# Policy Assessment for the Review of the Lead National Ambient Air Quality StandardsThis page is intentionally blank.EPA-452/R-14-001 May 2014



## Policy Assessment for the Review of the Lead National Ambient Air Quality Standards

U.S. Environmental Protection Agency Office of Air Quality Planning and Standards Health and Environmental Impacts Division Research Triangle Park, North CarolinaDISCLAIMER

This document has been reviewed by the Office of Air Quality Planning and Standards (OAQPS), U.S. Environmental Protection Agency (EPA), and approved for publication. This OAQPS Policy Assessment contains conclusions of the staff of the OAQPS and does not necessarily reflect the views of the Agency. Mention of trade names or commercial products is
not intended to constitute endorse ment or recommendation for use.ACKNOWLEDGMENTS

This Policy Assessment is the product of the Office of Air Quality Planning and Standards. It has been developed as part of the Environmental Protection Agency’s (EPA) ongoing review of the national am bient air quality standards ( NAAQS) for lead (Pb). The Pb NAAQS review team has been led by Dr. Deirdr e Murphy. For the chapte r on the health effects evidence and exposure/risk information, the prin cipal authors include Dr. Deirdre Murphy and Dr. Zach Pekar, and Dr. Murphy served as the pr incipal author for the ch apter on the primary Pb standard. For the chapters on welfare effects evidence and exposure/risk information and the secondary Pb standard, the principal author is Ms. Ginger Tennant. The principal author on the section discussing ambient air monitoring is Mr . Kevin Cavender. Cont ributors of emissions information and air quality analyses are Mr. Marc Houyoux, Mr. Josh Drukenbrod, Dr. Halil
Cakir and Mr. Mark Schmidt. Staff from othe r EPA offices, including the Office of Research and Development and the Office of General Coun sel, also provided valuable comments and
contributions.This page is intentionally blanki 

### TABLE OF CONTENTS

List of Figures ...............................................................................................................

................ iv

List of Tables ................................................................................................................

................. v
EXECUTIVE SUMMARY .................................................................................................... ES-1

1 INTRODUCTION................................................................................................................ 1- 1

1.1 PURPOSE .................................................................................................................... 1- 1
1.2 BACKGROUND ......................................................................................................... 1-3
1.2.1 Legislative Requirements ..................................................................................... 1-3 1.2.2 History of Lead NAAQS Reviews ....................................................................... 1-5 1.2.3 Current Lead NAAQS Review ............................................................................. 1-7 1.2.4 Related Lead Control Programs ........................................................................... 1-9
1.3 SCOPE OF CURRENT REVIEW: FA TE AND MULTIMEDIA PATHWAYS OF AMBIENT AIR LEAD ........................................................................................ 1-14
1.3.1 Environmental Distribution and Exposure Pathways......................................... 1-14 1.3.1.1 Human Exposure Pathways ....................................................................... 1-16 1.3.1.2 Ecosystem Exposure Pathways ................................................................. 1-18 1.3.2 Considerations Related to Historically Emitted Lead ........................................ 1-18
1.4 GENERAL ORGANIZATION OF THE DOCUMENT ........................................... 1-20
1.5 REFERENCES .......................................................................................................... 1-21

2 AMBIENT AIR LEAD ........................................................................................................ 2-1

2.1 SOURCES AND EMISSIONS TO AMBIENT AIR .................................................. 2-1
2.1.1 Temporal Trends on a National Scale .................................................................. 2-2 2.1.2 Sources and Emissions on National Scale - 2008 ................................................ 2-3 2.1.2.1 Stationary Sources ....................................................................................... 2-5 2.1.2.2 Mobile Sources ............................................................................................ 2-6 2.1.2.3 Natural Sources and Long-range Transport ................................................ 2-7 2.1.2.4 Previously Deposited Lead.......................................................................... 2-7 2.1.3 Sources and Emissions on Local Scale ................................................................ 2-9
2.2 AMBIENT AIR QUALITY ....................................................................................... 2-12
2.2.1 Air Monitoring ................................................................................................... 2-12 2.2.1.1 Lead NAAQS Surveillance Network ........................................................ 2-12 2.2.1.2 Other Lead Monitoring Networks ............................................................. 2-16 2.2.1.3 NAAQS Surveillance Monitoring Considerations .................................... 2-19 2.2.1.3.1 Sampling Considerations .................................................................... 2-19 2.2.1.3.2 Analysis Considerations ..................................................................... 2-21 2.2.1.3.3 Network Design Considerations ......................................................... 2-21 2.2.2 Ambient Concentrations ..................................................................................... 2-24 2.2.2.1 Temporal Trends ....................................................................................... 2-24 2.2.2.2 Current Concentrations ............................................................................. 2-26
2.3 AMBIENT AIR LEAD IN OTHER MEDIA ............................................................ 2-32
2.3.1 Atmospheric Deposition ..................................................................................... 2-32ii 2.3.2 Terrestrial Media ................................................................................................ 2-34 2.3.2.1 Indoor Household Dust ............................................................................. 2-34 2.3.2.2 Outdoor Dust in Areas of Human Activity ............................................... 2-35 2.3.2.3 Soil ............................................................................................................ 2-36 2.3.2.4 Biota .......................................................................................................... 2-38 2.3.3 Aquatic Media .................................................................................................... 2-39 2.3.3.1 Surface Waters .......................................................................................... 2-39 2.3.3.2 Sediments .................................................................................................. 2-40
2.3.3.3 Biota .......................................................................................................... 2-42
2.4 REFERENCES .......................................................................................................... 2-42

3 HEALTH EFFECTS AND EXPOSURE/RISK INFORMATION ................................. 3-1

3.1 INTERNAL DISPOSITION AND BIOMARKERS OF EXPOSURE AND DOSE .. 3-1
3.2 NATURE OF EFFECTS............................................................................................ 3-15
3.3 PUBLIC HEALTH IMPLICATIONS AND AT-RISK POPULATIONS ................ 3-29
3.4 EXPOSURE AND RISK ........................................................................................... 3-38
3.4.1 Conceptual Model for Air-Related Lead Exposure and Risk ............................ 3-39 3.4.2 Case Studies ....................................................................................................... 3-42 3.4.3 Analysis Approach ............................................................................................. 3-43 3.4.3.1 Estimating Exposure ................................................................................. 3-46 3.4.3.2 Air Quality Scenarios Include d in 2007 Assessment ................................ 3-49 3.4.3.3 Methods for Deriving Risk Estimates ....................................................... 3-51 3.4.3.3.1 Full Risk Model in 2007 REA .............................................................. 3-52 3.4.3.3.2 Air Quality Scenarios Re flecting the Current Standard ........................ 3-55 3.4.4 Challenges in Characterizing Air- related Exposure and Risk ............................ 3-56 3.4.5 Risk Estimates .................................................................................................... 3-58 3.4.6 Treatment of Variability ..................................................................................... 3-63 3.4.7 Characterizing Uncertainty ................................................................................ 3-64 3.4.8 Updated Interpretation of Risk Estimates .......................................................... 3-67
3.5 REFERENCES .......................................................................................................... 3-68

4 REVIEW OF THE PRIMARY ST ANDARD FOR LEAD .............................................. 4-1

4.1 APPROACH ................................................................................................................ 4-1
4.1.1 Approach Used in the Last Review ...................................................................... 4-2 4.1.1.1 Approach Regarding the Need for Revision ............................................... 4-3 4.1.1.2 Approach Regarding Elements of Revised Standard .................................. 4-5
4.1.2 Approach for the Current Review ...................................................................... 4-11
4.2 ADEQUACY OF THE CURRENT STANDARD .................................................... 4-14
4.2.1 Evidence-based Considerations .......................................................................... 4-14 4.2.2 Exposure/Risk-based Considerations ................................................................. 4-22 4.2.3 CASAC Advice .................................................................................................. 4-26
4.3 STAFF CONCLUSIONS ON THE PRIMARY STANDARD ................................. 4-28
4.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND DATA COLLECTION .............................................................................................. 4-36 4.5 REFERENCES .......................................................................................................... 4-39iii 5 WELFARE EFFECTS AND EXPOSURE/RISK INFORMATION ............................. 5-1

5.1 WELFARE EFFECTS INFORMATION ................................................................... 5-1
5.2 EXPOSURE AND RISK INFORMATION ............................................................. 5-16
5.2.1 Screening Assessment from Last Review ......................................................... 5-17 5.2.2 Screening Assessment Results and Interpretation ............................................. 5-20
5.3 REFERENCES .......................................................................................................... 5-25

6 REVIEW OF THE SECONDARY STANDARD FOR LEAD ....................................... 6-1

6.1 APPROACH ............................................................................................................... 6-1
6.1.1 Approach Used in the Last Review ..................................................................... 6-2 6.1.2 Approach for the Current Review ....................................................................... 6-3

6.2 ADEQUACY OF THE CURRENT STANDARD ..................................................... 6-5
6.2.1 Evidence-based Considerations ........................................................................... 6-5 6.2.2 Exposure/Risk-based Considerations .................................................................. 6-9 6.2.3 CASAC Advice ................................................................................................. 6-11

6.3 STAFF CONCLUSIONS ON THE SECONDARY
STANDARD ............................................................................................................. 6-12

6.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND
DATA COLLECTION ............................................................................................. 6-13

6.5 REFERENCES ......................................................................................................... 6-15

CHAPTER APPENDICES Appendix 2A. The 2008 NEI: Data Sour ces, Limitations and Confidence ........................... 2A-1 Appendix 2B. Recent Regulatory Actions on Stationary Sources of Lead ............................ 2B-1 Appendix 2C. Criteria for Air Quality Data Analysis ............................................................ 2C-1 Appendix 2D. Air Quality Data Analysis Summary .............................................................. 2D-1 Appendix 3A. Interpolated Risk Estimates for the Generalized (Local) Urban Case Study .. 3A-1 Appendix 5A. Additional Detail on 2006 Ec ological Screening Assessment ........................ 5A-1

ATTACHMENT Clean Air Scientific Advisory Committee Letter (June 4, 2013)iv LIST OF FIGURES

Figure 1-1. Pathways of human and ecosystem exposur e to lead from ambient air. .............. 1-16 Figure 2-1. Temporal trend in U.S. air emissions of Pb: 1970-2008. ....................................... 2-3 Figure 2-2. Geographic distribution of faciliti es and airports estimated to emit at least 0.50 tpy of Pb in 2008. ......................................................................................... 2-11 Figure 2-3. Map of Pb-TSP monitoring sites in curre nt Pb NAAQS monitoring network. .... 2-15 Figure 2-4. S ites near airports for which one year of Pb-TSP monitoring is required. ........... 2-16 Figure 2-5. Pb-PM 10 monitoring sites. .................................................................................... 2-17 Figure 2-6. Pb-PM 2.5 monitoring sites in CSN and IMPROVE networks (2012). ................. 2-19 Figure 2-7. Temporal trend in Pb -TSP concen trations: 1980-2010 (31 sites). ...................... 2-24 Figure 2-8. Temporal trend in Pb-TSP concentr ations: 2000-2012 (50 sites). ....................... 2-25 Figure 2-9. Airborne Pb -TSP concentrations (3-m onth average) at fi ve sites near roadways: 1979-2010. ......................................................................................... 2-26 Figure 2-10. Pb-TSP maximum 3-mont h means (215 sites), 2010-2012. ................................ 2-27 Figure 2-11. Distribution of maximum 3-mont h mean concentrations of Pb-TSP, Pb-PM 10 and Pb-PM 2.5 at different site types, 2010-2012. ................................................. 2-29 Figure 2-12. Distribution of annual m ean concentrations of Pb-TSP, Pb-PM 10 and Pb-PM 2.5 at different site types, 2010-2012. ........................................................................ 2-30 Figure 2-13. Distribution of maximum monthly mean concentrations of Pb-TSP, Pb-PM 10 and Pb-PM 2.5 at different site types, 2010-2012. ................................................. 2-31 Figure 2-14. Temporal trend in sediment Pb c oncentration from core sa mples in 12 lakes at eight National Parks or Preserves. ........................................................................ 2-41 Figure 3-1. Temporal trend in mean blood Pb levels for NHANES cohorts. ........................... 3-4 Figure 3-2. Human exposure pathways for air-related Pb. ..................................................... 3-40 Figure 3-3. Overview of analysis approach. ........................................................................... 3-45 Figure 3-4. Comparison of four concentra tion-response functions used in risk assessment. . 3-53 Figure 3-5. Parsing of air-related risk estimates. .................................................................... 3-57 Figure 4-1. Overview of approach for review of current primary standard. ........................... 4-13 Figure 5-1. Analytical approach for screening-level ecological risk assessment in the last review (2006 REA, Exhibit 2-6) .......................................................................... 5-19 Figure 6-1. Overview of approach for review of current secondary standard. ......................... 6-4v LIST OF TABLES

Table 2-1. U.S. Pb emissions by source categories es timated to emit at least 4 tpy. ............... 2-4 Table 2-2. Facilities estimated to emit at least 0.50 tpy of Pb in 2008. .................................. 2-10 Table 2-3. Dry deposition of Pb in large metropolitan areas. ................................................. 2-36

Table 3-1. Empirically derived air-to-blood ratios fo r populations inclusive of children. ..... 3-13 Table 3-2. Associations with neurocognitive function measures in analyses with child study group blood Pb levels <5 μg/dL. ................................................................. 3-23 Table 3-3. Summary of quantitative rela tionships of IQ and blood Pb for analyses with blood Pb levels closest to those of young children in the U.S. today. ................... 3-29 Table 3-4. Number of children aged 5 and under in areas of elevated ambient air Pb concentrations relative to the NAAQS. ................................................................. 3-37 Table 3-5. Population size near larger sour ces of Pb emissions. ............................................ 3-38 Table 3-6. Types of population exposures assessed. .............................................................. 3-43 Table 3-7. Summary of approaches used to estima te case study media concentrations. ........ 3-47 Table 3-8. Air quality scenarios assessed. .............................................................................. 3-51 Table 3-9. Comparison of total and incremental IQ loss estimates for blood Pb below 10 μg/dL based on the four concen tration-response functions. ............................. 3-53 Table 3-10. Estimates of air-related risk fr om 2007 risk assessment. ...................................... 3-60 Table 3-11. Estimates of air-related risk for th e generalized (local) urban case study, including interpolated estima tes for current standard. .......................................... 3-61This page is intentionally blankES-1 

### EXECUTIVE SUMMARY

This Policy Assessment (PA) has been prepar ed by staff in the Environmental Protection Agency’s (EPA) Office of Air Quality Planning a nd Standards (OAQPS) as part of the Agency’s ongoing review of the primary (health-based) and secondary (welfare-based) national ambient air quality standards (NAAQS) for lead (Pb). It pres ents analyses and sta ff conclusions regarding the policy implications of the key sc ientific and technical information that informs this review. The PA is intended to “bridge th e gap” between the relevant sc ientific evidence and technical information and the judgments required of the EPA Administrator in determining whether to
retain or revise the current standa rds. Development of the PA is al so intended to facilitate advice
and recommendations on the standards to the Ad ministrator from an independent scientific review committee, the Clean Air Scientific A dvisory Committee (CASAC), as provided for in the Clean Air Act (CAA). Staff analyses in this PA are based on the scientific assessment presented in the Integrated Science Assessment for Lead (ISA) prepared for this re view by the EPA’s Office of Research and Development (ORD) as well as scien tific and technical assessments from prior Pb NAAQS reviews. Such assessments include quan titative human health a nd ecological risk and exposure assessments (REAs) developed in the la st review as new health and ecological REAs
were not warranted based on staff’s and CASAC’s consideration of the evidence newly available in this review with regard to risk and exposur e assessment. For the purpose of review of the NAAQS in considering the scientific evidence a nd other technical informa tion available in this review, emphasis is given to consideration of th e extent to which the evidence newly available
since the last review alters conclu sions drawn in the last review w ith regard to health and welfare effects of Pb, the exposure levels at which they occur and the a ssociated at-risk populations and ecological receptors or ecosystems. The overarching questions in this review, as in all NAAQS reviews, regard the support provided by the currently availabl e scientific evidence and exposure/risk-based information for the adequacy of the current standards and the extent to which the scientific evidence and technical information provides supp ort for concluding that consider ation of alternative standards may be appropriate. The analyses presented in th is PA to address such questions lead to staff conclusions that it is appropria te to consider retaining the current primary and secondary standards without revision; accordingly, no potential alternative standards have been identified by staff for consideration in this review. Comments and recommendations from CASAC, and public comments, based on review of the draft PA, have informed staff conclusions and the presentation of information in this final document.ES-2 Current Lead NAAQS and Scope of Review
The NAAQS for Pb was initially set in 1978. Review of the 1978 NAAQS for Pb, completed in October 2008, resulted in substant ial revision based on the large body of evidence accumulated over the intervening three decades. In terms of the basic elements of the NAAQS,
the level of the primary standard was lowered by an order of magnitude from 1.5 μg/m 3 to 0.15 μg/m 3 and the averaging time was revised to a rolling three-m onth period (from a period based on calendar quarters) with a maximum (not-to-be exceeded) form , evaluated over a 3-year period. The indicator of Pb in total suspended particles (Pb-TSP) was retained, reflecting the evidence that Pb particles of all sizes pose health risks. The s econdary standard was revised to be identical in all respects to the revised primary standard. The multimedia and persistent nature of Pb c ontributes complexities to the review of the Pb NAAQS unlike issues addressed in other NAAQS reviews. Air-related Pb distributes from air to other media, including i ndoor and outdoor dusts, soil, food, drinking water, as well as surface water and sediments. As a result, revi ew of the Pb NAAQS considers the protection provided against the health and environmental e ffects of air-related Pb associated both with exposures to Pb in ambient air and with exposures to Pb that makes its way from ambient air into other media. Additional complexity derives from the recognition that exposure to Pb also results from nonair sources, including Pb in paint, tap wa ter affected by plumbing containing Pb, leadtainted products, as well as surface water discharg es and runoff from industrial sites. Such nonair sources contribute to the total burden of Pb in the human body and in the environment, making it much more difficult to assess independently the health and welfare effects attributable to air-related Pb that are the focus of the NAAQS. Further, the persistence of Pb in the human body and the environment is another important cons ideration in assessing the adequacy of the current Pb standards. In so doing, staff is mi ndful of the history of the greater and more widespread atmospheric emissions that occurred in previous y ears (e.g., under the previous Pb standard, and prior to establishmen t of any Pb NAAQS) and that cont ributed to the Pb that exists in human populations and ecosystems today. Like wise, staff also recogni zes the role of nonair sources of Pb, now and in the past, that also cont ribute to the Pb that ex ists in human populations and ecosystems today. As in the last Pb NAAQS review, this backdrop of environmental Pb exposure, and its impact on the populations and ecosystems which may be the subjects of the currently available scientific evidence, complicat es our consideration of the health and welfare protection afforded by the current NAAQS.ES-3 Characterization of Ambient Air Lead

Emissions to ambient air and associated air Pb concentrations have declined substantially over the past several decades. The most dramatic reductions in Pb emissions occurred prior to 1990 in the transportation sector due to the removal of Pb from gasoline. Lead emissions were further reduced substantially between 1990 and 2008, with significant reductions occurring in the metals industries at least in pa rt as a result of national emissions standards for hazardous air pollutants issued under Section 112 of the CAA. Additional reductions in stationary source emissions are also anticipated from further regulations which have been promulgated since 2008
under Section 112 of the CAA. As at the time of the last review, the major ity of Pb emissions nationally is associated
with combustion of leaded avia tion gasoline by piston-driven airc raft. The largest sources on a local scale are generally associated with metals in dustries. As a result of revisions to monitoring regulations stemming from the la st Pb NAAQS review, Pb NAAQS monitors are required near the largest Pb emissions sources, as well as at sites distant from such s ources in large population areas. Ambient air Pb monitoring data available t hus far from this expanded network continue to illustrate the source-related aspect of airborne Pb, with highest concentrations near large sources
and lowest in areas removed from sources. In addition, Pb monitoring data are also being collected over at least a one-year period near a set of airports iden tified as most likely to have
elevated Pb concentrations due to leaded aviatio n gasoline usage. These data will improve our understanding of Pb concentrations in ambient air near airports and condit ions influencing these
concentrations. These data will also inform EPA’s ongoing investigation into Pb emissions from piston-engine aircraft under S ection 231 of the CAA, separate from this Pb NAAQS review. Lead occurs in ambient air in particulate form and, with characteristics and spatial patterns influenced by a number of factors, depo sits from air to surfaces in natural and humanmade environments. By this deposition process and subsequent transfer processes, ambient air Pb is distributed into multiple human exposure pathways and environmental media in aquatic and terrestrial ecosystems. In areas remove d from large air emissi ons sources, currently
available information on Pb concentrations in nonair media includes numerous examples of
declines in surface concentrations reflective of the reductions in deposition over the past several decades. In areas near large ai r sources where emissions reductions have occurred, only very limited information is available, such as for re ductions in air and surf ace dust concentrations,
with even less information available on trends for other media such as surface soils.ES-4 Health Effects and Review of the Primary Standard Lead has long been recognized to exert an array of deleterious effects on multiple organ systems as described in the ISA for this review a nd consistent with conclusions of prior scientific
assessments. Over the three decades from the tim e the standard was initially set in 1978 through its revision with the NAAQS review comp leted in 2008, the evidence base expanded considerably in a number of areas, including with regard to effects on ne urocognitive function in young children at increasingly lower blood Pb levels. These effects formed the primary basis for the 2008 revisions to the primary standard. The current standard was set most specifically to provide appropriate public health protection from the effects of air-rel ated Pb on cognitive function (e.g., IQ loss) in young ch ildren. In so doing, the standa rd was judged to provide the requisite public health protection from the full array of health eff ects of Pb, consistent with the CAA requirement that the primary standard, in the judgment of the Administrator, based on the latest scientific knowledge, be re quisite to protect pub lic health with an adequate margin of safety. The health effects evidence newly available in this review, as critically assessed in the ISA in conjunction with the full body of evidence, reaffirms conclusions on the broad array of effects recognized for Pb in the last review. Furt her, staff observes the ge neral consistency of the
current evidence with the evidence available in th e last review, particularly with regard to key aspects of the evidence on which the current stan dard is based. These ke y aspects include those regarding the relationships between air Pb concen trations and the associated Pb in the blood of young children (i.e., air-to-blood ratios) as well as between total blood Pb levels and effects on neurocognitive function (i.e., concentration-resp onse (C-R) functions for IQ loss). Factors characterizing these two relationshi ps are the key inputs to the fr amework developed in the last
review to translate the available evidence into a basis for considering a primary Pb standard that would be requisite to protect agai nst this and other Pb-related hea lth endpoints. This framework is again considered in light of the currently available evidence. This Pb NAAQS review, like any NAAQS review, requires public health pol icy judgments. The public health policy judgments for this review include the public heal th significance of a give n magnitude of IQ loss in a small subset of highly exposed children (i.e ., those likely to e xperience air-related Pb exposures at the level of the standard), as well as how to consider the nature and magnitude of the array of uncertainties that are inherent in th e evidence and in the appli cation of this specific
framework. In also considering the quantitative risk es timates associated with the current standard,
based on the risk assessment conducted in the la st review, staff observe s that these estimates
indicate a level of risk that is roughly consiste nt with and generally s upportive of conclusions
drawn from the evidence usi ng the evidence-based air-rela ted IQ loss framework. StaffES-5 additionally recognizes the complexity of the mo deling done as part of that assessment and the
substantial limitations and uncertaintie s in the resulting risk estimates. Based on the above considerations, staff concludes that the currently available information supports a primary standard as prot ective as the current standard and that it is appropriate to consider retain ing the current standard withou t revision. In so doing, staff additionally notes that the final decision on the adequacy of the current standard is largely a public health policy judgment to be made by the Administrator, draw ing upon the scientific information as well as judgments about how to co nsider the range and magn itude of uncertainties
that are inherent in the scientific evidence a nd technical analyses. In this context, staff recognizes that the uncertainties and limitations associated with the many aspects of the relationship between air Pb concen trations and blood Pb levels and associated health effects are amplified with consideration of increasingly lower air concentrati ons. In staff’s view, based on the current evidence there is appreciable uncer tainty associated with drawing conclusions regarding whether there would be reductions in blood Pb levels a nd risk to public health from alternative lower levels as compar ed to the level of the current standard. Thus, staff concludes that the basis for any considera tion of alternative lower standard levels would reflect different public health policy judgments as to the approp riate approach for weighing uncertainties in the evidence and for providing requisite protection of public health w ith an adequate margin of safety. Accordingly, and in light of the staff c onclusion that it is approp riate to consider the current standard to be adequate , this document does not identify potential alternative standards
for consideration in this review.

Welfare Effects and Review of the Secondary Standard

Consideration of the welfare effects evidence and screening-level risk information in the last review (completed in 2008) led to the c onclusion that there was a potential for adverse
welfare effects occurrin g under the then-current Pb standard (set in 1978), although there were insufficient data to provide a qua ntitative basis for set ting a secondary standard different from the primary standard. Accordingly, the secondary standard was substantially revised to be identical in all respects to the newly revised primary standard. In assessing the currently available scientif ic evidence and the exposure/risk information with regard to support for the ad equacy of the protection afforded by the current standard, staff observes the general consistency of the current evid ence with that available in the last review, including that with regard to ecological effects associated with Pb exposure and the substantial limitations in the current evidence that complicat e conclusions regarding the potential for Pb emissions under the current, much lower standard to contribute to welfare effects. Such complications include the significant difficulties in interpreting effects evidence from laboratoryES-6 studies to the natural environmen t and linking those effects to ambient air Pb concentrations. Based on staff analysis, including the above considerations, staff concludes that the currently available evidence and exposure/risk information do not call into question the adequacy of the current standard to provide the re quisite protection for public welfar e. Thus, staff concludes that consideration should be given to retaining the current standa rd, without revision, and this document does not identify poten tial alternative standards for consideration in this review.1-1 

### 1 INTRODUCTION

1.1 PURPOSE The U.S. Environmental Protection Agency (EPA) is presently conducting a review of the primary (health-based) and secondary (welfare -based) national ambient air quality standards (NAAQS) for lead (Pb). The ove rall plan and schedule for this review were presented in the Integrated Review Plan for the National Ambient Air Qualit y Standards for Lead (IRP; USEPA, 2011a). The IRP also identified key policy-relevant issu es to be addressed in this review and discussed the key documents that generally in form NAAQS reviews, including an Integrated Science Assessment (ISA), Risk and Exposure Assessments (REAs), and a Policy Assessment (PA). The PA presents a staff evaluation of th e policy implications of the key scientific and
technical information in the ISA and REAs for EPA’s consideration. 1 The PA generally provides a transparent evaluation and staff conclusi ons regarding policy cons iderations related to reaching judgments about the adequacy of the cu rrent standards and, if revision is considered, what revisions may be a ppropriate to consider. The PA is intended to help “bridge the gap” between the Agency’s scientific assessments presented in the ISA and REAs and the judgm ents required of the EPA Administrator in determining whether it is appropriate to retain or revise the NAAQS. In evaluating the adequacy of current standards and whether it is appropria te to consider alternat ive standards, the PA focuses on information that is most pertinent to evaluating the basic elements of the NAAQS: indicator, 2 averaging time, form, 3 and level. These elements, whic h together serve to define each standard, must be considered collectively in evaluating the health and welfare protection afforded by the Pb standards. The PA integrates and interprets the information from the ISA and REAs to frame policy options for considerati on by the Administrator. In so doing, the PA recognizes that the selection of a specific appr oach to reaching final decisions on primary and secondary NAAQS will reflect the judgments of the Administrator.

1 The terms “staff” and “we” throughout this document refer to staff in the EPA’s Office of Air Quality Planning and Standards (OAQPS). In past NAAQS reviews, this document was referred to as the OAQPS Staff Paper.

2 The “indicator” of a standard defines the chemical species or mixture that is to be measured in determining whether an area attains the standard. The indicator for the Pb NAAQS is lead in total suspended particles.

3 The “form” of a standard defines the air quality statistic that is to be compared to the level of the standard in determining whether an area attains the standard. For example, the form of the annual NAAQS for fine particulate matter (PM 2.5 ) is the average of annual mean PM 2.5 concentrations for three consecutive years, while the form of the 8-hour NAAQS for carbon monoxide is the second-highest 8-hour average in a year.1-2 The development of the PA is also intended to facilitate advice to the Agency and
recommendations to the Administrator from an independent scientific review committee, the Clean Air Scientific Advisory Committee (CASAC), as provided for in the Clean Air Act. As discussed below in section 1.2.1, the CASAC is to advise not only on the Agency’s assessment of the relevant scientific information, but also on the adequacy of the existing standards, and to make recommendations as to any revisions of th e standards that may be appropriate. The EPA
facilitates CASAC advice and recommendations , as well as public input and comment, by requesting CASAC review and public commen t on one or more drafts of the PA. 4 In this PA for this review of the Pb NAAQS, we consider the scientific and t echnical information available in
this review as assessed in the Integrated Science Assessment for Lead (henceforth referred to as the ISA [USEPA, 2013a]), prepared by EPA’s Na tional Center for Environmental Assessment (NCEA), and the quantitative human exposure and h ealth risk and screeni ng-level ecological risk assessments performed in the last review . As discussed below in section 1.2.3, upon
consideration of the evidence newl y available in this review with regard to risk and exposure assessment, staff concluded that new health and welfare REAs were not wa rranted. Accordingly, the quantitative risk information considered in this PA is based on the quantitative human exposure and health risk and scre ening-level ecological risk asse ssments performed in the last review (the 2007 Health Risk Assessment Report or 2007 REA [USEPA, 2007a] and the 2006 screening-level Ecologic al Risk Assessment or 2006 REA [ICF , 2006]) and is interpreted in the context of newly available evidence in this review. The evaluation and staff conclusions presented in this PA for the Pb NAAQS have been informed by comments and advice received
from CASAC in their reviews of the draft PA and of other draft Agency documents prepared in this NAAQS review. Beyond informing the EPA Administrato r and facilitating the advice and recommendations of CASAC and the public, the PA is also intended to be a useful reference to all parties interested in the Pb NAAQS review. In these roles, it is intended to serve as a single source of the most policy-relevant information that informs the Agency’s review of the Pb NAAQS, and it is written to be unde rstandable to a broad audience.

4 The decision whether to prepare on e or more drafts of the PA is influenced by preliminary staff conclusions and associated CASAC advice and public comment , among other factors. Ty pically, a second draft PA has been prepared in cases where the available information calls into question the adequacy of the current standard and analyses of potential alternative standards are deve loped taking into consideration CASAC advice and public comment. In such cases, a seco nd draft PA includes preliminary staff conclusions regarding potential alternative standards and undergoes CASAC review and public comment prior to preparation of the final PA. When such analyses are not undertaken, a second draft PA may not be warranted.1-3 1.2 BACKGROUND

1.2.1 Legislative Requirements

Two sections of the Clean Air Act (CAA or the Act) govern the establishment and revision of the NAAQS. Section 108 (42 U.S.C. section 7408) directs the Administrator to identify and list certain air pollutants and then to issue air quality criteria for those pollutants.
The Administrator is to list thos e air pollutants that in her “judgm ent, cause or contribute to air pollution which may reasonably be anticipated to endanger public health or welfare;” “the presence of which in the ambient air results fr om numerous or diverse mobile or stationary sources;” and “for which . . . [the Administrator] plans to issue air quality criteria...” Air quality
criteria are intended to “accurately reflect the la test scientific knowledge useful in indicating the kind and extent of all identifiable effects on pub lic health or welfare which may be expected from the presence of [a] pollutant in the ambien t air . . .” 42 U.S.C. § 7408(b). Section 109 (42 U.S.C. 7409) directs the Admini strator to propose and promulga te “primary” and “secondary” NAAQS for pollutants for which air quality crite ria are issued. Secti on 109(b)(1) defines a primary standard as one “the attainment and maintenance of which in the judgment of the Administrator, based on such criter ia and allowing an adequate margin of safety, are requisite to protect the public health.” 5 A secondary standard, as defined in section 109(b)(2), must “specify a level of air quality the attainment and ma intenance of which, in the judgment of the Administrator, based on such crit eria, is requisite to protect the public welfare from any known or anticipated adverse effects asso ciated with the presence of [the ] pollutant in the ambient air.” 6 The requirement that primary standards provi de an adequate margin of safety was
intended to address uncertainties associated with inconclusive scientific and technical
information available at the time of standard set ting. It was also intende d to provide a reasonable degree of protection against hazards that research has not yet identified. See Lead Industries
Association v. EPA , 647 F.2d 1130, 1154 (D.C. Cir 1980), cert. denied , 449 U.S. 1042 (1980);
American Petroleum Institute v. Costle , 665 F.2d 1176, 1186 (D.C. Cir. 1981), cert. denied , 455 U.S. 1034 (1982); American Farm Bureau Federation v. EPA, 559 F. 3d 512, 533 (D.C. Cir. 2009); Association of Battery Recyclers v. EPA , 604 F. 3d 613, 617-18 (D.C. Cir. 2010). Both kinds of uncertainties are components of the risk associated with pollution at levels below those

5 The legislative history of section 109 indicates that a primary standard is to be set at “the maximum permissible ambient air level . . . which will protect the health of any [sensitive] group of the population,” and that for this purpose “reference should be made to a repres entative sample of persons comprising the sensitive group rather than to a single person in such a group” S. Rep. No. 91-1196, 91st Cong., 2d Sess. 10 (1970).

6 Welfare effects as defined in section 302(h) (42 U.S.C. § 7602(h)) include, but are not limited to, “effects on soils, water, crops, vegetation, man-made materials, anim als, wildlife, weather, visibility and climate, damage to and deterioration of property, and hazards to transportation, as well as ef fects on economic values and on personal comfort and well-being.”1-4 at which human health effects can be said to occur with reasonable scientific certainty. Thus, in selecting primary standards that provide an adeq uate margin of safety, the Administrator is seeking not only to prevent pollution levels that ha ve been demonstrated to be harmful but also to prevent lower pollutant levels that may pose an unacceptable risk of harm, even if the risk is not precisely identified as to nature or degree. The CAA does not require the Administrator to establish a primary NAAQS at a zero-risk leve l or at background concentration levels, see Lead
Industries v. EPA , 647 F.2d at 1156 n.51, but rather at a level that reduces risk sufficiently so as to protect public health with an adequate margin of safety. In addressing the requirement for an adequate margin of safety, the EPA considers such factors as the nature and severity of the health effects involved, th e size of sensitive population(s) at risk, 7 and the kind and degree of the uncertainties that must be a ddressed. The selection of any particular approach to providing an adequate marg in of safety is a policy choice left specifically to the Administrator’s judgment. See Lead Industries Association v. EPA , 647 F.2d at 1161-62. In setting primary and secondary standards that are “requisite” to protect public health and welfare, respectively, as provi ded in section 109(b), EPA’s task is to establish standards that are neither more nor less stringe nt than necessary for these purposes. In so doing, the EPA may not consider the costs of implementing the standards. See generally, Whitman v. American Trucking Associations , 531 U.S. 457, 465-472, 475-76 (2001). Likewise, “[a]ttainability and technological feasibility are not relevant considerations in the promulgation of national ambient air quality standards.” American Petroleum Institute v. Costle , 665 F. 2d at 1185. Section 109(d)(1) requires that “not later than Decemb er 31, 1980, and at 5-year intervals thereafter, the Admini strator shall complete a thor ough review of the criteria published under section 108 and th e national ambient air quality st andards . . . and shall make
such revisions in such criteri a and standards and promulgate such new standards as may be appropriate . . . .” Section 109(d)(2) requires th at an independent scie ntific review committee “shall complete a review of th e criteria . . . and the national primary and secondary ambient air quality standards . . . and sha ll recommend to the Administrato r any new . . . standards and revisions of existing criteria and standards as ma y be appropriate . . . .” Since the early 1980s, this independent review function has been pe rformed by the Clean Air Scientific Advisory Committee (CASAC). 8

7 As used here and similarly throughout this document, the term population (or group) refers to persons having a quality or characteristic in common, such as a speci fic pre-existing illness or a speci fic age or life stage. As discussed more fully in section 3.3 below, the identifica tion of sensitive groups (called at-risk groups or at-risk populations) involves consideration of susceptibility and vulnerability.

