# Review of the National Ambient Air Quality Standards for Lead:

Risk and Exposure Assessment Planning DocumentEPA-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 27711ii 

### 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 Ai r Quality Planning and Standards, U.S. Environmental Protection Agency. Any opinions, findings, conclusions, or recommendations are those of the authors and do not necessarily reflec t the views of the EPA. Mention of trade names or commercial products is not intended to cons titute endorsement or recommendation for use. Any questions or comments concerning human h ealth-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 Associat ed 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 Av ailable 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 Av ailable 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 Depo sition 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 Previ ous 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 Ri sk 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. ...................................................................................................................... 2-191-1 

## 1 INTRODUCTION

The U.S. Environmental Protection Agency (EPA) is conducting a review of the air quality criteria and the national ambient air qua lity 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 methodol ogies warrant the conduct of quantitative risk and exposure assessments (REAs) that might inform th is review. Also considered is the extent to which newly available evidence may refine our ch aracterization of exposure and risk estimates provided by the assessments conduc ted 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 cons ideration of the much-expanded health effects evidence on neurocognitive effects of Pb in ch ildren, EPA substantially revised the primary

standard from a level of 1.5 mi crograms per cubic meter (μg/m 3 ) to a level of 0.15 μg/m 3

. 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 μ g/m 3 was estimated to protect against air Pb-re lated IQ loss in the most highly exposed children, those exposed at the level of the standa rd. Results of the quant itative risk assessment were judged supportive of the evidence-based fram ework estimates. The averaging time was revised to a rolling 3-month period with a maxi mum (not-to-be-exceeded) form, evaluated over a 3-year period. 1 The indicator of Pb in total suspended particles (Pb-TSP) wa s retained, reflecting the evidence that Pb part icles 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 revi ew, EPA completed a quantitative assessment which estimated air-related Pb expos ure and the associated risk of IQ loss in children for a series of study areas. Risks were estimated for then-cur rent 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 analys is informed the EPA’s decision

to lower the level of the standard in the last review.

1 As compared to the previous aver aging time of calendar quarter, this re vision was considered to be more scientifically appropriate and more h ealth protective. The rolling average gives equal weight to all three-month periods, and the new calculation method gi ves 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 pe rtaining 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-relate d Pb to pose ecological risks of concern, limitations in available informa tion and tools precluded our ability to parse out estimates of air-related ecologica l risk associated with the th en-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 considerat ion 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 th e purpose of obtaining advice on EPA’s consideration of the recently available evid ence (information, methods, etc) with regard to its potential impact on quantitative exposure and ri sk analyses, both with regard to consideration

of the extent to which new assessments are warr anted in this review a nd with regard to our

consideration of the last assessm ent 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 em ployed for the last review, and on Agency experience with Pb exposure and risk assessmen t since that time, while also drawing from information presented in the May 2011 dr aft of the ISA for the current review.1-3 Background

Sections 108 and 109 of the Clean Air Act (A ct) govern the establishment and periodic review of the NAAQS. These st andards are established for pollutants that may reasonably be anticipated to endanger public health and welf are, and whose presence in the ambient air results from numerous or diverse mobile or st ationary 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 re view, 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 st andards, 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 committ ee advise the Administrator as part of this NAAQS review process, a functi on now performed by the CASAC.

EPA’s overall draft plan and sche dule for this Pb NAAQS review is presented in the draft Integrated Review Plan for the National Ambient Air Qualit y Standards for Lead

. 3 That plan discusses the preparation of key documents in the NAAQS re view process including an Integrated Science Assessment (ISA) and a Poli cy 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 a nd exposure assessments, that were performed for the review or for past reviews. Based on this eval uation, the Policy Assessment presents staff conclusions regarding standard-s etting options for the Administra tor to consider in reaching decisions on the NAAQS. 4

_________________________________ 1 Welfare effects, as defined in section 302(h) of the Ac t include, but are not limited to, ”effects on soils, water, crops, vegetation, man-made materials, animals, wild life, 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 heal th.” Section 109(b)(2) of the Act directs that a secondary standard is to Aspecify a level of air quality the attain ment 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 presen ce 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, consider ing evidence of effects asso ciated 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 informati on 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 a nd health risk assessments completed for the last review; and, (b) to what exte nt would an updated risk model ge nerate risk estimates that are substantially different from estim ates generated in the previous review (i.e., enhanced precision and/or confidence, coverage for additional sensit ive subpopulations and/or he alth endpoints)? In designing and implementing an assessment of exposure and risk asso ciated with Pb in ambient air, we are faced with significant li mitations and complexity that go far beyond the

situation for similar assessments typically performed for other crit eria pollutants. For example, unlike other criteria pollutants, ri sk associated with exposure to Pb originally rele ased 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 ambi ent 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 dietar y 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 rela tionship between Pb exposure and th e 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 an d not only exposure related to Pb released into ambient air. In addition, modeli ng some of the key pathways involved in Pb exposure (e.g., Pb loading of indoor residential dus t by ambient air Pb that penetr ates indoors and settles onto surface), can be complicated. These are some of the factors that make modeling exposure and

risk to Pb released into ambien t air a technically challenging task that often requires the use of simplifying assumptions and that is subject to a range of technical limita tions 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 to2-2 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 PR EVIOUS ASSESSMENT

This section provides an overview of the hum an 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 esti mating IQ loss in children due to exposure to Pb over the first seven years of life from a vari ety of sources, including, most importantly for purposes of this review, Pb released into ambien t air. The risk assessment focused on a set of

case studies. Due to limited data and models fo r 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. More over, 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 explic itly 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 th e 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 mo deling elements (e.g., monitor data, air quality models, indoor dust models, input datasets, c oncentration-response func tions), and section 2.1.4 describes particular challenges associated with differentiating air-related exposure and risk from those associated with nonair pa thways (section 2.1.4). Lastly in section 2.1.5, we describe key

uncertainties and limitations associ ated with the risk model.



### 2.1.1 Conceptual Model for Risk Associated with Air-related Lead

This section describes the con ceptual model developed for th e last review for assessment of public health risks associat ed with Pb from ambient air. The model identifies sources, pathways, routes, exposed populations, and health e ndpoints, with specific at tention to those that were explicitly addressed in th e risk assessment completed for th e 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 conceptualiz ation, these are exposures with the potential to be affected (over some time fram e) 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 ar e not bolded in Figure 2-1.2-3 Sources of Pb exposure include current and hi storical 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 substa ntial role in human expos ures, particularly for children. Additionally, Pb in house dust, which ma y be derived from Pb in outdoor dust and soil,

as well as from ambient air Pb is anot her 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 mobili zed 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 b ackground sources (e.g., Pb solder on water distribution pipes and Pb in materials used in food proces sing). Limitations in our data and modeling tools handicapped our ability to separate these contri butions 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 P b, 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 eff ects endpoints, the previous risk assessment focused on IQ loss in children up to age 7 years. This reflected consider ation of the evidence

which indicated that children r eceived elevated Pb exposure due to hand-to-mouth activity (i.e.,

incidental soil and indoor dust i ngestion) and that ambient air- related Pb has been shown to

contribute to Pb in outdoor so il 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 availa ble for the review (summarized in section 2.1.3 below) focused on simulating PbB concentra tions through the first 7 years of childhood. In terms of internal disposition and the biomet rics used to assess Pb exposure, PbB levels continue to be extensively used as an i ndex or biomarker of exposure by national and international health agencies. Th is reflects the association of Pb B with exposure, particularly recent exposure in young children, and the relative ease of collecting PbB measurement. Although bone Pb measurements have become easie r to collect and conseq uently, their use has been more widespread, epidemiological and toxico logical studies of Pb health effects and doseresponse relationships (particula rly for neurodevelopmental effects in children) tend to be dominated by PbB as the exposure metric. Th erefore, 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 estima tes presented for “tot al 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, wh ile lifetime average was estimated as the average

