestimate of risk for children livithe standard level). While it is areas across the U.S. that reflecgeneral urban study area (e.g., tchildren it may represent), this cimportant assessment of risk for that just meet the standard asseshigher-end risk associated with 

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 airrelated 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 (and data for Pb in other exposudrinking water and dietary itemwith refined central-tendency esand risk for the study areas, the need to be addressed to substanestimates of exposure and risk icorrelation between Pb exposurfor individuals experiencing elewhat extent is higher drinking wcorrelated with higher soil Pb exof elevated ambient air Pb expocorrelational information for mo
 2-21 

Limitation/Uncertainty in Risk 

Model 

Information Newly Available in this 

Review 

Consideration of Potential U

Quantitative Exposure/

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 iof measured Pb levels in exposumoderate to larger set of childreideally, this would include PbB can look in detail at the air-blooabsence of this improved informcorrelations between Pb exposuin a position to substantially imexposure and risk (including the fraction of risk), particularly for including those with elevated amexposures. 

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 (mechanisticempirical) 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 airrelated 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 

μm 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) stuinformation on cleaning efficienpotential for vacuuming to leavfloors, the utility of the study in hybrid dust model (e.g. additionefficiency) is limited by the fact Pb samples from Herculaneum focused on hard floors (and did flooring or any other textiles coenvironments). Given the site-smaterial (i.e., associated with practivity that includes a significacombined with repeated remedioriginating from the study, whilguiding remediation efforts and strategies for residences near Hreadily extrapolated to other urbPb exposure. Note, however, thfrom the study may be used quainterpret risk estimates generatereview. Specifically, the Hunt e
 2-22 

Limitation/Uncertainty in Risk 

Model 

Information Newly Available in this 

Review 

Consideration of Potential U

Quantitative Exposure/

dust Pb concentrations, which are needed for PbB simulation in IEUBK. 

identifies the potential for low-bestimates, if dust containing Pb ultimately in a finer form that is incidental ingestion by childrenstudy also identifies the potentiaresidences that lack carpets and relative cleaning efficiency rategeneralized urban setting (their higher than ours). Note, howev(2008) study exclusively focuseand not carpeting, and we woulhave substantially lower cleanin

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 specific locations provide insighdrive indoor dust Pb levels and important limitation of these stuinclude measurements of ambiethese studies do not provide expareas with elevated ambient air source can be of greater importaperformance assessing elements is limited. Had these studies incambient air Pb (including areas levels), then the utility of the stuthe risk assessment would be grNote, that as part of the risk assthe last review, we considered sEPA-sponsored National HumaSurvey (NHEXAS) in performasimulation of indoor dust Pb levExhibit G-6 of the Pb HEHR, U
 2-23 

Limitation/Uncertainty in Risk 

Model 

Information Newly Available in this 

Review 

Consideration of Potential U

Quantitative Exposure/

Estimating Exposure and PbB for Young Children 

F) Uncertainty in modeling multiplepathway 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. 

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. 

While the NHEXAS-Maryland Egeghy et al., (2005) study inclof exposure pathways (includindietary pathways, soil and drinkanalysis includes predominantly our child age range of interest, iinforming our consideration of pand potential correlation betweeaddition, the relatively small samindividuals), could potentially lassessment of the degree of corrpathways for different percentilpopulation with regard to PbB lnote, that in the Egeghy et al., 2Pb, while statistically associated was not associated directly with although this may reflect the facreflected residential areas with rair Pb, such that other factors (econdition of indoor paint and cdrove loadings of indoor dust P

G) Modeling PbB levels in young children given pathway-specific intake estimates (use of IEUBK).There is uncertainty both in the 

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 

It does not appear that there havdevelopments in the modeling osince the last review. While therused to update the GSDs used in 
 2-24 

Limitation/Uncertainty in Risk 

Model 

Information Newly Available in this 

Review 

Consideration of Potential U

Quantitative Exposure/

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 IEUBK-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 variabilchildren), without improved chapotential correlations between pestimates of higher percentile Pwill still be subject to substantiainability to reliably apportion tocontributing pathways (at those 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 havimprovements in our ability to m(including PbB levels) for adult populations. Furthermore, predilevels for older children and adurecent changes in ambient air Pbcomplicated significantly by the 
 2-25 

Limitation/Uncertainty in Risk 

Model 

Information Newly Available in this 

Review 

Consideration of Potential U

Quantitative Exposure/

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. 