8 Lists of CASAC members and of members of the CASAC Pb Review Pa nel are available at: http://yosemite.epa.gov/sab/sabproduct.nsf/WebCASAC/CommitteesandMembership?OpenDocument

.1-5 1.2.2 History of Lead NAAQS Reviews

Unlike pollutants such as particulate matter and carbon monoxide, ai r quality criteria had
not been issued for Pb as of the enactment of the Clean Air Act of 1970, which first set forth the requirement to set national ambient air quality st andards based on air quality criteria. In the years just after enactment of the CAA, the EPA did not intend to issue air quality criteria for Pb and accordingly had not listed Pb under Section 108 of the Act. The EPA had determined to control Pb air pollution through regulations to phas e out the use of Pb additives in gasoline and the EPA viewed those controls, and possibly additio nal federal controls, as the best approach to controlling Pb emissions (See 41 FR 14921 (April 8, 1976 ). However, the decision not to list Pb under Section 108 was challenged by environmen tal and public health groups and the U.S.
District Court for the Southern Di strict of New York concluded th at the EPA was required to list
Pb under Section 108. Natural Resources Defense Council v. EPA , 411 F. Supp. 864 21 (S.D. N.Y. 1976), aff’d , 545 F.2d 320 (2d Cir. 1978). Accordingly, on April 8, 1976, the EPA published a notice in the Federal Register that
Pb had been listed under Section 108 as a cr iteria pollutant (41 FR 14921) and on October 5, 1978, the EPA promulgated primary and secondar y NAAQS for Pb under Section 109 of the Act (43 FR 46246). Both primary and secondary standa rds were set at a level of 1.5 micrograms per cubic meter ( μ g/m 3 ), measured as Pb in total suspended particles (Pb-TSP), not to be exceeded by the maximum arithmetic mean concentrati on averaged over a calendar quarter. These standards were based on the 1977 Air Qu ality Criteria for Lead (USEPA, 1977).
The first review of the Pb standards was initiated in the mid-1980s. The scientific
assessment for that review is described in th e 1986 Air Quality Criteria for Lead (USEPA, 1986a), the associated Addendum (USEPA, 1986b) and the 1990 Supplement (USEPA, 1990a). As part of the review, the Ag ency designed and performed human exposure and health risk analyses (USEPA, 1989), the results of which were presented in a 1990 Staff Paper (USEPA, 1990b). Based on the scientific assessment and the human exposure and hea lth risk analyses, the 1990 Staff Paper presented recommendations for consideration by the Ad ministrator (USEPA, 1990b). After consideration of the documents de veloped during the review and the significantly changed circumstances since Pb was listed in 1976, the Agency did not propose any revisions to the 1978 Pb NAAQS. In a parallel effort, the Agency developed the broad, multi-program, multimedia, integrated U.S. Strategy for Reducing Lead Exposure (USEPA, 1991). As part of implementing this strategy, the Agency focused efforts primarily on regulatory and remedial clean-up actions aimed at reducing Pb exposures from a variety of nonair sources judged to pose more extensive public health ri sks to U.S. populations, as well as on actions to reduce Pb emissions to air, such as bringing more ar eas into compliance with the existing Pb NAAQS1-6 (USEPA, 1991). EPA continues this broad, multi- program, multimedia approach to reducing Pb exposures today, as describe d in section 1.2.4 below.
The last review of the Pb ai r quality criteria and standard s was initiated in November 2004 (69 FR 64926) and the Agency’s plans for preparation of the Air Quality Criteria Document and conduct of the NAAQS review we re presented in documents completed in 2005 and early 2006 (USEPAa, 2005; USEPA 2006a). 9 The schedule for completion of the review was governed by a judicial order in Missouri Coalition for the Environment v. EPA (No. 4:04CV00660 ERW, Sept. 14, 2005; and amended on April 29, 2008 and July 1, 2008), which specified a schedule for the review of duration substantially shorter than five years.
The scientific assessment for the review is described in the 2006 Air Quality Criteria for
Lead (USEPA, 2006b; henceforth referred to as the 2006 CD), multiple drafts of which received review by CASAC and the public. The EPA also conducted human exposure and health risk assessments and a pilot ecological risk assessment for the review, after consultation with CASAC and receiving public comment on a draft an alysis plan (USEPA, 2006c). Drafts of these quantitative assessments were reviewed by CASA C and the public. The pilot ecological risk assessment was released in December 2006 (ICF, 2006) and the final health risk assessment report was released in November 2007 (USEPA , 2007a). The policy assessment, based on both of these assessments, air quality analyses and key evidence from the 2006 CD, was presented in the Staff Paper (USEPA, 2007b), a draft of which also received CASAC and public review. The final Staff Paper presented OAQPS staff’s evalua tion of the public hea lth and welfare policy implications of the key studies and scientif ic information contained in the 2006 CD and presented and interpreted results from the quant itative risk/exposure anal yses conducted for this
review. Based on this evaluati on, the Staff Paper presented OAQ PS staff recommendations that the Administrator give consideration to subs tantially revising the primary and secondary standards to a range of le vels at or below 0.2 μg/m 3

. Immediately subsequent to completion of th e Staff Paper, the EPA issued an advance notice of proposed rulemaking (ANPR) that was signed by the Administrator on December 5, 2007 (72 FR 71488). 10 CASAC provided advice and recomme ndations to the Administrator with regard to the Pb NAAQS based on its review of the ANPR and the previously released final Staff Paper and risk assessment reports. The proposed decision on revisions to the Pb NAAQS was signed on May 1, 2008 and published in the Federal Register on May 20, 2008 (73 FR 29184). Members of the public provided bot h written and, at two public hear ings, oral comments and the

9 In the current review, these two documents have been combined in the IRP.

10 The ANPR was one of the features of the revised NAAQ S review process that EPA instituted in 2006. In 2009 (Jackson, 2009), this component of the process was replaced by reinstatement of a policy assessment prepared by OAQPS staff (previously termed the OAQPS Staff Paper).1-7 CASAC Pb Panel also provided advice and reco mmendations to the Administrator based on its review of the proposal notice. The final de cision on revisions to th e Pb NAAQS was signed on October 15, 2008 and published in the Federal Register on November 12, 2008 (73 FR 66964).
The November 2008 notice described EPA’s decision to revise the primary and secondary NAAQS for Pb, as discussed more fully in section 4.1.1 below. In consideration of the much-expanded health effects evidence on neur ocognitive effects of Pb in children, the EPA substantially revised the primary standard from a level of 1.5 μg/m 3 to a level of 0.15 μg/m 3

. The averaging time was revised to a rolling th ree-month period with a maximum (not-to-beexceeded) form, evaluated over a three-year pe riod. The indicator of Pb-TSP was retained, reflecting the evidence that Pb pa rticles of all sizes pose health risks. The secondary standard
was revised to be identical in all re spects to the revise d primary standards. 11 Revisions to the NAAQS were accompanied by revisions to the da ta handling procedures, the treatment of exceptional events and the ambient air monito ring and reporting requirements, as well as emissions inventory re porting requirements. 12 One aspect of the new data handling requirements
is the allowance for the use of Pb-PM 10 monitoring for Pb NAAQS attainment purposes in
certain limited circumstances at non-source-oriented sites. Su bsequent to the 2008 rulemaking,
additional revisions were made to the monitoring network requiremen ts as described in chapter 2
below.

1.2.3 Current Lead NAAQS Review

On February 26, 2010, the EPA formally initiate d its current review of the air quality criteria and standards for Pb, requesting the submission of recent scientific information on specified topics (75 FR 8934). Soon after this, the EPA held a science policy workshop to discuss the policy-relevant scie ntific information, which inform ed identification of key policy issues and questions to frame the review of the Pb NAAQS (75 FR 20843). Drawing from the workshop discussions, the EPA developed the draft IRP (USEPA, 2011b). The draft IRP was
made available in late March 2011 for consultati on with the CASAC Pb Review Panel and for public comment (76 FR 20347). This document was discussed by the Panel via a publicly accessible teleconference consultation on May 5, 2011 (76 FR 21346; Frey, 2011a). The final IRP, developed in consideration of the CASA C consultation and public comment, was released in November, 2011 (USEPA, 2011a; 76 FR 76972).

11 The current NAAQS for Pb are specified at 40 CFR 50.16.

12 The current federal regulatory measurement methods for Pb are specified in 40 CFR 50, Appendix G and 40 CFR part 53. Consideration of ambient air measurements with regard to judging attainment of the standards is specified in 40 CFR 50, Appendix R. The Pb monitoring network requirements are specified in 40 CFR 58, Appendix D, section 4.5. Guidance on the approach for implementation of the new standards was described in the Federal Register notices for the proposed and final rules (73 FR 29184; 73 FR 66964).1-8 In developing the ISA for this review, the EPA held a workshop in December 2010 to
discuss with invited scientific e xperts preliminary draft materials and released the first external
review draft of the document for CASAC re view and public comment on May 6, 2011 (USEPA, 2011c; 76 FR 26284). The CASAC Pb Review Pa nel met at a public meeting on July 20, 2011 to review the draft ISA (76 FR 36120). The CASAC provided comments in a December 9, 2011
letter to the EPA Administrato r (Frey and Samet, 2011). The s econd external review draft ISA
was released for CASAC review and public comment in February 2012 (USEPA, 2012b; 77 FR 5247) and was the subject of a public mee ting on April 10-11, 2012 (77 FR 14783). The CASAC provided comments in a July 20, 2012 letter (S amet and Frey, 2012). The third external
review draft was released fo r CASAC review and public comme nt in November 2012 (USEPA, 2012a; 77 FR 70776) and was the subject of a pu blic meeting on February 5-6, 2013 (78 FR 938). The CASAC provided comments in a June 4, 2013 letter (Frey, 2013a). The final ISA was
released in late June 2013 (USEPA, 2013a; 78 FR 38318). In June 2011, the EPA developed and re leased the REA Planning Document for consultation with CASAC and public comment (USEPA, 2011d; 76 FR 58509). This document presented a critical evaluation of the informa tion related to Pb human and ecological exposure and risk (e.g., data, modeling approaches) newl y available in this review, with a focus on
consideration of the extent to which new or substantially revise d REAs for health and ecological risk are warranted by the newly available evid ence. Evaluation of the newly available information with regard to designing and impl ementing health and ecological REAs for this review led us to conclude that the currently available information did not provide a basis for developing new quantitative risk and exposure assessments that would have substantially improved utility for informing the Agency’s cons ideration of health and welfare effects and evaluation of the adequacy of the current prim ary and secondary standa rds, respectively (REA Planning Document, sections 2.3 and 3.3, respec tively). The CASAC Pb Panel provided
consultative advice on that docum ent and its conclusions at a public meeting on July 21, 2011 (76 FR 36120; Frey, 2011b). Based on their co nsideration of the REA Planning Document analysis, the CASAC Pb Review Panel generally concurred with the conclusion that a new REA was not warranted in this review (Frey, 2011b; Fr ey, 2013b). In consideration of the conclusions reached in the REA Planning Document and CA SAC’s consultative advice, the EPA has not developed REAs for health and ecological risk for this review. Accordingly, this Policy Assessment considers the risk assessment finding s from the last review with regard to any appropriate further interpretati on in light of the evidence newl y available in this review. A draft of this Policy Assessment was re leased for public comment and review by CASAC in January 2013 (USEPA, 2013b; 77 FR 70776) and was the subject of a public meeting on February 5-6, 2013 (78 FR 938). Comments pr ovided by the CASAC in a June 4, 2013 letter1-9 (Frey, 2013b), as well as public comments received on the draft PA were considered in preparing
the final PA.

1.2.4 Related Lead Control Programs

States are primarily responsible for ensuring attainment and maintenance of the NAAQS. Under section 110 of the Act (42 U.S.C. 7410) and related provisions, states are to submit, for EPA approval, state implementation plans (SIP s) that provide for the attainment and
maintenance of such standards through control programs directed to sources of the pollutants involved. The states, in conjunc tion with EPA, also administer the prevention of significant deterioration program (42 U.S.C. 7470–7479) for th ese pollutants. In addition, federal programs provide for nationwide reductions in emissions of these and other air pollutants through the Federal Motor Vehicle Control Program under Title II of the Act (42 U.S.C. 7521–7574), which involves controls for automobile, truck, bus, moto rcycle, nonroad engine, and aircraft emissions; the new source performance standards under sect ion 111 of the Act (42 U.S.C. 7411); and the national emission standards for hazardous air pollut ants under section 112 of the Act (42 U.S.C. 7412). As noted in section 1.2.2 above, the NAAQS is only one component of EPA’s programs
to address Pb in the environment. Some recent actions expected to resu lt in air Pb emissions
reductions that are associated with other EPA programs, such as those recognized above, are more specifically recognized in section 2.1. The presentation below briefly summarizes additional ongoing activities that, although not directly pertinent to the review of the NAAQS, are associated with controlling e nvironmental Pb levels and human Pb exposures more broadly. Among those identified are EPA programs intende d to encourage exposure reduction programs
in other countries. Reducing Pb exposures has been recognized as a federal priority as environmental and public health agencies continue to grapple with soil and dust Pb leve ls from the historical use of Pb in paint and gasoline and from other sources. 13 A broad range of federal programs beyond those that focus on air pollution control provid e for nationwide reducti ons in environmental releases and human exposures. For example, pursuant to Section 1412 of the Safe Drinking Water Act (SDWA), EPA regulates lead in pub lic drinking water systems through corrosion

13 In 1991, the Secretary of the H ealth and Human Services (HHS) ch aracterized Pb poisoning as the “number one environmental threat to the health of children in the United States” (Alliance to End Childhood Lead Poisoning. 1991). In 1997, President Clinton created, by Executive Order 13045, the President’s Task Force on Environmental Health Risks and Safety Risks to Children in response to increased awareness that children face disproportionate risks from environmental health and safety hazards (62 FR 19885 ). By Executive Orders issued in October 2001 and April 2003, President Bush extended the work for the Task Force beyond its original charter (66 FR 52013 and 68 FR 19931). Reducing Pb poisoning in children was identified as the Task Force’s top priority.1-10 control and other utility actions which work together to minimize lead levels at the tap. (40 CFR 141.80-141.91). In addition, under Secti on 1417 of the Safe Drinking Water Act, pipes, fittings and fixtures for potable water ap plications may not be used or introduced into commerce unless they are considered “lead free” as defined by that Act (40 CFR 141.43). 14 Additionally, federal Pb abatement programs provide for the reduction in human exposures and environmental releases from in-place materials containing Pb (e.g., Pb-based paint, urban soil and dust, and contaminated waste sites). Federal regulations on disposal of Pb-based pain t waste help facilitate the removal of Pb-based paint from residences (68 FR 36487). Federal programs to reduce exposure to Pb in paint, dust, and soil are specified under the comprehensive federal regulatory framework deve loped under the Residen tial Lead-Based Paint Hazard Reduction Act (Title X). Under Title X (c odified as Title IV of the Toxic Substances Control Act [TSCA]), EPA has es tablished regulations and associ ated programs in the following six categories: (1) training, cer tification and work practice requi rements for persons engaged in lead-based paint activities (abatement, inspecti on and risk assessment); accreditation of training providers; and authorization of state and tribal lead-based paint programs; (2) training, certification, and work practice requirements for persons engaged in home renovation, repair and painting (RRP) activities; accreditation of RRP trai ning providers; and authorization of state and tribal RRP programs; (3) ensuring that, for mo st housing constructed before 1978, information about lead-based paint and lead -based paint hazards flows from sellers to purchasers, from landlords to tenants, and from renovators to owne rs and occupants; (4) es tablishing standards for identifying dangerous levels of Pb in paint, dust and soil; (5) providing grant funding to establish and maintain state and tribal lead-based pain t programs; and, (6) providing information on Pb hazards to the public, including steps that people can take to protect themselves and their families from lead-based paint hazards. Under Title IV of TSCA, EPA es tablished standards identifying hazardous levels of Pb in residential paint, dust, and soil in 2001. This regulation supports the implementation of other regulations which deal with worker training and certification, Pb h azard disclosure in real estate transactions, Pb hazard evaluation and control in federally-owned housing prior to sale and housing receiving federal assistan ce, and U.S. Department of Housing and Urban Development grants to local jurisdictions to perform Pb hazar d control. The TSCA Title IV term "lead-based paint hazard" implemented through this regulation identifies lead-based pa int and all residential lead-containing dust and soil regardless of the so urce of Pb, which, due to their condition and

14 In 2011, revisions to this section of the Safe Dr inking Water Act lowered the amount of Pb permitted in pipes, fittings, and fixtures; the changes became effectiv e in January 2014. More information is provided in “Summary of the Reduction of Lead in Drinking Water Act and Frequently Asked Questions” at http://water.epa.gov/drink/info/lead/index.cfm)1-11 location, would result in adverse human health eff ects. One of the underlying principles of Title X is to move the focus of public and private de cision makers away from the mere presence of lead-based paint to the presence of lead-based paint hazards, for which more substantive action
should be undertaken to control exposures, especially to young children. In addition, the success of the program relies on the volun tary participation of states a nd tribes as well as counties and cities to implement the programs and on propert y owners to follow the standards and EPA's requirements. On March 31, 2008, the EPA issued a new ru le (Lead: Renovation, Repair and Painting [RRP] Program, 73 FR 21692) to protect children from lead-based paint hazards. This rule applies to compensated renovators and main tenance professionals who perform renovation, repair, or painting in housi ng and child-care facilities built prior to 1978. Among its requirements is one that requires that firms that conduct RRP activities be certified; that their employees be trained; and that they follow protective work practi ce standards. These standards prohibit certain dangerous work practices, such as open flame bur ning or torching of lead-based paint. The required work practices also incl ude posting warning signs, restricting occupants from work areas, containing work areas to prev ent dust and debris from spreading, conducting a thorough cleanup, and verifying that cleanup was effective. The rule became fully effective in April 2010. The rule also specifies procedures fo r the authorization of states, territories, and
tribes to administer and enforce these standards a nd regulations in lieu of a federal program. In announcing this rule, EPA noted that approximately 37 million homes in the United States contain some lead-based paint, and that this rule’s require ments are key components of a comprehensive effort to eliminate childhood Pb poisoning. To foster adoption of the rule’s measures, EPA has been conducting an extensiv e education and outreach campaign to promote awareness of these new requirements among both the regulated entities and the consumers who hire them. In addition, the EPA is investigati ng whether lead hazards are also created by RRP activities in public and commercial buildings, an d if appropriate, to issue RRP requirements for this class of buildings. Programs associated with the Comprehensiv e Environmental Response, Compensation, and Liability Act (CERCLA or Superfund) a nd Resource Conservation Recovery Act (RCRA) also implement abatement programs, reducing ex posures to Pb and other pollutants. For example, EPA determines and implements protectiv e levels for Pb in soil at Superfund sites and
RCRA corrective action facilities. Federal programs, including those implementing RCRA, provide for management of hazardous substances in hazardous and municipal solid waste (see, e.g., 66 FR 58258). Federal regulations concerning ba tteries in municipal solid waste facilitate1-12 the collection and recycling or proper disposal of batteries containing Pb. 15 Similarly, federal programs provide for the reduction in environmental releases of hazardous substances such as Pb in the management of wastewater ( http://www.epa.gov/owm/ ). A variety of federal nonregul atory programs also provide for reduced environmental release of Pb-containing materials by encourag ing pollution prevention, promotion of reuse and recycling, reduction of priority and toxic chemicals in products and waste, and conservation of energy and materials. These include the Resource Conservation Challenge ( http://www.epa.gov/epaosw er/osw/conserve/index.htm ), the National Waste Minimization Program ( http://www.epa.gov/epaoswer/hazwaste/minimize/leadtire.htm ), “Plug in to eCycling” (a partnership between EPA and consumer electronics manufacturers and retailers; http://www.epa.gov/epaoswer/hazwas te/recycle/electr on/crt.htm#crts ), and activities to reduce the practice of backya rd trash burning ( http://www.epa.gov/msw/backyard/pubs.htm ). In addition to the Pb control programs summarized above, EPA’s research program identifies, encourages and conducts research needed to locate and assess serious risks and to develop methods and tools to characterize and help reduce risks. For example, EPA’s Integrated Exposure Uptake Biokinetic Model for Lead in Children (IEUBK model) is widely used and accepted as a tool that informs the evaluation of site-specific data. More recently, in recognition of the need for a single model th at predicts Pb concentrations in tissues for children and adults, EPA has been developing the All Ages Lead Mo del (AALM) to provide researchers and risk assessors with a pharmacokinetic model cap able of estimating blood, tissue, and bone
concentrations of Pb based on estimates of e xposure over the lifetime of the individual (ISA, section 3.6). EPA research activities on substanc es including Pb, such as those identified here, focus on improving our characterization of health and environmental effects, exposure, and control or management of environmental releases (see http://www.epa.gov/research/ ). Other federal agencies also participate in pr ograms intended to reduc e Pb exposures. For examples programs of the Centers for Disease Control and Prevention (CDC) provide for the tracking of children’s blood Pb levels in the U.S. and provide guidan ce on levels at which medical and environmental case management activities should be implemented (CDC, 2012; ACCLPP, 2012). 16 As a result of coordinated, intensive efforts at the national, state and local levels, including those programs described abov e, blood Pb levels in all segments of the population have continued to decline from levels observed in the past. For example, blood Pb

15 See, e.g., “Implementation of the Mercury-Containing and Rechargeable Battery Management Act” http://www.epa.gov/epaoswer/haz waste/recycle/battery.pdf and “Municipal Solid Waste Generation, Recycling, and Disposal in the United States : Facts and Figures for 2005” http://www.epa.gov/epao swer/osw/conserve/re sources/msw-2005.pdf.

16 The CDC guidance on blood Pb levels is described further in section 3.1 below.1-13 levels for the general population of children 1 to 5 years of ag e have dropped to a geometric
mean level of 1.17 μ g/dL in the 2009-2010 National Health and Nutrition Examination Survey (NHANES) as compared to the geometric mean in 1999-2000 of 2.23 μg/dL and in 1988-1991 of
3.6 μ g/dL (ISA, section 3.4.1; CD, AX4-2). Simila rly, blood Pb levels in non-hispanic black, Mexican American and lower socioeconomic groups , which are generally higher than those for the general population, have also declined (ISA, section 3.4.1; Jones et al, 2009). The EPA also participates in a broad range of international programs focused on reducing environmental releases and human exposures in other countries. For example, the Partnership for Clean Fuels and Vehicles program engages governments a nd stakeholders in developing
countries to eliminate Pb in gasoline globally. 17 From 2007 to 2011, the number of countries known to still be using leaded gaso line was reduced from just over 20 to six, with three of the six also offering unleaded fuel. All six were expected to eliminate Pb from fuel in the subsequent few years (USEPA, 2011e). The U. S. EPA is a contributor to the Global Alliance to Eliminate
Lead Paint , which is a cooperative in itiative jointly led by the World Health Organization and the United Nations Environment Programme (UNEP) to focus and catalyze the efforts to achieve international goals to prevent children’s Pb expos ure from paints containing Pb and to minimize occupational exposures to Pb paint. This allia nce has the broad objective of promoting a phaseout of the manufacture and sale of paints containi ng Pb and eventually to eliminate the risks that such paints pose. The UNEP is also engaged on the problem of managing wastes containing Pb, including lead-containing batteries . The Governing Council of the UNEP, of which the U.S. is a member, has adopted decisions focused on promo ting the environmentally sound management of products, wastes and contaminated sites containi ng Pb and reducing risks to human health and the environment from Pb and cadmium throughout the life cycles of t hose substances (UNEP Governing Council, 2011, 2013). EPA is also engage d in the issue of environmental impacts of spent lead-acid batteries inte rnationally through the Commissi on for Environmental Cooperation (CEC), where the EPA Administrator along with th e cabinet-level or equivalent representatives of Mexico and Canada comprise the CEC’s senior governing body (CEC Council). 18

17 International programs in which the U.S. participat es, including those identified here, are described at several web sites: http://epa.gov/international/air/pcfv.html, http://www.unep.org/transport/pcfv/
, http://www.unep.org/hazardoussubstances/Home/tabid/19 7/hazardoussubstances/LeadCadmium/PrioritiesforAction/ GAELP/tabid/6176/Default.aspx

18 The CEC was established to support cooperation among the North American Free Trade Agreement partners to address environmental issues of continental concern, including the environmental challenges and opportunities presented by continent-wide free trade.1-14 1.3 SCOPE OF CURRENT REVIEW: FATE AND MULTIMEDIA PATHWAYS OF AMBIENT AIR LEAD

The multimedia and persistent nature of Pb c ontributes complexities to the review of the Pb NAAQS unlike issues addr essed in other NAAQS reviews. 19 As described in section 1.1, NAAQS are established to protect public health with an adequate margin of safety, and public
welfare from known or an ticipated adverse effects, from ai r pollutants (substances emitted to ambient air). Since Pb distributes from air to other media and is persistent, our review of the NAAQS for Pb considers the pr otection provided against such effects associated both with exposures to Pb in ambient air and with exposur es to Pb that makes its way into other media from ambient air. Additionally, in assessing the adequacy of protection afforded by the current NAAQS, we are mindful of the long history of greater and more widespread atmospheric emissions that occurred in prev ious years (both before and after establishment of the 1978 NAAQS) and that contributed to the Pb that ex ists in human populations and ecosystems today. Likewise, we also recognize the role of other, nona ir sources of Pb now and in the past that also
contribute to the Pb that exists in human populations and ecosystem s today. As in the last Pb NAAQS review, this backdrop of environmental Pb exposure, and its impact on the populations and ecosystems which may be th e subjects of the currently available scientific evidence, complicates our consideration of the health and welfare protection afforded by the current NAAQS. In the first section below, we summar ize the environmental pathways of human and ecosystem exposures to Pb emitted to ambient air and associated complexities. The subsequent section briefly discusses the role of historically emitted Pb in our consideration of the adequacy of the current NAAQS for Pb.

1.3.1 Environmental Distribution and Exposure Pathways

Lead emitted to ambient air is transported thr ough the air and is also distributed to other media through the process of deposition, which ma y occur in dry conditions or in association with precipitation, as summarized further in section 2.3 below (ISA, section 2.7.2). Once deposited, the fate of Pb is influenced by the type of surface onto which the particles deposit and by the type and activity level of transport processes in that location. Prec ipitation and other natural, as well as human-influen ced, processes contribute to the fate of such particles, which affects the likelihood of subseque nt human and ecological exposur es, e.g., tracking into nearby houses or transport with surface runoff into near by water bodies (ISA, sections 2.3 and 3.1). For

19 Some aspects of the review of the secondary standa rd for oxides of nitrogen and sulfur (completed in 2012), which involved consideration of pollutant transport and fate in nona ir media with a fo cus on impacts to aquatic ecosystems, have some similarity to consideratio ns for Pb, while the Pb review also differs in other important aspects.1-15 example, Pb particles deposited onto impervious surfaces, such as roadway, sidewalk or other urban surfaces, may be more available for human contact while they remain on such surfaces or are transferred to other human environments, su ch as on clothing or through resuspension and infiltration (ISA, section 3.1.1.1). Deposited Pb can also be transported (by direct deposition or stormwater runoff) to water bodies and into asso ciated sediments, which may provide a storage function for Pb in aquatic ecosystems (ISA, sections 2.3.2 and 6.2.1). Lead deposited in terrestrial ecosystems can also be incorporated into vegetation and soil matrices (ISA, sections 2.3.3 and 6.2.1). Figure 1-1 illustrates, in summary fashi on, the pathways by which Pb emitted into
ambient air can be distributed in the envir onment, contributing to human and ecosystem exposures. As shown in this figure, the multimedia distribution of Pb emitted into ambient air (air-related Pb) contributes to multiple air-related pathways of human and ecosystem exposure (ISA, sections 3.1.1 and 3.7.1). 20 Figure 1-1 additionally illustrates that air-related pathways may involve media other than air, including indoor and outdoor dust, soil, surface water and sediments, vegetation and biota. As recognized by the figure and discussed more completely in the subsections below, Pb occurring in indoor and outdoor environments that has not passed through ambient air (nonair Pb) may complicate our consideration of ambient air related Pb exposures. Further, the persistenc e of Pb and the associated envi ronmental legacy of historical releases pose an additional complication, also disc ussed below, with regard to consideration of exposures associated with current Pb emissions.

20 The exposure assessment for children performed for the review completed in 2008 employed available data and methods to develop estimates intended to inform a characterization of these pathways, as described in the rulemaking notices for that review (73 FR 29184; 73 FR 66964) and the associated heal th risk assessment report (USEPA, 2007).1-16 Figure 1-1. Pathways of human and ecosystem exposure to lead from ambient air.

1.3.1.1 Human Exposure Pathways

Air-related Pb exposure pathways for human s include inhalation of ambient air or ingestion of food, water or other materials, includ ing dust and soil, that have been contaminated through a pathway involving Pb deposition from am bient air (ISA, section 3.1.1.1). Ambient air inhalation pathways include both inhalation of ai r outdoors and inhalation of ambient air that has
infiltrated into indoor en vironments. The air-related ingestio n pathways occur as a result of Pb passing through the ambient air, be ing distributed to other envir onmental media and contributing to human exposures via contact with and ingestion of indoor and outdoor dusts, outdoor soil, food and drinking water. The various inhalation and ingestion air-relate d pathways may vary with regard to the time in which they respond to changes in air Pb concentrations. For example, human exposure pathways most di rectly involving Pb in ambient air and exchanges of ambient air with indoor air (e.g., inha lation) can respond most quick ly, while pathways involving 

### Ecosystem Exposures 

## Ambient Air

Outdoor Dust and Soil

Indoor Air, Indoor Dust Surface Waters and Sediments

Wildlife, Livestock, Crops 

### Current Pb Emissions to Ambient Air

Human Population (body burden) * Compartments marked by asterisk may also include Pb emitted to air in the past and Pb from nonair sources (released now and in the past) . Depending on the compartment, nonair sources may include wastewater releases to surface water or Pb usage in paint, drinking water dist ribution or food processing/packaging. ‐‐‐‐‐‐‐ deposition ‐‐‐‐‐‐‐ resuspension

‐ ‐‐‐ deposition

‐‐‐

Note: Arrows indicate general pathways by which Pb distributes in environment and human populations. Individual pathway significance varies with lo cation- and receptor-specific factors. 

### * * *

* * Human Exposures (Inhalation and Ingestion)1-17 exposure to Pb deposited from ambient air into the environment (e.g., diet) may be expected to respond more slowly. The extent of this will be influenced by the magnitude of change, as well as – for deposition-related pathways - the extent of prior deposition and environment characteristics influencing availability of prior deposited Pb (section 1.3.1.2 below). Lead currently occurring in nonair media ma y also derive from sources other than ambient air (nonair Pb sources), as summarized further in section 2.3 be low (ISA, section 3.7.1). For example, Pb in dust inside some houses or ou tdoors in some urban areas may derive from the common past usage of leaded paint, while Pb in drinking water may derive from the use of leaded pipe or solder in dr inking water distribution systems (ISA, section 3.1.3.3). We also recognize the history of much greater air emissions of Pb in the past , such as that associated with leaded gasoline usage and highe r industrial emissions (as summ arized in section 2.1.1 below) which have left a legacy of Pb in other (nonair) media. The relative importance of different pathways of human exposure to Pb, as well as the
relative contributions from Pb resulting from recent and historic air emissions and from nonair sources, vary across the U.S. population as a result of both extrinsic factor s, such as a home’s proximity to industrial Pb sources or its history of leaded paint us age, and intrinsic factors, such as a person’s age and nutri tional status (ISA, sections 5.1, 5.2, 5.2.1, 5.2.5 and 5.2.6). Thus, the relative contributions from specific pathways is situation specific (IS A, p. 1-11), although a predominant Pb exposure pathway for very young ch ildren is the incidental ingestion of indoor dust by hand-to-mouth activity (ISA, section 3.1. 1.1). For adults, however, diet may be the primary Pb exposure pathway (2006 CD, section 3.4) . Similarly, the relative importance of airrelated and nonair-related Pb al so varies with the relative magnitudes of exposure by those pathways, which may vary with different circumst ances. For example, relative contributions to a child’s total Pb exposure from air-related expos ure pathways compared to other (nonair) Pb exposures depend on many factors, including ambien t air concentrations and air deposition in the area where the child resides (as well as in the area from which th e child’s food derives), as well as access to other sources of Pb exposure such as Pb paint, tap water affected by plumbing containing Pb, and lead-tainted pr oducts. Studies indica te that in the absence of paint-related exposures, Pb from other sources such as n earby stationary sources of Pb emissions may dominate a child’s Pb exposures (ISA, sec tions 3.1 and 3.1.3.2; 2006 CD, section 3.2.3). In other cases, such as children living in older housi ng with peeling paint or where renovations have occurred, the dominant source of Pb exposure may be dust from leaded paint used in the house in the past. Depending on Pb levels in a home’s tap water, drinking water can sometimes be a significant source. Lead exposure may also be the result of a mixture of contributions from multiple sources, with no one source dominating. Our understanding of the relative contribution of air-related Pb to ingestion exposure pathways is limited by the paucity of studies that parse1-18 ingestion exposure pathways with regard to air- related and nonair Pb. Our understanding of the
relative contribution of ai r-related Pb associated with histor ical emissions and that from recent emissions is similarly limited, as disc ussed further in section 1.3.2 below.

1.3.1.2 Ecosystem Exposure Pathways

The distribution of Pb from ambient air to ot her environmental media also influences the exposure pathways in terrestrial and aquatic eco systems. Exposure of terrestrial animals and vegetation to air-related Pb can occur by contact with ambient air or by contact with soil, water or food items that have been contaminated by Pb from ambient air (ISA, section 6.2). Transport of Pb into aquatic systems similarly provides for exposure of biota in those systems, and exposures may vary among systems as a result of differences in sources and levels of contamination, as well as characteristics of the sy stems themselves. In addition to Pb contributed by current atmospheric deposition, Pb may occur in aquatic systems as a result of nonair sources such as industrial discharges or mine-related drainage, of historical air Pb emissions (e.g., contributing to deposition to a wa ter body or via runoff from soils ne ar historical ai r sources) or combinations of different types of sources (e.g., resuspension of sediments contaminated by urban runoff and surface water discharges). The persistence of Pb contribu tes an important temporal aspe ct to lead’s environmental pathways, and the time (or lag) associated with re alization of the impact of air Pb concentrations on concentrations in other media can vary with the media (e.g., ISA, section 6.2.2). For example, exposure pathways most directly involving Pb in ambient air or surface waters can respond more quickly to changes in ambient air Pb concentrati ons while pathways involving exposure to Pb in soil or sediments generally res pond more slowly. An additiona l influence on the response time for nonair media is the environmental presence of Pb associated with past, generally higher, air concentrations. For example, after a reduction in air Pb concentrations, the time needed for
sediment or surface soil concentrations to indi cate a response to reduced air Pb concentrations might be expected to be longer in areas of more substantial past contamination than in areas with lesser past contamination. Thus, considering the Pb concentrati ons occurring in nonair media as a result of air quality conditions that meet the current NAAQS is a complexity of this review, as it also was, although to a lesser de gree, with regard to the prior standard in the last review.

1.3.2 Considerations Related to Historically Emitted Lead

In reviews of NAAQS, the overarching consider ation of each review is first focused on the general question as to whet her the currently available info rmation supports or calls into question the adequacy of the current standard(s). In addressing that consideration for the NAAQS for Pb, our focus is on Pb emitted to am bient air under conditions meeting the current standard and its potential to cause health or welfare effects as a result of e xposures to Pb in air or1-19 in other media. Our framing of the focus in this way differs from that for NAAQS reviews involving other pollutants. We frame the focus in this way in consideration of the multiple exposure pathways for Pb currently being emitted and in consideration of the persistence of Pb in the environment over time, a characteristic which does not affect reviews of other NAAQS. In considering the case for Pb, however , we recognize that, because of its persistence, both recent
emissions to ambient air and the substantial emissions of the pa st contribute to current Pb exposures (via multiple exposure pathways, as summarized in section 1.4.1 above). And we recognize that past Pb emissions contributed to many situations where air concentrations were
well in excess of the current Pb standard, and may continue to contribute to exposures even
where air concentrations are below the current st andard. Yet our task in this and every NAAQS review is focused on assessing the ad equacy of the current standard.
The substantial historical emissions to air and releases to nonair media contributed to human and environmental exposures in th e past (e.g., 1978 CD, 1986 CD, 2006 CD, ISA). Because of the persistence of Pb, historical e xposures associated with both air-related and
nonair-related sources have contri buted a legacy of Pb that is now stored within older humans and ecosystems. For example, concentrations of Pb in the bone and blood of older members of the U.S. population, who lived during the time of widespread air emissi ons associated with leaded gasoline usage (as well as higher indus trial emissions) under the previous Pb NAAQS or prior to establishment of any Pb NAAQS, are gr eater than what would result from air quality conditions allowed by the current, more restrict ive NAAQS. Epidemiologi cal studies of these populations, in which this exposure history is represented by current bone or blood Pb concentrations, contribute to the overall evidence base regarding lead-related health effects (as discussed in chapter 3 below). Such studies of these historically e xposed populations, however, are generally less informative in judging the ad equacy of the current primary standard (as discussed in chapter 3 below). This is in c ontrast to epidemiological studies of very young populations with much shorter and mo re recent exposure histories (also discussed in chapter 3). Substantial and widespread atmospheric emissions of Pb in the U.S. (as well as releases to other media) exte nd back through the 19 th century (Yohn et al, 2004; Jackson et al., 2004; Graney et al., 1995). These histor ical emissions contributed to th e distribution of Pb within and well beyond the U.S. (ISA, section 2.5.5; Re uer and Weiss, 2002; McConnell and Edwards, 2008). Although it has not been completely and to tally characterized, mu ltiple aspects of the legacy of this widespread distribution have been documented and described. The current concentrations of Pb in U.S. ecosystems thus re flect the influence of greater air emissions that occurred in the past, under the prior Pb NAAQS and prior to establis hment of any Pb NAAQS. 21

21 The current distribution of Pb in U.S. ecosyst ems also reflects histor ical nonair releases.1-20 As described further in section 2.3 below, media in ecosystems across the U.S. are still recovering from the past period of greater at mospheric emissions and deposition that is documented in media such as soil, aquatic se diments and peat bogs (2006 CD, section 2.3.1; ISA, section 2.6.2). Core samples of these medi a show a pattern of Pb concentrations in deposited material that peaks around the 1970s follo wed by marked decline in more recent years (2006 CD, section 2.3.1; ISA section 2.6.2). Indivi dual ecosystem responses differ with regard to their rates of change in media concentrations due to the extent of cont amination in individual systems as well as the influence of ecosystem-s pecific characteristics (f urther described in section 2.3 below). Thus, the time required for these ecosystem media to come to a condition that is relatively stable with time (i.e., “steady-st ate”) will also vary, and the resulting range of “steady-state” media concentrations in U.S. ecosystems under ambient air concentrations consistent with the current NAAQS are unknown. Future research may better inform our understanding in this area. In considering the array of eco logical effects evidence in th is review, we recognize that evidence of effects pertaining to th e concentrations associated with the past, higher emissions (as well as from nonair sources), while generally info rmative to our understanding of welfare effects associated with environmental Pb, does not direc tly inform our consideration of welfare effects that might be anticipated under th e current secondary standard a nd thus may be generally less informative in judging the adequacy of the current standard. The availability of information on whether adverse effects could be anticipated from the Pb in terrestrial and aquatic ecosystems that results from air quality conditions allowe d by the current, more restrictive NAAQS is discussed in chapter 5, with c onsideration of the current NAAQS discussed in chapter 6.