of PbB levels across the 7 year period. At the time of the last review, we noted th at limitations precluded prediction of changes in adult PbB levels (or bone Pb levels) given cha nges in ambient Pb levels. This reflects the fact that the presence of substantial hi storic Pb stores in most adults introduces uncertainty into the prediction of changes in blood or bone Pb in th ese adult populations resu lting from changes in ambient air Pb exposure. Additionally, in cons idering 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 th e 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 Inte lligence Quotient (IQ) used as the risk metric.2-5 Figure 2-1. Conceptual Model for Prev ious 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 studies 5,6 that generally represent two types of residential population exposures: (1) more highly ai r-pathway exposed young children (as described below) residing in small neighborh oods or localized residential areas with air

concentrations somewhat near the standard being evaluated, and (2) location-specific urban populations with a broader rang e of air-related exposures. The case studies representing the children mo st highly exposed via air-related pathways were the general urban case study and the primar y Pb smelter case study. The general urban case study was not based on a specific geographic location and reflected several simplifying assumptions in representing expos ure including uniform ambient ai r Pb levels associated with

the standard of interest ac ross the hypothetical study area and a uniform study population. Additionally, the method for simulating temporal variab ility in air Pb concentrations in this case study relied on national average estim ates of the relationships be tween air concentrations in

terms of the statistics considered for different forms of the standard being assessed and the

annual ambient air concentrations re quired for input to the PbB model. 7 Thus, while this case study provided characterization of risk to childr en 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 characterizati on of ambient air Pb levels and associated risk. The primary Pb smelter case study provides risk estim ates for children living in a specific area that is currently not in attainment with th e current NAAQS. We focused particularly on a

subarea within 1.5 km of the faci lity, where airborne Pb concen trations were closest to the

current standard and where child ren’s air-related exposures ar e 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 wa s 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 relationshi ps in the available air monitoring data between different statistical forms being considered for th e 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 Ange les to provide representations of urban populations with a broader range of air-related exposures due to spat ial gradients in both ambient air Pb levels and population density. For example, th e highest air concentrations in these case studies (i.e., those closest to the standard being a ssessed) were found in very small parts of the study areas, while a large majority of the case study popu lations resided in areas with much lower air concentrations. Based on the nature of the population exposures represented by the tw o categories of case study, the first category (the general urban a nd 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 leve l 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 meeti ng the then-current (at the time of the last review) NAAQS of 1.5 μ g/m 3 , 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 fo r Previous Review.

Air Quality Scenario Averaging Time (Form) Level (μg/m 3 ) Case Study

Then-current Standard

Calendar Quarter (maximum) 1.5 All

Current Conditions 0.87 (95 th 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 scen arios for other media and exposure pathways varied depending on the type of case study (as su mmarized below in section 2.1.3) and, in some2-8 cases (as summarized below in section 2.1.4), lim itations in the available data and modeling tools precluded the assessment from varying con centrations of some non air media across the air quality scenarios. For example, dietary and drin king 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 scenar ios, although as summarized in section 2.1.3, the methods used differed among the di fferent types of case studies.



### 2.1.3 Analysis Approach and Modeling Elements

This section describes the risk assessment appr oach (including discussion of key analysis steps), used in assessing risk fo r 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, in cluding the dispersion of Pb away from the point of release, (b) pr ediction of the resulting concentra tion of Pb in media of concern including outdoor air and indoor dust, (c) use of th ese Pb concentrations to gether 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-re sponse functions derived from epidemiology studies to estimate IQ loss associ ated with the estimated PbB levels. The modeling approach for the general urban case study and location-specific ur ban 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 urba n case study. Figure 2-2 id entifies 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 exposur e assessment, while the fourth is the risk assessment step (exposure assessment and risk asse ssment steps are discussed separately below).2-9 Figure 2-2. Overview of Analysis Approac h 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 ASSESSMENTRISK CHARACTERIZATION2-10 Exposure Assessment

Concentrations of Pb were estimated in ambient media and indoor dust using a combination of empirical data and modeling projectio ns. The use of empirica l data brings with it uncertainty related to the potenti al inclusion of bac kground 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 unce rtainties (e.g., model and parame ter uncertainties). Both of

these uncertainties are discussed below in Sec tion 2.1.5. Specific approaches used at the three case study locations are br iefly described below.

Characterization of Pb in ambient air relied on (a) dispersion modeling of facility-related (including fugitive) Pb emissions for the primar y Pb smelter case study, (b) the use of ambient monitor data for the location-sp ecific urban case studies, and (c) an assumption of uniform ambient air Pb levels (matching the standard le vel 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 patte rns of ambient air Pb over reside ntial areas in the vicinity of the facility, where ambient Pb levels were dominat ed 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 th ree urban areas in the U.S. By contrast, the general urban study area is designed to assess ex posure and risk for a smaller group of residents (e.g., neighborhood) exposed at the level of the sta ndard and therefore, di d 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 a ssociated with the facility, concentrations in the location-specific urban study areas, which reli ed on empirical (monitor-based) data to define ambient air Pb concentrations, reflected contribu tions from all contributing sources, be they currently active stationary or mobile sources, re suspension 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 us e of (a) existing site-specific measurements (primary Pb smelter case study), and (b) nationall y representative resident ial soil measurements obtained from the literature (general and location-sp ecific urban case studies). In the case of the primary Pb smelter case study, soil Pb concentrati on data were available for a zone close to the facility and statistical extrapol ation 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 rela te indoor dust to outdoor air Pb and/or outdoor soil Pb and (b) mechanistic models that predic t indoor dust Pb based on key mechanisms (e.g., infiltration of2-11 outdoor air indoors, deposition rates of Pb from indoor air to indoor surfaces, house cleaning rates). For the point source case study, a combin ation of regression-base d models obtained from the literature and developed ba sed 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 availabl e regression-based models had been developed largely based on residential e xposures near large point sour ces and were not considered representative of more genera l 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 concen trations 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, ind oor dust) using the Integrated Exposure and Uptake Biokinetic (IEUBK) m odel (Sections 3.2.1.1 and 5.2.4 of US EPA, 2007a). 8 However, rather than completing a fully-pr obabilistic 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 with in a given study area. We then combined this central-tendency estimate with a geometric stan dard 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 (u sing 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 concu rrent and lifetime-avera ge PbB metrics, although ultimately, we focused on the concurrent PbB metric in estimating risk. 10

8 In predicting PbB levels, we assumed that Pb con centrations 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 GS D to produce an population-distribution of PbB levels. However, for both the primary Pb sm elter and the location-specific urban st udy areas, smaller polygons within the larger study area (e.g., US Census bl ocks for the location specific urban st udy 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 asse ssment 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 cons idered ”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 gene rating a distribu tion of IQ loss estimates for

the set of children simulated in the exposure assessment. Specifi cally, 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 c oncentration-res ponse functions were selected to provide differe nt 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 5 th 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 lo ss in children, or they are derived from data presented in that study. The four functions are presented in Figur e 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 func tions is also provided below:

 Log-linear with cutpoint : log-linear function derived fr om 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 stra tification 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 leve ls. 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 Concentratio n-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-linearwith 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 ge nerated 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 50 th , 90 th and 95 th percentile modeled child ). This category of metric provides perspective on the distribution of IQ loss resulting from polic y-relevant exposure pathways, ranging from the typical or average child (50 th percentile, mean) to ch ildren experiencing higher exposures (90 th , 95 th 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 linearization2-14  Child frequency counts associated with specific ri sk percentiles : Number of children associated with each of the population percen tiles (e.g., the number of children predicted to have risk levels at or above the 95 th percentile). This risk me tric provides a perspective on the number of children associat ed with various levels of IQ loss for a particular case study.