than 7 years (the IEUBK limit), including teenagers.12

Regarding the potential for empirical air-toPbB 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 μg/m3). 

accumulated Pb in bone which clevels and can itself reflect Pb e

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 

The varied studies on associationow available do not provide a 

12 As noted in the draft ISA, EPA’s All Ages Lead Model is still in development, 
 2-26 

Limitation/Uncertainty in Risk 

Model 

Information Newly Available in this 

Review 

Consideration of Potential U

Quantitative Exposure/

the magnitude of IQ loss predicted for simulated children, particularly at lower total PbB levels (e.g., < 2.5 μg/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 μg/dL.13 However, there is limited representation of PbB levels below 3 μg/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 adjustresponse function. As noted in risk assessment for the last reviedifferent quantitative functions from the nonlinear function from for the concentration-response rlowest PbB level region (see tabThe new studies do not provide development of a quantitative fulevel region that falls outside of functions represented by these aOf the three studies (Chiodo et 2008; Kim et al., 2009) identifieonly Kim et al. (2009) provides blood-Pb IQ concentration-respPbB levels below 3 μg/dL. Furutilizes a Korean population and than the group modeled in the laWith this older population, therregarding the exposure conditioobserved response. Further, the established PbB model, the IEUused in the last assessment, doefor 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 evidencsupport for a quantitative characconcentration –response relationbehavioral endpoints is unclear. concentration-response function

13 Chiodo et al.(2007) and Jusko et al. (2008) will be included in the second draft ISA. 
 2-27 

Limitation/Uncertainty in Risk 

Model 

Information Newly Available in this 

Review 

Consideration of Potential U

Quantitative Exposure/

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 concentrationresponse 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 μg/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 μg/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 from epidemiological analyses tfunctions and not typically devecontinuous epidemiological anaregression analyses). There is rassociated with the information contributes additional uncertainresponse functions developed frSince most of the recent studies neurobehavioral endpoints do neffect estimates (e.g., quartile redo not provide strong support foresponse function for use in quaassessment. Additionally, some on older (teenage) children, and discussion (see prior row) of the study, EPA’s established childhIEUBK model, does not provide children. Regarding the other non-neurolrecognize that the evidence is urole of lead-induced changes in system, red blood cell function onset to puberty in eliciting or cimmunological, hematological ooutcomes. An improved underslinkages is needed to support quassessment for the impact of amin contributing to risk of outcomendpoints. 

14 Jedrychowski et al. (2008), Nigg et al. (2008), and Wang et al. (2008) will be included in the second draft ISA. 
 2-28 

Limitation/Uncertainty in Risk 

Model 

Information Newly Available in this 

Review 

Consideration of Potential U

Quantitative Exposure/

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 Pbassociated 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 et al., 2010). 

More detailed limitations associof recent non-neurological endpquantitative risk assessment varolder children, for which there iassociated with interpretations rconditions contributing to the mto the associated effects; focus omeasures of prenatal exposures which we are lacking in establistools; and, focus on non-U.S. pocharacteristics influencing Pb udiffer from U.S. populations. Aquantitative risk assessment for effects (e.g., kidney function) wincidence data the availability ofor 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 texposures during a lifetime (timmagnitudes) which contribute to outcomes continues to introduce to the simulation of adult health from changes in air Pb. This prdeveloping concentration-respo
 2-29 

Limitation/Uncertainty in Risk 

Model 

Information Newly Available in this 

Review 

Consideration of Potential U

Quantitative Exposure/

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 concentrationresponse relationships, a number of studies have investigated impacts at lower blood lead levels including those less than 5 μg/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 Pbrelated exposures. 

modeling potential adult health The absence of biokinetic modeadults also limits our ability to mendpoints as a component in a revaluating ambient air Pb. Our effect estimates for adult health non-occupational levels of Pb eour lack of a reliable means for between air-Pb levels (e.g., assopotential standards) and PbB levFurther, the contribution to blooendogenous Pb (e.g., stored in bhistorical Pb exposures complicblood lead as a biomarker of cuadults, and consequently contribinterpreting epidemiological stuPb exposures eliciting observed 
2-30 

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 
2-31 

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 
2-32 

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. 
3-1 

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 § 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 
3-2 

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 longterm 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, 2011b). 
3-3 

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 
3-4 

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. 
3-5 

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. 