1.4 GENERAL ORGANIZATION OF THE DOCUMENT Following this introductory chapter, this documen t is organized into th ree main parts: the characterization of ambient Pb; le ad-related health effects and the primary Pb NAAQS; and leadrelated welfare effects and the secondary Pb NAAQS. The characterization of ambient Pb is presented in Chapter 2 and includes information on Pb properties in ambient air, current Pb emissions and air quality patterns, historic trends, and background levels. Chapter 2 also describes the Pb NAAQS surveillance and other Pb monitoring networks. In recognition of the
multimedia nature of Pb and the distribution into other media of Pb emitted into the air, Chapter 2 also includes information on Pb in media other than air including outdoor dust, soil, surface water and sediment. This chapter provides a fr ame of reference for exposure and risk-related considerations and subsequent discussion of the Pb NAAQS. Chapters 3 and 4 comprise the second main part of this document, dealing with human health and the primary standard. These chapte rs are organized around a series of questions,1-21 building on those identified in the IRP, that address the key policy-relevant issues related to the primary standard. Chapter 3 presents an overview of key policy-relevant h ealth effects evidence and major health-related conclusions from the IS A; an examination of issues related to the quantitative assessment of health risks; key result s from quantitative assessments together with a discussion of uncertainty and va riability in the results; and di scussion of the public health implications of the evidence and exposure/r isk information. Chapter 4 includes staff’s consideration of the scientific evidence and exposure/risk information related to the primary
standard and associated conclusi ons related to the adequacy of the current primary standard. Chapters 5 and 6 comprise the third main pa rt of this document. These chapters are similarly organized around a series of questions , building on those identified in the IRP, that address the key policy-relevant i ssues related to the secondary st andard. Chapter 5 presents an
overview of welfare effects evidence related to these key policy-relevant issues and major
welfare effects-related conclusions from the IS A; an examination of issues related to the screening-level ecological risk assessment; and key results from the risk assessment together with a discussion of uncertainty and variability in the result s; and discussion of the public welfare implications of the quantitative assessment with regard to the current standard. The final chapter, chapter 6, includes staff’s conclusions re lated to the adequacy of the current secondary
standard.

1.5 REFERENCES

ACCLPP (2012) Low Level Lead Exposure Harms Children: A Renewed Call for Primary Prevention. Report of the Advisory Committee on Childhood Lead Poisoning Prevention of the Centers for Disease Control and Prevention. January 4, 2012. Available at: http://www.cdc.gov/nceh/lead/A CCLPP/blood_lead_levels.htm

CDC. (2012) CDC Response to Advisory Committee on Childhood Lead Poisoning Prevention Recommendations in “Low Level Lead Exposure Harms Children: A Re newed Call of Primary Prev ention.” Available at: http://www.cdc.gov/nceh/lead/A CCLPP/blood_lead_levels.htm

Frey, H.C. (2011a) Letter from Dr. H. Christopher Frey , Chair, Clean Air Scientif ic Advisory Committee Lead Review Panel, to Administrator Lisa P. Jackson. Re : Consultation on EPA’s Draft Integrated Review Plan for the National Ambient Air Quality Standards for Lead. May 25, 2011.

Frey, H.C. (2011b) Letter from Dr. H. Christopher Frey , Chair, Clean Air Scientif ic Advisory Committee Lead Review Panel, to Administrator Lisa P. Jackson. Re: Consultation on EPA’s Review of the National Ambient Air Quality Standards for Lead: Risk and Exposure Assessment Planning Document. October 14, 2011.

Frey, H.C. (2013a) Letter from Dr. H. Christopher Frey, Chair, Clean Air Sc ientific Advisory Committee and Clean Air Scientific Advisory Committee Lead Review Pane l, to Acting Administrator Bob Perciasepe. Re: CASAC Review of the EPA’s Integrated Science Asse ssment for Lead (Third External Review Draft – November 2012). June 4, 2013.

Frey, H.C. (2013b) Letter from Dr. H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee and Clean Air Scientific Advisory Committee Lead Review Pane l, to Acting Administrator Bob Perciasepe. Re:1-22 CASAC Review of the EPA’s Policy Assessment for Lead (External Review Draft – January 2013). June 4, 2013.

Frey, H.C. and Samet, J.M. (2011) Letter from Drs. H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee Lead Review Panel, and Jonathan M. Samet, Chair, Clean Air Scien tific Advisory Committee, to Administrator Lisa P. Jackson. Re: CASAC Re view of the EPA’s Integrat ed Science Assessment for Lead (First External Review Dr aft – May 2011). December 9, 2011.

ICF International. (2006) Lead Human Exposure and Hea lth Risk Assessments and Ec ological Risk Assessment for Selected Areas. Pilot Phase. Draft Technical Report. Prepared for the U.S. EP A's Office of Air Quality Planning and Standards, Research Triangle Park, NC. December.

Jackson, L. (2009) Memorandum from Administrator Lisa Jackson, Subject: Development of regulations and policies. September 11, 2009. Available at: http://www.epa.gov/ttn/naaqs/pdfs/N AAQSReviewProcessMemo52109.pdf

Samet, J.M. and Frey, H.C. (2012) Letter from Drs. Jona than M. Samet, Chair, Clean Air Scientific Advisory Committee and H. Christopher Frey, Ch air, Clean Air Scientific Adviso ry Committee Lead Review Panel, to Administrator Lisa P. Jackson. Re: CASAC Re view of the EPA’s Integrat ed Science Assessment for Lead (Second External Review Draft – February 2012). July 20, 2012.

UNEP Governing Council (2011) Proceed ings of the Governing Council/Globa l Ministerial Environment Forum at its twenty-sixth session. Decision number 26/3. UNEP/GC.26/19. 24 February 2011. Available at: http://www.unep.org/gc/gc26/docs/Pro ceedings/K1170817_E-GC26-19_Proceedings.pdf

UNEP Governing Council (2013) Decisions adopted by the Governing Council at its twenty-seventh session and first universal session. Decision 27/12: Chemicals and waste management. February 2013. Available at: http://www.unep.org/GC/GC27/Docs/deci sions/GC_27_decisions-English.pdf

U.S. Environmental Protection Agency. (1977) Air quality criteria for lead. Research Triangle Park, NC: Health Effects Research Laboratory, Criteria and Special Studies Office; EPA report no. EPA-600/8-77-017. Available from: NTIS, Springfield, VA; PB-280411.

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

U.S. Environmental Protection Agency. (1986b) Lead effe cts on cardiovascular functi on, early development, and stature: an addendum to U.S. EPA Air Quality Criteri a for Lead (1986). In: Air quality criteria for lead, v. 1. Research Triangle Park, NC: Office of Health an d Environmental Assessment, Environmental Criteria and Assessment Office; pp. A1-A67; EPA report no. EPA-600/8-83/028aF. Available from: NTIS, Springfield, VA; PB87-142378.

U.S. Environmental Protection Agency. (1989) Review of the national ambient air quality standards for lead: Exposure analysis methodology and validation: OAQPS staff report. Research Triangle Park, NC: Office of Air Quality Planning and Standards; report no. EPA-450/2-89/011. Available on the web: http://www.epa.gov/ttn/naaqs/standards/pb/data/rnaaqsl_eamv.pdf

U.S. Environmental Protection Agency. (1990a) Air quality criteria for lead: supplement to the 1986 addendum. Research Triangle Park, NC: Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office; report no. EPA/600/8-89/049F. Available from: NTIS, Springfield, VA; PB91-138420.

U.S. Environmental Protection Agency. (1990b) Review of the national ambient air quality standards for lead: assessment of scientific and technical information: OAQPS staff paper. Research Triangle Park, NC: Office1-23 of Air Quality Planning and Standards; report no. EPA-450/2-89/022. Available from: NTIS, Springfield, VA; PB91-206185. Available on the web: http://www.epa.gov/ttn/naaqs/standards/pb/data/rnaaqsl_asti.pdf

U.S. Environmental Protection Agency. (1991) U.S. EPA Strategy for Reducing Lead Exposure. Available from U.S. EPA Headquarters Library/Washington, D.C. (Library Code EJBD; Item Call Number: EAP 100/1991.6; OCLC Number 2346675). http://www.epa.gov/ttn/naaqs/s tandards/pb/s_pb_pr.html

U.S. Environmental Protection Agency. (2005a) Project Work Plan for Revised Air Quality Criteria for Lead. CASAC Review Draft. National Center for Enviro nmental Assessment, Research Triangle Park, NC. NCEA-R-1465. Available at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_pd.html

U.S. EPA (U.S. Environmental Protection Agency). (2005b) . All ages lead model (AALM) (Version Draft 1.05) [Computer Program]. Research Triangle Park, NC: U.S. Environmental Protection Agency, National Center for Environmental Assessment.

U.S. Environmental Protection Agency. (2006a) Plan for Re view of the National Ambient Air Quality Standards for Lead. Office of Air Quality Planning and Standard s, Research Triangle Park, NC. Available at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_pd.html

U.S. Environmental Protection Agency. (2006b) Air Quality Criteria for Lead. Washington, DC, EPA/600/R5/144aF. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr.html

U.S. Environmental Protection Agency. (2006c) Analysis Plan for Human Health and Ecological Risk Assessment for the Review of the Lead National Ambient Air Quality Standards. Office of Air Quality Planning and Standards, Research Triangle Park, NC. Available at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_pd.html

U.S. Environmental Protection Agency. (2007a) Lead: Huma n Exposure and Health Risk Assessments for Selected Case Studies, Volume I. Human Exposure and Hea lth Risk Assessments – Full-Scale and Volume II. Appendices. Office of Air Quality Planning and Stan dards, Research Triangle Park, NC. EPA-452/R-07- 014a and EPA-452/R-07-014b. http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_td.html

U.S. Environmental Protection Agency. (2007b) Review of the National Ambient Air Quality Standards for Lead: Policy Assessment of Scientific an d Technical Information, OAQPS St aff Paper. Office of Air Quality Planning and Standards, Research Triangle Park, NC. EPA-452/R-07-013. Available at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_sp.html

U.S. Environmental Protection Agency. (2011a) Integrat ed Review Plan for the National Ambient Air Quality Standards for Lead. Research Triangle, NC. EPA-452/R-11-008. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html

U.S. Environmental Protection Agency. (2011b) Integrat ed Review Plan for the National Ambient Air Quality Standards for Lead. External Review Draft. Research Triangle, NC. EP A-452/D-11-001. Available online
at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html

U.S. Environmental Protection Agency. (2011c) Integrated Science Assessment for Lead (First External Review Draft). Washington, DC, EPA/600/R-10/075A. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html

U.S. Environmental Protection Agency. (2011d) Review of the National Ambient Air Quality Standards for Lead: Risk and Exposure Assessment Planning Document. Office of Air Quality Planning and Standards, Research Triangle Park, NC. EP A/452/P-11-003. Available at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_pd.html1-24 U.S. Environmental Protection Agency. (2011e) Partnership for Clean Fuels and Vehicles: Evaluation of the Design and Implementation of the Lead Campaign. Final Report. Document number EPA-100-R-11-008. Office of Policy, Washington, DC. December 2011.

U.S. Environmental Protection Agency. (2012a) Integrated Science Assessment for Lead (Third External Review Draft). Washington, DC, EPA/600/R-10/075C. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_isa.html

U.S. Environmental Protection Agency. (2012b) Integrated Science Assessment for Lead (Second External Review Draft). Washington, DC, EPA/600/R-10/075B. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html

U.S. Environmental Protection Agency. (2013a) Integrated Science Assessment for Lead. Washington, DC, EPA/600/R-10/075F. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_isa.html

U.S. Environmental Protection Agency. (2013b) Policy Assessment for for the National Ambient Air Quality Standards for Lead. External Review Draft. Research Triangle, NC. EPA-452/P-13-001. Available online
at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_pa.html

.2-1 

### 2 AMBIENT AIR LEAD

The focus for this Pb NAAQS review is on Pb derived from sources emitting Pb to
ambient air. As noted in sect ion 1.3, air emissions contribute to concentrations in multiple environmental media, and the role of nonair media is enhanced by the persistent nature of Pb. Consequently this chapter discus ses our current unders tanding of both Pb in ambient air and of
ambient air-related Pb in other media. Lead emitted to the air is predominantly in pa rticulate form, with the particles occurring in various sizes (ISA, section 2.3). 1 Once emitted, particle-bound Pb can be transported long or short distances depending on particle size, whic h influences the amount of time spent in the aerosol phase. Consistent with previous evid ence, recent research on particulate matter with
mass median diameter of 2.5 and of 10 micrometers (PM 2.5 and PM 10 ) confirms the transport of airborne Pb in smaller particles appreciable di stances from its sources. For example, samples
collected at altitude over th e Pacific Ocean, as well as th e seasonal pattern of Pb-PM 2.5 at rural sites in the western U.S., indica te transport of Pb from sources in Asia, although such sources have been estimated to contribute less than 1 ng/m 3 to western U.S. Pb concentrations (ISA, sections 2.3.1 and 2.5.5; Murphy et al., 2007). In general, larger particles tend to deposit more quickly, within shorter distances from emissions poi nts, while smaller particles remain in aerosol phase and travel longer distan ces before depositing (ISA, sec tion 1.2.1). As summarized in section 2.2.2 below, airborne c oncentrations of Pb near sour ces are much higher, and the representation of larger particles generally greater, than atsites not directly influenced by

sources. In this chapter, we discuss the current info rmation on on sources and emissions of Pb to ambient air (section 2.1), current ambient air m onitoring methods and networks and associated measurements (section 2.2) and th e contribution of ambi ent air Pb to Pb in other media (section 2.3).

2.1 SOURCES AND EMISSIONS TO AMBIENT AIR In this section we describe the most recently available information on sources and
emissions of Pb into the ambient air. The sect ion does not provide a comprehensive list of all sources of Pb, nor does it provide estimates of emission rates or emission factors for all source categories. Rather, the discussion here is intended to identify the larger source categories, either

1 While in some circumstances Pb can be emitted in gaseous form, the Pb compounds that may be produced initially in vapor phase can be expected to condense into particles upon cooling to ambient temperature and/or upon oxidizing with mixing into the atmosphere (ISA, section 2.2.2.1; Gidney et al., 2010).2-2 on a national or local scale, and generally descri be their emissions and distribution within the
U.S. The primary data source for this discussion is the National Emissions Inventory (NEI) for
2008 2 . The NEI is a comprehensive and detailed es timate of air emissions of both criteria and hazardous air pollutants from air em issions sources. The NEI is ge nerally prepared at three-year intervals, such that the next NEI, for 2011, is cu rrently under development. The NEI is prepared by the EPA based primarily upon emission estimat es and emission model inputs provided by state, local, and tribal air agencies for sour ces in their jurisdictions, supplemented by data developed by the EPA. Some of these esti mates are required by regulation, while some are voluntarily reported. For example, states are required to report Pb emissions from facilities emitting more than 5 tons of Pb per year (tpy) and from facilities emitting greater than threshold amounts for other criteria pollutants (e.g., 100 tp y of particulate matter or volatile organic compounds; CFR 51, subpart A). Estimates of Pb emissions presented in this document (and in the ISA) are drawn from the 2008 NEI version 3. 3 As a result of various Clean Air Act requirements, emissions standards implemente d since 2008 for a number of industrial source categories represented in the NEI are projected to result in considerably lower emissions at the current time or in the near future. (Appendix 2A) The following sections present information relative to 2008 Pb emissions on a national and local scale. Lead is emitted from a wide variety of source types, some of which are small individually but for which the cumulative emissions are large, and some for which the opposite is true. For example, a source category may be composed of many sma ll (i.e., low-emitting) sources or of just a few very large (high-emitting) sources. Temporal trends in the national totals of Pb emissions are presented in Section 2.1.1. Information about the emissions source types or categories that are la rge on a national scale as of 2008 is presented in Section 2.1.2, while information on the sources that are large at th e local scale is presen ted in Section 2.1.3. Additional information on data sources for, limita tions of and our confidence in the information summarized here is described in Appendix 2B.

2.1.1 Temporal Trends on a National Scale

Figure 2-1 shows the substantial downward trend in Pb emissions that has occurred over the past several decades. The most dramatic re ductions in Pb emissions occurred prior to 1990 in the transportation sect or due to the removal of Pb from gasoline used in on-road vehicles.
Lead emissions were further reduced substa ntially between 1990 a nd 2008, with significant

2 http://www.epa.gov/ttn/chief/net/2008inventory.html

3 With regard to Pb emissions, the 2008 NEI, version 3 (January 2013) has been augmented with sources not included in the 2008 NEI, version 2.2-3 reductions occurring in the metals industries at le ast in part as a result of national emissions
standards for hazar dous air pollutants.

Figure 2-1. Temporal trend in U.S. air emissions of Pb: 1970-2008.

2.1.2 Sources and Emissions on National Scale - 2008

As indicated in Figure 2-1, the largest source sector emitting Pb into the atmosphere on a national scale is aviation gasolin e usage by piston engine driven aircraft. The next largest nationally is metal working and mining. Considering the national estimates at a more detailed scale, the largest source categories emitting Pb in to the atmosphere on a national scale, after emissions from aircraft operating on leaded fuel, are boilers and process heaters (fuel combustion). The latter indivi dually are generally small sources, which comprise a large category when aggregated nationally (Table 2-1). The next larges t categories are various metals industries, including lead-specific industries (Table 2-1). Together these and other sources were estimated to emit just under a thousa nd tpy of Pb in the U.S. in 2008.2-4 Table 2-1. U.S. Pb emissions by source categories estimated to emit at least 4 tpy.

Source Category Description 2008 Emissions (tons)
ALL CATEGORIES A 950 Aircraft operating on leaded fuel B 550 Industrial/Commercial/Institutional Boilers & Process Heaters 63 Utility Boilers 51 Iron and Steel Foundries 30 Integrated Iron and Steel Manufacturing 27 Steel Manufacturing: Electric Arc Furnaces 22 Secondary Lead Smelting 20 Primary Lead Smelting 19 C Primary Copper Smelting 17 Mining 15 Military Base 13 Cement Production 8 Glass Manufacturing 8 Battery Manufacturing 8 Secondary Non-ferrous Metals (other) 7 Primary Non-ferrous Metals (other) 7 Carbon Manufacturing 6 Pulp and Paper Production 6 Secondary Copper Smelting 5 Commercial Marine Vessels 5 Fabricated Metal Products Manufacturing 5 Residential Heating 5 Municipal Waste Incineration 4 Sewage Sludge Incineration 4 Mineral Products Manufacturing 4

A - Emissions estimate totals from 2008 National Emission s Inventory, version 3 (January 2013) for point sources and 2008 NEI version 2 for nonpoint sources (residential heating). B - This category includes Pb emitted at or near airports as well as Pb emitted in-flight. Lead emissions at or near airports comprise 46% of the total aircraft Pb emissi ons inventory. Emissions value based on EPA estimates. C - There is some uncertainty regarding the total emissions estimate for this source category in which there is one operational smelter, which ceased smelter operati ons at this site at the end of 2013 (USEPA, 2012).2-5 2.1.2.1 Stationary Sources

Since the last review of the Pb NAAQS, th e EPA has completed a number of regulations
which will result in reduced Pb emissions from stationary sources regulated under the Clean Air Act sections 112 and 129. For example, in January 2012, the EPA updated the National
Emission Standards for Hazardous Air Pollutants (NESHAP) for Secondary Lead Smelting (77 FR 555). These amendments to the original ma ximum achievable control technology standards apply to facilities nationwide that use furnaces to recover Pb from lead-bearing scrap, mainly from automobile batteries (15 ex isting facilities, one under construc tion). By the effective date in 2014, this action is estimated to result in a Pb emissions reduction of 13.6 tpy across the category (a 68% reduction). Also, the NESHAP s for Primary and Secondary Lead Smelting were revised in 2011 and 2012, respectively (76 FR 70834, 77 FR 555), as well as more than a dozen additional EPA actions taken in the past 5 years, which would not be reflected in the 2008 NEI estimates, will result in Pb emissions reductions (Appendix 2A). Explanation of aggregation approaches used for Tables 2-1 and 2-2:

Facilities have numerous processes that can fall into differ ent source categories and the NEI includes process-specific emissions estimates. Source categories are groups of faci lities that can be considered as the same type of emissions source. In order to present the emissions for source categor ies (e.g., secondary copper smelting) rather than for processes (e.g., Secondary Metal Production, Copper or Rotary Furnace) in Table 2-1, we aggregated processes for each facility and then present national estimates for source categories. T he source categories used were assigned using a three-tiered approach. First, processes known to be affected by sector-specif ic rules were set to the source categories. This was done for Utility Boilers, Portland Cement plants, Electric Arc Fur naces, Municipal Waste Combustors, and Taconite Ore facilities (mapped to Integrated Iron and Steel Manufacturing). Other sour ce categories did not use this first tier because the processes in the inventory have not yet been mapped to other rule s. Second, for processes that clearly map to source categories, the inventory process descrip tions (Source Classification Codes) were used to assign the source category. A good example of this is for Industrial, Commercial, and Institutional Boilers and Process Heaters. For all remaining processes, the Facility Type inventory field was mapped to a s ource category. Facility Types are the basis for aggregation used in Table 2-2. Facility Types in the NEI were set manually by EPA staff for facilities greater than 0.5 tons of Pb and using the North American Industrial Classification System (NAICS ) codes for smaller facilities. This (setting of the facility type) was done with consideration of the primary activity identif ied for the facility, which usually confirmed the NAICS code. A facility only has a single Facility Type but can have multip le processes and source categories. For example, some facilities are secondary metal processing plants for copper , aluminum, and non-ferrous metals, which divides their emissions into Secondary Copper and Secondar y Non-Ferrous metal source categories. In these cases, the facility website was reviewed to try to assess the predominant activity and the NAICS code was considered as well, and a Facility Type was set using the best judgement of EPA staff. However, th e emissions for these facilities are split across multiple processes as summed in Table 2-1. To prevent double counti ng of facility and state counts in Table 2-2, the Facility Type was used so that each facility shows up only once in this table.2-6 2.1.2.2 Mobile Sources

Forty years ago, combustion of leaded gasoline wa s the main contributor of Pb to the air. In the early 1970s, the EPA set national regulati ons to gradually reduce the Pb content in gasoline. In 1975, unleaded gasoli ne was introduced for motor vehi cles equipped with catalytic
converters. The EPA banned the use of leaded gasoline in highway vehicles after December
1995. Lead emissions from piston-engine aircraft operating on leaded fu el are currently the largest source of Pb air emissions on a national scale. Lead is adde d to aviation gasoline (commonly referred to as “avgas”) used in most pi ston-engine aircraft in order to boost octane and prevent engine knock. 4 The most commonly used avgas, 100 Octane Low Lead, contains up to 2.12 grams Pb per gallon (ASTM D 910). The Fe deral Aviation Administration estimates that in 2008, 248 million gallons of avgas were consumed in the U.S. 5 contributing an estimated 550 tons of Pb to the air that compri se 58% of the national Pb inventory. 6 Leaded avgas is used at approximately 20,000 airport facilit ies in the United States. The EPA is currently collecting and evaluati ng information regarding emissions and air concentrations of Pb resulting from avgas co mbustion by piston-engine aircraft (including monitoring data described in section 2.2.1.1 below). This is part of an ongoing investigation
under section 231 of the Clean Air Act into the potential for these emissions to cause or contribute to air pollution that may reasonably be anticipated to endanger public health or welfare. This evaluation by the EPA is occurr ing separate from the NAAQS review. The EPA’s investigation includes substant ial analytical work. The timeline for completion of this investigation and possible issuance of a final endangerment determination includes completion of necessary modeling and mon itoring information and other data, development of a proposal which will be published for public comment, review and analysis of comments received and
issuance of the final determination. If the EPA i ssues a positive determination that Pb emissions from aircraft engines cause or contribute to air pollution that may reason ably be anticipated to endanger public health or welfare, the EPA w ould then be required to propose and promulgate
emissions standards to control aircraft e ngine Pb emissions, and the Federal Aviation

4 Lead is not added to jet fuel used in commercial airc raft, military aircraft, or ot her turbine engine aircraft.

5 U.S. Department of Transportation Federal Aviat ion Administration Aviation Policy and Plans. FAA Aerospace Forecast Fiscal Years 2010-2030. p.99. Available at: http://www.faa.gov/about/offi ce_org/headquarters_offices/apl/aviatio n_forecasts/aerospa ce_forecasts/2010- 2030/media/2010%20Forecast%20Doc.pdf This document provides histor ical data for 2000-2008 as well as forecast data.

6 EPA (2010) Calculating Piston-Engine Aircraft Airport Inventories for Lead for the 2008 National Emissions Inventory. EPA-420-B-10-044. Available at: http://www.epa.gov/otaq/regs/nonroad/aviation/420b10044.pdf2-7 Administration would be required to promulgate regulations addr essing the fuel used by those
aircraft. More information about EPA’s actions is available at www.ep a.gov/otaq/aviation.htm. Vehicles used in racing are not regulated by the EPA under the Clean Air Act and can therefore use alkyl-Pb additives to boost octane . The National Association for Stock Car Auto Racing (NASCAR) formed a volunta ry partnership with the EPA with the goal of permanently removing alkyl-Pb from racing fuels used in the racing series now known as the Sprint Cup, the Nationwide Series and the Campi ng World Truck Series. The major NASCAR race series now
use unleaded fuels. Due to the presence of Pb as a trace contamin ant in gasoline, diesel fuel and lubricating oil, cars, trucks, and engines operating in nonroa d equipment, marine engines and jet aircraft emit small amounts of Pb (ISA, Section 2.2.2.6). A dditional mobile sources of Pb include brake wear, tire wear, and loss of Pb wheel weights (ISA, Section 2.2.2.6).

2.1.2.3 Natural Sources and Long-range Transport

Some amount of Pb in the air in the U.S. derives from natural sources, such as volcanoes, sea salt, and windborne soil particles from areas free of anthropogenic ac tivity and some may also derive from anthropogenic sources of airborne Pb located outside of the U.S. (ISA, section 2.5.5). Emissions estimates for th ese sources, as well as forest wildfires and biogenic sources, have not been developed for the NEI. Quantitative estimates for these processes remain an area of significant uncertainty . Based on several different approaches, the ISA identifies several
estimates of the concentration of airborne Pb derived from natural sources. The estimates extend no higher than 1 nanogram per cubic meter (ng/m 3 ), and extend down as low as 0.02 ng/m 3 (ISA, section 2.5.5). The data available to derive such an estimate ar e limited and such a value might be expected to vary geographically w ith the natural dist ribution of Pb.
Another contribution to U.S. ai rborne Pb concentrations is long-range transport such as
that associated with ai r masses carrying Pb from sources in Asia, where controls on Pb emissions have lagged those in the U.S. and Canada (ISA, section 2.5.5; Osterberg et al., 2008). The most recent estimates of contributions from Asia, how ever, conclude that the Asian contribution to
U.S. airborne Pb concentrations is generally less than 1 ng/m 3 (ISA, section 2.5.5; Murphy, 2007; Ewing et al., 2010).

2.1.2.4 Previously Deposited Lead

Lead-bearing particles that occur in outdoor dust on soil or built surfaces (e.g., streets and sidewalks) can be a source of airborne Pb as a result of particle re suspension (ISA, section 2.3.1.3). Proximity to major sources of Pb emi ssions, the extent of previous or historic deposition, and the effectiveness of natural and human removal pr ocesses dictate how important resuspension may be as a contribution to air Pb concentrations. In addition to resuspension and2-8 subsequent dispersion, surface water runoff (e.g., associated with rainfa ll) also plays a role in the movement of Pb-bearing particles from outdoor su rfaces to human-made or natural stormwater sediment catchments (ISA, sections 1.2.1, 2.3.1.3, 2.3.2 and 2.3.2.4; Wong et al., 2006). Mean
residence time of street dust has been estimat ed for a low-traffic st reet (approximately 30 vehicles/hour) to be several months but less than a year (ISA, sect ion 2.3.1.3; Allott et al 1990). Outdoor dust may be resuspended into th e air by wind or human-induced mechanical forces, such that the main drivers of particle re suspension are typically mechanical stressors such as vehicular traffic, constructi on and agricultural opera tions, and, generally to a lesser extent, the wind (ISA, section 2.3.1.3; 2006 CD, section 2.3.3). Wind resuspension, often defined in terms of a resuspension rate (the fraction of a surface contaminant released per unit time) is dependent on many factors, including wind speed, soil/surface moisture, particle size, presence of saltating particles and presence of vegeta tion; typical values range over se veral orders of magnitude (ISA, section 3.3.1.3; 2006 CD, section 2.3.3). Vehicular resuspension results from shearing stress of tires or turbulence generated by a passing vehicle and can be a ffected by a number of factors including vehicle size, vehicle speed, soil or su rface moisture, and partic le size (ISA, section 2.3.1.3; 2006 CD, section 2.3.3). Variabili ty and uncertainty in these f actors, and with regard to surface soil/dust composition, affect quantitative emissions estimates for these processes (2006 CD, section 2.3.3). 7 The relative importance of resuspension of pr eviously deposited dust particles as an influence on airborne Pb concentrations will depend on site-specific circumstances, such as the magnitude of Pb concentrations in the surface du st and air Pb contributions from nearby sources of new Pb emissions, as well as wi th variation in the forces that influence particle resuspension. For example, the highest air Pb concentrations as sociated with resuspension appear to occur in areas of highly contaminated su rface dust associated with histor ically active industrial sites, which may or may not be currently active (ISA, s ections 2.3.1.3). Air concentrations near such sites with currently active facili ties (e.g., metals industries) will reflect the impact of emissions from the current industrial activity in addition to that from resuspension of any previously deposited material (often a compone nt of “fugitive” emissions estimates 8 ). Accordingly, as might be expected, the limited da ta available for comparison indi cate the relative magnitude of

7 Quantitative estimates of resuspension-related emissions associated with many active industrial sources (particularly metals sources) are included within the NEI, although such emissions asso ciated with previously and no longer active Pb sources are not as generally included in the NEI.

8 For example, emissions factors have been establishe d to estimate fugitive emissions from resuspension of previously deposited material as a result of vehicular tr affic on facility roadways (U SEPA, 1996-2011). Where used, these estimates are combined with estimates for "process fugitives" (emissions that escape capture by control devices) to estimate total fugitive emissions from a fac ility. Accordingly, control of resuspension resulting from facility roadways, buildings or other property may be part of a strategy to meet regu latory emissions requirements (e.g., national emissions standards for hazardous air pollutants for secondary lead smelting, 77 FR 556).2-9 air Pb concentrations associated with no-longer-active industrial s ites to be generally lower than that for active sites yet greater than that in locations somewhat removed from industrial sources (section 2.2.2.2 below). Lead-bearing particulate matter in other, non-in dustrial, locations of appreciable historic Pb contamination, such as in soils or on surfaces in older urban areas or near older transportation corridors may, if disturbed, also become susp ended into the air and contribute to air Pb concentrations, although the availability of such ma terial for resuspension might be expected to
decline over time in most locations due to tr ansport and removal processes. In older transportation corridors or other locations not influenced by active industries, the significance of resuspension (e.g., in terms of resultant air Pb co ncentrations) appears to be much less than that
associated with active industries or now-closed i ndustries with substantial emissions in the past. 9 For example, the available data indicate that current Pb concentrati ons near roadways are substantially lower than those n ear large, currently ac tive industrial sources (see ISA, sections 2.3.1.3 and 2.5.1.2 and Figures 2-9 and 2-11 below). In general, air Pb concentrations at sites described as not influenced by an active industry are much lower than those near active sources (see ISA, section 2.5.1.2 and Figure 2-11 below).

2.1.3 Sources and Emissions on Local Scale

Based on the 2008 estimates, the highest emission s in specific situations locally are from different types of metals industries, 23 of wh ich had 2008 estimates greater than or equal to 1.0 tpy Pb (Table 2-2). The geogra phic distribution of the facilities summarized in Table 2-2 is presented in Figure 2-2.

9 Mass-balance analyses of emissions in southern Calif ornia newly available in the last review suggested that Pb in resuspended road dust may represent between 40% and 90% of Pb emissions in some areas (2006 CD, p. 2-65; ISA, section 3.2.2.7). Air Pb monitoring data near roadways, however, including those in California, indicate Pb concentrations well below those near significant industrial sources and below the current Pb NAAQS (e.g., ISA, section 3.5.1.2).2-10 Table 2-2. Facilities estimated to emit at least 0.50 tpy of Pb in 2008.

Facility Type Facilities emitting ≥ 1.0 tpy A,B Facilities emitting < 1.0 and ≥ 0.50 A,C No. Facilities No. States Facility Emissions () A No. Facilities No. States Primary Lead Smelting Plant 1 1 19.2 D Steel Mill 14 8 1.0 - 9.8 10 9 Primary Copper Smelting/Refining Plant 4 3 2.3 - 8.8 Military Base 4 3 1.4 - 7.2 3 3 Secondary Lead Smelting Plant 5 5 1.4 - 7.1 3 2 Carbon or Graphite Plant 1 1 6.3 Primar y Non-ferrous Metal Smeltin g

/Refinin g

Plant ( not Lead, Gold, Aluminum, or Co pp

er

) 1 1 5.4 Mines/Quarries 5 2 1.6 - 3.8 Ethanol Biorefineries 2 2 1.5 - 3.8 Portland Cement Manufacturing 1 1 3.3 Pulp and Paper Plant 2 2 2.5 - 3.0 2 2 Calcined Pet Coke Plant 1 1 2.5 Battery Plant 3 3 1.5 - 2.5 1 1 Wood Board Manufacturing Plant 1 1 2.3 Foundries, Iron and Steel 3 3 1.1 - 2.3 10 8 Foundries, Non-ferrous 3 2 1.2 - 2.0 2 2 Secondary Non-ferrous Metal Smelting/Refining Plant (not Lead, Aluminum, or Copper) 2 2 1.2 - 2.0 1 1 Coke Battery 2 2 1.0 - 1.8 Electricity Generation via Combustion 2 2 1.0 - 1.7 7 5 Chemical Plant 1 1 1.7 2 2 Airport 6 4 1.0 - 1.3 52 17 Automobile/Truck or Parts Plant 1 1 1.2 3 2 Wastewater Treatment Facility 1 1 1.0 2 2 Munition or Explosives Plant 1 1 1.0 2 2 Glass Plant 2 2 Fabricated Metal Products Plant 5 4 Municipal Waste Combustor 3 3 Lumber/Sawmill 2 1 Plastic, Resin, or Rubber Products Plant 1 1 Taconite Processing Plant 1 1 Petroleum Storage Facility (Bulk Station) 1 1
A

- Emissions totals from 2008 National Emissions Inventory, version 3 (January 2013), except in the case of airports for which EP A -specific estimates were used. B - This category includes facilities with total emissions estimates greater than or equal to 0.95 tpy. C - This category includes facilities with total emissions estimates greater than or equal to 0.495 and less than 0.95 tpy. D - There is additional uncertainty regarding this total emissions estimate for this facility, the only remaining operational p rimary Pb smelter in the U.S., which ceased smelter op erations at this site at the end of 2013 (USEPA, 2012).2-11Figure 2-2.Geographic distribution of facilities and airports estimated to emit at least 0.50 tpy of Pb in 2008.2-12 2.2 AMBIENT AIR QUALITY The EPA and state and local agencies have b een measuring Pb in the atmosphere since the 1970s. In response to reduced emissions (see section 2.1), Pb concentrations have decreased dramatically over that period. Currently, the highest concentrat ions occur near some metals
industries where some individual locations have concentrations that exceed the NAAQS. This
section describes the ambient Pb measurement methods, the sites and networks where these measurements are made, and how the ambient Pb concentrations va ry geographically and temporally.

2.2.1 Air Monitoring

Ambient air Pb concentrations are measured by five national monitoring networks. The
networks include the State a nd Local Air Monitoring Sites (S LAMS) intended for Pb NAAQS surveillance, the PM 2.5 Chemical Speciation Network (CSN ), the Interagency Monitoring of Protected Visual Environments (IMPROVE) networ k, the National Air Toxics Trends Stations (NATTS) network, and the Urban Air Toxics Mon itoring program. All of the data from these
networks are accessible via EPA’s Air Quality System (AQS): http://www.epa.gov/ttn/airs/airsaqs/ . In addition to these networks, various environmental organizations have operated other sampling site s yielding data (which may or may not be accessible via AQS) on ambient air concentrations of Pb, often for limited periods and/or for primary purposes other than quantification of Pb itself. The subsections below describe each
network and the Pb measurements made at these sites.

2.2.1.1 Lead NAAQS Surveillance Network

This section describes sample collection, analysis and network aspects for the Pb SLAMS network, the main purpose of which is survei llance for the Pb NAAQS. As such, the EPA regulates how this monitoring is conducted in order to ensure accurate and comparable data for determining compliance with the NAAQS. The code of federal regulations (CFR) at parts 50, 53 and 58 specifies required aspects of the ambi ent monitoring program for NAAQS pollutants. 10 In order to be used in NAAQS attainment designations, ambient Pb concentration data must be obtained using either the federal reference method (FRM) or a federal equi valent method (FEM). The indicator for the current Pb NAAQS is Pb-TSP. However, in some situations, 11 ambient Pb-

10 The FRMs for sample collection and analysis are specified in 40 CFR part 50, the procedures for approval of FRMs and federal equivalent methods are specified in 40 CFR part 53 and the rules specifying requirements for the planning and operatio ns of the ambient monitoring networ k are specified in 40 CFR part 58.