For the general urban case study, only the firs t type of risk metric, population risk percentiles, was developed because this case stud y is not location-specific. Child frequency counts are not applicable, since a specific location withassociated 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 tw o air-related (policy relevant) categories, referred to as “recent air” and “pas t 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 es timates for the air-re lated 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 inf iltration 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 pla ced into the “past air” category. These include ingestion of Pb in outdoor dust/so il 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 estimat es for the air-related and background categories is the apportionmen t 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 th is 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). Th e inclusion of indoor pain t Pb as a component of "other" indoor dust Pb (and conse quently as a component of the “p ast air” category) represents a source of potential high bias in ou r prediction of exposure and risk associated with the “past air” category because, conceptually, exposure to indoo r paint Pb is considered part of background exposure. At the same time, Pb in ambient air do es contribute to the exposure pathways included in the “background” category (drinki ng water and diet), and is likel y a substantial contribution to diet. We could not separate the air contribu tion from the nonair contributions, and the total2-15 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 poten tial low bias in our predic tions of air-related risk. Further, we note that in simulating reductio ns in exposure associated with reducing ambient air Pb levels through alternative NAAQS (and increases in exposure if the current NAAQS was reached in certain ca se studies) only the exposure path ways categorized as “recent air” (inhalation and ingestion of that portion of indoor dust asso ciated with outdoor ambient air) were varied with changes in ai r 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 subs equent decrease in exposure thr ough 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 th e assessment design, data and modeling tools, our risk estimates for the “past air” category in clude both risks that ar e truly air-related and potentially, some background risk. Because we c ould 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 limita tion leads to a slight overestimate of the risks in the “past air” category. At the same time, as discussed above, the "r ecent air" category does not fully represent the risk associ ated with all air-relat ed pathways. Thus, we considered the risk

attributable to air-related e xposure 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 fo r 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 th ere was uncertainty associated w ith the model and its output. For example, because of the evidence for a non linear response of PbB to exposure and also the nonlinearity reflected in the C–R functions fo r estimation of IQ loss, the assessment first

estimated total PbB levels and associated ri sk (i.e., for air- and nonair-related exposure pathways), and then separated out those estimate s of PbB and associated risk for pathways of interest in this review. We separated out the esti mates of total (all-pathway) PbB and IQ loss into a background category and two air-related categ ories (“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 and2-16 background categories. As disc ussed above, we believe these limitations led to a slight overestimation of the risks for the past-air catego ry and to an under representation of air-related pathways for the recent-air category. Thus, we ch aracterized the risk attr ibutable to air-related exposure pathways to be bounded by the estimat es developed for past-air and recent-air categories. Additional limitations, assumptions and uncerta inties, which were recognized in various ways in the assessment and presen tation of results, are listed be low, beginning with those related to design of the assessment or case studies, fo llowed by those related to estimation of Pb concentrations in ambient air, indoor dust, out door 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 ar e adjusted to match the age of the child).

 General Urban Case Study: The design for this cas e study employs assumptions regarding uniformity that are reasonable in the co ntext of a small neighborhood population, but would contribute significant uncertainty to extrapolation of these estimates to a specific urban location, particul arly a relatively large one. Thus, the risk estimates for this general urban case study, wh ile 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 gradient s 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-cur rent 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 studie s, as well as the uncertainty in simulation of conditions associated with the implementation of em issions 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 cha nging 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 th e degree of correlati on between high-end Pb exposures across pathways (e.g., the degree to which an individual experiencing high drinking water Pb exposure would also potenti ally experience high Pb paint exposure and high ambient air-related Pb exposure). Our inab ility to characterize potential correlations between exposure pathways (particularly at th e higher percentile exposure levels) limited our ability to (a) effectively model high-end Pb risk and (b) apportion that risk between different exposure pathways, includ ing 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 NEWL Y AVAILABLE EVIDENCE

This section evaluates the info rmation, methods and models ne wly available since the last review (as summarized in the first draft Pb ISA) to assess the extent to wh ich it has the potential