 
3-6 

Figure 3-1. Conceptual Model for Ecological Risk Assessment During the Last Review. 
3-7 

3.1.2 Overview of Analytical Approach 

The screening-level assessment in the last NAAQS 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). 
3-8 

Figure 3-2. Analytical Approach for Screening-level Assessment in the Last Review. 

 
3-9 

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., 
3-10 

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, EcoSSLs, 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 of Pb 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] 
3-11 

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 “[a]lthough 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 
3-12 

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, locationspecific 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 
3-13 

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 (2011a) 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 
3-14 

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, 2011c) 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. 

 
3-15 

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. 

 Bioavailability, 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. 
4-1 

4 REFERENCES 

Braun, J. M., Kahn, R. S., Froehlich, T., Auinger, P., & Lanphear, B. P. (2006). Exposures to 

environmental toxicants and attention deficit hyperactivity disorder in U.S. children. 

Environmental Health Perspectives, 114, 1904-1909. http://dx.doi.org/10.1289/ehp.9478

Chiodo L.M., Covington C., Sokol R.J., Hannigan J.H., Jannise J., Ager J., Greenwald M., DelaneyBlack V. (2007) Blood lead levels and specific attention effects in young children. 

Neurotoxicol Teratol, 29(5):538-46 

De Vries, W., and J.E. Groenenberg. 2009. Evaluation of approaches to calculate critical loads for 

forest ecosystems. Env. Poll. 157: 3422-3432. 

Dixon, S. L., Gaitens, J. M., Jacobs, D. E., Strauss, W., Nagaraja, J., Pivetz, T., . . . Ashley, P. J. 

(2009). Exposure of US children to residential dust lead, 1999-2004: II. The contribution of 

lead-contaminated dust to children's blood lead levels. Environmental Health Perspectives, 

117(3), 468-474. http://dx.doi.org/10.1289/ehp.11918

Egeghy, P. P., Quackenboss, J. J., Catlin, S., & Ryan, P. B. (2005). Determinants of temporal 

variability in NHEXAS-Maryland environmental concentrations, exposures, and 

biomarkers. Journal of Exposure Science and Environmental Epidemiology, 15(5), 388-397. 

http://dx.doi.org/10.1038/sj.jea.7500415 

Gaitens, J. M., Dixon, S. L., Jacobs, D. E., Nagaraja, J., Strauss, W., Wilson, J. W., & Ashley, P. J. 

(2009). Exposure of US children to residential dust lead, 1999-2004: I. Housing and 

demographic factors. Environmental Health Perspectives, 117(3), 461-467. 

http://dx.doi.org/10.1289/ehp.11917

Huel, G., Sahuquillo, J., Debotte, G., Oury, J. F., & Takser, L. (2008). Hair mercury negatively 

correlates with calcium pump activity in human term newborns and their mothers at 

delivery. Environmental Health Perspectives, 116(2), 263-267. 

http://dx.doi.org/10.1289/ehp.10381

Hunt, A., Johnson, D. L., Brooks, J., & Griffith, D. A. (2008). Risk remaining from fine particle 

contaminants after vacuum cleaning of hard floor surfaces. Environmental Geochemistry 

and Health, 30(6), 597-611. http://dx.doi.org/10.1007/s10653-008-9183-8 

ICF International. (2006) Lead Human Exposure and Health Risk Assessments and Ecological Risk 

Assessment for Selected Areas. Pilot Phase. Draft Technical Report. Prepared for the U.S. 

EPA's Office of Air Quality Planning and Standards, Research Triangle Park, NC. 

December. Available at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_td.html 

Jedrychowski, W., Perera, F., Jankowski, J., Rauh, V., Flak, E., Caldwell, K.L., Jones, R.L., Pac, 

A., Lisowska-Miszczyk, I. (2008). Prenatal low-level lead exposure and developmental 

delay of infants at age 6 months (Krakow inner city study). Int J Hyg Environ Health , 211: 

345-351. 
4-2 

Jedrychowski, W., Perera, F., Maugeri, U., Rembiasz, M., Flak, E., Mroz, E., . . . Zembala, M. 

(2011). Intrauterine exposure to lead may enhance sensitization to common inhalant 

allergens in early childhood: A prospective prebirth cohort study. Environmental Research, 

111(1), 119-124. http://dx.doi.org/10.1016/j.envres.2010.11.002 

Jusko, T.A., Henderson, C.R., Lanphear, B.P., Cory-Slechta, D.A., Parsons, P.J., Canfield, R.L. 