11 The Pb-PM 10 measurements may be used for NAAQS mo nitoring as an alternative to Pb-TSP measurements in certain conditions defined in 40 CFR part 58 Appendix C, section 2.10.1.2. These conditions include where Pb concentrations are not expected to equal or exceed 0.10 micrograms per cubic meter as an2-13 PM 10 concentrations may be used in judging non attainment. Accordingly, FRMs have been
established for Pb-TSP and for Pb-PM 10 . The current FRM for the measurement of Pb-TSP is provided in 40 CFR part 50 Appendix G. This FRM includes sampling using a high-volume TSP sampler that meets the design criteria identi fied in 40 CFR part 50 Appendix B and sample analysis for Pb content using flame atomic absorption. There are 24 FEMs currently approved
for Pb-TSP. 12 All 24 FEMs are based on the use of hi gh-volume TSP samplers and a variety of approved equivalent analysis methods.
A new FRM for Pb-PM 10 was promulgated as part of the 2008 review (40 CFR part 50 Appendix Q). This FRM is based on the PM 10 sampler defined in 40 CFR part 50 Appendix J coupled with x-ray fluorescence (XRF) anal ysis. In addition, one FEM for Pb-PM 10 has been finalized for the analysis of Pb-PM 10 based on inductively coupled plasma mass spectroscopy (ICP-MS). The current Pb monitoring network desi gn requirements for NAAQS compliance purposes (40 CFR part 58, Appendix D, paragraph 4.5) include two types of monitoring sites – source-oriented monitoring site s and non-source-oriented monito ring sites. Source-oriented monitoring sites are required near sources of air Pb emissions which are exp ected to or have been
shown to contribute to ambient air Pb concentr ations in excess of the NAAQS. At a minimum,
there must be one source-oriented site locate d to measure the maximum Pb concentration in ambient air resulting from each non-airport Pb so urce estimated to emit 0.50 or more tons of Pb per year and from each airport estimated to emit 1.0 or more tons of Pb per year. 13 The EPA Regional Administrators may require additi onal monitoring beyond the minimum requirements where the likelihood of Pb air qualit y violations is signif icant. Such locations may include those near additional industrial Pb sources, recently cl osed industrial sources and other sources of resuspended Pb dust, as well as airports where piston-engine aircraft em it Pb (40 CFR, part 58, Appendix D, section 4.5(c)). Monitoring agencies are also required, unde r 40 CFR, part 58, Appendix D, to conduct non-source-oriented Pb monitoring at the NCore sites required in metropolitan areas with a population of 500,000 or more. 14 NCore is a network of multipollutant monitoring stations

arithmetic three-month mean and where the source of Pb emissions is expected to emit a substantial majority of its Pb in the size fraction captured by PM 10 monitors.

12 A complete list of FEM can be found at the following webpage - http://www.epa.gov/ttn/am tic/files/ambient/criteria/refere nce-equivalent-methods-list.pdf

13 The Regional Administrator may waive the requirement in paragraph 4.5(a) for monitoring near Pb sources if the State or, where appropriate, local agency can demonstrate the Pb source will not contribute to a maximum three-month average Pb concen tration in ambient air in excess of 50 percent of the NAAQS level based on historical monitoring data, modeling, or other means (40 CFR, part 58, Appendix D, section 4.5(a)(ii)).

14 Defined by the US Census Bureau - http://www.census.gov/population/ www/metroareas/metroarea.html2-14 intended to meet multiple monitoring objectives th at formally began in January 2011. The NCore
stations are a subset of the st ate and local air monitoring stati ons network and are intended to support long-term trends analysis, model evalua tion, health and ecosystem studies, as well as NAAQS compliance. The complete NCore networ k consists of approximately 60 urban and 20 rural stations, including some existing SLAMS s ites that have been modified for additional
measurements. Each state will contain at least one NCore station, and 46 of the states plus Washington, DC, will have at least one urban station.
Either Pb-TSP or Pb-PM 10 monitoring may be performed at these sites. Of 50 NCore sites measuring Pb concentra tions as of April 2014, 28 are m easuring Pb in TSP and 24 are measuring Pb in PM 10 (two sites are measuring both Pb in TSP and Pb in PM 10 ). While nonsource-oriented monitoring data can be used fo r purposes of NAAQS attainment designations, a main objective for non-source-oriented monitori ng is to gather information on neighborhoodscale Pb concentrations that are typical in urba n areas in order to bett er understand ambient airrelated Pb exposures for populations in these areas.
Source-oriented monitors near sources estima ted to emit 1.0 tpy Pb were required to be operational by January 1, 2010, and the remainde r of the newly required source-oriented monitors were required to be operational by December 27, 2011 (75 FR 81126). Currently, approximately 260 Pb-TSP monitors are in opera tion; these are a mixture of source- and nonsource-oriented monitors. Figure 2-3 shows th e geographic distribution of these monitors (in addition to the airport study monitors descri bed below) in the Pb NAAQS surveillance network, 15 with the Pb-TSP monitors existing at the time of the 2008 rulemaking indicated separately from the newly sited Pb-TSP monitors.

15 This figure reflects Pb-TSP monitors in AQS as of September 2012.2-15 Figure 2-3. Map of Pb-TSP monitoring sites in current Pb NAAQS monitoring network.

The current regulations also required one year of Pb-TSP monitoring (using FRM or FEM methods) near 15 specific airports in or der to gather additional information on the likelihood of NAAQS exceedances n ear airports due to the combustion of leaded aviation gasoline (75 FR 81126). These airports were se lected based on three criteria: annual Pb inventory between 0.5 ton/year and 1.0 ton/year, ambient air within 150 meters of the location of maximum emissions (e.g., the end of the runway or run-up location), and airport configuration and meteorological scenario that leads to a gr eater frequency of operations from one runway.
These characteristics were select ed because they are expected, co llectively, to identify airports with the highest potential to have ambient Pb concentrations approaching or exceeding the Pb NAAQS. Data from this monitoring study will be used to assess the need for additional Pb monitoring at airports. These 15 s ites (Figure 2-4) were intended to be operational no later than December 27, 2011, although delays in monitor siting extended the installation of some of these
monitors into late 2012.2-16 Figure 2-4. Sites near airports at which one year of Pb-TSP monitoring is required. 16

2.2.1.2 Other Lead Monitoring Networks

The NATTS network, designed to monitor c oncentrations of ha zardous air pollutants including Pb compounds, included 25 sites measuring Pb-PM 10 as of 2012. Most of these sites (20) are in urban areas (Figure 2-5). In addi tion to the NATTS network, as of 2012, states were collecting Pb-PM 10 at an additional 22 sites (most as pa rt of the Urban Air Toxics Monitoring program). All collect particulate matter as PM 10 for toxic metals analysis using either a highvolume PM 10 sampler or a low volume PM 10 sampler, typically on a 1 in 6 day sampling schedule. Most of these monitoring locations are not measuring usi ng FRM/FEM methods at this time. Lead in the collected sample is generally quantified via an ICP/MS method. The standard operating procedure for me tals by ICP/MS is available at:

16 The 15 Airports are: Merrill Field (Anchorage, AK), Pryor Field Regional (Limestone, AL), Palo Alto Airport of Santa Clara County and Reid -Hillview (both in Santa Clara, CA), McClellan-Palomar and Gillespie Field (both in San Diego, CA), San Carlos (San Mateo, CA), Nantucket Memorial (Nantucket, MA), Oakland County International (Oakland, MI), Republic and Brookhaven (both in Suffolk, NY), Stinson Municipal (Bexar, TX), Northwest Regional (Denton, TX), Harvey Field (Snohomish, WA), and Auburn Municipal (King, WA).2-17 http://www.epa.gov/ttn/amtic/airtox.html . As noted in section 2.2.1.1 above, non-sourceoriented Pb monitoring using FR M/FEMs that is required at the 51 NCore sites with a population of 500,000 or more (shown in Figure 2-5) may be Pb-PM 10 . As shown in Figure 2-5, there are
some cases where states have addressed their NATTS and NCore Pb monitoring needs with the use of a single monitoring site or may have nearby sites.

Figure 2-5. Pb-PM 10 monitoring sites. 17

17 Presented on this map are all NCore sites where FR M/FEM Pb monitoring is required along with other sites actively monitoring Pb-PM 10 (by any method) based on having 2012 data in AQS as of September 2012.2-18 Two networks measure Pb in PM 2.5 , the EPA CSN and the IMPROVE network. The CSN consists of 53 long-term trends sites (co mmonly referred to as the Speciation Trends Network or STN sites) and appr oximately 150 supplemental sites, all operated by state and local monitoring agencies. Most STN sites operate on a 1 in 3 day sampling schedule, while most supplemental sites operate on a 1 in 6 day samp ling schedule. All sites in the CSN network
determine Pb concentrations in PM 2.5 samples. Lead is quantified via the XRF method. 18 Data are accessible through AQS. The locations of the CS N are shown in Figure 2-6. Nearly all of the CSN sites are in urban areas, often at the location of highest known PM 2.5 concentrations. The first CSN sites began operation around 2000. The IMPROVE network is administered by th e National Park Service, largely with funding by the EPA, on behalf of federal land mana gement agencies and state air agencies that
use the data to track trends in rural visibility. Lead in PM 2.5 is quantified via the XRF method, as in the CSN. Data are managed and made accessible mainly through the VIEWS website ( http://vista.cira.colostate.edu/views/ ) but are also available via AQS. Samplers are operated by several different federal, state, and tribal host agencies on the same 1 in 3 day schedule as the STN. In the IMPROVE network, PM 2.5 monitors are placed in “Class I” areas (including National Parks and wilderness areas) and are mostly in rural locations (Fig ure 2-6). The oldest of these sites began operation in 1988, while many others began in the mid 1990s. There are 110 formally designated IMPROVE sites, which are locat ed in or near nationa l parks and other Class I visibility areas, virtually all of these being ru ral. Approximately 80 additional sites at various urban and rural locations, requested and funded by various parties, are also informally treated as part of the network.

18 The standard operating procedure for metals by XRF is available at: http://www.epa.gov/ttnamti1/files/ambient/pm25/spec/xrfsop.pdf

.2-19 Figure 2-6. Pb-PM 2.5 monitoring sites in CSN and IMPROVE networks (2012).

2.2.1.3 NAAQS Surveillance Monitoring Considerations

In this section, aspects of the methods for sa mpling and analysis of the Pb are reviewed, and the current NAAQS surveillance network of monitoring locations are considered. The methods for sampling and analysis are considered in light of the indicator for the Pb NAAQS, and conclusions regarding the current NAAQS and associated indicator appear in chapter 4. Consideration of the ambient air monitoring ne twork generally informs the interpretation of
current data on ambient air concentrations and helps identify whether the monitoring network is adequate to determine compliance with the NAAQS . This section disc usses considerations related to these aspect s of the ambient air m onitoring program for Pb. 19

2.2.1.3.1 Sampling Considerations

As described in section 2.2.1.1 above, consistentwith the Pb NAAQS indicator being PbTSP, the FRM for Pb, which is required at all so urce-oriented sites, is measurement of Pb-TSP using a high-volume TSP sampler meeting the design criteria specifie d in 40 CFR part 50

19 The code of federal regulations (CFR) at parts 50, 53 and 58 specifies required aspects of the ambient monitoring program for NAAQS pollutants. The FRMs for sample collection and analysis are specified in 40 CFR part 50, the procedures for approval of FRMs and FEMs are specified in 40 CFR part 53 and the rules specifying requirements for the planning and operatio ns of the ambient monitoring networ k are specified in 40 CFR part 58.2-20 Appendix B. During the review of the Pb NAAQS completed in 2008, CASAC noted the variability in high-volume TSP sample measuremen ts associated with the effects of wind speed
and wind direction on collection effi ciency in their comments regard ing the indicator. However, at the time of the 2008 review, no alternative TSP sampler designs were identified that had an adequate characterization of thei r collection efficiency over a wide range of particle sizes. The existing high-volume sampler was retained as the sampling approach for the Pb-TSP FRM and
FEMs. Since promulgation of the 2008 Pb NAAQS, the EPA has initiated an effort to review alternative sampler designs in an effort to de velop a new sampler to replace the current highvolume Pb-TSP sampler. Efficient collection of particles much larger than 10 μm is considerably more challenging b ecause the greater inertia and hi gher settling velocities of Pb particles hinder their efficient intake by sample rs. The sampling difficulties and the long history of research to develop adequate sampling t echnology for large particles have been thoroughly reviewed (Garland and Nicholson, 1991). Some existing commercia lly available sampler inlets are designed to collect particles larger than 10 μm with greater than 50% efficiency (Kenny et al., 2005), and these inlets can be tested as potential replacemen ts for TSP sampling. However, no alternatives to the FRM TSP sampler have be en identified that have been adequately
characterized.
The EPA has initiated efforts to characteri ze the collection effici ency of alternative sampler designs through wind tunnel testing as a necessary step towards the development of a new sampler capable of sampling particles larger than PM 10 without the noted wind speed and wind direction biases. Important considerations in specifying a sampler design with these desired features include the feasibility and challe nges to collection of particles much larger than 10 μm; some existing alternative sample collectio n methods are discussed in ISA (ISA, section 2.4.1.1). Also important to consider are physical limitations in the ability to generate and transport ultra-coarse particles that affect the abil ity to adequately characterize the new sampler. Although all sizes of airborne Pb particles are of interest, th e factors identified above are expected to ultimately limit the upper cut-poin t of potential samplers to the range of 18-20 micrometers. Following characterization in a wind tunnel, field testing of promising candidates would be required to evaluate performance and to make comp arisons to the existing Pb-TSP samplers. This effort is expected to take seve ral years to complete, and, as such, it is unlikely that this new sampler will be available in time for consideration during this NAAQS review due to the activities which will need to be completed to adequately characteri ze its performance both in the laboratory and the field. We expect the new sampler to be available for consideration in a future review and consequently do not expect to consider new alternatives for sampling methods for Pb-TSP as part of this review.2-21 In addition to the FRM for Pb-TSP, there is also, as noted in section 2.2.1.1 above, a
FRM for Pb-PM 10 (40 CFR part 50 Appendix Q), based on the PM 10 sampler defined in 40 CFR part 50 Appendix J coupled with XRF analysis. The Pb-PM 10 measurements may be used as an
alternative to Pb-TSP measuremen ts in certain conditions define d in 40 CFR part 58 Appendix C paragraph 2.10. These conditions include where Pb concentrations are not expected to equal or exceed 0.10 micrograms per cubic meter on an arith metic 3-month mean and where the source of Pb emissions is expected to emit a subs tantial majority of its Pb in the PM 10 size fraction. At this time, we believe the low-volume FRM sampler for Pb-PM 10 to be adequate for this application. Hence, we do not expect to consid er new sampling methods for Pb-PM 10 as part of this review.

2.2.1.3.2 Analysis Considerations

Due to reduced availability of laborator ies capable of performing flame atomic absorption analyses and general a dvances in analysis methods, the EPA has initiated an effort to expand FRM analysis methods beyond atomic absorp tion to include the more modern analysis method, ICP-MS. A consultation with the CASAC Ambient Air Monitoring and Methods Subcommittee was held on September 15, 2010 (Russell and Samet, 2010), and the EPA plans to propose a new FRM for Pb-TSP based on this more modern analysis method in 2013. In addition, the EPA has approved several new FEMs (for ICP-MS and other analysis methods) since the last Pb NAAQS review was completed in 2008. With regard to Pb-PM 10 samples, in addition to the FRM analysis method (XRF), two FEMs have been accepted for Pb-PM 10 analysis since the 2008 Pb NAAQS rulemaking. These
methods are based on ICP-MS and are consistent with analysis methods used for the NATTS
network. The EPA will continue to cons ider new FEMs for analysis of Pb-PM 10 and Pb-TSP as applications are received, although no ne w FRMs (beyond the Pb-TSP FRM for ICP-MS discussed above) are expected during this NAAQS review.

2.2.1.3.3 Network Design Considerations

Significant revisions to the Pb network de sign requirements (40 CFR part 58, Appendix D) were made as part of the 2008 Pb NAAQS review and an associ ated revision to the requirements in 2010. As summarized in se ction 2.1.1.1 above, the current Pb monitoring network design requirements (40 CFR part 58, A ppendix D, paragraph 4.5) include two types of monitoring sites – source-oriented monitoring site s and non-source-oriented monitoring sites - as well as the collection of a year of Pb-TSP measurements at 15 sp ecific airports. This section describes the design considerations for the Pb NAAQS surveillance network. Source-Oriented Monitoring. Since the phase out of Pb in on-road gasoline, Pb is widely recognized as a source-oriented air pollutant . As summarized in the ISA, variability in air Pb concentrations is highest in areas including a Pb sour ce, “with high concentrations2-22 downwind of the sources and low concentration at areas far from sources” (ISA, p. 2-92).
Recent data summarized in section 2.2.2.2 belo w indicates that the highest ambient Pb concentrations are found near large Pb sources, usually metals industries (see, for example, Figures 2-11 through 2-13 below). Analysis of the monitoring network during the last Pb NAAQS review with regard to adequacy of monitoring near su ch sources found that monitors were lacking near many of the larger Pb emissions sources, leading the EPA to conclude that the monitoring network existing at that time was in adequate to determine compliance with the revised Pb NAAQS (73 FR 29262). Findings and conclu sions of that analysis led to revisions of network design requirements fo r source-oriented monitorin g, begun with the 2008 Pb NAAQS rulemaking (73 FR 66964). Additional revisions were completed as part of a reconsideration of the monitoring requirements in December 2010 (75 FR 81126). The current requirements for source-oriented monitoring include placement of monitor
sites near sources of air Pb emissions which are e xpected to or have been shown to contribute to
ambient air Pb concentrations in excess of th e NAAQS. At a minimum, there must be one
source-oriented site located to measure the maxi mum Pb concentration in ambient air resulting from each non-airport Pb source which emits 0.50 or more tons of Pb per year and from each airport which emits 1.0 or more tons of Pb per year. 20 The expansion of the network, including these source-oriented sites, is shown in Figur e 2-3. Comparison of Figure 2-3 (monitors) with Figure 2-2 (sources) illust rates the coverage which the mon itoring network provides, as of 2012, of large Pb emissions sources.
The emissions threshold for source-oriented monitoring sites, 0.50 tpy, was developed based on an analysis intended to estimate the lowest emission ra te that under reasonable worstcase conditions (e.g., meteorological and emission rele ase conditions that lead to poor dispersion
and associated elevations in Pb concentrations) could l ead to Pb concentrations exceeding the Pb NAAQS (Cavender, 2008). This an alysis included three approaches . The first two of the three approaches included a simple scaling of the hist oric 5 tpy emission threshold applied to the old 1.5 μg/m 3 Pb NAAQS, and a simplified modeling effort using a screening model. The third approach relied on design values based on Pb monitoring data surrounding large sources (1 tpy or greater) of Pb. At the time of the 2008 re view, complete 3-year design values were only available for seven source-monitor pairs. As more recent data become available, an alysis of the updated and expanded dataset will inform evaluation of the appropriateness of th e current requirements. Since the analysis

20 The Regional Administrator may waive the requirement in paragraph 4.5(a) for monitoring near Pb sources if the State or, where appropriate, local agency can demonstrate the Pb source will not contribute to a maximum Pb concentration in ambient air in excess of 50 percent of the NAAQS (based on historical monitoring data, modeling, or other means).2-23 performed during the 2008 review, over 150 addi tional source-oriented monitors have been installed. At this time, the full set of these ne w monitors have not coll ected a complete 3-year dataset, which is needed for the development of complete design values for the new sourceoriented monitors

. For monitors installed in response to the 2008 revisions (near sources estimated to emit 1.0 tpy or more of Pb), 3-year s of certified data would be expected to have been available in spring 2013. Three-years of cer tified data for the monito rs required in the 2010 regulations will be available in spring 2015. As is seen from Figures 2-11 through 2-13 below, Pb concentrations very widely across the sour ce oriented monitors. This variation is not unexpected given potential for appreciable differences in source characte ristics beyond estimated annual Pb emissions that would be exp ected to affect airborne Pb concentrations. Such characteristics include source or industry ty pe and associated processes and work practices, proximity of emissions points to source bounda ries, extent of fugitive emissions. One-year Airport Monitoring. In addition to the above source-oriented monitoring requirement for airports estimated to emit more than 1 tpy of Pb (40 CFR part 58, Appendix D, 4.5(a)) and the Regional authority to require mo nitoring near airports where piston-engine aircraft emit Pb (40 CFR part 58, Appendix D, 4.5(c )), one year of monito ring was required near 15 specific airports in order to gather a dditional information on the likelihood of NAAQS
exceedances due to the combustion of leaded aviation gasoline (75 FR 81126; 40 CFR part 58, Appendix D, 4.5(a)(iii)). Given delays in monito r siting, monitor installation at some of these sites extended into late 2012. Accordingly, the timing for completion of the year of monitoring
has varied across the 15 locations. As describe d further in section 2.1.2.2 above, these airport monitoring data along with other data gath ering and analyses will inform EPA’s ongoing investigation into the potential for Pb emissi ons from piston-engine aircraft to cause or contribute to air pollution that may reasonably be anticipated to endanger public health or welfare. This investigation is occurring under Section 231 of the Clean Air Act (CAA), separate from the Pb NAAQS review. As a whole, the various data gathering and anal yses are expected to improve our understanding of Pb concentrations in ambient air near airports and conditions influencing these concentrations. Non-Source-Oriented Monitoring. Monitoring agencies are also required to conduct non-source-oriented monitoring NCore sites w ith a population of 500,000 or more, as noted
above. 21 Currently, all 50 NCore site s are operational and measuri ng Pb concentrations, with 28 measuring Pb in TSP and 24 measuring Pb in PM 10 (2 sites are measuring both Pb in TSP and Pb
in PM 10 ). While non-source-oriented monitoring data can be used for designation purposes, an alternative objective stated fo r these sites is the collection of data on neighborhood-scale Pb

21 Defined by the US Census Bureau - http://www.census.gov/population/ www/metroareas/metroarea.html2-24 concentrations that are typical in urban areas to inform our unde rstanding of ambient air-related Pb exposures for the general population. The da ta available as of April 2014 for these sites
indicate little variation in concentrations, with a range from less than 0.01 to 0.06 μg/m 3 in terms of maximum 3-month average concentration (of Pb-PM 10 or Pb-TSP), with the vast majority of sites showing concentrations less than 0.03 μg/m 3 . In recognition of the limited extent of this data analysis, we have not drawn conclusions here on the usefulness of these data for purposes of characterizing neighborhood-scale con centrations. We additionally note the existence of other monitoring networks that, alt hough not required by regulation, provide data on Pb in PM 10 , and
also in PM 2.5 , at non-source-oriented urban sites. These include the NATTS for PM 10 and the
CSN for PM 2.5 , as described in section 2.2.1.2 above.

2.2.2 Ambient Concentrations

2.2.2.1 Temporal Trends

Ambient air concentrations of Pb in the U.S. have declined substantially over the past 30 years. Figure 2-7 illustrates this decline in terms of site-specific maximum 3-month average
concentrations at the set of 31 monitoring sites that have been operating across this period. The median of this dataset has declined by more than 90% over the 30-year period, and the average by 89%. Over the past 12 years, a larger datase t of 50 sites operating across that period also indicates a decline, which is on the order of 50% for the average of that dataset (Figure 2-8). 22

Note: Based on annual maximum 3-month average at 31 sites.
Figure 2-7. Temporal trend in Pb -TSP concentrations: 1980-2010 (31 sites).

22 In Figures 2-7 and 2-8, the top of the blue band is the 90 th percentile among sites, the bottom is the 10 th percentile, and the white line is the average. http://www.epa.gov/air/airtrends/lead.html2-25 Note: Based on annual maximum 3-month average at 50 sites.
Figure 2-8. Temporal trend in Pb-TSP con centrations: 2000-2012 (50 sites).

The role of the phase-out of leaded ga soline for on-road vehicles on declining concentrations is evident from temporal trends in air Pb concentrati ons near roadways, as illustrated in Figure 2-9 which presents data for five monitors sited near roadways during the years 1979 through 2010. 23 These sites additionally indicate the concentrations currently common at such sites, with the maximum 3-month av erage concentrations at all five sites falling below 0.03 μg/m 3 in the most recent years.

23 In selecting these sites, the objective was to identify sites near roadways that do not appear to be near other (stationary) sources of Pb emissions. In addition to consideration of information in national emissions inventories, the areas around the sites were examined us ing satellite pictures (in Google Maps) for signs of current or historical industrial activity.2-26 Monitor locations: Los Angeles, CA (06-037-4002), Riverside, CA (06-065-1003), Cook, IL (17-031-0052, 17-031-6003), Suffolk, M A (25-025-0002).
Figure 2-9. Airborne Pb -TSP concentrations (3 -month average) at five sites near roadways: 1979-2010.

2.2.2.2 Current Concentrations

As a result of revisions to the Pb NAAQS surveillance monitoring requirements (described in section 2.2.1 above), Pb monitoring sites have been in transition over the last few years as indicated by Figure 2-3. For presentation in this do cument, we have focused on the most recent period for which adequately comp lete data are available, 2010-2012, recognizing that the dataset developed for this period includes many but not all of the monitors newly required by the December 2010 regulations described in section 2.2.1.1 above. Lead concentrations, in te rms of maximum 3-month aver age Pb-TSP concentration, at monitoring sites active across the U.S. during the period 201 0-2012, and for which sufficient data are available to meet completeness criteri a described in Appendix 2C, are presented in Figure 2-10. 24 Highest concentrations occur in the vi cinity of large metals industries, as
discussed in section 2.1.2.1. 25 Note that due to differences in data completeness criteria which reflect the different purposes of th e analyses (characteri zation of air quality at different types of monitoring sites vs identifica tion of sites exceeding the NAAQ S), Figure 2-10 (and Figures 2-11 through 2-13) do not include some sites which may have been reported elsewhere (e.g., with “design values” which are used for comparison to the NAAQS level). 26

24 Criteria for development of the 2010-2012 air Pb-TSP, Pb-PM 10 and Pb-PM 2.5 datasets discussed in this section are described in Appendix 2C. Data summaries are included in Appendix 2D.

25 Information regarding areas of U.S. designated no nattainment with the Pb NAAQS is available at: http://www.epa.gov/air/oaqps/greenbk/mindex.html

. 26 Design values for the 2010-2012 period are available at: http://www.epa.gov/airtrends/values.html 0 0.2 0.4 0.6 0.8

1 1.2 1.4 1.6 1.8January‐79October‐79July‐80April‐81January‐82October‐82July‐83April‐84January‐85October‐85July‐86April‐87January‐88October‐88July‐89April‐90January‐91October‐91July‐92April‐93January‐94October‐94July‐95April‐96January‐97October‐97July‐98April‐99January‐00October‐00July‐01April‐02January‐03October‐03July‐04April‐05January‐06October‐06July‐07April‐08January‐09October‐09July‐10Concentration(μg/m3)

060374002

060651003

170310052

170316003

2502500022-27Figure 2-10.Pb-TSP maximum 3-monthmeans (215 sites), 2010-2012.2-28 Figures 2-11 through 2-13 illustrate differen ces in Pb-TSP concentrations, in terms of three different metrics (maximum 3-month me an, annual mean, and maximum monthly mean), among sites near and more distant from emissions sources. 27 The Pb-TSP sites indicate the much greater site and temporal variab ility in concentrations at sour ce-oriented and previous sourceoriented sites as compared to non-source-oriented sites. Across the Pb-TSP sites, as would be expected, the highest concentratio ns are observed at the source-or iented sites, followed by the previous source-oriented sites. This is the case for all three metrics analyzed (maximum 3- month mean, maximum monthly mean and annual mean). Figures 2-11 through 2-13 additionally present distributions of Pb-PM 10 and Pb-PM 2.5 concentrations in urban and rural locati ons where they are monitored. The Pb-PM 10 and PbPM 2.5 networks are described in section 2.2.1.2 and s hown in Figures 2-5 and 2-6, respectively. It is important to note that there ar e few sites in these recent datase ts with colocated monitors for
the different size fractions. As described in the IS A, at 18 urban sites (without specification as to proximity to Pb sources) with at least 30 co-located Pb-TSP and Pb-PM 10 samples collected during various time periods (nearly all between 1990 and 2000), approximately 80% of the Pb mass, on average, is captured by the Pb-PM 10 measurements (ISA, sections 2.5.3.1 and 2.8.4). The data distributions in Figures 2-11 through 2-13 indicate reduced variability in concentration for non-source-oriented sites and for part iculate Pb of smaller size fractions. 28

27 In the Figures 2-11 through 2-13, the whiskers indicate the 5 th and 95 th percentiles, the box indicates the 25 th 50 th and 75 th percentiles and the star indicates the arithmetic mean.

28 The number of observations for some categories of monitoring site varies among the three figures due to the impact of data completeness criteria used for the three different concentration metrics (see Appendix 2C).2-29Figure 2-11.Distribution of maximum 3-month meanconcentrations of Pb-TSP, Pb-PM10and Pb-PM2.5at different site types,2010-2012.0.00.10.20.30.40.50.60.70.80.91.01.11.21.3

Concentration (μg/m 3 )Pb-TSPall sites(n=236)Pb-TSPsource-oriented(non-airport) sites(n=119)Pb-TSPnot source-orientedsites (n=93)Pb-TSPprevious sourceoriented sites(n=11)Pb-PM10urban sites(n=45)Pb-PM2.5urban CSNsites (n=193)Pb-PM2.5non-urbanIMPROVE sites(n=102)Pb-TSPsource-oriented(airport) sites(n=13)2-30Figure 2-12.Distribution of annual mean concentrations of Pb-TSP, Pb-PM10and Pb-PM2.5at different site types, 2010-2012.0.00.10.20.30.40.50.6Pb-TSPall sites(n=242)Pb-TSPsource-oriented(non-airport) sites(n=121)Pb-TSPnot source-orientedsites (n=96)Pb-TSPprevious sourceoriented sites(n=11)Pb-PM10urban sites(n=54)Pb-PM2.5urban CSNsites (n=195)Pb-PM2.5non-urbanIMPROVE sites(n=104)

Concentration (μg/m 3 )Pb-TSPsource-oriented(airport) sites(n=15)2-31Figure 2-13.Distribution of maximum monthly meanconcentrations of Pb-TSP, Pb-PM10and Pb-PM2.5at different site types,2010-2012.0.00.10.20.30.40.50.60.70.80.91.01.11.21.31.41.51.61.71.8

Concentration (μg/m 3 )Pb-TSPall sites(n=243)Pb-TSPsource-oriented(non-airport) sites(n=121)Pb-TSPnot source-orientedsites (n=96)Pb-TSPprevious sourceoriented sites(n=11)Pb-PM10urban sites(n=54)Pb-PM2.5urban CSNsites (n=184)Pb-PM2.5non-urbanIMPROVE sites(n=104)Pb-TSPsource-oriented(airport) sites(n=15)2-32 2.3 AMBIENT AIR LEAD IN OTHER MEDIA Lead emitted into the ambient air, depending on its chemical and physical characteristics, deposits out of air onto surfaces in the environmen t. The environmental fate of atmospherically emitted Pb, once deposited, is influenced by the type of surface onto which the particles deposit and by the type and activity level of transport fo rces in that location. Deposited Pb can be incorporated into soil matrices in terrestrial ecosystems or transported (by direct deposition or stormwater runoff) to water bodies and into a quatic sediments, which may serve as aquatic ecosystem sinks. Particles deposited onto impe rvious surfaces, such as urban surfaces or roadways, are more available for human contac t while they remain on such surfaces. For example, particles on urban surfaces may be availa ble for adherence onto skin or they may be resuspended into the air and inhaled. Preci pitation and other natura l, as well as humaninfluenced, processes contribute to the fate of such particles and their potential transport to areas or environments of lesser or greater likelihood for human contact, e.g., transport with surface runoff into nearby water bodies or tracki ng into nearby houses (ISA, section 2.3).
Lead from current and histori cal air emissions sources, in addition to a range of nonair sources (e.g., land disposal of wastes as well as surface runoff and releases to surface waters), contribute to Pb in outdoor dust, soil and aquatic systems. Because of its persistence, Pb from all
of these sources can contribute to media concentra tions into the future. The pattern of resulting Pb concentrations changes over time in respons e to changes in new Pb contributions to the systems (e.g., in types and rates of addition), as well as environmental processes (chemical, biological and physical) particular to each type of media and ecosystem. Accordingly, media and ecosystems differ with regard to Pb concentr ations and the changes in those concentrations in response to airborne Pb. These differences re late to ecosystem processes as well as Pb source or emissions characteristics and proximity. The initial section below (s ection 2.3.1) summarizes sali ent information regarding atmospheric deposition and how it is monitored. Subsequent sections describe the current information related to the pres ence of ambient air Pb in nonair media and what it indicates regarding impacts of current patterns of Pb in and being emitted to ambient air, including relationships to impacts in the past and to ot her Pb sources. Section 2.3.2 focuses on terrestrial media, while section 2.3.3 discusses aquatic media.

2.3.1 Atmospheric Deposition

Deposition is the pathway by which Pb partic les are removed from the atmosphere and
transferred to other environmental media. Ther e are several approaches by which atmospheric deposition, or the transfer of Pb from the atmos phere to soil or water bodies, can be assessed.
These include measurements of Pb in rainfall (wet deposition) and on collection surfaces during2-33 dry periods (dry deposition); dry deposition is also estimated from measurements of airborne Pb particles coupled with estimates of deposition ve locity (see 2006 CD, Sec tion 2.3.2). Less direct approaches include monitoring changes in Pb co ncentration in various biological or physical media such as lichen or mosses, snowpack, soil and aquatic sediments (ISA, sections 2.6.2, 2.6.4 and 2.6.6). Approaches for the latter three media may involve repeated measurements of surface samples over time or core samples coupled with isotope dating. To gain information on atmospheric deposition unaffected by contributions from direct nonair environmental releases, such studies are generally conducted in somewhat remote areas. As there are currently no nationwide Pb atmospheric deposition monitori ng programs, the discussion of atmospheric deposition in this and subsequent sections is drawn from this range of approaches (2006 CD, sections 2.3, 8.2.2 and AX7.1.2.3; ISA, sections 2.3.1.2 and 2.6 ). Geographic differences in deposition generally relate to differences in the amount and size distribution of airborne Pb particles in that location, as well as meteorology a nd other site-specific factors. For example, the size of particles, as well as solubility in rainwa ter, can also influence wet deposition rates (ISA, section 2.3.1.2; 2006 CD, p. 2-59). Factors that pa rticularly influence dry deposition are the level of atmospheric turbulence, especially in the layer nearest the ground, particle size distributions and density, and the nature of the surface itself, such as smooth or rough (2006 CD, pp. 2-55 to 2-57). Evidence for the temporal pattern of U.S. Pb deposition generally indicates a peak during the middle twentieth century (e.g., 1940s through 1970s) followed by substantial declines in the latter part of the century (IS A, section 2.3.1; 2006 CD section 2.3.1; Jackson et al., 2004). This pattern reflects the increased use of Pb in the in dustrial age (including its use in gasoline in the twentieth century) and declines in response to environmental controls on gasoline and metals
industries in the latte r part of the twentieth cen tury. Studies continue to document declines in atmospheric deposition since the 1980s in lo cations remote from industrial areas (e.g., Watmough and Dillon, 2007). As would be expecte d, stationary sources of Pb continue to contribute to relatively higher de position rates in industrial areas as compared to other areas, although rates in those areas app ear to have also declined si nce the 1970s-80s (ISA, section 2.3.1.2; Sabin and Schiff, 2008). In addition to records of atmospheric deposit ion in the U.S., evidence also documents the long-range atmospheric transport and distribution of the substantial emissions of Pb from the U.S. and other developed countries to regions well beyond those source count ries. For example, evidence provided by isotopic analyses of rainwate r and surface water in th e North Atlantic and ice cores in Greenland have documented the long -range transport and dist ribution of Pb from North American and European sources (IS A, section 2.5.5; 2006 CD, p. AX7-141; 1977 CD, section 6.3.1; Veron et al., 1998). The historical record provided by those cores indicate the2-34 period of most substantial deposition to that remote region during the 1960s and 1970s followed by a dramatic decline (ISA, section 2.5.5; Mc Connell and Edwards, 2008). These and other records of long-range transport indicate the wide spread distribution of historically emitted Pb (e.g., 2006 CD, section 2.3.1).

2.3.2 Terrestrial Media

Lead in the terrestrial media discussed here may originate from current or historical air
emissions or other sources. Other sources to th ese media include historic al use of indoor and outdoor leaded paint, more preval ent in areas with ol der buildings, and the processing of leadcontaining materials. Further, the concentrations of Pb in each media, as well as the relative contributions from various types of sources to those concentrations , vary among media and among locations for any one media. Differences among locations in media concentrations of airrelated Pb are generally related to the current and historical magnitude of Pb emissions and deposition at that location, as well as locati on- and media-specific removal factors.