to address these limitations and uncertainties. Ta ble 2-3 (a) identifies limit ations and sources of uncertainty in the risk assessment model develo ped in the last Pb NAAQ S review, (b) identifies the evidence newly available since the last re view that may address these uncertainties or limitations (in those instances where new informati on 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 limita tion. Based on the information provided in Table 2-3, EPA staff co nclusions regarding the potentia l 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 2.3.2-19Table 2-3. Assessment of Information (including methods, models, etc.) Newly Available in this Review.Limitation/Uncertainty in RiskModelInformation Newly Available in thisReviewConsideration of Potential Utility and Impact onQuantitative Exposure/Risk AssessmentCharacterizing Exposure PathwaysA) Characterizing spatial gradientsin ambient air Pb levels in the urbancontext.Limitations in our monitoringnetwork and in studies of smaller scalespatial gradients in ambient Pb levelsin the urban setting introduceduncertainty into our characterization ofexposure levels and risk for residentialpopulations modeled for the locationspecific urban study areas. Similarly,limitations in our characterization ofambient air Pb levels prevented usfrom characterizing areas across theU.S. with the attributes associated withthe general urban study area.Section 3.5.1.2 (Intra-urban Variability) of thedraft ISA observes that evidence from anumber of studies suggests that there issubstantial intra-urban variability in ambientair Pb levels with elevated levels beingassociated with proximity to specific sources(and often captured by source-orientedmonitors), while lower levels are oftenassociated with more generalized urban areas.However, the monitoring network in place isgenerally not refined enough to providecomprehensive coverage for an urban areasuch that the nature of the spatial gradient canbe well-characterized on a more localized(neighborhood) level. The draft ISA alsohighlights the fact that monitors fromdifferent networks can capture different sizegradients for particles containing Pb, whichcan make it hard to compare monitored levelsacross monitors (i.e., if they are from differentnetworks).In the last risk assessment, we used monitoring data totry and identify the fraction of monitor locations withambient air Pb levels near the current standard level (oralternative lower standard levels) which, therefore,could have potential risks at or near those estimated forthe general urban study area. However, without havingmore information on the gradient in air Pb levels nearthose higher source-oriented monitors, any assessmentof the size of populations experiencing those elevatedair Pb levels is highly uncertain. The newly availableinformation does not appear to provide substantiallyimproved data for characterizing gradients at this morerefined spatial scale. We also note, that even if we didhave highly-refined information on ambient air Pbgradients in urban areas, in order to complete moredetailed residential Pb-risk modeling, we would alsoneed more detailed information on other aspects of Pbexposure specific to those residential areas (e.g., indoordust Pb concentrations, soil concentrations, anddrinking water Pb concentrations). Availability of thislevel of refined exposure information for the urbanareas that might be of interest is likely limited orlacking. In addition, we would still be hampered bylimitations in our ability to apportion total risk betweenair and nonair pathways especially for individualsexposed to higher pathway-specific Pb levels, as wouldbe associated with this type of specific residentiallocation (i.e., we do not have information on the degreeof correlation among Pb exposure pathways).2-20Limitation/Uncertainty in RiskModelInformation Newly Available in thisReviewConsideration of Potential Utility and Impact onQuantitative Exposure/Risk AssessmentB) Limitations in our ability tosimulate alternative (lower)standard levels (implementingrollback).Significant uncertainty isassociated with the prediction ofreductions in ambient air Pb levels,reflecting potential actions by urbanareas to attain alternative (lower)standards.Section 2.1.1 (Sources, Fate and Transport ofAmbient Lead) and section 3.3 (Fate andTransport of Lead) of the draft ISA note thatPb associated with coarse PM will tend todeposit near sources, while Pb associated withfiner PM will tend to be transported further.The draft ISA also notes that the cycle ofdeposition and resuspension for even coarsephase Pb can be substantial leading todiffusion in the urban context. This moregeneralized information on the relationshipbetween Pb particle size and deposition helpsus to better understand and frameconceptually the issue ofspatial gradients inreduction around sources. However, theredoes not appear to be new research orinformation on how ambient air Pb levelsmight decrease given reductions in Pbemissions from specific sources, or categoriesof sources.It does not appear that we have substantially improvedinformation to support design of our rollback strategiesfor specific case studies. However, it is also importantto note that the general urban study area does notrequire this type of representative characterization ofsimulated reduction in ambient air Pb levels, since thatcase study assumes that ambient air Pb levels are at thestandard level being assessed (i.e., it provides anestimate of risk for children living in an area at or nearthe standard level). While it is difficult to characterizeareas across the U.S. that reflect key aspects of thegeneral urban study area (e.g., to estimates how manychildren it may represent), this case study provides animportant assessment of risk for children living in areasthat just meet the standard assessed (i.e., a reasonablehigher-end risk associated with a particular standard).C) Characterizing Pb levels in otherexposure media, including soil,drinking water and dietary items(indoor dust is discussed separatelybelow – see entry “D”). Limitations inour ability to characterize Pb levels inother media (besides ambient air) anddifferentiate those levels for differentsubsets of urban populations in thelocation-specific urban study areasevaluated, introduces uncertainty intothe analysis.Section 3.6.1 (Soils) of the draft ISA providesa table (3-9) identifying soil Pb levels inurban areas from the literature, including anumber of values from studies publishedsince the previous review yet conductedacross a broad range of years back to 1976.Therefore, depending on the availability ofinformation to clarify the context for thesemeasurements particularly with regard to airrelated and other sources, these may includenew data to inform the characterization ofurban soil Pb levels for the risk assessment.Section 4.1.1.3 of the draft ISA describesIt is important to note that while improved soil Pb data(and data for Pb in other exposure media includingdrinking water and dietaryitems) would provide uswith refined central-tendency estimates of Pb exposureand risk for the study areas, the key factor that wouldneed to be addressed tosubstantially improve ourestimates of exposure and risk is the degree ofcorrelation between Pb exposure pathways, particularlyfor individuals experiencing elevated exposure (e.g., towhat extent is higher drinking water Pb exposurecorrelated with higher soil Pb exposure and with areasof elevated ambient air Pb exposure). This type ofcorrelational information for more highly Pb exposed2-21Limitation/Uncertainty in RiskModelInformation Newly Available in thisReviewConsideration of Potential Utility and Impact onQuantitative Exposure/Risk Assessmentinformation on Pb in drinking water(including studies on the role of differentdrinking water systems in releasing Pb frompipes) and Pb in dietary items (Pb in crops,fish and game).children will only be availableif we have matched setsof measured Pb levels in exposure media for amoderate to larger set of children (as noted below,ideally, this would include PbB measurements so wecan look in detail at the air-blood ratios). In theabsence of this improved information on the nature ofcorrelations between Pb exposure pathways, we are notin a position to substantially improve our estimates ofexposure and risk (including the ambient air-relatedfraction of risk), particularly for higher PbB children,including those with elevated ambient air-sourced Pbexposures.D) Modeling the relationshipbetween ambient air Pb (outdoors)and indoor dust Pb (focusing onuncertainties related to applicationof the hybrid indoor dust model).Elements of the hybrid (mechanisticempirical) indoor dust model aresubject to uncertainty including: (a) thesimulation of the interplay between airexchange rates (ambient outdoor andindoor), loading to indoor surfacesfrom indoor air and removal throughcleaning, (b) estimating the fraction ofindoor dust Pb that originates from oldpaint versus the fraction originatingfrom ambient outdoor air Pb (combinesmechanistic modeling for ambient airrelated indoor dust with empirical dataon total dust Pb, including the fractionfrom indoor paint), and (c) convertingestimates of indoor dust Pb loading toSection 4.1.1.2. (Exposure to Lead in Soiland Dust) of the draft ISA discusses researchpublished since the last review focused onassessing risk reductions associated withvacuuming of surfaces with Pb dust (Hunt etal., 2008). This study suggests that, whilevacuuming may clean much of the soil massdeposited onto hard surface flooring, Pb dustin a relatively fine form (1-3μm particles,which may be more accessible throughincidental hand-to-mouth activity by children)remains. While this study providesinformation on cleaning efficiency, it isimportant to note that the soil Pb used in theanalysis was sourced from the Herculaneumlocation and the study focused exclusively onhard-surface flooring, providing no newinformation regarding cleaning efficienciesfor indoor environments with additional typesof surfaces (e.g., fabrics).While the Hunt et al. (2008) study provides someinformation on cleaning efficiency and highlights thepotential for vacuuming to leave fine-particle Pb onfloors, the utility of the study in providing inputs to thehybrid dust model (e.g. additional data on cleaningefficiency) is limited by the fact that the study used soilPb samples from Herculaneum and the fact that itfocused on hard floors (and did not evaluate carpetedflooring or any other textiles common in indoorenvironments). Given the site-specific nature of thismaterial (i.e., associated with primary Pb smeltingactivity that includes a significant historical signalcombined with repeated remediation activity), dataoriginating from the study, while potentially useful inguiding remediation efforts and house cleaningstrategies for residences near Herculaneum, cannot bereadily extrapolated to other urban scenarios involvingPb exposure. Note, however, that information obtainedfrom the study may be used qualitatively to further helpinterpret risk estimates generated in the previousreview. Specifically, the Hunt et al., 2008 study2-22Limitation/Uncertainty in RiskModelInformation Newly Available in thisReviewConsideration of Potential Utility and Impact onQuantitative Exposure/Risk Assessmentdust Pb concentrations, which areneeded for PbB simulation in IEUBK.identifies the potential for low-bias in our riskestimates, if dust containing Pb that is not cleaned isultimately in a finer form that is more accessible toincidental ingestion by children. Conversely, the Huntstudy also identifies the potential for high-bias inresidences that lack carpets and other fabrics, if theirrelative cleaning efficiency rates hold in a moregeneralized urban setting (their rates are generallyhigher than ours). Note, however that the Hunt et al.,(2008) study exclusively focused on hard floor surfacesand not carpeting, and we would expect carpeting tohave substantially lower cleaning efficiency.E) Modeling the relationshipbetween ambient air Pb (outdoors)and indoor dust Pb and then relatingthese to PbB levels (focusing heremore broadly on the relationshipbetween ambient air Pb and PbB,with indoor dust Pb as the primarylinkage).There is uncertainty inrelating changes in ambient air Pb tochanges in indoor dust Pb and PbB.Any data characterizing thisrelationship between ambient air Pband PbB (including matched data setsfor a group of children) could be usedin performance assessing and possiblycalibrating, the exposure component ofthe risk assessment.Section 4.5.2. (Environmental Lead-BloodLead Relationships) discusses studies basedon the CDC’s National Health and NutritionExamination Survey (NHANES) data from1999-2004. These studies assess therelationship between residential dust Pb andPbB levels in children (e.g., Gaitens et al.,2009 and Dixon et al., 2009). However, thesestudies do not account for ambient air Pb (andits potential relationship with indoor dust Pband consequently, total Pb exposure).While NHANES-based studies and other studies ofspecific locations provide insights into which factorsdrive indoor dust Pb levels and PbB levels, animportant limitation of these studies is that they doinclude measurements of ambient air Pb. Becausethese studies do not provide explicit coverage for urbanareas with elevated ambient air Pb levels (where this Pbsource can be of greater importance), their utility inperformance assessing elements of the risk assessmentis limited. Had these studies included consideration forambient air Pb (including areas with elevated air Pblevels), then the utility of the studies in the context ofthe risk assessment would be greater.Note, that as part of the risk assessment completed forthe last review, we considered studies based on theEPA-sponsored National Human Exposure AssessmentSurvey (NHEXAS) in performance evaluatingsimulation of indoor dust Pb levels (see Appendix G,Exhibit G-6 of the Pb HEHR, USEPA, 2007a).2-23Limitation/Uncertainty in RiskModelInformation Newly Available in thisReviewConsideration of Potential Utility and Impact onQuantitative Exposure/Risk AssessmentEstimating Exposure and PbB for Young ChildrenF) Uncertainty in modeling multiplepathway exposure to Pb in youngchildren, with consideration for thedegree of correlation betweenpathways.If we had detailed surveydata on pathway exposures for a set ofchildren (including ambient air Pb,indoor dust, soil Pb and dietary Pblevels for each child), we could thenuse those data to enhance oursimulation of total Pb exposure for theurban case studies. This kind ofmatched pathway-specific data for aset of children would allow us, inparticular, to define potentialcorrelations between Pb exposurepathways (e.g., the extent to whichchildren with high drinking water Pbare also exposed to high indoor dust Pband ambient air Pb). This, in turn,would potentially improve our abilityto simulate risk for children withelevated Pb exposures and parse outthe fraction associated with ambient airPb.Section 4.1.1 (Pathways for Lead Exposure)in the draft ISA discusses research based onthe EPA-sponsored National HumanExposure Assessment Survey (NHEXAS)dataset. For example, Egeghy et al., 2005,used a dataset for Maryland location toexamine determinants of variability in PbBlevels (including ambient air Pb, dust Pb anddietary Pb levels). While this analysis did usea matched dataset for a group of 80individuals, an important attribute of the studyis that all individuals are >6 yrs of age (i.e.,ranging older than the age group modeled inour risk assessment). Additionally, the air Pbmeasurements were restricted to particlessmaller than 10 microns potentially affectingconclusions regarding pathways involvingdeposition of larger particles. The shortsampling period (8 days) also may preclude arepresentative sample.While the NHEXAS-Maryland dataset used in theEgeghy et al., (2005) study includes data for a varietyof exposure pathways (including ambient air Pb,dietary pathways, soil and drinking water), because theanalysis includes predominantly individuals outside ofour child age range of interest, it is of reduced utility ininforming our considerationof pathways of exposureand potential correlation between those pathways. Inaddition, the relatively small sample size (80individuals), could potentially limit any more detailedassessment of the