(2008) Blood lead concentrations < 10 microg/dL and child intelligence at 6 years of age. 

Environ Health Perspect, 116(2):243-8. 

Karmaus, W., Brooks, K. R., Nebe, T., Witten, J., Obi-Osius, N., & Kruse, H. (2005). Immune 

function biomarkers in children exposed to lead and organochlorine compounds: A crosssectional study. Environmental Health: A Global Access Science Source, 4(5), 1-10. 

http://dx.doi.org/10.1186/1476-069X-4-5 

Kim, H. K., Yoon, E. K., Jang, J., Hwang, M., Kim, J., Ha, J. H.,...Park, K. L. (2009). Assessment 

of heavy metal exposure via the intake of oriental medicines in Korea. Journal of 

Toxicology and Environmental Health, Part A: Current Issues, 72(21-22), 1336-1342. 

http://dx.doi.org/10.1080/15287390903212485

Krieg, E. F., Jr., Butler, M. A., M-h, C., Liu, T., Yesupriya, A., Dowling, N., & Lindegren, M. L. 

(2010). Lead and cognitive function in VDR genotypes in the Third National Health and 

Nutrition Examination Survey. Neurotoxicology and Teratology, 32(2), 262-272. 

http://dx.doi.org/10.1016/j.ntt.2009.12.004

Lanphear, B. P., Hornung, R., Khoury, J., Yolton, K., Baghurst, P., Bellinger, D. C.,... Roberts, R. 

(2005). Low-level environmental lead exposure and children's intellectual function: An 

international pooled analysis. Environmental Health Perspectives, 113, 894-899. 

http://www.ncbi.nlm.nih.gov/pubmed/16002379 

Leggett, R. W. (1993) An Age-Specific Kinetic Model of Lead Metabolism in Humans. Environ 

Health Perspect. 101: 598-616. 

MacDonald, D.D., Ingersoll, C.G., and Berger, T.A. 2000. Development and evaluation of 

consensus-based sediment quality guidelines for freshwater ecosystems. Archives of 

Environmental Contamination and Toxicology 39: 20-31. 

 MacDonald, D.D., Ingersoll, C.G., Smorong, D.E. Lindskoog, R.A., Sloane, G., and Biernacki, T. 

2003. Development and Evaluation of Numerical Sediment Quality Assessment Guidelines 

for Florida Inland Waters. British Columbia: MacDonald Environmental Sciences, Lt. 

Columbia, MO: U.S. Geological Survey. Prepared for: Florida Department of 

Environmental Protection, Tallahassee, FL. 

Nigg, J.T., Knottnerus, G.M., Martel, M.M., Nikolas, M., Cavanagh, K,, Karmaus, W., Rappley, 

M.D. (2008) Low blood lead levels associated with clinically diagnosed attentiondeficit/hyperactivity disorder and mediated by weak cognitive control. Biol Psychiatry, 

63(3):325-31. 

Rodrigues, E. G., Virji, M. A., McClean, M. D., Weinberg, J., Woskie, S., & Pepper, L. D. (2010). 

Personal exposure, behavior, and work site conditions as determinants of blood lead among 

bridge painters. Journal of Occupational and Environmental Hygiene, 7(2), 80-87. 

http://dx.doi.org/10.1080/15459620903418316
4-3 

Sarasua, S. M., Vogt, R. F., Henderson, L. O., Jones, P. A., & Lybarger, J. A. (2000). Serum 

immunoglobulins and lymphocyte subset distributions in children and adults living in 

communities assessed for lead and cadmium exposure. Journal of Toxicology and 

Environmental Health, Part A: Current Issues, 60, 1-15. 

http://dx.doi.org/10.1080/009841000156556 

U.S. Environmental Protection Agency. (1998). Methodology for Assessing Health Risks 

Associated with Multiple Pathways of Exposure to Combustor Emissions. Cincinnati, OH: 

Update to EPA/600/6-90/003, EPA/NCEA (EPA 600/R-98/137). Available at 

oaspub.epa.gov/eims/eimscomm.getfile?p_download_id=427339. 

U.S. Environmental Protection Agency. (2003). Guidance for Developing Ecological Soil Screening 

Levels (Eco-SSLs), Attachment 1-4: Exposure Factors and Bioaccumulation Models for 

Derivation of Wildlife Eco-SSLs. Washington, DC: Office of Solid Waste and Emergency 

Response. OSWER Directive 9285.7-55. November. Available at 

http://rais.ornl.gov/homepage/ecossl.pdf. 