2.3.2.1 Indoor Household Dust

Household dust arises from particulate matter generated indoors and outdoors, and Pb in
household dust can reflect a combination of these sources. 29 Airborne particles can be transported indoors with ambient air, while par ticles deposited outdoors from ambient air may be carried in on humans and their clothing or ot her items transported indoor s. Depending on factors such as the proximity of the residence to curren t or historical metals industries, leaded paint usage, and age of the residence (which informs c onsideration of potential fo r presence of leaded paint), Pb in indoor residential dust can reflect current or histor ical atmospheric Pb or nonairrelated sources, such as leaded paint. Another indoor source is tobacco smoking (ISA, section 3.1.3.2; Gaitens et al., 2009; 2006 CD, p. 3-15; Manni no et al., 2003). The ag e of the residence may be an indicator of the potential for the pres ence of leaded paint and, in areas of significant levels of airborne Pb in the past, such as near mining or smelting industries, may also indicate the potential for the residual presence of hist orically emitted Pb (ISA, sections 3.1.1 and 3.1.3.2; 2006 CD section 3.2.3). A study of households in the Baltimore metropolitan area (in which there are no areas designated non-atta inment for the current Pb NAAQS) 30 indicated indoor air Pb concentrations to be signifi cantly associated with outdoor air Pb concentrations but did not show a statistically significant relationship of outdoor air Pb with indoor dust Pb (ISA, 3.1.3.2; Egeghy et al., 2005). Rather, indoor dust Pb was associated with Pb concentration in soil and

29 As discussed in chapter 4 below, indoor dust is a major pathway for air-related Pb exposure for preschool children, largely related to prevalent hand-to-mouth behavior at that age.

30 http://www.epa.gov/air/oaqps/greenbk/mnc.html2-35 several factors related to housing age, perhaps indi cating the greater role of sources other than air Pb for those households (Egeghy et al., 2005).

2.3.2.2 Outdoor Dust in Areas of Human Activity

Lead in particulate matter occurring on outdoor surfaces (outdoor dust) may reflect
current or historical Pb emissions , as well as the historical uses of Pb in products on buildings and infrastructure in surrounding areas. The concen trations of air-related Pb in outdoor dust and
the relative contribution of air-r elated Pb to the total Pb conc entrations in outdoor dust vary depending on the location-specific characteristics of air–related (and other) Pb sources. The role
of air-related sources in outdoor dust Pb has been documented in areas near industrial sources, such as smelters, where Pb concentrations in outdoor dust have been doc umented to decline in response to reduced emissions. For example, out door dust Pb concentrations in a long-time Canadian smelter town were found to track smelter Pb emissions, as a new smelting technology which reduced airborne Pb concentrations by 75% resulted in a 50% re duction in outdoor dust Pb loading rate and concentrations (2006 CD, p. 3-23; Hilts, 2003). The residence time of settled dust Pb (e.g., on sidewalks and other public surfaces ) and thus the response of settled dust Pb concentrations to changes in emissions and associ ated atmospheric deposition of Pb particles are expected to reflect site-specific rates of trans port or removal processes, such as stormwater runoff and atmospheric resuspension and tran sport (ISA, sections 2.3.1.3 and 2.3.2.4; Allott et al., 1990; Wong et al., 2006). Rates of dry deposition of Pb in large metropo litan areas during the past decade are much lower than those reported for the 1970s (ISA, sections 2.3.1 and 2.6.1; Table 2-4, below). For example, dry deposition of Pb into Los A ngeles harbor during 2002-2006 was more than an order of magnitude lower than rates reported for the same location in 1975 (ISA section 2.3.1.2; Sabin and Schiff, 2008; Lim et al., 2006). Across the Los Angeles metropolitan area, average rates generally ranged from 10 to 32 micr ograms per square meter per day (μg/m 2 /day) and down to 0.3 μg/m 2 /day for the non-urban site of Malibu dur ing 2002-2003 (Lim et al., 2006). Rates within this range are reported from studies in Manhattan and a non-industria l area of New Jersey, with a somewhat higher rate reported for a majo r industrial location with in the New York City metropolitan area (Yi et al., 2006; Caravanos et al., 2006a). Although rates have not been reported recently for smelter locations in the U.S ., the outdoor dustfall depos ition rate reported in a smelter town in British Columbia, Canada, afte r the installation of ne w technology that reduced average airborne Pb-TSP concentrations to a leve l still at least twice the current U.S. NAAQS (0.3 μg/m 3 from prior average of 1.1 μg/m 3 ) was several orders of ma gnitude higher than those reported for New York, Los Angeles and Chicag o urban areas (Hilts, 2003; Lim et al., 2006; Sabin et al., 2006; Yi et al., 2006; Caravanos et al., 2006a).2-36 From the few studies reporting levels of Pb loading or concentration in outdoor dust within the past decade or so, loading to surfaces of pedestrian traffic signals in New York City was on average approximately 15% of the loading reported on sidewalks in older, residential areas of downtown Baltimore (e.g., approximately 250 ug/ft 2 as compared to 1500 ug/ft 2 ) and an order of magnitude or more below that report ed in the long-time Canadian smelter town (Caravanos et al., 2006b; Farf el et al 2005; Hilts, 2003).

Table 2-3. Dry deposition of Pb in large metropolitan areas.

Description Average (or Median*) Dry Deposition Rate ( μ g Pb/m 2 /day) A Study

Los Angeles Harbor, June-Nov 2006 14* B Sabin and Schiff, 2008 Los Angeles Harbor, 2002-2003 C 15 Lim et al., 2006 Los Angeles Harbor, 1975 300* Sabin and Schiff, 2008 Los Angeles, metropolitan area urban sites, 2002-2003 C

10-32 Lim et al., 2006 Los Angeles, metropolitan area, non-urban site Malibu, 2002- 2003 C

0.3 “ Los Angeles, I-405, near Westwood (downwind side), spring 2003 D

24 Sabin et al., 2006 Los Angeles, I-405, near Westwood (upwind side), spring 2003 D 7.3 “ Jersey City, NJ, 2001- 2002 50 Yi et al., 2006 New Brunswick, NJ, 2001- 2002 8 “ Manhattan, NYC, 2 nd

story rooftop (unprotected), 2003-2005 27 Caravanos et al., 2006a Chicago, 1993-95 E 38-71 Yi et al 2001; Paode et al., 1998

A

– Methods generally involved collection and analysis of samples of deposited particulate matter; details provided in references cited. B - Rates for rest of off-shore transact from Santa Barbara to S an Diego Bay ranged from 0.52 (Oxnard) – 3.3 (San Diego Bay) μ g/m 3

. C - Average Pb-TSP range= 0.0056-0.017 μg/m 3 for urban sites; 0.0022 at Malibu site. D - Average Pb-TSP at downwind site over sampling period ~0.02 μg/m 3

. E – This time period is the most recent for which such data are reported for this metropolitan area.

2.3.2.3 Soil

As is the case for Pb in outdoor dust, Pb o ccurring in surface soils can be derived from current or historical emissions, as well as leaded paint usage on older buildings and other
structures. The relative role of these sources may vary with the type of environment and proximity to industry and population centers. In forested areas away from old urban ar eas, the role of leaded gasoline in soil contamination is illustrated by the documented reduc tions in Pb in surface soils subsequent to the phase-out of leaded gasoline for on-road vehicl es. For example, forest surface soil (litter)
concentrations in a transect from Vermont thr ough Maine and up to Gaspe in Quebec, which in 1979 exhibited a significant spatial trend ranging from 200 milligrams per kilogram, dry weight2-37 (mg/kg dw) at its southernmost point down to 60 mg/kg dw at its northernmost and most remote point in Quebec, declined to 32-66 mg/kg dw (w ith no spatial trend) by 1996 (ISA, section 2.6.1; Evans, 2005). In forests from the mid-Atlantic to southern New England, a reduction in litter Pb
concentration was observed between 1978 and 2004- 05 (ISA, section 2.6.1; Johnson and Richter, 2010). In the latter study, the au thors observed less change in con centration in the more northern sampling sites, which they attribute to reduced rates of organic matter decomposition in those colder temperature areas. Sim ilarly, an additional New England study by Kaste et al (2006) also documented a pattern in temporal reductions in soil Pb (O-horizon) re lated to decomposition activity. These recent findings are generally consiste nt with findings reported in the last review which indicated the gradual migration of depos ited Pb into mineral soils (e.g., Miller and Friedland, 1994; Kaste et al., 2003; Wang and Benoit, 1997; Johnson et al., 1995; Zhang, 2003). Few studies have investigated temporal trends of surface soil Pb concentrations in more populated areas in relation to re ductions in usage of leaded gasoline and paint. Current concentrations in areas of past heavy traffic powered by leaded gasoline are generally elevated above areas more distant from these areas (ISA, section 2.6.1). Current roadway-related sources of Pb (e.g., wear of vehicle parts), while substant ially less significant th an the historic use of leaded gasoline, may continue to provide some contribution to surface dust/soil in these areas (ISA, section 2.2.2.6). Surface soil and dust concentr ations are much higher in such areas in large, older cities than surrounding suburban ar eas (ISA, section 2.6.1). In older residential areas, the presence of leaded hous e paint is another contributor to surface soil concentrations (ISA, sections 2.6.1; Yesiloni s et al., 2008; Brown et al ., 2008; Clark et al., 2006). Areas of long-term Pb emissions from point sources appear to be the areas of highest surface soil Pb concentrations (ISA, secti ons 2.6 and 2.6.1). For example, Pb surface soil concentrations within approxima tely 100-250 meters of long-established Pb smelters have been five to ten times higher than those at 3-5 km distance (ISA, section 2.6.1; 2006 CD, Table 3-4).
Surface soil concentrations of Pb near U.S. mine s that are no longer active have also been found to be elevated above more distant areas (2006 CD , Table 3-6). Information described in the 2006 CD for areas surrounding smelters after implem entation of pollution cont rols, although showing
declines in Pb concentrations in outdoor dustfall, stre et dust and indoor dustfa ll, has not indicated
a noticeable decline in soil Pb concentrations (2006 CD, pp. 3-23 to 3-24). The continued Pb emissions in such industrial areas likely influence the dynamics of Pb concentrations in the soil, affecting any response to emissions reductions. Es timates of associated steady-state surface soil Pb concentrations or the expected longer-term tem poral pattern for this situation have not been
made. In summary, findings to date indicate th at many of those systems less influenced by current point sources have and may still be resp onding to reduced Pb deposition rates associated2-38 with reduced atmospheric emissions of Pb, incl uding those associated wi th the phase-out of leaded gasoline for on-road vehicles, while poten tial responses of soils near point sources and those involving historically depos ited Pb near roadways are less well characterized, but might be expected to have longer time horizons.

2.3.2.4 Biota

Terrestrial plants can take up Pb from soils in to roots and then transport it to other plant tissues, as well as absorb deposited Pb into above-ground plant tissues (ISA, section 3.1.3.3; 2006 CD, section 2.3.7; 1986 CD, sections 6.5.3 a nd 7.2.2.2.1). The relative contributions of these pathways to the different plant tissues di ffer with the physiology of different plants, the chemical and physical characteristics of the so il, and the relative leve ls of Pb in soil and atmospheric deposition (ISA, section 3.1.3.3). Te rrestrial animals may take in Pb through ingestion of vegetation, vegetation- consuming animals or soil, as we ll as directly from air. The
relative contributions from these terrestrial animal e xposure pathways vary with contamination level of the different items, as well as with sp ecies-specific factors, in cluding intake rates. The availability of data to document temporal trends in Pb concentrations in terrestrial
biota is somewhat limited. Measurements of Pb in some biota indicate re ductions in biologically available Pb over the past 30 years in some remote locations. For example, measurements of Pb
in lichen from Golden Lake in Mount Ranier National Park (2005) and Emerald Lake basin in Sequoia/Kings Canyon National Parks (2004) indicat e significant reductions (approximately 3-5- fold) since samples were previously collected in those locations in 1984 (ISA, section 2.6.6; Landers et al., 2008). Further, Pb in teeth of ju venile and adult moose in Isle Royale National Park in northern Michigan have also declined substantially (IS A, section 2.6.8; Vucetich et al., 2009).
Few recent data are available to characterize terrestrial biota Pb contamination levels associated with current air Pb deposition. In one example, however, Pb deposition associated with hauling mining materials has substantially increased Pb concentrations in moss within 10
meters of a road in the remo te wilderness areas of Cape Krusenstern National Monument,
Alaska. 31 In this example, the median Pb concentra tion measured within 10 meters of the haul road in summer 2001 was more than 20 times higher than at sites at great er distance from the road and nearly three orders of magnitude grea ter than those reported for this moss in other Alaska locations in 1990-1992 ( ISA, sect ion 2.3.1.2; Hasselbach et al., 2005). The composition of human and wildlife diet s (and associated contamination levels) influences the relative magnitude of dietary Pb intake, which may derive from currently existing

31 Red Dog mine is a zinc and Pb mine initiated in 1987. The materials are transported from the mine to a port on the Chukchi Sea via a 52-mile long haul road.2-39 or historic air sources in the U.S. or in countries that export food to the U.S. As noted in section 1.3.1.1 above, U.S. dietary Pb may also derive fr om nonair sources, such as through processing steps.

2.3.3 Aquatic Media

2.3.3.1 Surface Waters

In addition to delivery by atmospheric depositio n directly to surface waters, Pb is also
carried into surface waters via wa stewater effluent from munici palities and industry, stormwater runoff, erosion, and accidental discharges (2006 CD , p. AX7-142; ISA section 2.3.2). As a result of the phasing out of leaded gasoline for use in on -road vehicles, reductions in Pb concentrations
have been documented in surface waters of the North Atlantic Ocean, as well as the relatively less remote areas of the Great Lakes (2006 CD, p. 7- 23). The availability of studies investigating historical trends in surface waters is limited, in pa rt due to analytical issu es that challenged many monitoring programs in the past (2006 CD, AX7.2.2.2). Thus, temporal trends reported in many aquatic systems are based on sediment analyses (see section 2.3.3.2 below). Most Pb occurring in aquatic systems is associ ated with particles, with the distribution between particle-bound and dissolved form bei ng influenced by water chemistry as well as suspended sediment levels (ISA, 2.3.2; 2006 CD, pp. AX7-117 to AX7-118, Section AX7.2.2).
Water columns have been described as “transie nt reservoirs” for pollutants (2006 CD, p. 2-75). Once deposited to sediments, whether Pb is av ailable for resuspension back into the water column with potential transport further down a watershed versus being buried into deeper sediments depends on the aquatic system (ISA, s ection 2.7.2). In open oc ean waters (generally characterized by depth and distance from continenta l sources), resuspension to surface waters is unlikely. In more shallow systems, and those influenced by land sources (e.g., stormwater runoff as well as point sources), resusp ension may play a role in wate r column concentrations. For example, studies in San Francisco Bay, the southe rn arm of which has an average depth of 2 m, have indicated that Pb particles may be rem obilized from surface sediments into the water column (2006 CD, AX7-141). The distribution of Pb dissolved in many U. S. surface waters has been reported by the United States Geological Survey (USGS) National Water-Quality Assessment (NAWQA) program. The NAWQA data set referenced in the ISA (ISA, section 2.6) encompasses data
collected from 1991-2003 on Pb concentrations in flowing surface waters for more than 50 river basins and aquifers throughout the country (2006 CD, Section AX7.2.2.3). Th ese data indicate a
mean dissolved Pb concentrati on in U.S. surface waters of 0.66 μ g/L (range 0.04 to 30 μ g/L) in waters affected by a combined contribution of na tural and anthropogenic sources, as compared to
a mean of 0.52 μ g/L (range 0.04 to 8.4 μ g/L) for waters in “forest” , “rangeland”, and “reference”2-40 sites (2006 CD, Section AX7.2.2.3). The highest su rface water Pb concentrations were observed in sites impacted by land uses such as mi ning (2006 CD, p. AX7-131). The role of surface runoff in delivering contamination to waters ne ar such land uses, as well as near metals industries, presents a challenge to the task of disentangling the rela tive contributions from atmospheric deposition as compared to those associated with surface runoff.

2.3.3.2 Sediments

Many studies have investigated temporal tre nds in sediment Pb concentrations, using
sediment cores or surface sediment Pb concentr ation, with declines documented in many systems and usually attributed to the pha sing out of leaded gasoline for on-road vehicles and industrial emissions reductions (ISA, sections 2.6.2 and 2.7.5; 2006 CD, section AX7.2.2). Several studies documenting the increased Pb deposition of the industrial age, includi ng specifically leaded gasoline usage, and the subsequent declines associated with on-ro ad leaded gasoline phase-out were reported in the 2006 CD. They include investigations i nvolving sediment cores from the Okefenokee Swamp in Georgia as well as from 35 reservoirs and lakes in urban and reference locations (ISA, section 2.6.2; 2006 CD, p. AX7-141). In the latter, the median reduction in Pb mass accumulation rate in the cores, adjusted for background concentrations, was 246%, with the largest decreases in lakes located in dense urban watersheds (ISA , section 2.6.2; 2006 CD, p. AX7-141; Mahler et al, 2006). A third study of sediment core s in 12 lakes in the Great Lakes area also documented a peak in Pb concentrations consistent with peak us e of leaded gasoline in the U.S. in the mid 1970s and declining concentr ations in most lake sediments through the mid 1990s (2006 CD, p. 2-55; Yohn et al., 2004). Sediment surveys by the USGS NAWQA have reported the highest Pb concentrations in Ida ho, Utah, and Colorado, with seven of the highest
concentrations at sites classified as mining land use (2006 CD, p. AX7-133). Among the more recent investigation of temporal trends in aquatic sediments described in
the ISA is that associated with the Western Ai rborne Contaminants Assessment Project which
documented Pb in sediment cores from 14 lakes in eight U.S. national parks in western states, including three in Alaska (ISA, section 2.6.2; Lande rs et al., 2010). Among the Alaska cores, in which concentrations were genera lly on the order of 20 μg/kg dw, th ere was little variation in Pb concentration, flux or enrichment factor. The ot her park cores, with few exceptions, generally
exhibited an increase in concentration comme ncing in the mid-nineteenth century, which transitioned to declining trends in the past few decades, with lower concentrations in more recent, surface material. The highest concentra tion was recorded at core depth corresponding to2-41 the mid-1970s, in one of the Sequoia/Kings Canyon lake cores (Figure 2-16; ISA, section 2.6.2; Landers et al., 2010 32 ).

Figure 2-14. Temporal trend in sediment Pb concen tration from core samples in twelve lakes at eight National Parks or Preserves.

Analyses of cores taken in several lake s and reservoirs along the Apalachicola, Chattahoochee, and Flint River Basin from north of the Atlanta, GA metropolitan area to the Gulf of Mexico indicate changes in sediment c oncentration both with time and in relation to influence of the large metropol itan area of Atlanta (ISA, s ection 2.6.2; Callender and Rice, 2000). Highest concentrations were documented ju st downstream from Atlanta at the core depth corresponding to the 1975-1980 tim e period; the corresponding concentration for the most recent time period (1990-1995) at that location was approximately 50% lower (ISA, section 2.6.2; Callender and Rice, 2000). These data may re flect changes in surface water discharges of Pb in the Atlanta area, during this time period, as well as changes in air deposition. The smaller

32 Figure created from database for Landers et al (1980); http://www.nature.nps.gov/air/ Studies/air_toxics/wacap.cfm

. 0 25 50 75 100 125

1800 1830 1860 1890 1920 1950 1980 2010Pb Concentration (mg/kg, DW)

Year Material Deposited Sequoia/Kings Canyon-Pear (mid California) Sequoia/Kings Canyon-Emerald (mid California) Mt Ranier-Golden (mid Washington) Mt Ranier-LP19 (mid Washington) Glacier-Snyder (Montana) Glacier-Oldman (Montana) Rocky Mnt-Lone Pine (Colorado) Rocky Mtn-Mills (Colorado) Olympic (Washington) Denali (mid Alaska) Gates of the Arctic (n. Alaska) Noatak (n. Alaska)2-42 reduction (on the order of 20%) observed across the 20-year time period at the upstream site is likely more generally reflective of changes in air deposition.

2.3.3.3 Biota

Aquatic biota can contain Pb that may be de rived from historic or current atmospheric deposition in the watershed, from historic or cu rrent direct water discharges or from natural sources (ISA, section 6.2.1). In near-shore sy stems and populated watersheds, all of these sources may play a role in observed Pb concentra tions, complicating consider ation of the role of ambient air Pb deposition. Additional challenge s are presented by available data for mobile species such as fish (e.g., IS A, section 2.6.8; 2006 CD, section AX 7.2.2.2). A 20-year record of
Pb concentrations in blue and zebra mussels and oysters in U.S. coastal waters provides varying evidence on temporal trends that may reflect patter ns in site-specific environmental releases as well as other ecosystem impacts on Pb fate a nd transport over that pe riod (ISA, section 2.6.7; Kimbrough et al., 2008).

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Wang, E. X.; Benoit, G. (1997) Fate and transport of contaminant lead in spodosols: a simple box model analysis. Water Air Soil Pollut. 95: 381-397.2-45 Watmough, SA; Dillon, PJ. (2007). Lead biogeochemistry in a central Ontario forested watershed. Biogeochemistry 84: 143-159. http://dx.doi.org/10.1007/s10533-007-9110-6

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### 3 HEALTH EFFECTS AND EXPO SURE/RISK INFORMATION

This chapter presents key aspects of the curr ent evidence of lead-rel ated health effects and presents exposure/risk information from th e quantitative assessment performed in the last review in the context of the currently available evidence. Staff has drawn from EPA’s synthesis of the scientific evidence presented in the Integrated Science Assessment for Lead (USEPA, 2013; henceforth referred to as the ISA) and 2006 Air Quality Criteria Document for Lead (USEPA, 2006; henceforth referred to as th e 2006 CD), and from the documentation of the 2007 human exposure and health risk assessment (doc umented in USEPA, 2007a; henceforth referred to as the 2007 REA). The chapter is organize d into sections considering the information on blood Pb as a biomarker (section 3.1), the nature of Pb effects on health (section 3.2), public health implications and at-risk populations (s ection 3.3), and exposure and risk information (section 3.4). Presentation within these sections is organized to address key policy-relevant questions for this review concerning the evid ence and exposure/risk information, building upon the questions included in th e IRP (IRP, section 3.1).

3.1 INTERNAL DISPOSITION AND BIOMARK ERS OF EXPOSURE AND DOSE The health effects of Pb, di scussed in detail in the IS A and summarized in section 3.2 below, are remote from the portals of entr y to the body (i.e., the respiratory system and gastrointestinal tract). Consequent ly, the internal disposition and di stribution of Pb is an integral aspect of the relationship between exposure a nd effect. As discussed below, blood Pb has traditionally been used as a biomarker of Pb exposure and of internal dose, with relationships
between air Pb concentrations and blood Pb c oncentrations informing consideration of the NAAQS for Pb. Information available in this revi ew continues to support c onclusions in the last review with regard to these relationships. Lead associated with inhaled particles may, depending on particle si ze and Pb solubility, be absorbed into the systemic circ ulation or transported with particles to the gastrointestinal tract (ISA, section 3.2.1.1). The absorption efficiency of Pb from the gastrointest inal (GI) tract varies
with characteristics associated with the ingested Pb (e.g., particle size and chemical form or matrix), as well as with an i ndividual’s physiology (e.g., maturity of the GI trac t), nutritional status (e.g., iron, calcium, and zinc deficiencies increase absorption) , and the presence of food in the GI tract (ISA, section 3.2.1.2). Once in th e blood stream, where appr oximately 99% of the Pb is associated with red blood cells (mostly bound to aminolevulinic acid dehydratase, the predominant ligand), Pb is quickly distribu ted throughout the body (e.g., within days) and is available for exchange with the soft and skeletal tissues, conceptually viewed as the fast and slow turnover pools, respectivel y (ISA, section 3.2.2). Skeletal tissue serves as the largest3-2 storage compartment, with much less Pb stored in soft tissues (e.g., kidne y, liver, brain, etc.) (ISA, section 3.2.2.2). The role of the bone as the main storage comp artment is related to the ability of Pb to form stable complexes with phosphate and repl ace calcium in the salt comprising the primary crystalline matrix of bone (ISA, section 3.2.2.2). In infants le ss than a year old, the bone is estimated to contain approximately 60% of th e total body burden of Pb (ISA, section 3.2.2.2; Barry, 1975). Circulating Pb is taken up into the bone regions of active calcification. Accordingly, during early childhood there is rapi d uptake of Pb into mineralizing bone, with somewhat more than 70% of total body burden Pb estimated to reside in bone of children aged 2 to 16, increasing up to more than 90% by adul thood (ISA, section 3.2.2.2; Barry, 1975). The net accumulation of Pb in bone over a person’s lifetime results in bone lead concentrations generally increasing with age (ISA, section 3.2.2.2).
The distribution of Pb in the body is dynamic. Throughout life, Pb in the body is exchanged between blood and bone and between blood and soft tissues (ISA, sections 3.3.5 and 3.2.2; 2006 CD, section 4.3.2). The rates of thes e exchanges vary with age, exposure and various physiological variables. For example, resorption of bone, which results in the
mobilization of Pb from bone in to the blood, is a somewhat ra pid and ongoing process during childhood and a more gradual process in late r adulthood (ISA, sec tions 3.2.2.2, 3.3.5 and 3.7.2). Resorption rate is appreciably in creased in pregnant or nursing women and in association with osteoporosis in postmenopausal women or, to a lesser magnitude, in older men (ISA, sections 3.3.5.2). Changes in Pb exposure circumstances can also influence these exchanges, e.g., when exposure levels are substantially reduced, the relative contributi on of Pb from bone to blood Pb concentration increases (ISA, section 3.3.5). The st udies that address the relative contributions of bone Pb and current Pb exposure to blood Pb are limited to a few human studies during the 1980s and early 1990s, when leaded gasoline usage was common, and a study in non-human primates. These studies indicate an appreciable contribution from bone Pb stores to Pb in blood,
on the order of 40-70% of blood Pb contribu ted from bone, under circumstances with higher concurrent exposure than exposures common t oday (ISA, section 3.3.5; Smith et al., 1996; Gulson et al., 1995; Manton, 1985; Franklin et al., 1997). During bone resorption that occu rs in pregnancy, Pb is released from bone, increasing the bone contribution to maternal blood Pb levels, an d maternal Pb circulates across the placenta, posing risk to the developing fetus and provi ding the fetal body burden (ISA, sections 3.2.2.4, 3.3.5, 3.7.2 and 3.7.3; 2006 CD, 6.6.2; Chuang et al., 2001). The relative size of contributions of maternal bone Pb and current maternal exposur e to maternal blood Pb and fetal body burden are influenced by the relative magnitude of curre nt and historical expos ures. In various study populations with mean maternal blood Pb levels ranging from 1.7 to 8.6 μg/dL, average blood Pb3-3 concentration in the umbilical co rd (as representative of newbor n blood) has been reported to range from 70% to 100% of av erage maternal blood Pb (ISA, section 3.2.2.4); the range is similar for four study populations with mean maternal blood Pb level below 4 μg/dL (Amaral et al., 2010; Patel and Prabhu, 2009; Lagerkvist et al., 1996; Jedrychowski et al., 2011). The relationship between cord blood Pb and maternal blood Pb concentrations is more variable for individual mother-child pairs. In a low-income population with mean maternal blood Pb of 1.9 μg/dL, factors associated with occurrences of relatively higher cord-to-maternal blood Pb ratios included higher maternal blood pressure and alco hol consumption, while f actors associated with relatively lower cord-to-maternal blood Pb ra tios included higher maternal hemoglobin and sickle cell trait presence (Harvill e et al., 2005). As a result of th e contributions of maternal bone Pb to maternal blood Pb during pregnancy, the contribution to fetal body burden from maternal
bone Pb relative to maternal conc urrent exposure can be appreciab le. This maternal bone Pb contribution to fetal body burden is likely to vary, however, in response to differences between maternal historical exposures and those dur ing pregnancy, among othe r factors (2006 CD, sections 4.3.1.5 and 4.3.2.5; ISA, section 5.1; Chuang et al., 2001; Gulson et al., 1999; Gulson et al., 2003; Gulson et al., 2004a; Ro thenberg et al., 2000).
Limited data indicate that blood Pb levels in some newborns may decline during the period extending through the first few months of life; the extent to which this may occur may be influenced by the magnitude of blood Pb level at birth and of subseque nt exposure during early infancy (ISA, section 3.4.1; Carbone et al., 199 8; Simon et al., 2007; Gulson et al., 1999, 2001). As infants become more mobile and engage in hand-to-mouth behavior, blood Pb levels then commonly increase to a peak ar ound one to two years of age (ISA, sections 3.4.1 and 5.2.1.1).

 Does the current evidence continue to support blood Pb level as a useful indicator of Pb exposure and dose for purposes of characterizing Pb health effects, with well-recognized strengths and limitations? To what extent does the evidence suggest alternatives? As discussed in past CDs and in the ISA, blood Pb is the most commonly used indicator of human Pb exposure. Given th e association with exposure and the relative ease of collection, blood Pb levels are extensively used as an index or biomarker of exposure by national and international health agencies, as well as in epidemiological and toxi cological studies of Pb health effects and dose-response relationships (ISA, sections 3.3.2, 3.4.1, 4.3, 4.4, 4.5, 4.6, 4.7, and 4.8). While bone Pb measurements are also used in epidemiological studies as an indicator of cumulative Pb exposure, blood Pb measurements remain the predominant, well-established and well-characterized exposure approach.3-4 Since 1976, the U.S. Centers for Disease Control and Prevention (CDC) has been monitoring blood Pb levels nationally through th e National Health and Nutrition Examination Survey (NHANES). This survey has documented the dramatic decline in mean blood Pb levels in all ages of the U.S. population that has occu rred since the 1970s, as shown in Figure 3-1, and
that coincides with actions on l eaded fuels, leaded paint, l ead in food packaging, and leadcontaining plumbing materials that have reduced Pb exposure in the U.S. (ISA, section 3.4.1; Pirkle et al., 1994; Schwemberger et al., 2005). This decline ha s continued over the more recent past. For example, the 2009-2010 geometric mean blood Pb level in U.S. children aged 1-5 years is 1.17 μg/dL, as compared to 1.51 μg /dL in 2007-2008 (ISA, section 3.4.1) and 1.8 μg/dL in 2003-2004, the most recent data available at the time of the last review (73 FR 67002).
Somewhat less dramatic declines ha ve been reported in the upper tails of the distribution and in different groups with higher blood Pb levels th an the general child population (ISA, Figures 3-17 and 3-19).

Source: Adapted from data fr om the NHANES (NCHS, 2010) Note: The means of log blood Pb were weighted to represent national averages. Data were from the publically available NHANES II , NHANES III (1988-1991 and 1992-1994), and the continuous NHANES (1999-2000 , 2003-2004, 2005-2006, 2007-2008). Continuous NHANES data f rom 2001-2002 and 2009-2010 are not included because there were only 551 blood Pb samples in each of those data sets. The year plot ted for exam year was the reported exam year for NHANES II, the middle year of each of the phases of NHANES III, and the second year of each of the continuous NHANES. Figure 3-1. Temporal trend in mean blood Pb leve ls for NHANES cohorts (ISA, Figure 3- 18).3-5 The CDC, and its predecessor agencies, have for many years used blood Pb level as a metric for identifying highly exposed children at risk of adverse health effects for whom recommendations might be made for their protection (e.g., CDC, 1991; CDC, 2005). In 1978, when the Pb NAAQS was initially established, the CDC recognized a blood Pb level of 30 μ g/dL as a level warranting individua l intervention (CDC, 1991). In 1985, the CDC recognized a level
of 25 μ g/dL for intervention, and in 1991, they adopt ed a multi-tier approach that recommended
individual intervention ac tions at a level of 15 μ g/dL and implementation of more general community-wide preventi on activities if many children in a community have blood Pb at or
above 10 μ g/dL (CDC, 1991; CDC, 2005). In 2005, CDC revised their statement on Preventing Lead Poisoning in Young Children , specifically recognizing the ev idence of adverse health
effects in children with blood Pb levels below 10 μ g/dL and emphasizing the importance of preventive measures (CDC, 2005). 1 Consistent with this statement, the CDC revised their approach in 2012 to one that relies on the 97.5 th percentile of blood Pb c oncentrations in U.S. children aged one to five years of age (currently 5 μg/dL) 2 as a reference level for identifying young children for whom they recommend particular follow-up actions (CDC, 2012). Unless influenced by a recent elevation in exposure, blood Pb measurements are a reflection of total body burden. Accordingly, Figure 3-1 illustrates the reduction in Pb body burden in the U.S. population over th e past 40 years. Associations of health effects with blood Pb measurements indicate relationships with body burden and may, in some cases, indicate relationships with recent exposures. The exte nt to which blood Pb measurements represent current or recent exposure circumstances, howev er, may be uncertain, particularly where histories include exposures largel y different from those occurring more recently (ISA, sections 3.3 and 3.3.2). This uncertainty may be greate r for blood Pb measurements taken in older
children 3 and adults than those for young children as a result of their longer exposure histories. For example, the Pb in bone of adults may have accumulated over decades of Pb exposure (with past exposures often greater than current ones for current U.S. populations) such that the bone may be a significant source of Pb in blood in later years of life, after expos ure has ended or been appreciably reduced. Thus, in a dult and older child populations w ith past exposures that were

1 With the 2005 statement, CDC identified a variety of reasons, reflecting both scientific and practical considerations, for not lowering the 1991 level of concern, including a lack of effective clinical or public health interventions to reliably and consistently reduce blood Pb levels that are already below 10 μ g/dL, the lack of a demonstrated threshold for adverse effects, and concerns for deflecting resources from children with higher blood Pb levels (CDC, 2005).

2 CDC intends to update the value every 4 years using the two most recent NHANES surveys (CDC, 2012).

3 There is a paucity of experimental measurements of Pb biomarkers during adolescence to inform our characterization of Pb biokinetics (and relative roles of rece nt vs historic exposure on blood Pb levels) during this lifestage, in which individuals undergo rapid changes in sexual development, growth, food and water intake, bone growth and turnover, behavior, etc. (ISA, section 3.3).3-6 appreciably elevated in comparison to more r ecent exposures, current blood Pb levels may predominantly reflect their exposur e history rather than their cu rrent exposures (ISA, sections 3.3.5, 3.3.5.2 and 3.4.1). Accordingly, the extent to wh ich studies using cro ss-sectional blood Pb measurements as the exposure biomarker info rm our understanding of relationships between recent Pb exposures and various health effects can differ across age groups and is greatest for very young children, as discu ssed in section 3.3 below. The relationship of children’s blood Pb to r ecent exposure may reflect their labile bone pool, with their rapid bone turnove r in response to rapid childh ood growth rates (ISA, section 3.3.5). The relatively smaller skeletal compartm ent of Pb in children (particularly very young children) compared to adults is subject to mo re rapid turnover. As a result the blood Pb concentration of children can more quickly reflec t changes in their tota l body burden (associated with their shorter exposure hist ory) and can also reflect chan ges in recent exposures (ISA, section 3.3.5). Multiple studies of the relationship between Pb exposure and blood Pb in children (e.g., Lanphear and Roghmann 1997; Lanphear et al., 1998) have shown young children’s blood Pb levels to reflect Pb exposures, including exposures to Pb in surface dust. These and studies of child populations near sour ces of air Pb emissions, such as metal smelters, further demonstrate
the effect of airborne Pb on interior dust and on blood Pb (ISA, sections 3.4.1, 3.5.1 and 3.5.3; Hilts, 2003; Gulson et al., 2004b). Accordingly, blood Pb level was the index of exposure for children in the risk assessment performed in the last Pb NAAQS review (described in section 3.4 below). A well-recognized strength of using childre n’s blood Pb to investigate relationships between Pb exposure and health effects is the rela tively lesser uncertainty in the causality aspects of such relationships than might be associated with such relationships based, for example, on media concentration. Blood Pb is an integrated marker of aggregate Pb exposure across all pathways. The blood Pb concentration-response relationships described in epidemiological studies of lead-exposed populati ons do not distinguish among di fferent sources of Pb or pathways of Pb exposure (e.g., inhalation, ingesti on of indoor dust, ingestion of dust containing leaded paint). Given our focus on ambient air contributions to Pb e xposures, discussion in response to the question below considers the av ailable information re garding relationships
between Pb in ambient air and the associated Pb in blood. Additionally, the exposure component of the risk assessment performed for the last Pb NAAQS review (and de scribed in section 3.4 below) employed biokinetic modeling to estimate blood Pb levels associated with aggregate Pb exposure to inform our estimates of contributions to blood Pb arising fr om ambient air-related
Pb.3-7 Alternative biomarkers of Pb exposure incl ude bone Pb, teeth Pb, and hair Pb (ISA, section 3.3.1, 3.3.3 and 3.3.4). Given the role of bone as the repository of more than 90% of an adult body’s Pb burden, bone Pb levels are re cognized as indicators of body burden and cumulative lifetime exposure (ISA, sections 3.2.2.2, 3.3 and 3.3.5). The currently available evidence does not, however, indicate these or any othe r alternatives to be superior to blood Pb in young children or as commonly used for the purpose s of tracking recent Pb exposures and for assessing potential health risk for this age group (ISA, sectio n 3.7.3). In summary, the current evidence continues to support our conclusions from the last review regarding the use of blood Pb levels as an internal biomarker of Pb exposure and dose informative to characterize Pb health effects in young children.