degree of correlation betweenpathways for different percentiles of the studypopulation with regard to PbB level. It is interesting tonote, that in the Egeghy et al., 2005 study, outdoor airPb, while statistically associated with indoor air Pb,was not associated directly with indoor dust Pb levels,although this may reflect the fact that their datasetreflected residential areas with relatively low ambientair Pb, such that other factors (e.g., home age,condition of indoor paintand construction material)drove loadings of indoor dust Pb.G) Modeling PbB levels in youngchildren given pathway-specificintake estimates (use of IEUBK).There is uncertainty both in theSection 4.6 (Biokinetic Models of LeadExposure-Blood Lead Relationships) of thedraft ISA observes, that while modeling ofhuman Pb exposures and biokinetics hasIt does not appear that there have been significantdevelopments in the modeling of PbB levels in childrensince the last review. While there are data that could beused to update the GSDs usedin the risk assessment to2-24Limitation/Uncertainty in RiskModelInformation Newly Available in thisReviewConsideration of Potential Utility and Impact onQuantitative Exposure/Risk Assessmentprediction of central-tendency PbBlevels as well as the application ofgeometric standard deviations (GSDs)for characterizing populationvariability in PbB levels around thosecentral-tendency estimates. As notedin the risk assessment, we did notcomplete a probabilistic simulation ofPbB variability based on modelingPbB levels for each simulatedindividual using IEUBK and, instead,relied on GSDs to characterizevariability around the IEUBK-modeledcentral tendency PbB level for aparticular study population.advanced considerably during the past severaldecades, there have been relatively fewdevelopments since the 2006 Pb AQCD(USEPA, 2006a) was published in the lastreview (draft ISA, p. 4-93).Regarding newer data characterizingpopulation variability in PbB levels (i.e.,sources for updating the GSDs used tocharacterize population variability in PbBlevels in the risk assessment), there areupdated characterizations of PbB variabilityin children for the U.S. based on the 2005-2008 NHANES data (see section 4.4.1 - Leadin Blood – in the draft ISA). In addition,recent studies of Pb effects in children couldprovide characterization of variability in PbBlevels for smaller (more localized) groups ofchildren (for example, see section 5.3.3.1.Epidemiologic Studies of Behavioral Effectsin Children - in the draft ISA).characterize population variability in PbB levels (forchildren), without improved characterization of thepotential correlations between pathways, updatedestimates of higher percentile PbB levels (and IQ loss),will still be subject to substantial uncertainty due to aninability to reliably apportion total risk between thecontributing pathways (at those higher-end total Pbexposure levels).Estimating Exposure for Other Populations/LifestagesH) Estimating exposure for otherpopulations/lifestages.Limitations inour ability to relate changes in recentair Pb-related exposure to PbB levelsin adults was one of the reasons thatadult health endpoints were not part ofthe assessment for the last review. AAs noted above, section 4.6 (BiokineticModels of Lead Exposure-Blood LeadRelationships) of the draft ISA does notidentify substantial improvements in PbBprediction models, including models forsimulating changes in PbB (or otherbiometrics) for adults and for children olderIt does not appear that there have been significantimprovements in our ability to model exposure(including PbB levels) for adult or older childpopulations. Furthermore, predicting changes in PbBlevels for older children and adults resulting fromrecent changes in ambient air Pb-related exposures iscomplicated significantly by the presence of2-25Limitation/Uncertainty in RiskModelInformation Newly Available in thisReviewConsideration of Potential Utility and Impact onQuantitative Exposure/Risk Assessmentcritical source of uncertainty inmodeling adult PbB is the complexrole played by the storage of Pb invarious compartments (mainly in bone)over a person’s lifetime, as well as themobilization of this Pb during certainphysiological conditions. Thisaccumulated Pb in adults derives fromearlier exposures when both Pb intakeand environmental concentrations, mayhave been substantially higher.The models available for children olderthan 7 yrs (the age limit of IEUBK)and into adulthood (e.g., Leggett,1993) have not been routinely used bythe EPA in supporting regulatory riskassessment or subjected to theextensive and rigorous performanceevaluation which has been sothoroughly reported for IEUBK(AQCD, section 4.4.10). In addition,some of the same uncertaintiesidentified above for adults also pertainto some extent in modeling olderchildren/teenagers.than 7 years (the IEUBK limit), includingteenagers.12Regarding the potential for empirical air-toPbB models, section 4.5.1.2 of the Pb ISA,which addresses the availability of recentstudies in this area, describes an occupationalexposure study. The study size was relativelysmall with occupational exposureconcentrations well above those common inambient air (the geometric mean Pbconcentration over the two week period was58 μg/m3).accumulated Pb in bone which can contribute to PbBlevels and can itself reflect Pb exposure earlier in life.Estimating Risk for Young ChildrenI) Modeling IQ loss in youngchildren.Uncertainty associated withThe ISA (Section 2.8.2) summarizes thecurrent evidence that informs characterizationThe varied studies on associations between IQ and PbBnow available do not provide a strong foundation for12As noted in the draft ISA, EPA’s All AgesLead Model is still in development,2-26Limitation/Uncertainty in RiskModelInformation Newly Available in thisReviewConsideration of Potential Utility and Impact onQuantitative Exposure/Risk Assessmentthe magnitude of IQ loss predicted forsimulated children, particularly atlower total PbB levels (e.g., < 2.5μg/dL) reflects the appreciably lessextensive information available onwhich to base our characterization ofthe concentration-response function atlower PbB levels levels.of concentration-response relationships forthose health endpoints for which suchevidence is most well established. Theserelationships are for PbB levels in childrenwith cognitive deficitsand PbB levels inadults with increased blood pressure,mortality, and indicators of nephrotoxicity.With regard to studies published since the lastreview that might inform our understandingof the concentration-response relationship forPb associated IQ loss, three studies (Chiodo etal., 2007; Jusko et al., 2008; Kim et al., 2009)report effect estimates for IQ loss in studypopulations with mean PbB levels at or below5 μg/dL.13However, there is limitedrepresentation of PbB levels below 3 μg/dL inChiodo et al. (2007) and Jusko et al. (2008).In comparison to these two studies, Kim et al.(2008), which involved South Koreanchildren aged 8-11 years of age, includes alower distribution of PbB levels.development of a new or adjusted concentrationresponse function. As noted in section 2.1.3 above, therisk assessment for the last review included fourdifferent quantitative functions (based on or extendingfrom the nonlinear function from Lanphear et al 2005)for the concentration-response relationship in thelowest PbB level region (see table 2-2 and figure 2-3).The new studies do not provide support fordevelopment of a quantitative function for this PbBlevel region that falls outside of the range of C-Rfunctions represented by these approaches.Of the three studies (Chiodo et al., 2007; Jusko et al.,2008; Kim et al., 2009) identified since the last review,only Kim et al. (2009) provides information on theblood-Pb IQ concentration-response relationship forPbB levels below 3 μg/dL. Further, Kim et al. (2009)utilizes a Korean population and an age group olderthan the group modeled in the last risk assessment.With this older population, there is greater uncertaintyregarding the exposure conditions associated with theobserved response. Further, the Agency’s wellestablished PbB model, the IEUBK model, which wasused in the last assessment, does not provide estimatesfor ages beyond 7 years.J) Modeling other endpoints inyoung children. The assessment forthe last review did not quantitativelyassess risk of health endpoints otherthan IQ loss primarily due toThe ISA (Section 2.8.2) describes the currentevidence that informs characterization ofconcentration-response relationships for thosehealth endpoints for which such evidence ismost well established. These relationships areThe extent to which the evidence provides strongsupport for a quantitative characterization of theconcentration –response relationship for non-IQbehavioral endpoints is unclear. Further,concentration-response functions utilized in13Chiodo et al.(2007) and Jusko et al. (2008) will be included in the second draft ISA.2-27Limitation/Uncertainty in RiskModelInformation Newly Available in thisReviewConsideration of Potential Utility and Impact onQuantitative Exposure/Risk Assessmentlimitations in the available informationor an absence of relevant informationfor developing informativeconcentration-response functions.for PbB levels in children with cognitivedeficits and PbB levels in adults withincreased blood pressure, mortality, andindicators of nephrotoxicity.With regard to the evidence for concentrationresponse relationships of neurobehavioraloutcomes (other than IQ), a number of recentstudies have investigated impacts on cognitivedomains at lower PbB levels including thoseless 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) inchildren. Among these studies, some involvechild populations ranging in age up to 15 or16 years of age. Additionally they variouslyprovide continuous and/or noncontinuouseffect estimates and some analyzeassociations of prenatal exposure (based oncord blood measurements).14The ISA also recognizes evidence forassociations of renal, immune system,hematological, and reproductive effects withPbB levels below 5 μg/dL in childpopulations (draft ISA, Tables 2-2 and 2-3).However, the evidencefor these effects haslimited applicability for a quantitativeassessment of the risk of specific healthquantitative risk assessment are typically developedfrom epidemiological analyses that report continuousfunctions and not typically developed from noncontinuous epidemiological analyses (e.g., quartileregression analyses). There is reduced resolutionassociated with the information from the latter whichcontributes additional uncertainty to concentrationresponse functions developed from these analyses.Since most of the recent studies of non-IQneurobehavioral endpoints do not include continuouseffect estimates (e.g., quartile regression analysis), theydo not provide strong support for a concentrationresponse function for use in quantitative riskassessment. Additionally, some of these studies focuson older (teenage) children, and as noted in thediscussion (see prior row) of the Kim et al. (2009)study, EPA’s established childhood PbB model, theIEUBK model, does not provide estimates for olderchildren.Regarding the other non-neurological endpoints, werecognize that the evidence is unclear regarding therole of lead-induced changes in individual immunesystem, red blood cell function indicators and delayedonset to puberty in eliciting or contributing toimmunological, hematological or reproductive healthoutcomes. An improved understanding of theselinkages is needed to support quantitative riskassessment for the impact of ambient air Pb exposurein contributing to risk of outcomes related to theseendpoints.14Jedrychowski et al. (2008), Nigg et al. (2008), and Wanget al. (2008) will be included in the second draft ISA.2-28Limitation/Uncertainty in RiskModelInformation Newly Available in thisReviewConsideration of Potential Utility and Impact onQuantitative Exposure/Risk Assessmentoutcomes. The recent studies include: anNHANES analysis (Fadrowski et al., 2010),which reports associations between PbB and akidney function indicator in adolescents aged12-20 years; some studies reporting Pbassociated changes in specific immune systemindicators in child populations ranging in agefrom 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) withallergic sensitization in young children(Jedrychowski et al., 2011); a study reportingan association of low cord PbB levels withdecreased calcium-magnesium ATPaseactivity in newborn red blood cells (Huel etal., 2008); and, two studies reporting anassociation of childhood PbB with delayedonset of puberty (e.g., Hauser et al., 2008;Williams et al., 2010).More detailed limitations associated with applicabilityof recent non-neurological endpoint studies forquantitative risk assessmentvariously include: focus onolder children, for which there is increased uncertaintyassociated with interpretations regarding the exposureconditions contributing to the measured PbB levels andto the associated effects; focus on associations withmeasures of prenatal exposures (e.g., cord blood) forwhich we are lacking in established PbB modelingtools; and, focus on non-U.S. populations for whichcharacteristics influencing Pb uptake (e.g., diet) maydiffer from U.S. populations. Additionally,quantitative risk assessment for some of the identifiedeffects (e.g., kidney function) would require baselineincidence data the availability of which may be limitedfor the age groups studied.Estimating Risk for Other Populations/LifestagesK) Modeling endpoints for adultcohorts.The assessment for the lastreview did not quantitatively assess therisk of health endpoints that have beenassociated with PbB levels in adults inepidemiological studies primarily dueto uncertainties regarding the role ofThe draft ISA (Section 2.8.2) describes thecurrent evidence that informs characterizationof concentration-response relationships forthose health endpoints for which suchevidence is most well established. Amongadults, these relationships with blood leadlevels are increased blood pressure, mortality,Lack of information regarding the specific Pbexposures during a lifetime (time periods andmagnitudes) which contribute to the observed healthoutcomes continues to introduce substantial uncertaintyto the simulation of adult health outcomes resultingfrom changes in air Pb. This prevents us fromdeveloping concentration-response functions for2-29Limitation/Uncertainty in RiskModelInformation Newly Available in thisReviewConsideration of Potential Utility and Impact onQuantitative Exposure/Risk Assessmenthistorical exposures in eliciting thesehealth outcomes.Additionally, we are limited in ourcapabilities for simulating the impactof changes in ambient air Pb levels onadult PbB levels (or bone Pb) (seeentry “H” above).and indicators of nephrotoxicity.With regard to the evidence for concentrationresponse relationships, a number of studieshave investigated impacts at lower blood leadlevels including those less than 5 μg/dL withneurobehavioral 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 tobe associated with the interpretation of adultepidemiology studies as to the role ofhistorical exposures in eliciting the healthoutcomes observed and with regard to the roleof endogenous Pb in influencing concurrentblood or bone Pb measurements.Furthermore, ongoing research has notsubstantially reduced uncertainty related topredicting changes in PbB or bone Pbassociated with reductions in ambient air Pbrelated exposures.modeling potential adult health endpoints.The absence of biokinetic models specifically coveringadults also limits our ability to model adult healthendpoints as a component in a risk assessmentevaluating ambient air Pb. Our consideration of anyeffect estimates for adult health endpoints occurring atnon-occupational levels ofPb exposure is limited byour lack of a reliable means for estimating relationshipsbetween air-Pb levels (e.g., associated with alternatepotential standards) and PbB levels in adulthood.Further, the contribution to blood lead fromendogenous Pb (e.g., stored in bone) that can reflecthistorical Pb exposures complicates the utilization ofblood lead as a biomarker of current exposures inadults, and consequently contributes uncertainty ininterpreting epidemiological studies with regard to thePb exposures eliciting observed health outcomes.2-30 