U.S. Environmental Protection Agency. (2005). Guidance for Developing Ecological Soil Screening 

Levels. Washington, DC: Office of Solid Waste and Emergency Response. OSWER 

Directive 9285.7-55. November. 

U.S. Environmental Protection Agency. (2006a) Air Quality Criteria for Lead. Washington, DC, 

EPA/600/R-5/144aF. Available online at: www.epa.gov/ncea/

http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=158823 

U.S. Environmental Protection Agency. (2006b). Analysis Plan for Human Health and Ecological 

Risk Assessment for the Review of the Lead National Ambient Air Quality Standards. 

Draft. Office of Air Quality Planning and Standards, Research Triangle Park, NC. May 31, 

2006. 

U.S. Environmental Protection Agency. (2007a) Lead: Human Exposure and Health Risk 

Assessments for Selected Case Studies, Volume I. Human Exposure and Health Risk 

Assessments – Full-Scale and Volume II. Appendices. Office of Air Quality Planning and 

Standards, Research Triangle Park, NC. EPA-452/R-07-014a and EPA-452/R-07-014b. 

http://www.epa.gov/ttn/naaqs/standards/pb/data/20071101_pb_ra_body.pdf

http://www.epa.gov/ttn/naaqs/standards/pb/data/20071101_pb_ra_app.pdf

http://www.epa.gov/ttn/naaqs/standards/pb/data/20080515_pb_ra_errata.pdf 

U.S. Environmental Protection Agency. (2007b) Review of the National Ambient Air Quality 

Standards for Lead: Policy Assessment of Scientific and Technical Information, OAQPS 

Staff Paper. EPA-452/R-07-013. Office of Air Quality Planning and Standards, Research 

Triangle Park, NC. http://www.epa.gov/ttn/naaqs/standards/pb/data/20071101_pb_staff.pdf

http://www.epa.gov/ttn/naaqs/standards/pb/data/20080515_pb_sp_errata.pdf 

U.S. Environmental Protection Agency. (2007c). Review of the National Ambient Air Quality 

Standards for Lead: Policy Assessment of Scientific and Technical Information. OAQPS 

Staff Paper. Office of Air Quality Planning and Standards, Research Triangle Park, NC. 

EPA-452/R-07-013 November 2007 

U.S. Environmental Protection Agency. (2008). Integrated Science Assessment (ISA) for Oxides of 

Nitrogen and Sulfur Ecological Criteria (Final Report). U.S. Environmental Protection 

Agency, Washington, DC, EPA/600/R-08/082F, 2008. 
4-4 

U.S. Environmental Protection Agency. (2009). Risk and Exposure Assessment for Review of the 

Secondary National Ambient Air Quality Standards for Oxides of Nitrogen and Oxides of 

Sulfur. U.S. Environmental Protection Agency, Office of Air Quality Planning and 

Standards, Research Triangle Park, NC. EPA-452/R-09-008a. September 2009 

U.S. Environmental Protection Agency. (2011a). Integrated Science Assessment for Lead (First 

External Review Draft). U.S. Environmental Protection Agency, Washington, DC, 

EPA/600/R-10/075A, 2011. http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_isa.html

U.S. Environmental Protection Agency. (2011b). Integrated Review Plan for the National Ambient 

Air Quality Standards for Lead, External Review Draft. U.S. Environmental Protection 

Agency, Office of Air Quality Planning and Standards, Research Triangle Park, NC. EPA452/D-11-001. June 2011. 

U.S. Environmental Protection Agency. (2011c). Policy Assessment for the Review of the 

Secondary National Ambient Air Quality Standards for Oxides of Nitrogen and Oxides of 

Sulfur. U.S. Environmental Protection Agency, Office of Air Quality Planning and 

Standards, Research Triangle Park, NC. EPA-452/R-11-005a. February, 2011. 

Wang, H.L., Chen, X.T., Yang, B., Ma, F.L., Wang, S., Tang, M.L., Hao, M.G., Ruan, D.Y. (2008) 

Case-Control Study of Blood Lead Levels and Attention-Deficit Hyperactivity Disorder in 

Chinese Children. Environ Health Perspect, 116(10). p.1401-6. 
 
United States Office of Air Quality Planning and Standards Publication No

Environmental Protection Health and Environmental Impacts Division June 2011 Agency Research Triangle Park, NC