 To what extent has new information alt ered scientific conclusions regarding the relationships between Pb in ambient air and Pb in children’s blood? As described above, blood Pb is an integrat ed marker of aggregate exposure across all pathways and a reflection of exposure history. Thus, our interpretation of the health effects evidence for purposes of this review necessitates characterization of the relationships between Pb from those sources and pathways of interest in this review (i.e., those related to Pb emitted into the air) and blood Pb. The evidence in this re gard derives from analyses of datasets for populations residing in areas w ith differing air Pb concentrations, including datasets for
circumstances in which blood Pb levels have ch anged in response to changes in air Pb. The
control for variables other than air Pb that can affect blood Pb varies across these analyses.
Lead in ambient air contributes to Pb in blood by multiple exposure pathways by both inhalation and ingestion exposure routes (ISA, section 3.1.1). The qua ntitative relationship between ambient air Pb and blood Pb, which is often termed a slope or ratio, describes the increase in blood Pb (in μg/dL) estimated to be a ssociated with each unit increase of air Pb (in μg/m 3 ). Ratios are presented in the form of 1:x, with the 1 representing air Pb (in μg/m 3 ) and x representing blood Pb (in μg/dL). Description of rati os as higher or lower re fers to the values for x (i.e., the change in blood Pb pe r unit of air Pb). Slopes are pres ented as simply the value of x.
At the conclusion of the last review in 2008, the EPA interpreted the evidence as providing support for use (in informing the Admini strator’s decision on st andard level) of a range “inclusive at the upper end of estimates on the order of 1:10 and at the lower end on the order of 1:5” (73 FR 67002). This conclusion refl ected consideration of the air-to-blood ratios presented in the 1986 CD 4 and associated observations regardin g factors contribu ting to variation in such ratios, ratios reported subsequently and ratios estimate d based on modeling performed in the REA, as well as advice from CASA C (73 FR 66973-66975, 67001-67002). The information

4 The 2006 CD did not include an assessment of then-current evidence on air-to-blood ratios.3-8 available in this review, which is assessed in the ISA and largely, al though not completely, comprises studies that were available in the la st review, does not alter the primary scientific
conclusions drawn in the last re view regarding the relationships between Pb in ambient air and
Pb in children’s blood. The ratios summarized in the ISA in this review span a range generally consistent with the range concl uded in 2008 (ISA, section 3.5.1). The air-to-blood ratios for children, or for popul ations inclusive of children, discussed in the ISA for this review are summarized in Table 3-1. The evidence pertaining to this quantitative relationship between air Pb and children’s blood Pb is now, as in the past, limited by
the circumstances in which the data are collected. These estimates are generally developed from studies of populations in a va riety of Pb exposure circumstances. Accordingly, there is significant variability in air-to-blood ratios among the differe nt study populations exposed to Pb through different air-related exposur e pathways and at different expos ure levels. This variability
in air-to-blood estimates can relate to the representation of air-related pathways and study populations, including, for example, relatively narro w age ranges for the population in order to reduce age-related variability in blood Pb, or including populations with narrowly specified dietary sources. It can relate to the study popul ation exposure and blood Pb levels (ISA, section 3.7.4). It can also relate to the precision of air and blood measurements and of the study circumstances, such as with regard to spatial an d temporal aspects. Additionally, in situations where exposure to nonair sources covaries with air-related exposures that are not accounted for in deriving ratio estimates, uncertainties may relate to the potential for confounding by nonair exposure covariance (ISA, section 3.5). Most st udies have reported the relationship as either log-log or linear (Table 3-1; ISA, section 3.7.4). As was noted in the last review, age is an important influence on the magnitude of air-toblood ratio estimates derived. Ratios for children are generally higher than those for adults, and higher for young children than olde r children, perhaps due to behavi oral differences between the age groups, as well as their shor ter exposure history. Similarl y, given the common pattern of higher blood Pb levels in pre-sc hool aged children than during the rest of childhood, related to
behaviors that increase environm ental exposures (e.g., hand-to-mouth activity), ratios would be expected to be highest in earlier childhood. A dditionally, estimates of air-to-blood ratios that include air-related ingestion pa thways in addition to the inhalation pathway are “necessarily higher,” in terms of blood Pb response, than those estimates based on inhalation alone (USEPA 1986, p. 11-106). Thus, the extent to which studi es account for the full set of air-related inhalation and ingestion exposure pathways affect s the magnitude of the resultant air-to-blood estimates, such that including fewer pathways as “air-related” yields lowe r ratios. Estimates of air-to-blood ratios can also be influenced by population characteristics th at may influence blood3-9 Pb; accordingly, some analyses include adjustments. Most of the studies in Table 3-1 include ratios derived from linear analyses, while a subset are derived from nonlinear models. Given the recognition of young children as a ke y at-risk population in section 3.3 below, as well as the influence of age on blood Pb levels , the studies presented in Table 3-1 are grouped with regard to the extent of their inclusion of children younger than or barely school age (less than or equal to five years of age). Among the first group of studies, focused exclusively on young children, only one study dates from the end of or after the phase-out of leaded gasoline usage (namely, Hilts, 2003). This study reports cha nges in children’s blood Pb levels associated
with reduced Pb emissions and associated air con centrations near a Pb smelter in Canada (for children through age five). Give n the timing of this study, after the leaded gasoline phase-out, and its setting near a smelter, the ambient air Pb in this study may be somewhat more comparable to that near sources in the U.S. t oday than other studies di scussed herein. The study authors report an air- to-blood ratio of 1:6. 5 An EPA analysis of th e air and blood data reported for 1996, 1999 and 2001 results in a ratio of 1:6.5, and the analysis focused only on the 1996 and 1999 data (pre- and post- the new technology) yiel ds a ratio of 1:7 (ISA, section 3.5.1; Hilts, 2003). 6 The two other studies that focused on chil dren of age 5 or younger analyzed variations
in air Pb as a result of varia tions in leaded gasoline usage in Chicago, Illinois. The study by Hayes et al. (1994) compared patterns of ambient air Pb reductions and blood Pb reductions for large numbers of children, aged 6 months to 5 years, in Chicago between 1974 and 1988, a period when significant reductions occurred in bot h measures. The study re ported a better fit for the log-log model which describes a pattern of hi gher ratios with lower ambient air Pb and blood Pb levels (Hayes et al., 1994). Based on the log-log model, the ratio derived for the relationship of quarterly mean air concentra tion with blood Pb during the period is 1:8 (Table 3-1). Another analysis for a Chicago dataset, performed by Schwartz and Pitcher (1989) focused on the

5 Sources of uncertainty include the role of factors other than ambient air Pb reduction in influencing decreases in blood Pb (ISA, section 3.5.1). The author cited remedial programs (e.g., community and home-based dust control and education) as potentially responsible for some of the blood Pb reduction seen during the study period (1997 to 2001), although the author notes that these programs were in place in 1992, suggesting they are unlikely to have contributed to the sudden drop in blood Pb levels occurring after 1997 (Hilts, 2003). Other aspects with potential implications for ratios include the potential for children with lower blood Pb levels not to return for subsequent testing, and the age range of 6 to 36 months in the 2001 blood screening compared to ages up to 60 months in earlier years of the study (Hilts, 2003).

6 This study considered changes in ambient air Pb levels and associated blood Pb levels over a five-year period which included closure of an older Pb smelter and subsequent opening of a newer facility in 1997 and atemporary (3 month) shutdown of all smelting activity in the summer of 2001. The author observed that the air-toblood ratio for children in the area over the full period was approximately 1:6. The author noted limitations in the dataset associated with exposures in the second time peri od, after the temporary shutdown of the facility in 2001, including sampling of a different age group at that time and a shorter time period (3 months) at these lower ambient air Pb levels prior to collection of blood Pb levels. Consequently, EPA calculated an alternate air-to-blood Pb ratio based on ambient air Pb and blood Pb reductions in the fi rst time period, after opening of the new facility in 1997 (ISA, section 3.5.1).3-10 association of blood Pb in black ch ildren (aged < 5 years) with the use of leaded gasoline from 1976 through 1980. Given that leaded gasoline exposure occurs by air-related pathways, additional analyses have related th e leaded gasoline usage for this period to air concentrations. The resulting relationship of bl ood Pb with air Pb (adjusted fo r age and a number of other covariates) yields a ra tio of 1:8.6 (ISA, table 3-12, section 3.5.1). The blood Pb concentrations in the two leaded gasoline studies are appreciably higher (a factor of two or more) than those in the study near the smelter (Hilts, 2003). The second group of studies in Table 3-1 (compr ising studies includi ng but not limited to children less than or equal to five years of age) includes a co mplex statistical analysis and
associated dataset for a cohort of children born in Mexico City from 1987 through 1992 (Schnaas et al., 2004). This study, which was not assessed in the last review, en compasses the period of leaded gasoline usage and further informs our understanding of f actors influencing the quantitative relationship between air Pb and children’s blood P b. Air-to-blood ratios developed from this study are influenced by a number of f actors and appear to range from roughly 2 to 6, in addition to an estimate of 9 (ISA, section 3.5.1), although the latter is derived from a data set
restricted to the latter years of the study when little change in air Pb concentra tion occurred, such that the role of air Pb may be more uncertai n. Estimates associated with the developmental period of highest exposure (e.g., age 2 years) range up to approximately 6, illustrating the influence of age on the ratio (ISA, section 3.5.1). Also in the s econd group in Table 3-1 are two much older studies of populations with age range s extending well beyond 6 years. The first is the review and meta-analysis by Brunekreef (198 4) using datasets avai lable at the time for variously aged children as old as 18 years with identified air monitoring methods and reliable
blood Pb data for 18 locations in the U.S. and internationally. 7 The author discusses potential confounders of the relationship between air Pb and blood Pb, recognizing the desirability of taking them into account when deriving an air- to-blood relationship from a community study but noting that was not feasible in such an anal ysis. Two models were produced, one based on the full pooled dataset and a second limited to blood Pb-a ir Pb data pairs with blood Pb levels below 20 μg/dL (r 2 values were 0.692 and 0.331, respecti vely). From these two log n -log n models, airto-blood ratio estimates were derived for air concentrations corresponding to the geometric means of the two sets of data pairs. At those concentrations (1.5 and 0.54 μg/m 3 , respectively), the resultant ratios both round to 5. The study by Schwartz and Pitcher (1989) described above also analyzed the relationship between U.S. NH ANES II blood Pb levels for white subjects, aged

7 In the dataset reviewed by Brunekreef (1984), air-to-blood ratios from the subset of those studies that used quality control protocols and presented adjusted slopes include values of 3.6 (Zielhuis et al., 1979), 5.2 (Billick et al., 1979, 1980); 2.9 (Billick et al., 1983), and 8.5 (Brune kreef et al, 1983). The studies cited here adjusted for parental education (Zie lhuis et al., 1979), age and race (Billick et al., 1979, 1980) and air Pb monitor height (Billick et al., 1983); Brunekreef (1984) used multiple regression to control for several confounders (73 FR 66974).3-11 <74 years, and national usage of leaded gasoline. A separate, less specifically described, air Pb
dataset was used to convert the relationship of blood Pb with gas Pb to one for blood Pb with air Pb, with a resultant ratio on th e order of 9, adjusted for age and other covariates (Henderson, 2007a, pp. D-2 to D-3; ISA, Table 3-12).
The last two studies included in Table 3-1 ar e focused on older children (ages 6-11). The
methods for characterization of air Pb concentr ations (and soil Pb for Ranft et al., 2008) also
differ from other studies in Table 3-1. The firs t study regressed average blood Pb concentrations for multiple locations around Mumbai, India on averag e air Pb concentrations at those locations (Tripathi et al., 2001). The valu es in the linear regression we re 13 pairs of location-specific geometric means of all the da ta collected over the 13-year period from 1984 to 1996; the reported slope was 3.6 (Tripathi et al., 2001). The location-spec ific geometric mean blood Pb levels in this study (8.6-14.4 μg /dL) indicate blood Pb distribu tions in this age group much higher than those pertinent to similarly aged children in the U.S. today. The second study analyzed air, soil and children’s blood Pb concentrations in Duisburg, Germany, during the leaded gasoline phase-out (Ranft et al., 2008). Av erage blood Pb levels declined over the nearly 20-year study period from 9 μg/dL in 1983 (345 child ren average age of 9 years) to 3 μg/dL in 2000 (162 children average of 6 years). 8 Average air Pb concentr ation declined from 0.45 μg/m 3 to 0.06 μg/m 3 over the same period, with the largest re duction occurring between the first study year (derived from tw o monitoring sites for full study area ) and the second study year, 1991, for
which air concentrations were derived from a combination of dispersion modeling and the two monitoring sites. 9 For a mean air Pb concentration of 0.1 μg/m 3 , the study’s multivariate loglinear regression model predicted air-to-blood ratios of 3.2 and 6.4 for “background” blood Pb concentrations of 1.5 and 3 μg/dL, respectively. In this study, background referred to Pb in blood from other sources; the bl ood Pb distribution over the study pe riod, including levels when air Pb concentrations are lowest, indicates 3 μg /dL may be the better es timate of background for this study population. Inclusion of soil Pb as a variable in the model may have contributed to an
underestimation of the these blood Pb-air Pb ratios for this study because some of the Pb in soil likely originated in air and the blood Pb-air Pb slope does not in clude the portion of the soil/dust Pb ingestion pathway that derive s from air Pb. Using univariat e linear, log-log and log-linear
models on the median air and blood Pb concentrati ons reported for the five years included in this study, the ISA also derived air-to-blood ratio estimates ranging from 9 to 17 (ISA, p. 3-126;

8 Blood Pb measurements were available on a total of 843 children across five time periods, in the first of which the average child age was 9 years while it was appr oximately 6 years in each of the latter years: 1983 (n=356), 1991 (n=147), 1994 (n=122), 1997 (n=56), and 2000 (n=162) (Ranft et al., 2008).

9 The 1983 air Pb concentrations were based on two monitoring stations, while a combination of dispersion modeling and monitoring data was used in the later year s. Surface soil Pb measuremen ts were from 2000-2001, but geo-matched to blood Pb measurements across full study period (Ranft et al., 2008).3-12 Ranft et al., 2008, Table 2). Uncerta inties related to this study’s estimates include those related
to the bulk of air concentrat ion reduction occurring between th e first two time points (1983 and 1991) and the difference among the year’s air datase ts (e.g., two data sources [air monitors] in 1983 and multiple geographical points from a combination of the monitors and modeling in subsequent years).3-13 Table 3-1. Empirically derived air-to-b lood ratios for populations inclusive of children.

Study Information Quantitative Analysis Air-to-Blood Ratio A Focused on children < 5 years old
Children, 0.5-5 yr (n = 9,604), average age 2.5 yr Chicago, IL, 1974-1988 Urban area with lead-emitting industries, leaded gasoline usage Hayes et al. (1994) log n -log n regression: quarterly median PbB and quarterly mean PbA [unadjusted] PbB: 10-28 μg/dL (quarterly median) PbA: 0.05-1.2 μg/m 3 (quarterly mean) 8.2 (@ 0.62) B

Children, 0.5-5 yr (1996-1999), 0.5-3 yr (2001) (n = 200-500) Trail, BC, 1996-2001; Small town before/after cleaner technology on large metals smelter (at end of/after leaded gasoline phase-out) Hilts (2003) linear regression: annual GM PbB and AM PbA [unadjusted] PbB: 4.7-11.5 μg/dL (annual GM) PbA: 0.03-1.1 μg/m 3 (annual AM) 6- 7.0 C

Black children, <5 yr (n = 5,476) Chicago, IL, Feb 1976- Feb 1980 Area with lead-emitting industries, leaded gasoline usage Schwartz an d Pitcher (1989), U.S. EPA (1986a) linear regression: quarterly mean PbB with gasoline Pb (usage) [ adjusted for demographic covariates] combined with gasoline Pb – air Pb relationship. PbB: 18-27 μg/dL (quarterly mean, adjusted) PbA – gas Pb relationship based on annual U.S. means of per-site maximum quarterly means (0.36-1.22 μg/m 3 ) 8.6 D

Larger age range, inclusive of children < 5 years old Children, 96 groups of various age ranges, (n>190,000) Various countries (18 locations), 1974-1983 urban or near lead-emitting industries, leaded gasoline usage Brunekreef (1984) Meta-analyses (log n -log n regression of group means): (1) all children, (2) children <20 μg/dL [unadjusted] PbB: 5-76 μg/dL (study group means) PbA: 0.1-24 μg/m 3 (location means) Full dataset: 4.6 (@1.5) E <20μg/dL: 4.8 (@ 0.54) F Children, born 1987-92 (n = 321); Mexico City, 1987-2002 Average age increased over study period: <3yrs (1987-1992), and increased by a year each year after that Urban area during/after leaded gasoline usage Schnaas et al. (2004) Linear , log n -log n regressions: annual mean PbB and PbA [unadjusted] PbB: 5-12 μg/dL (annual GM), aged 0.5-10 yr PbA: 0.07-2.8 μg/m 3 (AM); 0.1-0.4 over last 6 years Linear: 9.0 (0.1-0.4) 2.5 (full range) Log-log: 4.5 (@ 0.4) C

U.S. NHANES II white subjects, 0.5-74 yr, Feb 1976-1980 National survey during time of leaded gasoline usage Schwartz an d Pitcher (1989), U.S. EPA (1986a) Linear regression: PbB with mass Pb in gasoline as described above. [adjusted for demographic covariates] PbB: 11-18 μg/dL (mean per gas Pb, adjusted) PbA – gas Pb relationship based on annual U.S. means of per-site maximum quarterly means (0.36-1.22 μg/m 3 ) 9.3 D

Focused on children > 6 years old Children, 6-10 yr (n = 544) Mumbai, India, 1984-1996 Large urban area, leaded gasoline usage Tripathi et al. (2001) Linear regression: 13-year location-specific GM PbB and PbA [unadjusted] PbB: 8.6-14.4 μg/dL (location GM) PbA: 0.11-1.18 μg/m 3 (location GM); 0.45 (overall GM) 3.6

Children, 6-11 yr (n=843); average: ~9.5 yr (1983), ~6.5 (others) Duisburg, Germany–5 areas: 1983, 1991, 1994, 1997, 2000 Industrial urban area during/after leaded gasoline usage Ranft et al. (2008) Linear, log n -log n, log-linear regressions: annual mean PbB and air Pb [unadjusted] PbB: 3.33-9.13 μg/dL (AMs of 5 study years) PbA: 0.06-0.45 μg/m 3 (5 AMs), 0.10 (overall median) Log-linear G 6.4, 3.2

A - Predicted change in blood Pb (μg/dL per μg/m3) over range ± 0.01 μg/m 3 from study’s central air Pb, which is provided in μg/m 3 in parentheses. For linear models, this is simply the air Pb coefficient. B - ln(PbB) = ln(PbA) x 0.24 +3.17 (ISA, Table 3-12; Hayes et al., 1994) C - See discussion in text and ISA, section 3.5.1. D - Based on data for U.S. (1986 CD). See ISA, section 3.5.1. Log-lin = log-linear model. E - ln(PbB) = ln(PbA) x 0.3485 +2.853 F - ln(PbB) = ln(PbA) x 0.2159 + 2.620 G -Derived from regressions with separate soil Pb variable, cont ributing to underestimation of contribution from air Pb (see te xt and ISA, section 3.5.1). GM, geometric mean; AM, arithmetic mean; GSD, geometric standard dev iation; PbB, blood Pb concentration, μg/dL; PbA, air Pb con centration, μg/m 33-14 In the 2008 Pb NAAQS review, in addition to considering the evidence presented in the published literature and that reviewed in the 198 6 CD, we also considered air-to-blood ratios derived from the exposure assessment (73 FR 66974; 2007 REA, section 5.2.5.2). In the exposure assessment (summarized in section 3.4 be low), current modeling tools and information on children’s activity patterns, behavior and physio logy were used to estimate blood Pb levels associated with multimedia and multipathway Pb exposure. The results from the various case studies assessed, with considerati on of the context in which they were derived (e.g., the extent to which the range of air-related pathways was simu lated, and the limitations associated with those simulations), and the multiple sources of un certainty (see section 3.4.7 below) are also informative to our understanding of air-to-blood ratios. Estimates of air-to-blood ratios for the two REA case studies that represent localized po pulation exposures exhibited an increasing trend across air quality scenarios representing decreasing air concentrations. For example, across the
alternative standard levels a ssessed, which ranged from a cale ndar quarter average of 1.5 μg/m 3 down to a monthly average of 0.02 μg/m 3 , the ratios ranged from 1:2 to 1:9 for the general urban case study, with a similar trend al though of generally higher ratio for the primary smelter case study subarea. This pattern of model-derived rati os is generally consiste nt with the range of
ratios obtained from the literature. We continue to recognize a number of sources of uncertainty
associated with these model-derived ratios which may contribute to high or low biases. 10 The evidence on the quantitativ e relationship between air Pb and air-related Pb in blood is now, as in the past, limited by the circumstan ces (such as those related to Pb exposure) in
which the data were collected. Previous reviews have recognized the significant variability in
air-to-blood ratios for different populations exposed to Pb thr ough different air-related exposure pathways and at different air and blood levels, with the 1986 CD noting that ratios derived from studies involving the higher bl ood and air Pb levels pertaini ng to occupationally exposed workers are generally smaller than ratios from studies involving lower blood and air Pb levels (ISA, p. 3-132; 1986 CD, p. 11–99). Consistent with this observation, slopes in the range of 3 to

10 For example, the limited number of air-related pathways (inhalation and indoor dust ingestion) simulated to change in response to changes in ambient air Pb reductions in these case studies could have implications for the air-to-blood ratios. Additionally, with regard to the urba n case study, the relationship between dust loading and concentration, a key component in the hybrid dust model used in estimating indoor dust Pb levels, is based largely on a housing survey dataset reflecting dust Pb in housing constructed before 1980 (as described in the 2007 REA, Volume II, Appendix G, Attachment G-1). The use of leaded paint in some housing constructed before 1980 contributes some uncertainty due to the potential role of indoor Pb paint (compared to ambient air Pb) in the relationship. The empirically-based ambient air Pb – dust Pb relationships used in the primary Pb smelter (subarea) case study may contribute to a potential for the ratios from this case study to more fully capture the impact of changes in ambient air Pb on indoor dust Pb, and consequently on blood Pb. Some have suggested, however, that the regression used may not accurately reflect the tempor al relationship between reduct ions in ambient air Pb and indoor dust Pb and as a result may overestimate the dust Pb reduction per ambient air Pb reduction, thus contributing a potential high bias to the air-to-blood Pb ratios.3-15 5 were estimated for child population datasets assessed in the 1986 CD (ISA, p. 3-132; 1986 CD p. 11–100; Brunekreef, 1984; Tripathi et al., 2004). Additional studies considered in the last review and those assessed in the ISA provide ev idence of ratios above th is older range (ISA, p. 3-133). For example a ratio of 6.5-7 is indicate d by the study by Hilts (2003), one of the few
studies that evaluate the air Pb-b lood Pb relationship in conditions that are closer to the current state in the U.S. ( ISA, p. 3-132). We additionally note the variety of factors identified in the ISA that may potentially affect estimates of va rious ratios (including potentially coincident reductions in nonair Pb sources during the course of the studies), and for which a lack of complete information may preclude any adjustment of estimates to account for their role (ISA, section 3.5). In summary, as at the time of the last review of the NAAQS for Pb, the currently
available evidence includes estimates of air-to-bl ood ratios, both empirically- and model-derived,
with associated limitations and related uncertain ties. These limitations and uncertainties, which are summarized here and also noted in the ISA, usually include uncertainty associated with reductions in other Pb sources during the study period. The limited amount of new information
available in this review has not appreciably altered the scientific conclusions reached in the last review regarding relationships between Pb in ambient air and Pb in children’s blood or with regard to the range of ratios. The currently available evidence conti nues to indicate ratios relevant to the population of young children in th e U.S. today, reflecti ng multiple air-related pathways in addition to inhalation, to be generall y consistent with the approximate range of 1:5 to 1:10 given particular atten tion in the 2008 NAAQS decision, incl uding the “generally central estimate” of 1:7 (73 FR 67002, 67004; ISA, pp. 3-132 to 3-133).

3.2 NATURE OF EFFECTS Lead has been demonstrated to exert a broad array of deleterious effects on multiple organ systems as described in the assessment of the evidence available in this review and consistent with conclusions of past CDs (ISA, section 1.6; 2006 CD, section 8.4.1). A sizeable
number of studies on Pb health effects are newly available in th is review and are critically assessed in the ISA as part of the full body of evidence. The ne wly available evidence reaffirms conclusions on the broad array of effects recognized for Pb in the last review (see ISA, section 1.10). 11 Consistent with those conclusions, in th e context of pollutant exposures considered

11 Since the last Pb NAAQS review, the ISAs which have replaced CDs in documenting each review of the scientific evidence (or air quality crite ria) employ a systematic framework for weighing the evidence and describing associated conclusions with regard to causality, using established descriptors (“causal” relationship with relevant exposure, “likely” to be causal, evidence is “suggestive” of causality, “inadequate” evidence to infer causality, “not likely”) (ISA, Preamble).3-16 relevant to the Pb NAAQS review, 12 the ISA determines that causal relationships 13 exist for Pbwith effects on the nervous system in childr en (cognitive function decrements and the group of externalizing behaviors comprisi ng attention, impulsivi ty and hyperactivity), the hematological system (altered heme synthesis and decreased red blood cell survival and function), and the cardiovascular system (hypertension and cor onary heart disease), and on reproduction and development (postnatal development and male reproductive function) (ISA, table 1-2). Additionally, the ISA desc ribes relationships between Pb and effects on the nervous system in adults, on immune system function and with cancer 14 as likely to be causal 15 (ISA, table 1-2, sections 1.6.4 and 1.6.7). In some categories of health effects, there is newly available evidence regarding some aspects of the effects described in the last review or that stre ngthens our conclusions regarding aspects of Pb toxicity on a pa rticular physiological system. Am ong the nervous system effects of Pb, the newly available evidence is consistent wi th conclusions in the previous review which recognized that “[t]he neurotoxi c effects of Pb exposure are am ong those most studied and most extensively documented among human population groups” (2006 CD, p. 8-25). Nervous system effects that receive prominence in the current review, as in previous reviews, include those

12 With regard to consideration of pollutant exposures for studies included in the ISA, the ISA states the following (ISA, pp. lx-lxi). In drawing judgments regarding causality for the criteria air pollutants, the ISA focuses on evidence of effects in the range of relevant pollutant exposures or doses, and not on determination of causality at any dose. Emphasis is placed on evidence of effects at doses (e.g., blood Pb concentration) or exposures (e.g., air concentrations) that are relevant to, or somewhat above, those currently experienced by the population. The extent to which studies of higher concentrations are considered varies by pollutant and major outcome category, but generally includes those with doses or exposures in the range of one to two orders of magnitude above current or ambient conditions. Studies that use higher doses or exposures may also be considered to the extent that they provide useful information to inform understanding of mode of action, interspecies differences, or factors that may increase risk of effects for a population. Thus, a causality determination is based on weight of evidence evaluation for health, ecological or welfare effects, focusing on the evidence from ex posures or doses generally ranging from current levels to one or two orders of magnitude above current levels.

13 In determining there to be a causal relationship for Pb with specific health effects, EPA has concluded that “[e]vidence is sufficient to conclude that there is a causal relationship with relevant pollutant exposures (i.e., doses or exposures generally within one to two orders of magnitude of current levels)” (ISA, p. lxii)

14 Lead has been classified as a probable human ca rcinogen by the International Agency for Research on Cancer, based mainly on sufficient anim al evidence, and as reasonably antici pated to be a human carcinogen by the U.S. National Toxicology Program (ISA, section 4.10). In this assessment, EPA concludes that a causal relationship is likely to exist between Pb exposure and cancer, based primarily on consistent, strong evidence from experimental animal studies, but inconsistent epidemiological evidence (ISA, section 4.10.5).

15 In determining that there is likely to be a causal relationship for Pb with specific health effects, EPA has concluded that “[e]vidence is sufficient to conclude that a causal relationship is likely to exist with relevant pollutant exposures, but important uncertai nties remain” (ISA, p. lxii).3-17 affecting cognitive function and behavior in childre n (ISA, section 4.3), with conclusions that are consistent with findings of the last review. Across the broad array of Pb effects for sy stems and processes other than the nervous system, the evidence base has been augmented with additional epidemiological investigations in a number of areas, including developmental outcome s, such as puberty onset, and adult outcomes related to cardiovascular function, for which se veral large cohorts have been analyzed (ISA, Table 1-8 and sections 4.4 and 4.8). Conclusi ons on these other systems and processes are
consistent with conclusions reached in the last review, while also extending our conclusions on some aspects of these effects. For example, evidence in this review for the cardiovascular system includes information on the role of inte ractions of cumulative Pb exposure with other factors, such as stress in contributing to hypert ension, and on a role for Pb in contributing to coronary heart disease (ISA, section 4.4 and Table 1-8).
Based on the extensive assessmen t of the full body of evidence available in this review, the major conclusions drawn by the ISA regarding health effects of Pb in children include the following (ISA, p. lxxxvii). Multiple epidemiologic studies conducted in diverse populations of children consistently demonstrate the harmful effe cts of Pb exposure on cognitive function (as measured by IQ decrements, decreased academic performance and poorerperformance on tests of executive function).... Evidence suggests that some Pbrelated cognitive effects may be irre versible and that the neurodevelopmental effects of Pb exposure may persist into adulthood (Section 1.9.4). Epidemiologic studies also demonstrate that Pb exposure is associated with decreased attention, and increased impulsivity and hyperactivity in children (externalizing behaviors). This is supported by findings in anim al studies demonstrating both analogous effects and biological plausibility at re levant exposure levels. Pb exposure can also exert harmful effects on blood cells and blood producing organs, and is likely to cause an increased risk of symptoms of depression and anxiety and withdrawn behavior (internalizing behaviors),decrea ses in auditory and motor function, asthma and allergy, as well as conduc t disorders in children and young adults. There is some uncertainty about the Pb exposures contributing to the effects and blood Pb levels observed in epidemiol ogic studies; however, these uncertainties are greater in studies of older child ren and adults than in studies of young children (Section 1.9.5).

Based on the extensive assessmen t of the full body of evidence available in this review, the major conclusions drawn by the ISA regarding health effects of Pb in adults include the following (ISA, p. lxxxviii). A large body of evidence from both epidemiologic studies of adults and experimental studies in anim als demonstrates the effect of long-term Pb exposure on increased blood pressure (BP) and hype rtension (Section 1.6.2). In addition to its effect on BP, Pb exposure can also lead to coronary heart disease and death3-18 from cardiovascular causes and is associ ated with cognitive function decrements, symptoms of depression and anxiety, and immune effects in adult humans. The extent to which the effects of Pb on the cardiovascular system are reversible is not well-characterized. Additional ly, the frequency, timing, level, and duration of Pb exposure causing the effects observed in adults has not been pinpointed, and higher past exposures may contribute to the development of health effects measured later in life.

As in prior reviews of the Pb NAAQS, this review is focused on those effects most pertinent to ambient air Pb exposures. Given th e reductions in ambient air Pb levels over the past decades, these effects are ge nerally those associated with th e lowest levels of Pb exposure that have been evaluated. Additionally, we recognize the limitations on our ability to draw conclusions regarding the exposure conditions cont ributing to the findings from epidemiological analyses of blood Pb levels in populations of olde r children and adults, particularly in light of their history of higher Pb exposures. In the la st review, while recognizi ng the range of health effects in variously aged populati ons related to Pb exposure, we focused on the health effects for which the evidence was strongest with regard to relationships with the lowest exposure levels, neurocognitive effects in young childre n. The policy-relevant questions on health effects for this review (identified in the IRP) were framed in r ecognition of the conclusions of the last review.
Our consideration of the health effects evidence in this review is framed by policy-relevant questions building on those identified in the IRP.

 To what extent is there new scientif ic evidence available to improve our understanding of the health effects associ ated with various time periods of Pb exposures at various stages of life? As in the last review, we base our current und erstanding of health effects associated with different Pb exposure circumstances at various stages of life on the full body of available evidence which includes epidemiological studies of health effects associated with population Pb biomarker levels as well as laboratory animal st udies in which the effects of different exposures on different lifestages are assessed under controlled conditions. Th e epidemiological evidence is overwhelmingly comprised of studies that rely on blood Pb for the exposure metric, with the remainder largely including a focus on bone Pb. Because these metrics reflect Pb in the body (e.g., as compared to Pb exposure concentratio ns) and, in the case of blood Pb, reflect Pb available for distribution to targ et sites, they strengthen th e evidence base for purposes of drawing causal conclusions with regard to Pb generally. The complexity of Pb exposure pathways and internal dosimetry tends to limit the extent to which these types of studies inform our more specific understanding of the Pb exposure circumstances (e.g., timing, duration, frequency and magnitude) elici ting the various effects.3-19 The specific exposure circumstances, including timing during the lifetime, that contribute to the blood Pb (or bone Pb) measurements with which associations have been analyzed in epidemiological studies are unknown. This is particularly the case with regard to the contributing role of recent exposures for which uncer tainty is greater in a dults and older children than in younger children (ISA, sections 1.9.4). Fo r example, a critical as pect of much of the epidemiological evidence, particularly that focu sed on older adults in the U.S. today, is the backdrop of generally declining environmental Pb exposure (fro m higher exposures during their younger years) that is common across many stud y populations (ISA, p. 4-2). An additional factor complicating the interpretation of health effect associations with blood Pb measurements in older children and younger a dults is the common behaviors of younger children (e.g., hand-tomouth contact) which generally c ontribute to relatively greater environmental exposures earlier in life (ISA, sections 3.1.1, 4.2.1). Such exposur e histories complicate our ability to draw conclusions regarding critical time periods and lifestages for Pb exposures eliciting the effects
with which associations with Pb biomarkers ha ve been observed in populations of adults and older children (e.g., IS A, section 1.9.6). 16 As at the time of the last review, assessm ent of the full evidence base, including evidence newly available in this review, demonstrates that Pb exposure prenatally and also in early childhood can contribute to neurocognitive impact s in childhood, with evidence also indicating the potential for effects pers isting into adulthood (ISA, s ections 1.9.5, 1.9.6, and 1.10). In
addition to the observed associatio ns of prenatal and childhood bl ood Pb with effects at various ages in childhood, there is also evidence of lead-related cogni tive function effects in nonoccupationally exposed adults (ISA, section 4.3.11) . This includes eviden ce of associations of
such effects in adulthood with childhood blood Pb levels and, in other cohorts, with concurrent (adult) blood Pb levels (ISA, sections 4.3.2.1, 4.3.2.7 and 4.3.11). As the studies finding
associations of adult effects with childhood blood Pb levels did not examine adult blood Pb levels, the relative influence of adult Pb exposure cannot be ascertained, and a corresponding lack of early life exposure or biomarker measurem ents for the latter studies limit our ability to draw conclusions regarding spec ific Pb exposure circumstances eliciting the observed effects (4.3.11). Findings of stronger associations fo r adult neurocognitive effects with bone Pb,

16 The evidence from experimental animal studies can be informative with regard to key aspects of exposure circumstances in eliciting specific effects whic h can inform our interpretation of the epidemiological evidence. For example, the animal evidence base with regard to Pb effects on blood pressure demonstrates the etiologically-relevant role of long-term (as compared to sh ort-term) exposure (ISA, section 4.4.1). This finding then informs consideration of epidemiological studies of adu lt populations for whom historical exposures were likely more substantial than concurrent ones to suggest that the observed effects may be related to the past exposure (ISA, section 4.4.1). For other health effects, the animal evidence base may or may not be informative with regard to the role of specific exposure circumst ances in eliciting those effects.3-20 however, indicate the role of historical or cumulative exposu res for those effects (ISA, section 4.3). Given the relatively short exposure histories of young children, there is relatively reduced uncertainty regarding the lifestages in which expos ures contribute to effects for associations of early childhood effects with early childhood bl ood Pb levels (ISA, sections 1.9.4, 1.9.6 and 4.3.11). In considering our understanding of the relative impact on neurocognitive function of additional Pb exposure of children by school ag e or later we recognize increasing uncertainty associated with limitations of the currently avai lable evidence, including epidemiological cohorts with generally similar temporal patterns of e xposure. We take note, additionally, of evidence from experimental animal studies and a small body of epidemiological studies that indicates that Pb exposures during different lifestages can induce cognitiv e impairments. The limited epidemiological evidence is of populations with blood Pb levels that are not strongly correlated over time and that can, accordingl y, address the issue of the role of exposure subsequent to the earliest lifestages (ISA, sect ion 4.3.11; Hornung et al., 2009). Some animal evidence demonstrates impaired learning with infancy only, from infancy into adulthood, and postinfancy only Pb exposure (Rice, 1990; Rice and Gilbert 1 990; Rice, 1992). Further, evidence that Pb exposure presents a risk during different lifestages is also consistent with our broader understanding that nervous system developm ent continues throughout childhood. The limited analyses of this issue that are newly availabl e in this review do not appreciably change our understanding or conclusions on th is from those of the prior review (ISA, section 4.3.11). As in the last review, there is also substant ial evidence of other neurobehavioral effects in children, such as reduced atten tion span, increased impulsivit y, hyperactivity, conduct disorders and effects on internalizing behaviors. The ev idence for many of these endpoints, as with neurocognitive effects, also includ es associations of effects at various ages in childhood and, for some effects, into adulthood, with blood Pb levels reflective of several different lifestages (e.g., prenatal and several different ages in childhood ) (ISA, sections 4.3.3 and 4.3.4). There is similar or relatively less extensive evidence to inform our understanding of such effects associated with specific time periods of exposure at specific lifestages than is the case for effects on cognitive
function. Across the range of Pb effects on physiologi cal systems and processes other than the nervous system, the full body of evidence on etiologi cally relevant circumst ances of Pb exposure eliciting increases in blood pre ssure and hypertension is somewhat more informative than is the case with regard to many other effects. In the case of lead-induced in creases in blood pressure,
the evidence indicates an im portance of long-term exposure (ISA, sections 1.6.2 and 4.4.7.1). In summary, as in the last review, we con tinue to recognize a numb er of uncertainties regarding the circumstances of Pb exposure, in cluding timing or lifestage s, eliciting specific3-21 health effects. Consideration of the evidence newly available in this review has not appreciably changed our understanding on this topic. The relationship of long-term exposure to Pb with hypertension and increased blood pressure in adu lts is substantiated despite some uncertainty regarding the exposures circumstances (e.g., magn itude and timing) contributing to blood Pb levels measured in epidemiological studies. Ac ross the full evidence base, the effects for which our understanding of relevant exposure circumstances is greatest are neur ocognitive effects in young children. Thus, we continue to recognize and gi ve particular attenti on to the role of Pb exposures relatively early in childhood in c ontributing to neurocognitive effects which may persist into adulthood.