### 2.3 KEY OBSERVATIONS AND CONCLUSIONS

Information presented in Table 2-3 reflects EP A staff assessment of the degree to which research published since the last Pb NAAQS re view (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 uncer tainty 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 assessmen t 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 revi ew. 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 consider ations. With regard to the latter, to the extent to which a de cision is made not to develop a new version of the risk model to generate new exposure and risk estimates, sta ff 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 comprehe nsive new assessment of exposure and risk

associated with air-related Pb for this review fo cuses 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 fr om estimates generated for the previous review. In this context, “substantial ly different” would mean that the degree of uncertainty is substantially reduce d, or bias is addressed, such th at 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 not ed above, in the event that a new exposure and risk assessment is not warrant, newly available ev idence may still be used to qualitatively or semi-quantitatively interpret exposur e and risk estimates generated fo r the last review, in order to enhance their potential utility in informing the current review. Key observations regarding th e 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 charact erization of ambient air Pb le vels in the context of the urban study areas, including our simulation of current and al ternative 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 th is 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 drinki ng water), we do not have updated data for improving our characterization of the degr ee of correlation between pathways in2-31 modeling total Pb exposure and risk. This mean s that, even if we were to incorporate improved data on urban soil Pb and dri nking water Pb, estimates of higher-end exposures (which are of particul ar interest in the risk asse ssment) would still be subject to uncertainty reflecting our inability to representatively characterize the degree to which pathway exposures are correlated (p articularly at higher-percentiles of exposure).