 At what levels of Pb exposure do heal th effects of concern occur? Is there evidence of effects at expo sure levels lower than previously observed and what are important uncertaintie s in that evidence? In considering the question posed here, we r ecognize, as discussed in section 3.1 above, that the epidemiological evidence base for our co nsideration in this review, as in the past,
includes substantial focus on intern al biomarkers of exposure, such as blood Pb, with relatively less information specific to exposure levels, includ ing those derived from air-related pathways. Given that blood and bone Pb are integrated ma rkers of aggregate expo sure across all sources and exposure pathways, our interpretation of stud ies relying on them is informed by what is known regarding the historical context and expos ure circumstances of the study populations. For example, a critical aspect of much of the epidemiological evid ence is the backdrop of generally declining Pb exposure over the past severa l decades. Thus as a generality, recent epidemiological studies of populatio ns with similar characteristics as those studied in the past tend to involve lower overall Pb exposures and accordingly lower blood Pb levels (e.g., ISA, sections 2.5 and 3.4.1; 2006 CD, section 3.4). This ha s been of particular not e in the evidence of blood Pb associations with nervous system effect s, particularly impacts on cognitive function in children, for which we have seen associations with progressively lower childhood blood Pb levels across past reviews (ISA, sec tion 4.3.12; 1986 CD; USEPA, 1990; 2006 CD; 73 FR 66976). The evidence currently available with rega rd to the magnitude of blood Pb levels associated with neurocognitive effects in children is generally consistent with that available in the review completed in 2008. Nervous system effects in children, sp ecifically effects on cognitive function, continue to be the effects that are best substantiated as occurring at the lowest blood Pb concentrations (ISA, pp. lxxxvii-lxxxviii). Associations of blood Pb with effects on cognitive function measures in children have b een reported in many studies across a range of3-22 childhood blood Pb levels, including study group (m ean/median) levels ranging down to 2 μg/dL (e.g., ISA, p. lxxxvii and section 4.3.2). 17 Studies in which such findings were re ported for childhood study group blood Pb levels below 5 μg/dL are summarized in Table 3-2. 18 In recognition of the influence of age on blood Pb levels, the analyses in Table 3-2 are li sted in order of age at which the blood Pb measurements were taken. Findings for studies newly available in this review are indicated in bold text. Although the analyses fr om Lanphear et al (2005) listed in Table 3-2 were available in the last review, the information presented in Table 3-2 for sample size and mean blood Pb concentration has been updated to reflect reca lculations using data corrected for recently identified errors, as described further in the next section below (Kirrane and Patel, 2014).

17 The value of 2 μg/dL refers to the regression analysis of blood Pb and end-of-grade test scores, in which blood Pb was represented by categories for integer values of blood Pb from 1 μg/dL to 9 and >10 μg/dL from large statewide database. A significant effect estimate was repo rted for test scores with all blood Pb categories in comparison to the reference category (1 μg/dL), which incl uded results at and below the limit of detection. Mean levels are not provided for any of the categories (Miranda et al., 2009).

18 Two additional studies (both newly available) that report such associations with blood Pb levels for which the mean is equal to 5.0 μg/dL. The first is a study of 506 children in Detroit, MI (born, 1982-1984) at age 7 years which observed a significant negativ e association with concurrent blood Pb levels for which the mean equals 5.0 μg/dL (8.9% of childen with concurrent blood Pb above 10 μg/dL) (ISA, sections 4.3.2.1 and 4.3.3.1; Chiodo et al., 2007). The second study focuses on 174 of the Rochester cohort children at age 6 years, reporting significant negative associations with FSIQ for four different blood Pb metrics: concurrent (mean = 5.0 μg/dL), lifetime average (mean=7.2 μg/dL), infancy averag e (mean = 7.1 μg/dL) and peak (mean = 11.4 μg/dL) (Jusko et al., 2008).3-23Table 3-2.Associations with neurocognitive function measures in analyses with childstudy group blood Pb levels <5 μg/dL.MeasureAStudy Group Dataset DescriptionBlood Pb LevelsAdditional Information on AnalysesAgeMeanB(μg/dL)RangeB(μg/dL)NCStudies discussed in ISA (section 4.3.2) with findings of effects on neurocognitive measuresreported for childhood study groupPbB < 5 μg/dL(ordered by age of blood Pb measurements)FSIQBoston, prospective, age 5 yrSubgroup with peak PbB <10 μg/dLBellinger and Needleman 200324 mo 3.8 1 - 9.348Regression, PbB as continuous variable; statistically significant negativeassociationBSID/MDIMexico City, age 24 mo,Tellez-Rojo et al.,2006Subgroup with PbB<5 μg/dLFull dataset24 mo“ “2.94.30.8 – 4.90.8 - 9.8193294Regression, PbB as continuous variable; statistically significant negativeassociationAcadPerfNorth Carolina, 4thgraders4thgrade reading scores, Full datasetMiranda et al., 20099-36 mo 4.8 1-16 57,678Linear and quantal regressions with integer PbB as categorical variable(PbB-1=reference category, includes LOD). Linear analysis: statistically significant effectfor all comparison categories. Quantal analysis: statistically significant effect in allreading score quantiles for PbB categories greater than integer PbB=3; largesteffect in lower quantiles. Means not reported for PbB categories.AcadPerfAvon, United Kingdom, age 7-8 yrstandard assessment scores, Full dataset,Chandramouli et al., 200930 mo 4.2221% <252% 2-521% 5-10488DRegressions with PbB as continuous and categorical variables:continuousanalysis (statistically significant negative association); categorical (significantlyreduced scores for 5-10 μg/dL vs reference group [ 0-2 μg/dL])FSIQRochester, prospective cohort, age 5 yrSubgroup with peak PbB <10 μg/dLCanfield et al., 20035 yr 3.320.5 – 8.4(LOD=1)71Regression, PbB as continuous variable; statistically significant negativeassociationFSIQPooled International, age 6-10 yrSubgroup with peak PbB <7.5 μg/dLLanphear et al 2005E5-7 yr 3.3 0.9 – 7.4 118Regression, PbB as continuous variable; statistically significant negativeassociationFSIQLM, EFAcadPerfNew England, 2 areas, age 6-10, ,Full dataset,Surkan et al., 20076-10 yr 2.3 1 – 10 389Regression, PbB grouped into categories; statistically significant negativeassociation for high subgroup (5-10μg/dL, n=32) compared to reference PbBsubgroup (1-2μg/dL, n=286).FSIQKorea, 4 areas, age 8-11 yrFull datasetKim et al., 20098-11 yr 1.73 0.4 – 4.9 261Regression, PbB analyzed as quartiles; statistically significant difference amongquartiles; statistically significant negative association in continuous analysis of fulldataset and high blood manganese groupLMAcadPerfNHANES III (1988-1994)Lanphear et al., 20006-16 yr 1.9 4,853Continuous (unadjusted) and categorical (adjusted) analysis; significant differenceamong PbB quartiles (< 1, 1.1-1.9, 2.0-3.0, >3.0μg/dL), and neg assoc PbB <5.0.LMAcadPerfNHANES III (1991-1994)Krieg et al., 201012-16 yr 1.95 766-80Regression analysis; PbB as continuous variable; statistically significant negativeassociation.A- FSIQ = Full Scale Intelligence Quotient; BSID = Bayley Scalesof Development; MDI= MentalDevelopment Index; LM=Learning andMemory; EF= Executive Function; AcadPerf= Academic Performance.B - Blood Pb level (PbB) information provided here is in some cases augmented bystudy authors (Bellinger, 2008; Canfield, 2008a,b; Hornung, 2008a,b; Tellez-Rojo, 2008; Kirrane and Patel, 2014).C - Bolded measures and studies are newly available in this review.D - In practice, 337-425 cases were includedin analysis (Chandramouli et al., 2009).E - Blood Pb measurements of subgroup with peak PbB <7.5μg/dL comprised of 24.6% age 5 (Boston, Cleveland), 58.5% age 6 (Rochester), 16.9% age 7 (Yugoslavia, Mexico, Cincinnati). IQ assessed at age 5 for thesingle member of this subgroupfrom Cleveland cohort. This analysis includes blood Pb data from Rochester and Boston cohorts, although for different ages (6 and 5 years, respectively) than the ages analyzed in Canfieldet al 2003 and Bellinger and Needleman 2003. For full dataset analysis (n=1333), IQ assessed at ages 5-10 yr, median blood Pb(at ages 5-7 yr) of 9.7 μg/dL and 5th -95th percentile of 2.5-33.2 μg/dL.3-24 Among the analyses of lowest study group blood Pb levels at the youngest ages in Table 3-2 are analyses available in the last review of Pb associations with neurocognitive decrement in study groups with mean levels on the order of 3- 4 μg/dL in children aged 24 months or ranging from 5 to 7 years (73 FR 66978-66969; ISA, sections 4.3.2.1 and 4.3.2.2; Bellinger and Needleman, 2003; Canfield et al., 2003; Lanphe ar et al., 2005; Tellez-Rojo et al., 2006; Bellinger, 2008; Canfield, 2008; Tellez-R ojo, 2008; Kirrane and Patel, 2014). 19 Newly available
in this review are two studies re porting association of blood Pb leve ls prior to three years of age with academic performance on standardized test s in primary school; mean blood Pb levels in these studies were 4.2 and 4.8 μg/dL (ISA, s ection 4.3.2.5; Chandramouli et al., 2009; Miranda et al., 2009). One of these two studies, which re presented integer blood Pb levels as categorical variables, indicated a small eff ect on end-of-grade reading score of blood Pb levels as low as 2 μg/dL, after adjustment for age of measurement, race, sex, enrollment in free or reduced lunch program, parental education, and sch ool type (Miranda et al., 2009). In a newly available study of blood Pb leve ls at primary school age, a significant association of blood Pb in children aged 8-11 years and concurrently measured full scale IQ (FSIQ) was reported for a cross- sectional cohort in Korea with a mean blood Pb level of 1.7 μg/dL and range of 0.43-4.91 μg/dL (Kim et al., 2009). 20 In considering the blood Pb levels in this study, we note that blood Pb le vels in children aged 8-11 are generally lower than those in pre-school children, for reasons related to beha vioral and other factors (ISA, sections 3.3.5, 3.4.1 and 5.2.1.1). 21 It is likely that the blood Pb levels of this study group at earlier ages, e.g., prior to school entry, were higher and the available inform ation does not provide a basis to judge whether the blood Pb levels in this study represent lowe r exposure levels than those experienced by the younger study groups. In still older children, a la rge cross-sectional investigation of blood Pb
association with effects on memo ry and learning that was available in the last review was focused on children aged 6-16 years, born during 1972-1988, with a mean blood Pb of 1.9 μg/dL. A study newly available in this review, focused on a subset of the earlier study cohort

19 The tests for cognitive function in these studies include age-appropriate Wechsler intelligence tests (Lanphear et al., 2005; Bellinger and Needleman, 2003), the Stanford-Binet intelligence test (Canfield et al., 2003), and the Bayley Scales of Infant Develo pment (Tellez-Rojo et al., 2006). The Wechsler and Stanford-Binet tests are widely used to assess neurocognitive function in children and adults. These tests,however, are not appropriate for children under age three. For such children, studies gene rally use the age-appropriate Bayley Scales of Infant Development as a measure of cognitive development.

20 Limitations of this study included a lack of consid eration of potential confounding by parental caregiving quality or IQ (ISA, Table 4-3).

21 This study also investigated the potential role of ma nganese (Mn) in the blood Pb associated effects. When the cohort was subdivided based on Mn blood Pb levels, using the median Mn level (14 μg/L) as the break point, the significant association of intelligence quotient (I Q) with Pb persisted in the higher Mn group but was no longer significant in the lower Mn group (ISA, section 4.3.2). Separate analysis of the full study group found a significant negative association of IQ with blood Mn (Kim et al., 2009).3-25 (ages 12-16, born during 1975-1982), also reports a si gnificant negative association of blood Pb with learning and memory test results with mean blood Pb levels of approximately 2 μg/dL (ISA, section 4.3.2.3; Lanphear et al., 2000; Krieg et al., 2010). In considering these study findings with regard to the question of exposure levels eliciting effects, we recognize, however, that blood Pb levels are, in general, lower among teenagers than young children and also that, for these subjects specifically, the ma gnitude of blood Pb levels dur ing the earlier childhood (e.g., preschool ages) was much higher. For example, the mean blood Pb levels for the 1-5 year old age group in the NHANES 1976-80 sample was 15 μg/dL, declining to 3.6 μg/dL in the NHANES 1988-1991 sample (Pirkle et al., 1994; ISA, section 3.4.1). With regard to other nervous system effects in children, the evidence base at lower blood
Pb levels is somewhat extended since the last review with re gard to the evidence on Pb and effects on externalizing behavi ors, such as attention, impul sivity, hyperactivity and conduct disorders (ISA, section 4.3.3 and table 4-17). Seve ral newly available studies investigating the
role of blood Pb levels in olde r children (primary school age and ol der) have reported significant
associations for these effects with concurrent bl ood Pb levels, with mean levels generally on the order of 5 μg/dL or higher (ISA, section 4.3.3) . One exception is the newly available crosssectional, categorical analysis of the NHANES 2001-2004 sample of children aged 8-15 years, which found higher prevalence of conduct disorder in the subgr oup with concurrent blood Pb levels of 0.8-1.0 μg/dL as compared to the <0.8 μg/dL group (ISA, section 4.3.4 and Table 4- 12). As noted above, we recognize that many of these children, born between 1986 and 1996, are likely to have had much hi gher Pb exposures (and associated blood Pb levels) in their earlier years than those commonly experienced by young children today, thus precluding a conclusion regarding evidence of effects as sociated with lower exposure levels than provided by evidence previously available. As summarized earlier in this section, blood Pb has been associated with a range of health effects on multiple organ systems or processes. As is the case for studies of nervous system effects in children, newly available studies of ot her effects in child a nd adult cohorts include
cohorts with similar or somewhat lower mean blood levels than in previous ly available studies. Categories of effects for which a causal relati onship has been concluded in the ISA and for which there are a few newly available epidemiol ogical studies indicating blood Pb associations with effects in study groups with somewhat lower blood Pb levels than previously available for these effects include effects on development (delayed puberty onset) and reproduction (male reproductive function) and on the cardiovascular system (hypertension) (ISA, sections 4.4 and 4.8; 2006 CD, sections 6.5 and 6.6). With regard to the former category, study groups in the newly available studies include groups comprised of older child ren ranging up to age 18 years, for which there is increased uncertainty regardin g historical exposures and their role in the3-26 observed effects. 22 An additional factor that handicaps our consideration of exposure levels associated with these findings is the appreciabl e uncertainty associated with our understanding of Pb biokinetics during this lifestage (ISA, s ections 3.2, 3.3, and 4.8.6). The evidence newly available for Pb relationships w ith cardiovascular effects in adu lts include some studies with
somewhat lower blood Pb levels than in the last review. The long expos ure histories of these cohorts, as well as the generally higher Pb exposures of the past complicate conclusions regarding exposure levels that may be elicit ing observed effects (ISA, sections 4.4.2.4 and 4.4.7). 23 In summary, our conclusions regarding exposure levels at which Pb health effects occur, particularly with regard to such levels that might be common in the U.S. today, are complicated now, as in the last review, by seve ral factors. These factors include the scarcity of information in epidemiological studies on cohort exposure histories, as well as by the backdrop of higher past exposure levels which frame the history of some study cohorts. Recognizing the complexity, as well as the potential role of higher exposure levels in the past, we continue to focus our consideration of this questi on on the evidence of effects in young children for which our understanding of exposure hi story is less uncertain. 24 Within this evidence base, we recognize the lowest study group blood Pb levels to be associated with effects on cognitive function measures, indicating that to be the most sensitive endpoint. As described above, and summarized in Table 3-2, the evidence available in this review is generally consistent with that available in the last review with regard to blood Pb levels at which such effects had been reported (ISA, section 4.3.2; 2006 CD, section 8.4.2.1; 73 FR 66976-66979). As blood Pb levels are a reflection of exposure hi story, particularly in early childhood (ISA, section 3.3.2), we conclude, by extension, that the currently available evidence does not indicate Pb effects at exposure levels appreciably lower than recognized in the last review. We additionally note that, as in the last re view, a threshold blood Pb level with which nervous system effects, and specifically neurocognitive effects, occur in young children cannot be discerned from the currently availa ble studies (ISA, sections 1.9.3 and 4.3.12). Epidemiological analyses have reported blood Pb associations with neurocognitive effects (FSIQ

22 Several of these studies involve NHANES III cohorts for which early childhood exposures were generally much higher than those common in the U.S. today (ISA, section 4.8.5).

23 Studies from the late 1960s and 1970s suggest that adult blood Pb levels during that period ranged from roughly 13 to 16 μ g/m 3 and from 15 to 30 μg/dL in children aged six and younger (ISA, section 4.4.1).

24 In focusing on effects associated with blood Pb levels in early childhood, however, we additionally recognize the evidence across cat egories of effects that relate to blood Pb levels in older child study groups (for which early childhoood exposure may have had an influence) which provides additional support to an emphasis nervous system effects (ISA, sections 4.3, 4.4, 4.5, 4.6, 4.7, 4.8).3-27 or BSID MDI 25 ) for young child population subgroups (age five years or younger) with individual blood Pb measurements as low as appr oximately 1 μg/dL and mean concentrations as low as 2.9 to 3.8 μg/dL (ISA, section 4.3.12; Bellinger and Needleman, 2003; Bellinger, 2008; Canfield el al., 2003; Canfield, 2008; Tellez-Rojo et al., 2006; Tellez-Rojo et al., 2008). As concluded in the ISA, however, “the current ev idence does not preclude the possibility of a threshold for neurodevelopmental effects in childr en existing with lower blood levels than those currently examined” (ISA, section 4.3.13). Important uncertainties associated with the ev idence of effects at low exposure levels are similar to those recognized in the last review, incl uding the shape of the concentration-response relationship for effects on neurocognitive function at low blood Pb levels in today’s young children. Also of note is our interpretation of a ssociations between blood Pb levels and effects in epidemiological studies, with wh ich we recognize uncertainty w ith regard to the specific exposure circumstances (timing, duration, magnitude and frequency) that have elicited the observed effects, as well as uncertainties in re lating ambient air concentrations (and associated air-related exposures) to blood Pb levels in early childhood, as discussed in section 3.1 above. We additionally recognize uncertainties associated with conclusions drawn with regard to the nature of the epidemiological associations w ith blood Pb (e.g., ISA, section 4.3.13), but note that,
based on consideration of the full body of evidence for neurocognitive effects, the EPA has determined a causal relationship to exist between relevant blood Pb levels and neurocognitive impacts in children (ISA, section 4.3.15.1).

 To what extent does the newly availabl e evidence alter our understanding of the concentration-response relationship for neur ocognitive effects (IQ) with blood Pb levels in young children? Based primarily on studies of FSIQ, the assessm ent of the currently available studies, as was the case in the last review, continues to recognize a nonlinear rela tionship between blood Pb and effects on cognitive function, with a greater incremental effect (greater slope) at lower relative to higher blood Pb levels within the range thus far stud ied, extending from well above 10 μg/dL to below 5 μg/dL (ISA, section 4.3.12). Th is was supported by the evidence available in the last review, including the an alysis of the large pooled inte rnational dataset comprised of blood Pb measurements and IQ test results from seven prospective cohor ts (Lanphear et al., 2005; Rothenberg and Rothenberg, 2005; ISA, se ction 4.3.12). The blood Pb measurements in this pooled dataset that were conc urrent with the IQ tests ranged from 2.5 μg/dL to 33.2 μg/dL. The study by Lanphear et al (2005) additionally presented analyses that stratified the dataset

25 Bayley Scales of Infant Development, Mental Development Index. The Bayley MDI is a wellstandardized and widely used assessment measure of infant cognitive development. Scores earlier than 24 months are not necessarily correlated with later FSIQ scores in children with normal development (ISA, section 4.3.15.1).3-28 based on peak blood Pb levels (e.g., with cutpoints of 7.5 μg/dL and 10 μg/dL peak blood Pb)
and found that the coefficients from linear mode ls of the association for IQ with concurrent blood Pb were higher in the lower peak blood Pb level subsets than th e higher groups (ISA, section 4.3.12; Lanphear et al., 2005). We note that since the completion of the ISA, two errors have been identified with the pooled dataset analyzed by Lanphear et al ( 2005) (Kirrane and Patel, 2014). A recent publication and EPA have separate ly recalculated the statistics and mathematical models of Lanphear et al (2005) using th e corrected pooled data set (Kirrane and Patel, 2014). While the magnitude of the loglinear and linear regression coefficients are modified slightly based on the corrections, the conclusions draw n from these coefficients, in cluding the finding of a steeper slope at lower (as compared to higher) blood Pb concentrations are not affected (Kirrane and Patel, 2014). In other publications, stratifie d analyses of several indi vidual cohorts also observed higher coefficients for blood Pb re lationships with meas ures of neurocognitive function in lower as compared to higher blood Pb subgroups (ISA, section 4.3.12; Canfield et al., 2003; Bellinger and Needleman, 2003; Kordas et al., 2006; Tell ez-Rojo et al., 2006). Of these subgroup analyses, those involving the lowe st mean blood Pb levels and cl osest to the current mean for U.S. preschool children are li sted in Table 3-3 below (drawn from Table 3 of the 2008 final rulemaking notice [73 FR 67003], and Kirrane and Pa tel, 2014). These analyses were important inputs for the evidence-based, air-related IQ loss framework which informed decisions on a
revised standard in the last review (73 FR 67005), discussed in section 4.1.1 below. As the
framework focused on the median of the four slopes in Table 3- 3, the change to the one from Lanphear et al (2005) based on the recent r ecalculation described above has no impact.3-29 Table 3-3. Summary of quantitative relationships of IQ and blood Pb for analyses with blood Pb levels closest to those of young children in the U.S. today.

Blood Pb Levels (μg/dL)

Study/Analysis Average Linear Slope A (IQ B points per μg/dL) Geometric Mean Range (min-max)

2.9 0.8 – 4.9 Tellez-Rojo et al (2006) B , subgroup with concurrent blood Pb <5 μ g/dL -1.71 3.3 0.9 – 7.4 Lanphear et al (2005) C , subgroup with peak blood Pb <7.5 μ g/dL -2.53 3.32 0.5 – 8.4 Canfield et al (2003) C , subgroup with peak blood Pb <10 μ g/dL -1.79 3.8 1 - 9.3 Bellinger and Needleman (2003) C , subgroup with peak blood Pb <10 μ g/dL -1.56 Median value -1.75

A

- A verage linear slope estimates here are generally for relationship with IQ assessed concurrently with blood Pb measurement. As exceptions, Bellinger & Needleman (2003) slope is relationship for 10 year old IQ with blood Pb levels at 24 months, and the da ta for Boston cohort included in Lanphear et al 2005 slope are relationship for 10 year old IQ with blood Pb levels at 5 years. B -The slope for Tellez-Rojo et al 2006 is for BSID (MDI), a measure of cognitive development appropriate to study population a ge (24-mos). C - The Lanphear et al. (2005) pooled International study also includes blood Pb data from the Rochester and Boston cohorts, al though for different ages (6 and 5 years, respectively) than the ages analyzed in Canfield et al. (2003) and Bellinger and Needleman (2003 ). Thus, the ages at the blood Pb measurements used in derivation of the linear slope for the Lanphear et al (2005) subgroup shown here are 5 to 7 years. The blood Pb levels and coefficient presented here reflect the recalculation using the corrected pooled dataset (Kirrane and Pa tel, 2014).

Several studies newly available in the current review have, in all but one instance, also found a nonlinear blood Pb-cognitive function relati onship in nonparametric regression analyses of the cohort blood Pb levels analyzed (ISA, section 4.3.12). These studies, however, used statistical approaches that did not produce qua ntitative results for each blood Pb group (ISA, section 4.3.12). Thus, newly available studies ha ve not extended the range of observation for quantitative estimates of this relationship to lo wer blood Pb levels than those of the previous review. The ISA further notes that the potential for nonlinearity has not been examined in detail within a lower, narrower range of blood Pb levels than those of the full cohorts thus far studied in the currently available evidence base (ISA, section 4.3.12). Such an observation in the last review supported the cons ideration of linear slopes with rega rd to blood Pb levels at and below those represented in Table 3-3. In summary, the newly available evidence does not substantively alter our understanding of the concentration-response relati onship (including quantitative aspects) for neurocognitive impact, such as IQ with blood Pb in young children.

3.3 PUBLIC HEALTH IMPLICATIONS AND AT-RISK POPULATIONS There are several potential publ ic health impacts associated with Pb exposure. In recognition of effects causally related to blood Pb levels somewhat near those most recently reported for today’s population and for which the wei ght of the evidence is greatest, the potential public health impacts most prominently rec ognized in the ISA are population IQ impacts associated with childhood Pb exposure and preval ence of cardiovascular e ffects in adults (ISA,3-30 section 1.9.1). With regard to the latter category, as discussed above, the full body of evidence indicates a role of long-term cumulative exposur e, with uncertainty re garding the specific exposure circumstances contributing to the eff ects in the epidemiologi cal studies of adult populations, for whom historical Pb exposures we re likely much higher than exposures that commonly occur today (ISA, section 4.4). There is less uncertainty re garding the exposure patterns contributing to the blood Pb levels re ported in studies of younger populations (ISA, sections 1.9.4, 1.10). Accordingly, we focus the disc ussion of public health implications relevant to this review predominantly on nervous system effects, including IQ de crements, in children. We focus this discussion on IQ in recogniti on of IQ being a well-established, widely recognized and rigorously standardized measure of neurocognitive function, as well as a global measure reflecting the integrati on of numerous processes (ISA, section 4.3.2; 2006 CD, sections 6.2.2 and 8.4.2). We recognize, however, that IQ is one of several measures of cognitive function negatively associated with Pb exposur e. Other examples include other tests of intelligence and cognitive development and tests of other cognitive abilities, such as learning, memory, and executive functions, as well as academic performance and achievement (ISA, section 4.3.2). In consid ering the public health significance of neurocognitive effects of Pb in children, we recognize that, althoug h some may be transient, so me effects may persist into adulthood (ISA, section 1.9.5). 26 We also note that deficits in neurodevelopment early in life may have lifetime consequences as “[n]eurodeve lopmental deficits meas ured in childhood may set affected children on trajectories more pr one toward lower educational attainment and financial well-being” (ISA, section 4. 3.14). Thus, population groups for which neurodevelopment is affected by Pb exposure in early childhood are at risk of related impacts on
their success later in life. There are important distinctions between population and individual risk such that “[s]mall shifts in the population mean IQ can be highly significant from a public health perspective” (ISA, p. xciii). For example, if l ead-related decrements are manifested uniformly across the range of IQ scores in a population, “a small shift in the population mean IQ may be significant from a public health perspective because such a shift could yield a larger proportion of individuals functioning in the low range of the IQ distribution, which is associated with increased risk of educational, vocational, and social failure” as well as a decrease in the proportion with high IQ scores (ISA, section 1.9.1).

26 The ISA states that the “persisten ce of effects appears to depend on the duration and window of exposure as well as other factors that may affect an individual’s ability to recover from an insult”, with some evidence of greater recovery in children reared in households with more optimal caregiving characteristics and low concurrent blood Pb levels (ISA, p. 1-77; Bellinger et al., 1990).3-31 In the discussion below, we use the term at-risk populations 27 to recognize populations that have a greater likelihood of experiencing lead-related health eff ects, i.e., groups with
characteristics that contribute to an increased risk of Pb-related h ealth effects. These populations are also sometimes referred to as sensitive groups, as in section 1.2.1 above. This increased
likelihood of lead-related effects can result from many factors, in cluding lifestage or age, sex, race or ethnicity, diet, pre-existing disease stat e, or increased exposure (ISA, chapter 5). Accordingly, in identifying factors that increase risk of lead-related health effects, there has been consideration of evidence rega rding factors contributing to in creased susceptibility (i.e., physiological or intrinsic factor s contributing to a greater resp onse for the same exposure), and those contributing to increased exposure (inclu ding that resulting from behavior leading to increased contact with contaminated media). As noted in the ISA, “definitions of susceptibility and vulnerability vary across studies, but in most instances ‘susceptibility’ refers to biological or intrinsic factors (e.g., age, sex) while ‘vulnerabi lity’ refers to nonbiologica l or extrinsic factors (e.g., socioeconomic status [SES])” and the terms “at-risk” and “sensitive” populations have in various instances been used to encompass these concepts more generally (ISA, p. 5-1). Although we emphasize the term “at-risk”, we rely on the othe r terms in particular instances below; in so doing, our usage is consistent with these definitions.
Factors that increase risk of lead-related effects include , among others, behavioral and physiological factors. A behavior al factor of great impact on Pb exposure is the incidence of hand-to-mouth activity that is prevalent in very young children and by which they transfer Pb in settled particles to their mouths (ISA, secti ons 3.7.1 and 5.2.1.1). Physiol ogical factors include both conditions contributing to a gr oup’s increased risk of effects at a given blood Pb level, and
those that contribute to blood Pb levels higher than those otherw ise associated with a given Pb exposure (ISA, sections 5.3 and 5.1, respectively). We also considered evidence encompassing situations of elevated exposure, such as residi ng in old housing with Pb-containing paint or near sources of ambient Pb, as well as socioeconomic f actors, such as reduced access to health care or low socioeconomic status (SES) that can contribute to increased risk of adverse health effects from Pb (ISA, sections 1.9.7, 5.2, and 5.4).

 Has new information altered our understanding of human populations that are particularly at risk of health effects from Pb exposures? The information newly available in this review has not substa ntially altered our understanding of at-risk populations . As in the last review, the factor most prominently

27 In the context of “at-risk populations”, the term population refers to persons having one or more qualities or characteristics including, for example, a specific pre-ex isting illness or a specific age or lifestage, with lifestage referring to a distinguishable time frame in an individual’s life characterized by unique and relatively stable behavioral and/or physiological characteristics that are associated with development and growth.3-32 recognized to contribute to increas ed risk of Pb effects is age (ISA, section 1.9.6). As noted in section 3.2 above, although the specific ages or life stages of greatest susceptibility or risk have not been established (e.g., ISA, section 4.3.11) , the at-risk status of young children to the neurodevelopmental effects of Pb is we ll recognized (e.g., ISA, sections 1.9.6, 4.3, 5.2.1, 5.3.1, and 5.4). The evidence indicate s that prenatal blood Pb levels are associated with nervous system effects, including mental development in very young childre n and can also be associated with cognitive decrements in older children (ISA, section 4.3). The coincidence during early childhood of behaviors that increase exposure, such as hand-to-mouth contact, and the development of the nervous system contributes increased risk during th is time (ISA, sections 4.3.2.6, 5.2.1.1, and 5.3.1.1). The evidence also indicates a relationship of postnatal blood Pb levels (through early childhood to school age) with cognitive function decrement in older children and adolescents (ISA, section 4.3). In ep idemiological studies, associations have been observed of neurocognitive, and some other nervous system effects, at various ages from early childhood to school age with prenatal, early-ch ildhood, lifetime average, and concurrent blood
Pb levels as well as with childhood tooth Pb levels (ISA, section 4.3). Consideration of epidemiological study results for different lifestages of exposure, particularly later in childhood, is complicated by the fact that blood Pb leve ls in children, although highly affected by recent exposure, are also influenced by their history of Pb exposure due to rapid growth-related bone turnover in children (ISA, section 3.3.5). Thus, bl ood Pb level in children also may reflect past Pb exposures and, to some extent, maternal Pb, w ith relative contributions varying with child and maternal exposure history (ISA, sect ion 3.2.2.4, 3.4.1 and 4.3.15; 2006 CD, section 6.6.2). Collectively, however, the evidence indicates both the susceptibility of the developing fetus and early postnatal years, as well as the potentia l for continued susceptib ility through childhood as the human central nervous system continues to ma ture and be vulnerable to neurotoxicants (ISA, sections 1.9.5 and 4.3.15; 2006 CD, section 6.2.12). In the collective body of eviden ce of nervous system effects in children, it is difficult to distinguish exposure in later lif estages (e.g., school age) and its associated risk from risks resulting from exposure in prenatal and ear ly childhood (ISA, section 4.3.11). While early childhood is recognized as a time of increased susceptibility, a diffi culty in identifying a discrete period of susceptibility from epidemiological stud ies has been that the period of peak exposure, reflected in peak blood Pb leve ls, is around 18-27 months when hand-to-mouth activity is at its maximum (ISA, section 3.4.1 and 5.2.1.1; 2006 CD, p. 6-60). The task is additionally complicated by the role of maternal exposure history in cont ributing Pb to the developing fetus (ISA, section 3.2.2.4.). Epidemiological analyses evaluating risk of ne urocognitive impacts (e.g., reduced IQ) associated with different blood Pb metrics in cohorts with differing exposure patterns (including those for which blood Pb levels at different ages were not highly correlated)3-33 indicate associations with blood Pb measuremen ts concurrent with FSI Q tests at ages of approximately 6-7 years, alt hough the analyses did not conclu sively demonstrate stronger findings for early (e.g., age 2 years) or c oncurrent blood Pb (ISA, section 4.3.11). The experimental animal evidence additionally indica tes early life susceptibility (ISA, section 4.3.15 and p. 5-21). Thus, the full evidence base cont inues to indicate prenatal and early childhood lifestages as periods of increased lead-related risk . In summary, while uncertainties remain with regard to the role of Pb exposures during a part icular age of life in eliciting nervous system effects, such as cognitive function decrements, the evidence continues to indicate the at-risk status of pre- and postnatal childhoo d lifestages (ISA, sections 4.3.11 and 4.3.15). Several physiological factors incr ease risk of lead-related hea lth effects by contributing to
increased blood Pb levels over those otherwise associated with a given Pb exposure (ISA, sections 3.2, 3.3 and 5.1). These include nutritiona l status, which plays a role in Pb absorption from the GI tract (ISA, section 3.2.1.2). For exampl e, diets deficient in ir on, calcium or zinc can contribute to increased Pb absorption and asso ciated higher blood Pb levels (ISA, sections 3.2.1.2, and 5.1). Evidence is suggestive of some gene tic characteristics as potential risk factors, such as presence of the δ -aminolevulinic acid dehydratase-2 (ALAD-2) allele which has been
indicated to increase blood Pb levels or l ead-related risk (ISA, s ections 3.3.2 and 5.1). Risk factors based on increased exposure in clude spending time in proximity to sources
of Pb to ambient air or other environmenta l media (e.g., large active metals industries or locations of historical Pb contamination) (IS A, sections 3.7.1 and 5.2.5). Residential factors associated with other sources of Pb exposure (e .g., leaded paint or plumbing with Pb pipes or solder) are another exposure-rel ated risk factor (ISA, secti ons 3.7.1 and 5.2.6). The role of socioeconomic status (SES) with regard to lead-r elated risk is somewhat complicated. SES often
serves as a marker term for one or a combin ation of unspecified or unknown environmental or
behavioral variables. Lower SES has been asso ciated with higher Pb exposure and higher blood Pb concentration (ISA, sections 5.3.16, 6.2.4 and 6.4) . Further, it is independently associated with an adverse impact on neurocognitive development, and a few studies have examined SES as a potential modifier of the a ssociation of childhood Pb exposure with cognitive function with inconsistent findings regarding lo w SES as a potential risk factor. Although the differences in blood Pb levels among children of lower as compar ed to higher income levels have lessened, blood Pb levels continue to be higher among lo wer-income children i ndicating higher exposure and/or greater influence of fact ors independent of exposure, su ch as nutritional factors (ISA, sections 1.9.6, 5.2.1.1 and 5.4). In considering risk factors associated with increased Pb exposure or increased blood Pb levels, we note that the currently available ev idence continues to support a nonlinear relationship between neurocognitive effects and blood Pb that indicates incrementally greater impacts at3-34 lower as compared to higher blood Pb levels (IS A, section 4.3.12), as described in section 3.2 above. An important implication of this findi ng is that while children with higher blood Pb levels are at greater risk of lead-related effects than children with lower blood Pb levels, on an incremental basis (e.g., per μg/dL), the risk is greater for children at lower blood Pb levels. This was given particular attention in the last review of the Pb NAAQS, in which the standard was
revised with consideration of the incremental impact of air-related Pb on young children in the U.S and the recognition of greater impact for those children with lower absolute blood Pb levels (73 FR 67002). Such consideration included a fo cus on those C-R studies involving the lowest blood Pb levels, as described in section 4.1.1 below. Some racial or ethnic backgr ounds have been identified as fa ctors that may increase risk of lead-related health effects (ISA, secti ons 1.9.6, 5.2.3 and 5.3.7). For example, although blood Pb levels in the U.S. general population (e.g., geom etric mean level in children aged 1-5) have declined, mean levels reported in recent NHANE S samples continue to differ among children of different ethnic backgrounds, w ith higher levels in non-white pe rsons as compared to whites (ISA, sections 3.4.1, 5.2.1.1 and 5.2.3). Additionally, a study of lead-related risk of hypertension among adults reported greater risk associated with blood Pb levels above 1 μg/dL among Mexican Americans and non-Hispanic blacks th an among non-Hispanic whites (ISA, section 5.3.7; Muntner et al., 2005). The ev idence available in the current review, consis tent with that in the last, also suggests that health status or pre-existing disease is potentially a phys iological risk
factor for lead-related effects (ISA, section 1.9.6). Populations with pre-existing health conditions, such as hypertension, may be more susceptible than those without such conditions for particular Pb-associated effects (IS A, section 5.3.4). For example, increased risks of lead-related renal effects and heart rate variability have been reported among hype rtensive individuals compared to those that are normotensive (ISA, section 1.9.6). Additionally, African Americans, as a group, have a higher frequency of hypertension than the larger U.S. population as a whole and than other ethnic groups (NCHS, 2011) and, as a result, may face a greater risk of adverse health impact from Pb-associated cardiovascular effects.
Older adulthood has been identified as a life stage of potentially gr eater risk of leadrelated health effects based primarily on the eviden ce of increases in blood Pb levels during this lifestage (ISA, sections 5.2.1.2, 5.3.1.2, and 5.4). Cont ributing to blood Pb levels in the studied populations of older adults are likely to be their exposure hi stories, which included younger years during the time of leaded gasoline usage and other sources of Pb exposures which were more prevalent in the past than today (e.g., ISA, Figure 2-1 and section 2.5.2). Exposure history has a contributing role to blood Pb levels th roughout life, and the in creased rate of bone remodeling during later adulthood increases contributions of Pb from bone stores into the systemic circulation during that lifestage (IS A, sections 3.3.5 and 5.2.1.2). Additionally, limited3-35 animal evidence has indicated specific brain path ology in older animals that had substantial Pb exposures earlier in life (ISA, sections 4.3.9.1 and 5.3.1). Further, the full body of evidence
includes observed associations of some cardiovascular and neurol ogical effects with bone and blood Pb in older populations, with biological plausibility for the role of Pb provided by experimental animal studies (ISA, sections 4.3.5, 4.3.7 and 4.4). In summary, the information newly available in this review has not appreciably altered our understanding of human populations that are part icularly sensitive to Pb exposures. In the current review, as at the time of the last re view of the Pb NAAQS, we recognize young children as an important at-risk populat ion, with sensitivity extending to prenatal exposures and into childhood development. Additional risk factors in clude deficiencies in dietary minerals (iron, calcium and zinc), some racial or ethnic b ackgrounds, and spending ti me in proximity to environmental sources of Pb or residing in ol der houses. The evidence for SES continues to
indicate increased blood Pb levels in lower income children, although its role with regard to an
increased health risk for same blood Pb level is unclear. Additionally, the currently available evidence continues to suggest a pote ntial for increased risk associat ed with several other factors, including older adulthood, pre- existing disease (e.g., hypertension) , variants for certain genes
and increased stress.