 Simulation of urban dust Pb le vels using the hybrid model: New information characterizing the cleaning efficiency of vacuuming on hard surface floors (and associated information on the size of Pb par ticles left behind) may be informative to our interpretation of the dust modeling and a ssociated urban residential risk estimates developed in the last review. However, the new data are not directly applicable in the context of updating or even quantitativel y performance-evaluati ng 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 st udies in specific locations provide insights on factors related to PbB levels in children, including detailed assessment of housing characteristics linked to indoor dus t 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 di rect use of these studies to either update elements of the risk assessment, or quantit atively 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 popu lation reflected in the risk assessment). For these reasons, while inform ation from these studies is not conducive to updating the risk model, in some instances, the information may be useful in further interpreting risk estimates genera ted 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 c ontrast, there are newe r 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 uncertain ty (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 interpreti ng risk estimates generated fo r 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 th e 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 eviden ce continues to support the association of this endpoint with the lowest blood levels studied. These findings reaffirm our emphasis on this endpoint as ri sk metric for quantifying the impact of Pb2-32 exposure on neurocognitive function in young chil dren (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 populat ions/lifestages: The newly available studies for additional endpoints in children that are r ecognized 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 cons idered in the subsequent Policy Assessment for this review. However, these stud ies do not appear to provide support for quantitative risk assessment for these endpoint s. For example, as noted in Table 2-3 above, there is uncertainty in interpreting the relationshi p of some of the immune system and red blood cell function indicators with health outcomes. Additionally, our capability for quantitatively assessing endpoi nts 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 cohor ts. Our ability to model risk of lead-induced health outcom es in older children and adults in epidemiological studies is limited by uncertainti es regarding the role of past exposures in eliciting the health outcomes associat ed with current PbB levels (as well as influencing current PbB levels). In the case of adult studies, the ro le of past exposures, which are likely higher, contributes partic ular uncertainty regarding the specific Pb exposures eliciting the observed outcomes. Th ere is also uncertain ty associated with simulation of changes in adult PbB levels (or bone Pb) resulting from reductions in exposure to Pb originally sourced from ambi ent 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 inte rpreting risk estimates generated for the previous review, there by enhancing their utility in in forming the current review. However, we do not believe that the informati on newly available in th is 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 uncer tainty 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. Notwith standing our consideratio n here of the use of newly available information in a new or updated ri sk assessment, we note the need to carefully consider the newly available information (as charac terized 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 consider ations in the Policy A ssessment for this review.3-1 

## 3 ECOLOGICAL RISK ASSESSMENT

The evaluation of information newly availa ble in this review is structured around

consideration of tw o 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 ava ilable 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 whic h the available information supports a new quantitative risk assessment likely to contribute to substantive ne w 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 pr otection 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 e ffects on soil, water, crops, vege tation, and manmade materials, “whether caused by transformation, conversion, or combination with other pollutants.” Because of the broad range of effects that must be c onsidered in the design and implementation of an assessment of exposure and risk associated with P b, we are faced with a level of complexity that is substantially greater than for similar asse ssments typically performed for other criteria pollutants. For example, unlike most other criteri a pollutants, risk associated with exposure to Pb originally released to ambient air is multimed ia 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 previ ous Pb NAAQS or under those prio r 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 ambi ent air, such as land and water disposal of wastes, leaching of solder used in water dist ribution systems into wa ter that flows through

wastewater treatment facilities and land uses such as mining. The screening-level ecological risk assessmen t 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 standard s. These findings supported similar, largely3-2 qualitative, conclusions drawn from consider ation 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 e ffects on organisms was generally extrapolated to ecosystem effects. Taken together, the Ag ency concluded that the available data and evidence, primarily qualitative, suggested the potentia l for adverse environmental impacts under

the then-current standar d. While lacking data to provide a quantitative ba sis for setting a secondary standard different from the primar y, 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 stan dard. 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 eviden ce of direct effects of Pb from ambient air under conditions meeting the then-current st andard 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 eviden ce to support a more refined understanding of the direct and indirect effects of deposited ambien t Pb on ecosystems and organisms and of the longterm behavior of deposited Pb. We focus most sp ecifically on the ability of current data sets to characterize exposure of ecosystems in the U.S. to ambient Pb being de posited under the current

standard. Critical to this focus is considerati on of the extent to which the available information improves our understanding of ecolo gical effects attributable to Pb deposited from ambient air

under conditions associated with the current standa rd in light of other sources of current and

historic Pb in the environment. We also look to any new scie ntific evidence that might be available to provide additional in sight into the responsiveness of ecosystems to changes in Pb deposition. As part of this eval uation we consider the adequacy of any new scientific evidence on critical loads that might be used in assess ing ecosystems potentially vulnerable to Pb on a scale that is large enough to provide informati on 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 expos ure 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 IS A 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 in form our consideration of the adequacy of the current standard. Key observations and conclusions drawn from th is 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 associ ated endpoints and risk metric s (Figure 3-1). This model provided a framework in which to consider the ev idence for Pb in designing the approach for the

assessment. Central to this model is the asse ssment of terrestrial a nd aquatic exposures and, specifically within the context of the NAAQS revi ew process, the portion of these exposures that

are associated with ambient air concentra tions 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 environmenta l Pb (including mining activities, contaminat ed landfills, etc.)

also contribute to Pb concentrations in environmen tal media. Of most interest in the quantitative analysis for the review were present and past em issions to air and the as sociated deposition to sensitive ecosystems. Ecologically significant pathways of exposure to air-related Pb are predominantly those involving deposition of Pb from air to other me dia (soils, surface waters, and sediments). Exposure to Pb in air has been considered a re latively less significant ecological exposure/risk pathway. Accordingly, the analysis develope d for the last review focused primarily on deposition and resulting concentrat ions in enviro nmental media. Those organisms in contact with Pb-contaminat ed 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 expos ed organisms in the environment. There is limited evidence for biomagnification of Pb in food chains, but sens itivities 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 and3-4 population levels thereby altering ecosystem proce sses. Known effects of elevated Pb exposure include changes in growth, development and reproduction, hematological effects, neurobehavioral effects, and incr eased mortality rates among some organisms. These effects, in turn, can adversely impact comm unity structure, biodiversity a nd ecosystem functions. In a general sense, changes in the functioning of ecosystems can im pact services provided by an ecosystem to human populations. 15 In planning the quantitative analysis for the la st review, staff considered the potential for developing risk metrics descrip tive of individual, popul ation, and ecosystem effects estimated to result from Pb exposures. Given data and ot her 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 us ed to develop the screening levels used in the assessment performed during the previous review. On an ecosystem scale, an approach for integrating the consid eration of exposure pathways and risk for multimedia pollutants such as Pb is represented by critical loads analyses. 16 Application of this type of approach re quires 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 cri tical 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 lo ads have not been validated for Pb” and that “[m]any of the methods neglect the speciation of Pb when estimating criti cal 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, ecol ogical services has been reco gnized as a useful tool for assessing adverse impacts to public welfare (USEPA, 2011).

16 In the 2006 AQCD, critical loads were defined as thre shold deposition rates of air pollutants that current knowledge indicates will not cause long-term adverse effect s 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 le vel of biological harm that is defined by a critical limit in the sentinel parameter for the targeted pollutant and type of ecosyste m 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 ut ility 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 m odels, and include validations of the assumptions used by the models (AQCD, p. 7-46). Accordingly, the qua ntitative assessment for the last Pb NAAQS review did not involve critical load analyses.3-6 Figure 3-1. Conceptual Model for Ecological Ri sk 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). Thre e quantitative case studies were designed to estimate the potential for ecological risks associated with exposures to Pb emitted

into ambient air in three situa tions: areas surrounding a primar y 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 iden tification and descripti on of the location as

well as consideration of literat ure 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 so il, surface water, and/or sedi ment were estimated for the three case studies from available monitoring data or modeling analysis and then compared to ecological screening benchmarks (e.g. Ecologi cal 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 at mospheric 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 concentratio n 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 Screenin g-level Assessment in the Last Review.3-9 The measures of exposure in the screening asse ssment for the last review were total Pb concentrations in soil, dissolved Pb concentratio ns 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 sc reening 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 concentratio ns 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 wi th atmospheric Pb deposition, rather than with nonair sources, such as r unoff 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 highway s, 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 estimate s of Pb associated with historical deposition.

 In the national-scale surface wa ter 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 use d. Air emissions, water discharge, and land

use data for the areas surroundi ng these locations were asse ssed to identify locations where atmospheric Pb deposition may be expect ed to contribute to potential ecological impacts. The exposure assessment focused on these locations.

The tools used for assessing th e potential for effects include d ecological screening values, derived from the Ecological Soil Screening Levels (Eco-SSLs) developed by the EPA’s Superfund program (USEPA 2003, 2005c), EPA’s r ecommended ambient water quality criteria (AWQC), and sediment screening values deve loped by MacDonald and others (2000, 2003). A hazard quotient (HQ) was calculated for various recep tors 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 calculate d 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 ecotoxici ty 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 me dia where it can contribute to ecological risks, they were severely limited in the extent to whic h they could inform an understanding of the role of atmospheric deposition under cond itions associated with the NAAQS. 19

 The ecological risk screen was limited to spec ific case study locations and other locations

for which Pb data were available. The limite d availability of U.S. locations for which

recent measurements of Pb concentrations were available even with the reliance of national databases to identify ecosystems a nd 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 s ources might have actually contributed to the Pb exposure estimates, and the extent to whic h air-attributable cont ributions represented

conditions when the then-current standard was not met.

 Additionally, the screening-le vel tools used for effects assessment (e.g., AWQC, EcoSSLs, sediment criteria) and/ or the media-specific paramete rs available for the media concentration estimates in the assessment did not accommodate a more rigorous or detailed consideration of bioavailability charac teristics influential to Pb toxicity in these media (USEPA, 2007c). The screening assessment results included seve ral locations where concentrations of Pb in soil, surface water and sedi ments exceeded screening values for these media, indicating the potential for adverse effects asso ciated 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 pr actices (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 contemporar y 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 im pacts 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 th ese cases is unknown. While it was not possible to dissect the contri butions of air Pb emissions from other sources, and it is likely that, at least for the long-operating primary smelte r, the air contribution is significant, the Pb source at that location had been in operation we ll 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 th e available evidence, were severely limited in their ability to inform quantitative conc lusions regarding the secondary standard.



### 3.2 CONSIDERATION OF NEWL Y 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 lim ited the quantitative assessment that could be developed in that review as well as conclusions that could be draw n 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 w ith 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 ne w 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 de veloping quantitative analyses that would substantively and quantitatively inform considera tion of the adequacy of the current secondary NAAQS. Further, beyond these four areas, we not e 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 cultura l 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 environmenta l factors affect the

distribution of Pb in the environment and Pb bioavailability and, accordingly, Pb-induced toxicity and associated ecol ogical risk (2006 AQCD, summarized in Section 8.7; draft ISA,

section 2.6.1. The first draft ISA discusses the current evidence re garding 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 previo us Pb AQCDs that biol ogical effects of Pb on terrestrial organisms vary with species and life stage, duration of exposure, form of Pb, and soil3-12 characteristics (draft ISA, p. 2-29). The evid ence reviewed in secti ons 7.2.3 and 7.2.4 of the

draft ISA used as the basis for the conclusion de monstrates that “many f actors, including species and various soil physiochemical properties, inter act strongly with Pb c oncentration to modify those effects” (ISA, p. 2-30). Newly available evidence on Pb bioavailabil ity from sediments and soils to aquatic and terrestrial vegetation, resp ectively, indicates Pb to be relativ ely more bioavailable in sediment than in soil (draft ISA, 7.3.10.2). Currently availa ble models for predicting bioavailability in aquatic systems focus on acute toxicity and do not consider all possible r outes 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 spec ies sensitivity to Pb, and many environmental variables (e.g., pH, organic matter) determine the bi oavailability 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, informati on 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 comp lexities associated with the movement of Pb in those systems, particularly vertical transp ort 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 insi ghts 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 transpor t 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, secti on 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). Additiona lly, 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 informati on on the movement of Pb among ecosystem compartments, the draft ISA concludes that despit e our increasing knowledge there is a lack of3-13 information not only on bioavailabil ity, as affected by the specific characteristics of the receiving ecosystem, but also on the kinetics of Pb di stribution 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 at tributable to atmospheric sources.



### 3.2.3 Relative Roles of Atmospheric Depo sition 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 ma tter, 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 1 st draft ISA (2011a) reviews the sour ces 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 larges t 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. Nationa l 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 agri culture and industry. A clear

decline in Pb concentrations in sediments afte r the discontinued use of leaded on-road gasoline

was observed in sediment cores at almost all WACAP locations. Althoug h, Pb was measured in snow, water, sediment, lichen and fish during th e 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 ev idence, the draft ISA concludes that there is

“limited evidence to relate ambient air concentr ations of Pb to levels of deposition onto terrestrial and aquatic ecosystems and subseque nt movement of atmospherically-deposited Pb though environmental compartments (e.g., soil, se diment, water, biota),” and the relative contribution from atmospheric versus other sources in studies reporting on Pb accumulation in biota is usually not known (dra ft 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 fo r both terrestrial and aquatic systems available at the time of the la st review (AQCD, 2006) did not account for Pb bioavailability within the system, fluxes with in systems, or focused solely on atmospheric3-14 deposition, ignoring other contributions. This was considered a main limita tion 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, “sin ce the 2006 Pb AQCD there is no new significant information on critical loads of Pb in aqua tic systems” (draft ISA, p. 7- 112).

Since the last review our unde rstanding of how CL can be used in the context of the NAAQS review process has improved. A CL mo del was utilized in the recently completed review of the Secondary National Ambient Air Qu ality Standards for Oxides of Nitrogen and Oxides of Sulfur (US EPA 2008, 2009, 2011c) and th e overall approach was reviewed favorably by the CASAC committee. As noted above, that a ssessment was based on the well-established state-of-knowledge and location-specific data, de veloped over the past four decades, on nitrogen and sulfur deposition and their ro le on ecosystem acidification in the U.S., with resulting impacts to various ecosystem services. Thus, while since th e last review we have gained experience with critical loads modeling, and in the case of Pb our understandi ng 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 ade quately 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 (Sec tion 7.2.7), did include fluxes of Pb within a system, one area previously considered a limitation in the mode l, 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 bioavail ability, speciation, sources and fluxes at a local scale, which could be applie d in a large-scale assess ment 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 draf t ISA describes evidence that expands our knowledge of the movement and potential adve rse 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 th e development of exposure-re sponse 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 asse ss 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 n ecessary components (f lux, 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 affecti ng the disposition and toxicity of Pb in the environment, the information and methods to su pport a quantitative assess ment of the role of atmospheric Pb in the U.S are limited. Specific constraints include the limited availability of location-specific data describi ng a range of U.S. ecosystems a nd their pertinent environmental characteristics. These data gaps and areas of uncertainty in the curren t evidence restrict our ability to assess quantitatively the relationship be tween concentrations of Pb in ambient air and terrestrial and/or aquatic system s, 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 avai lable regarding areas that are critical to developing quantitative estimates of ecosystem risk a ssociated 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 de veloping 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 

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