 Is there new evidence on health effect s beyond neurocognitive endpoints in children that suggest additional at-ris k populations should be given increased focus in this review? The evidence newly available in this revi ew supports or strengthens our previous conclusions regarding the broad array of health effects of Pb (see ISA, section 1.10 which compares key conclusions drawn in the last re view with conclusions drawn in the current assessment). Additionally, in some categories of health effects, the newly available studies extend the evidence for some aspects of the health effects described in the last review. For example, among the nervous system effects, th e newly available eviden ce continues to support
the conclusions from the last review regarding Pb and neuroc ognitive and behavioral effects (ISA, section 4.3). Across the array of neurocogn itive and behavioral effects, we recognize the sensitivity of the prenatal period and severa l lifestages of childhood, and we particularly recognize young children as an im portant at-risk population in li ght of current environmental exposure levels. As discussed in section 3.2 above, the blood Pb levels of populations studied in newly available epidemiological studies that report associations of bl ood Pb with effects for systems and processes other than the nervous syst em (e.g., cardiovascular, developmental and reproductive) are similar to or, in a few cases, so mewhat lower than those assessed in the last review (ISA, sections 4.4, 4.6, 4.7, and 4.8). Th e greater uncertainties regarding the time,3-36 duration and magnitude of expos ure contributing to these obser ved health effects complicate identification of sensitive lifestages and associat ed exposure patterns that might be compared with our understanding of the sensitivity of young children to neurocognitive impacts of Pb. Thus, while augmenting the evidence base on th ese additional endpoints, the newly available evidence does not lead us to identify a health en dpoint expected to be more sensitive to Pb exposure than neurocognitive endpoints in children, l eading us to continue to conclude that the appropriate primary focus for our review is on neurocognitive e ndpoints in children. In summary, there are a vari ety of ways in which lead-exposed populations might be
characterized and stratified for cons ideration of public health impact s. Age or lifestage was used to distinguish potential groups on which to focus in the last review in re cognition of its role in exposure and susceptibility, and young children were selected as the priority population for the risk assessment (see section 3.4 below) in consider ation of the health eff ects evidence regarding endpoints of greatest public hea lth concern and in recognition of effects on the developing nervous system as a sentinel endpoint for public health impacts of P b. This identification continues to be supported by the eviden ce available in th e current review.

 What does the information about air Pb concentrations available in this review indicate with regard to the size of a t-risk populations and their distribution across the U.S.? The magnitude of a public health impact is dependent upon the size of populations affected, as well as type or se verity of the effect. As summarized above, the population group that may be most at risk of health effects asso ciated with exposure to Pb is young children. The 2010 census indicates nearly 310 million people re siding in the U.S., approximately 74 million
of whom are children under the age of 18, with some 20 million under the age of five years. Children at greatest risk from air-related Pb ar e those children with highest air-related Pb exposure which are considered to be those living in areas of higher ambient air Pb
concentrations. The discussion below consider s the information available to inform our understanding of areas of children potent ially at risk from air-related Pb. In considering the extent of this at-risk populat ion, we turn first to consideration of those
areas in the U.S. with air Pb concentrations above the current sta ndard (e.g., section 2.2.2.2 above). Using the available monitoring data a nd U.S. census information, Table 3-4 summarizes the size of populations within 0.5 km of monitors in our current Pb NAAQS surveillance network at which Pb concentrations were highe r than the current standard during the recent period from 2009-2011. The distance to which co ncentrations exceeding the standard might extend will vary with the magnitude of the Pb concentrations and particle size, among other factors; a half-kilometer distance was selected fo r purposes of illustration here. This analysis indicates that approximately 2,400 children aged 5 or under reside within 0.5 km of monitors3-37 exceeding the current standard. To also account for the population in areas with air concentrations just at (or very near) the curren t standard, we have also identified an additional nine Pb-TSP monitors with 3-month average conc entrations within 10% of, but not exceeding, the current standard (Appendix 2D). Based on the 2010 U.S. census, 265 children aged 5 or
under reside within 0.5 km of these additional sites.

Table 3-4. Number of children aged 5 and under in areas of elevated ambient air Pb concentrations relative to the NAAQS.

Population within 0.5 km of monitors with maximum 3-month Pb concentration greater than 0.15 μ g/m 3 (2009-2011)

Number of Counties Number of States or Territories Total population Children, 5 and under

All sites >0.15 μ g/m 3 29 20 25,344 2,416
Subset of sites >0.5 μ g/m 3 11 9 11,753 1,018
Data Sources: U.S. Bureau of the Census, 2010 Census of Population and Housing and recent Pb-TSP dataset presented in Figure 2-10 above (dataset criteria and su mmaries included Appendices 2C and 2D, respectively). Section 2.2.1.1 above describes the surveillance monitoring network required for identifying locations with the potential to exceed the NAAQS.

As the air quality data set analyzed in sect ion 2.2.2 above may not be inclusive of all of the newly sited monitors, as discussed in sec tion 2.2.1 above, we recognize there may be other areas of the country where concentrations are ab ove or just meet the current standard but for which such data are not yet availabl e. To consider the potential fo r there to be a dditional, not yet identified, areas with elevated Pb concentratio ns, we have separately quantified the size of young child populations residing in areas near large Pb sources in Table 3-5. In so doing, we recognize uncertainties and potential limitations associat ed with these emissions estimates for these purposes, uncertainties both with regard to the accu racy of such estimates and also with regard to the role of specific source char acteristics and meteorology, not expl icitly considered here, in influencing ambient air Pb concentrations and c ontributing to substantia l variation in air Pb
concentrations at source locations (e.g., Figure 2-11 above). Acco rdingly, while the summary in Table 3-5 is informative in considering the pot ential prevalence of airborne Pb emissions and potential exposure of human populations, it is lim ited with regard to its ability to identify populations living in areas of elevat ed ambient air Pb concentrations . We interpret this analysis to indicate that fewer than about 7,800 young child ren (aged 5 or younger) live in areas with air
Pb concentrations near or above the current standard, with the current mon itoring data indicating the size of this population to be approximately 2,700.3-38 Table 3-5. Population size near larger sources of Pb emissions.

Population Within 0.5 km of Sources Emitting at Least 0.5 tpy in 2008

Facilities (other than airports) Airports All

Number of Locations Population, all ages Population, aged 5 and

younger Number of Locations Population, all ages Population, aged 5 and

younger Population, aged 5 and

younger Facilities/Airports estima ted to emit > 5.0 tpy 8 484 61 0 0 0 61 Facilities/Airports estimate d to emit 1.0 - 4.9 tpy A 53 12,143 731 6 6,261 266 997 Facilities/Airports estimate d to emit 0.50 – 0.95 tpy B 63 12,934 1,143 52 76,105 6,699 7,842 A - Facilities estimated to emit at least 1.0 tpy (after rounding to 1 decimal place) and less than 5.0 (after rounding to 1 de cimal place). B - Facilities estimate to emit at least 0.50 tpy (after rounding to 2 decimal places) and less than 1.0 (after rounding to 1 d ecimal place). Sources: Population counts from U.S. Bureau of the Census, 2010 Census of Population and Housing. Emissions estimates for facilities other than airports drawn from 2008 NEI, version 3 (Dec ember 2012); estimates for airports re flect EPA’s best estimates of piston-eng ine aircraft emissions. Piston-engine aircraft emissions inventory is available at: http://www.epa.gov/ttn/chief/net/200 8neiv2/2008_ne iv2_tsd_draft.pdf

.

3.4 EXPOSURE AND RISK
The risk information available for this revi ew and described here is based primarily on the exposure and risk assessment developed in th e last review of the Pb NAAQS (henceforth referred to as the 2007 REA [USEPA, 2007a]), as c onsidered in the cont ext of the evidence newly available in this review (as presented in the ISA). As described in the REA Planning Document, careful consideration of the information newly available in this review, with regard to designing and implementing a full REA for this review , led us to conclude that performance of a
new REA for this review was not warranted. We did not find the information newly available in this review to provide the means by which to de velop an updated or enhanced risk model that would substantially improve the utility of risk estimates in informing the current Pb NAAQS review (REA Planning Document, section 2.3). Based on their cons ideration of the REA Planning Document analysis, the CASAC Pb Re view Panel generally concurred with the
conclusion that a new REA was not wa rranted in this review (Frey, 2011). 28 Accordingly, the information described here is drawn primarily from the 2007 REA, augmented by a limited new case study-specific analysis focused on risk associated with the current standard, as described in
section 3.4.3.3 below.

28 In our evaluation presented in the REA Planning Document and in consultation with CASAC, we indicated our conclusion that the information newly availabl e in this review did not provide the means by which to develop an updated or enhanced risk model that would substantially improve the utility of risk estimates in informing the current Pb NAAQS review. In their review of the draft PA, the CASAC Pb Review Panel reenforced their concurrence with EPA’s decision not to develop a new REA (Frey, 2013).3-39 The focus for the risk assessment and associated estimates presented here is on Pb derived from sources emitting Pb to ambient air. As discussed in section 1.3 above (and conceptually illustrated in Figure 1-1), the multimedia and persistent nature of Pb, the role of multiple exposure pathways, and the contributions of nonair sources of Pb to human exposure media all present challenges and co ntribute significant additional complexity to the health risk assessment that goes far beyond the situation for similar assessments typically performed for other NAAQS pollutants (e.g., that focus only on th e inhalation pathway). Limitations in the
available data and models affected our character ization of the various complexities associated with exposure to ambient air Pb. As a result , the assessment includes a number of simplifying assumptions in a number of areas and, as descri bed in section 3.4.4 below, our estimates of airrelated Pb risk are approximate and ar e characterized by upper and lower bounds. The conceptual model developed to in form planning for the 2007 REA, including identification of key exposure media, target population, health endpoint and risk metric is
described in section 3.4.1. The 2007 REA relied on a case study approach to provide estimates that inform our understanding of air-related exposure and risk in different types of air Pb exposure situations; the case stud ies included are described in s ection 3.4.2. In section 3.4.3, the analysis approach and general aspects of expos ure and risk assessment methods are summarized, and the air quality scenarios simulated are desc ribed. In section 3.4.3, we also summarize the 2007 REA risk model and the interpolation approach used in the limited new analyses performed for purposes of this review. Section 3.4.4 identifi es key aspects of the exposure assessment and risk estimates are presented in section 3.4.5. Treat ment of key sources of variability in exposure
and risk estimates is described in section 3.4.6 and the characterizati on of uncertainty is summarized in 3.4.7. An updated inte rpretation of the risk estimates for our purposes in this Pb NAAQS review section is presented in section 3.4.8.

3.4.1 Conceptual Model for Air-Rela ted Lead Exposure and Risk

In considering public health risks associated w ith Pb from ambient air, the focus is on Pb derived from those sources emitting Pb to ambient air. The multimedia and persistent nature of Pb, illustrated in Figure 1-1 above, as well as the existence of many nonair sources of Pb to the environment, contribute multiple complexities to the consideration of exposure and risk for ambient air-related Pb. The conceptual model that informed planning for the 2007 REA identified sources, pathways, routes, exposed populations, and health endpoints, focusing on those aspects of Pb exposure most relevant to th e review, while also recognizing the role of Pb exposure pathways unrelated to Pb in ambient air (2007 REA, section 2.1).3-40 As recognized in section 1.3 above, sources of human Pb exposure include current and historical air emissions sources, as well as mis cellaneous nonair sources, wh ich can contribute to multiple exposure media and associated pathways (e.g., inhalation of ambi ent air, ingestion of indoor dust, outdoor soil/dust and diet or drinking water). 29 Figure 3-2 illust rates these human exposure pathways from an analytical perspec tive, drawing on the con ceptual model for the assessment (2007 REA, Figure 2-1). 30 As shown in Figure 3-2, in addition to airborne emissions (recent or those in the past), so urces of Pb to these pathways also include old leaded paint, including Pb mobilized indoors dur ing renovation/repair activities, and contaminated soils. Lead in diet and drinking water may have air pathway- related contributions as well as contributions from nonair sources (e.g., Pb solder on water dist ribution pipes and Pb in materials used in food processing). Limitations in our data and modeling tools handicappe d our ability to separate the nonair contributions to Pb exposure from estim ates of air-related Pb exposure and risk. 31

Figure 3-2. Human exposure pathways for air-related Pb.

29 We did not explicitly consider Pb exposure related to consumer products (e.g., toys, cosmetics, dishes) in the 2007 REA.

30 We additionally note that Pb in children at birth is from maternal exposures, recent or historical, as recognized in section 3.1 above, and that ingestion of maternal breast milk may be a Pb exposure pathway for infants in some cases (ISA, section 3.1.3.3).

31 The assessment grouped the exposure and risk estimates for Pb in diet and drinking water together and combined them with the other pathways in estimates presen ted for “total Pb exposure”. Characterization of the risk assessment results in the rulemaking recognized the cont ribution, albeit unquantified, from air-related pathways within this category. 

### Pb in ambient air

Indoor air

Indoor dust Outdoor soil/dust Food (crops/ livestock) Drinking water

Paint Pb Historic Pb Deposition outdoors

Deposition

indoors Pb from distribution /processing

* Green ovals indicate nonair or historic sources. Sources unrelated to environmental pathways (e.g., jewelry, mini-blinds) not shown. Infiltration



### Inhalation of ambient air Pb

(outdoors or

indoors) Ingestion of indoor dust Pb Ingestion of outdoor soil/dust Pb Ingestion of Pb in diet/drinking water Resuspension

Resuspension

Water discharges Land releases 

### *3-41 Identification of exposure populations, exposur e/dose metric, health effects endpoint and
risk metric to be included in the 2007 REA we re based on consideration of the then-currently
available evidence as assessed in detail in th e 2006 CD. As discussed in the REA Planning Document (USEPA, 2011), these selections continue to be supported by the evidence now
available in this review as described in the ISA. In the REA, we focused on IQ loss in childre n exposed up to age 7 years. This focus reflected the evidence for young children with re gard to air-related exposure pathways and susceptibility to Pb health impacts (e.g., ISA, sections 3.1.1, 4.3, 5.2.1.1, 5.3.1.1, and 5.4). For example, the hand-to-mouth activity of young child ren contributes to their Pb exposure (i.e.,
incidental soil and indoor dust ingestion) and ambient air-related Pb has been shown to
contribute to Pb in outdoor soil and indoor house dust (ISA, s ections 3.1.1 and 3.4.1; 2006 CD, section 3.2.3). Blood Pb is commonly used as an integrated index or biomarker of exposure due to both its association with exposure, particularly recent exposure in young ch ildren, and the relative ease of the measurements, as discussed in se ction 3.1 above. Although bone Pb measurements have become easier to collect and conseque ntly, their use has been more widespread, epidemiological and toxicological studies of Pb health effects and dose-response relationships (particularly for neurodevelopmental effects in child ren) tend to be dominated by blood Pb as the exposure metric. Therefore, we focused on modeling blood Pb in young children, developing
estimates for two blood Pb metrics: “concurrent ” and “lifetime average”. For the former we estimated blood Pb at age 7 years, while lifetime average was estimated as the average across the 7-year period. 32 In addition, our focus on young children reflects the evidence that the developing nervous system in children is among, if not, the most sensitive of the endpoints associated with Pb exposure (ISA, sections 1.6 and 1.10). At the time of the last re view, we noted that limitations precluded prediction of changes in adult blood Pb levels (or bone Pb levels) given changes in ambient Pb levels. This reflects the fact that the pr esence of substantial historic Pb stores in most adults introduces uncertainty in to the prediction of changes in blood or bone Pb in these adult populations resulting from changes in ambient ai r Pb exposure. Additionally, in considering concentration-response relationships for adu lt blood Pb and adult health outcomes, we recognized the uncertainty with rega rd to the role of historic co mpared to recent exposures in eliciting the observed outcomes. Based on conc lusions regarding the scientific evidence available in the last review (presented in th e 2006 CD), the assessment focused on risk to the

32 The pathways represented in this modeling included childhood inhalation and ingestion pathways, as well as maternal contributions to newborn body burden (2007 REA, Appendix H, Exhibit H-6).3-42 central nervous system in chil dhood as the most sensitive effect that could be quantitatively assessed, with decrement in IQ used as the risk metric.

3.4.2 Case Studies

Lead exposure and associated risk were esti mated for multiple case studies that generally represent two types of re sidential population exposures to ai r-related Pb (see Table 3-6): (1) location-specific urban populati ons of children with a broad ra nge of air-related exposures, reflecting existence of urban con centration gradients; and, (2) child ren residing in localized areas with air-related exposures representing air con centrations specif ically reflecting the standard level being evaluated. Thus, the two types of case studies differed with regard to the extent to which they represented population variability in air-related Pb e xposure (as discussed further in section 3.4.7 below). Three location-specific ur ban case studies focused on residential areas within Cleveland, Chicago, and Los Angeles, pr oviding representations of urban populations with a broad range of air-related exposures due to spatial gradient s in both ambient air Pb levels and population density. For example, the highest air concentrations in these case studies (i.e.,
those closest to the standard be ing assessed) were found in very small parts of the study areas, while a large majority of the case study populati ons resided in areas with much lower air concentrations. The case studies representing th e children most highly exposed via air-related pathways were the generalized (local ) urban case study (also referred to as general urban case study ) and the primary Pb smelter case study subarea. The generalized (loc al) urban case study was not based on a specific geographic location an d reflected several simplifying assumptions in representing exposure incl uding uniform ambient air Pb levels associated with the standard of interest across the hypot hetical study area and a uniform st udy population. The primary Pb smelter case study provides risk estimates for child ren living in a specific area within which some locations, at the time of the 2007 REA, were not meeting the then-current standard. In addition to characterizing risks within a 10 km ra dius area surrounding the smelter (full area), we focused particularly on a subarea within 1.5 km of the facility, where airbor ne Pb concentrations were closest to the then-current standard (a maximum calendar quarter average concentration of 1.5 μg/m 3 Pb-TSP) and where children’s air-relate d exposures are most impacted by emissions
associated with the Pb smelter from which air Pb concentrations were estimated. Based on the nature of the population exposures represen ted by the two categor ies of case study, the generalized (local) urban and primary Pb smelte r case study subarea includ e populations that are relatively more highly exposed by way of air pathwa ys to air Pb concentrations near the standard3-43 level evaluated, compared with th e populations in the th ree cities or the fu ll area of the primary smelter case study. 33,34

Table 3-6. Types of population exposures assessed.

Type of Population Exposure Case Study 1

Broad range of air-related exposures Part of metropolitan area with spatially varying air concentrations, inclusive of location at standard or conditions being evaluated Multiple exposure zones, larger populations Location-specific urban: Cleveland, Chicago, Los Angeles

As above, with dominant, historically active metals industry as ambient air Pb source Primary Pb smelter (full area)

Generalized, high end of air-related exposure Localized residential area with air concentrations generally representing the standard or conditions evaluated Single exposure zone without enumerated population Generalized (local) urban

A few exposure zones with small population Primary Pb smelter (subarea)

3.4.3 Analysis Approach

The approach to assessing exposure and risk for the two categories of case studies was comprised of four main analytic al steps: (a) estimation of ambi ent air Pb concentrations, (b) estimation of Pb concentrations in other key ex posure media, including outdoor soil and indoor dust, (c) use of exposure media Pb concentrations, with other pathway Pb intake rates (e.g., diet), to estimate blood Pb levels in children using bi okinetic modeling, and (d ) use of concentrationresponse functions derived from epidemiology studi es to estimate IQ loss associated with the blood Pb levels. In implementing these st eps for the primary smelter case study, air concentrations were estimated using dispersi on modeling; indoor dust concentrations were estimated for the case study subarea using a site-s pecific regression model. The approach for the generalized (local) urban case study and location-specific urba n case studies was somewhat

33 An additional case study (the secondary Pb smelter case study) was also developed in the 2007 REA, however, significant limitations associated with the use of dispersion modeling to predict ambient air, dust and soil Pb levels near the facility contributed to large uncertain ties in the risk estimates (2007 REA, section 4.3.1).

34 In addition to the case studies included in the 2007 REA, the pilot phase of the 2007 REA also included a near-roadway case study, focused on subset of urban population exposed immediately near roadways (ICF International, 2006). Based on the pilot results and advi ce from CASAC, however, this case study was not carried into the full-scale analysis. As an alternative, we deve loped the generalized (local) urban case study to represent urban residents in a localized area ex posed to air-related Pb associated with the standard being assessed.3-44 simpler, since it did not involve fate and transp ort modeling for air conc entration estimates and, instead, used ambient monitor leve ls to characterize the gradient in air Pb levels across the study area. All steps are somewhat simpler in the generalized (local) urba n case study which included a single exposure zone. Figure 3-3 identifies the key input data sets, modeling steps and intermediate model output in each of the four analytical steps. The first three steps were employed in the exposure assessment (discussed in section 3.4.3.1), while the fourth is the risk assessment step (discussed in section 3.4.3.3).3-45 Drawn from 2007 REA, Figure 3-3 (USEPA, 2007).

Figure 3-3. Overview of analysis approach. 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 case 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 functions (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 CHARACTERIZATION3-46 3.4.3.1 Estimating Exposure

Concentrations of Pb were estimated in ambient media and indoor dust using a combination of empirical data and modeling projectio ns. The use of empirica l data brings with it uncertainty related to the potential inclusion of nonair source si gnals in these measurements (e.g., house paint contributions to indoor dust and outdoor soil Pb). Conversely, the use of modeling
tools introduces other uncerta inties (e.g., model and parameter uncertainties). The characterization of uncertainty a ssociated with the risk assessment is discussed in section 3.4.7. Table 3-7 summarizes the exposur e modeling approaches and data used to characterize Pb concentrations or input associated with each exposure pathway for each of the case studies.
Characterization of Pb in ambient air relied on (a) dispersion modeling of facility-related (including fugitive) Pb emissions for the 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 generalized (local) urban case study. The use of dispersion modeling for the primary Pb smelter case study allowed us to capture more spatially re fined patterns of ambient air Pb over residential areas in the vicinity of the facility, where am bient Pb levels were dominated by Pb released from the facility. For the location-specific urban case studies, we used Pb monito rs within each of the urban study areas to characterize spatial grad ients. By contrast, the genera lized (local) urban case study is designed to assess exposure a nd risk for a smaller group of residents (e.g., neighborhood) exposed at the level of the standa rd and therefore, did not rely on monitor data in characterizing levels, since ambient air Pb was fixed at the standard being assessed. While ambient air Pb concentrations in the primary Pb smelter case st udy reflected only contributions from direct and fugitive emissions associated with the facility, co ncentrations in the location-specific urban study areas, which relied on empirical (monitor-based) da ta to define ambient air Pb concentrations,
reflected contributions from a ll contributing sources, be they currently active stationary or mobile sources, resuspension of previously de posited Pb or other. Additional detail on estimation of ambient (outdoor) and indoor air con centrations is presented in section 5.2.2 and Appendices A through D of the 2007 REA.
Characterization of Pb concentrations in outdoor surface soil/dust resulting from deposition of airborne Pb was based on the us e of (a) existing site-specific measurements (primary Pb smelter case study) and (b) nationall y representative reside ntial 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 extrapolat ion from these data was used to predict soil levels for portions of the study area beyond this zone. Additional detail on estimation of Pb concentrations in outdoor surface soil or dust is presented in sec tions 3.1.3 and 5.2.2.2 and Appendix F of 2007 REA.3-47 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 of outdoor air indoors, deposition rates of Pb from indoor air to indoor surfaces, house cleaning rates). For the point source case study, we us ed a combination of regression-based models obtained from the literature and developed base d on site-specific data and we developed a customized hybrid empirical-mechanistic model fo r the general and locati on-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 ge neralized (local) urban case study. Additional
detail on estimation of Pb concentrations in indoor dust is presente d in sections 3.1.4 and 5.2.2.2 and Appendix G of 2007 REA.

Table 3-7. Summary of approaches used to estima te case study media concentrations.

Simulation of

air quality

impacts Media category Generalized (local) urban case study Location-specific urban case study Primary Pb smelter case study (1.5 km subarea

and 10 km full area)

Concentrations for these media were varied across air quality scenarios (see section

3.4.3.2). Ambient air Pb levels Single ambient air Pb level assumed across entire study area (single exposure zone) Source and non-source monitors describe concentration gradient (6 to 11 exposure zones per case study) Dispersion modeling of smelter-related emissions (22 census block groups and 115 blocks)

Indoor dust Pb levels Hybrid model: dynamic aspect relates ambient air Pb concentrations to indoor dust Pb; empirical aspect represents Pb from other sources (e.g., paint, historical air, Pb carried indoors with people) For subarea - regression of site-specific air, dust data. For full area - regression of air, dust, soil data from other, historical locations. Concentrations were constant across air

quality scenarios (data/modeling

limitations) Outdoor soil Pb levels National datase t (HUD, for houses constructed between 1940 and 1998). Site-specific data (for subarea) Dietary Pb intake National datasets for Pb residue data (US FDA Total Diet Study) and food consumption data (NHANES) Drinking water Pb intake US and Canada datasets for residential water Pb concentrations and ingestion rates

Blood Pb levels were predicted from estimat es of Pb contained in various media (e.g., ambient air, diet, water, indoor dust) and estimates of Pb intake from dietary and drinking water pathways, using the Integrated Exposure and Uptake Biokinetic (IEUBK) model (2007 REA,3-48 sections 3.2.1.1 and 5.2.4). 35 Diet and drinking water intake an d concentrations, as well as other model inputs, were based on the most current information (2007 REA, Appendix H). Detail on
methods used to characterize media Pb concentr ations and all IEUBK inputs for each case study are in the 2007 REA, sections 3.1, 3.2, 5.2.3 and 5.2.4 and appendices C through H. As the shortest temporal scale accepted for inputs to the IEUBK is a y ear, all model inputs, developed for each exposure zone in each case study, were a nnual average values. For media concentration inputs, the same values were used for each ye ar of the seven-year simulation. Other model inputs varied as appropriate with the age of the simulated child (2007 REA, Appendix H). To simulate population variability in Pb inta ke and uptake, we used the IEUBK model to first generate a central-tendency estimate of the blood Pb levels for the group of children within a given exposure zone of a study area. 36 Outside the IEUBK model, we then combined this centraltendency estimate with a geometric standard de viation (GSD) reflecting variability in blood Pb levels for groups of children to generate a dist ribution of blood Pb levels for a study area. The procedure for combining the IEUBK-based centr al tendency blood Pb estimate with a GSD to generate a population dist ribution of blood Pb levels differs somewhat for the categories of case studies. The approach for the gene ral urban case study is fairly simp le in that we have a single IEUBK-based estimate of blood Pb levels, and this is, in turn, combined with the GSD selected for this study area to produce a population distribution of blood Pb levels. For both the primary Pb smelter and the location-specific urban study areas, multiple polygons within the larger study area (e.g., U.S. Census blocks for the location spec ific urban study areas) are used as the basis for generating distributions of blood Pb levels fo r the child population in each study area. These distributions are generated using a Monte Ca rlo-based population-weig hted sampling method with U.S. Census child counts for each polygon and an adjustment fact or distribution based on the chosen GSD (see 2007 REA, sections 3.2.2 and 5.2.2.3). The GSD reflects a number of factors which ope rate together to pr oduce interindividual variability in blood Pb levels, including: (a) bi okinetic variability (differences in the uptake, distribution or clearance of Pb), (b) differences in behavior rela ted to Pb exposure (e.g., varying hand-to-mouth activity, tap water ingestion rate s, and time spent playing indoors) and (c)

35 In predicting PbB levels, we assumed that Pb con centrations in exposure media remained constant throughout the 7 year simulation period.

36 In typical IEUBK applications, th e GSD is applied within the IEUBK model as part of the modeling process in order to generate percentiles of PbB distribution for the population simulated. However, for the NAAQS REA, we used IEUBK only for generating the central-tendency PbB value for a given exposure zone and then probabilistically combined that estimate with the GSD outs ide of the IEUBK model. This allowed us, in the case of the primary Pb smelter and the location-specific urban case studies (as noted below) to generate individual population-level PbB distributions for each exposure zone which could then be population-weighted and combined using Monte Carlo sampling to generate a single populatio n-distribution for each study area. This was not possible with the typical application of the GSD within the IEUBK model.3-49 differences in environmental Pb exposure concen trations (e.g., spatial gr adients in ambient Pb levels of a resolution beyond that simula ted in each case study, differences in cleaning/vacuuming rates a nd air exchanges rates). 37 For all of the study areas, we assumed that pathway apportionment of blood Pb levels base d on the modeling of the central-tendency blood Pb level (using IEUBK) holds fo r all percentiles of blood Pb le vels derived by combining that central tendency estimate with the GSD. Blood Pb modeling completed for all case studies
included estimates of both concurrent and lifetim e-average blood Pb metrics, although ultimately
we focused on the concurrent blood Pb metric in estimating risk (2007 REA, section 2.1.5). 38

3.4.3.2 Air Quality Scenarios Included in 2007 Assessment The air quality scenarios assessed in the 2007 REA for the case st udies identified in Table 3-6 above included conditions just meetin g the NAAQS that was current at the time of the last review (1.5 μ g/m 3 , maximum calendar quarter average) and conditions meeting several alternative, lower standards. Additionally, scenarios for current conditions (2003-2005) were
also included for the three loca tion-specific urban case studies. 39 These air quality scenarios are characterized by quarterly or monthly averaging times and a not-to-be-exceeded form. Once the air quality dataset representing each scenario was developed, the associated annual average concentrations for each exposure zone were deri ved for input to the IEUBK model, which does not accept air quality inputs of a temporal scal e shorter than a year (2007 REA, Appendix H). 40 As a result of the differing air quality condi tions of the location-sp ecific case studies, there were differences among them with regard to the scenarios assessi ng the then-existing or alternative standards (see Table 3-8). To simulate the previous (1978) standard at the primary Pb

37 We specified GSDs for each of the case studies th at reflected differences in the study areas and underlying study populations, as well as the availability of blood Pb measurement data (see 2007 REA, sections 3.2.3 and 5.2.2.3).

38 As discussed in section 2.1.5 of the 2007 REA, the concurrent PbB measurement (i.e., PbB measurements at the time of IQ test) and the lifetime-average blood level (i.e ., average of measurements taken over child’s first 6-7 years) were considered stronger predictors of lead ’s effect on IQ than were peak and early childhood levels.

39 For the location-specific urban cas e studies of Cleveland, Chicago and Los Angeles, the maximum monthly average concentration was 0.56, 0.31 and 0.17 μg/m 3 , respectively, and the maximum calendar quarter average concentration was 0.36, 0.14 and 0.09 μg/m 3 , respectively, (2003-2005 data; 2007 REA, Appendix O).

40 Although many different patterns of temporally vary ing air concentration will just meet a given potential alternative standard, the shortest ti me step accommodated by the blood Pb model is a year. Thus, the air Pb concentration inputs to the blood Pb model for each air qu ality scenario are annual average air Pb concentrations. For the generalized (local) urban case study, the national Pb-TSP monitoring dataset wa s analyzed to characterize the distribution of site-specific relationships between metrics reflecting the averaging time and form for the air quality scenarios being assessed (Table 3-5) and the annua l average. The IEUBK annual average input was then derived by multiplying the level for a given air quality scenario by the ratio for the averaging time and form for that air quality scenario. For the location-specific case studies, the full temporally varying air Pb concentration dataset for each exposure zone was used to derive the average annual concentration for the IEUBK input.3-50 smelter location, at which then-current monitoring data indicated exceedance of that standard, a proportional roll-down was performed across the ar ea to achieve conditions that just met that standard. Additionally, although it was considered an extremely unlikely scenario that air
concentrations in urban areas across the U.S. that were well below the previous NAAQS would increase to just meet that sta ndard (e.g., by way of expansion of existing sources or congregation of multiple sources in adj acent locations), we simulated this scen ario in all case studies. In so doing, the air Pb concentrations were rolled up proportionally across the lo cation-specific urban study areas to conditions just meeting the standa rd. No other scenario simulations involved rolling concentrations up. For the primary Pb smelter case study, air Pb concentrations were proportionally rolled down to conditions just mee ting each of the potentia l alternativ e standards assessed. In the three location-specific urban cas e studies, the temporally and spatially varying concentrations were rolled down to conditions ju st meeting each of the potential alternative standards that they exceed ed (2007 REA, section 5.2.2.1). 41 For the generalized (local) urban case study, wh ich has a single expos ure zone in which air Pb concentrations do not vary spatially, we derived a single air Pb concentration estimate to meet the standard assessed (e.g., specified maximu m monthly or quarterly average). To reflect the variability in air Pb concentrations that occur over time scales less than a year as a result of temporal changes in meteorology and source and em ission characteristics, the annual average air concentration (input for IEUBK and dust model) was derived for the maximum monthly and quarterly average metrics assessed using relati onships based on the ava ilable Pb-TSP monitoring data for large U.S. urban ar eas (2007 REA, Appendix A).

41 When concentrations in the exposure zone (within th e study area) that has the highest Pb concentrations (in terms of the metric being assessed) achieve a maximum quarterly or monthly average of the specified level, the potential standard is “just met”.3-51 Table 3-8. Air quality scenarios assessed.

Air Quality Conditions Just Meeting ... Case Studies Where Simulated

Generalized (local) Urban A Location Specific Maximum Quarterly Average (μg/m 3 ) Maximum Monthly Average (μg/m 3 ) Primary Smelter Cleveland Chicago Los Angeles

1.5 B √ √ √ √ √
0.2 C √ √

0.5 √ √ √ 0.2 √ √ √ √ 0.05 √ √ √ √ √ 0.02 √ √ √ √ √ A - Conditions were set to meet the standards assessed in the single exposure zone of this case study. B - Concentrations were proportionally rolled down to conditions just meeting the previous standard in the primary Pb smelter case study; concentrations in the three urban location- specific case studies were proportionally rolled up to just meet this standard. C - Concentrations were proportionally rolled down to just meet this and the other potential alternative standards.

The approaches for estimating Pb concentratio ns in other media varied depending on the type of case study (see section 3.4.3.1 above). Li mitations in the available data and modeling tools precluded simulation of linkages between some media and air Pb, such that the full impact of changes in air Pb conditions associated with attainment of lower stan dards was not simulated. For example, dietary and drinking water Pb con centrations, as well as soil Pb concentrations, were not varied across the air quality scenarios in any case study (see Tabl e 3-7). For all case studies, however, indoor dust Pb concentrations were simulated to change with the different air quality scenarios that also provided differing ambient air Pb concentrations (outdoors and indoors).

3.4.3.3 Methods for Deriving Risk Estimates

In this section, we first summarize the fu ll risk model employed in the 2007 REA for estimating risk for a broad range of air qual ity scenarios (section 3.4.3.3.1). Then, in section 3.4.3.3.2, we summarize approaches by which we have identified risk estima tes pertaining to the current standard, the second of which involves an analysis newly completed in this review in which risk estimates are interpolated for th e current standard based on the 2007 REA risk
estimates.3-52 3.4.3.3.1 Full Risk Model in 2007 REA

The risk characterization step employed in the 2007 REA involved generating a distribution of IQ loss estimates for the set of children simulated in the exposure assessment. Specifically, estimated blood Pb levels for the concurrent blood Pb metric 42 were combined with four blood Pb concentration-response (C-R) func tions for IQ loss based on the analysis by Lanphear et al (2005) of a pool ed international dataset of blood Pb and IQ (see 2007 REA, section 5.3.1.1). Four different C-R functi ons were selected to provide different characterizations of behavior at low exposures. Th e decision to use four different functions is in recognition of uncertainty related to modeling this endpoint, particul arly at lower blood Pb levels for which there is limited repres entation in the Lanphear et al (2005) pooled dataset; the 5th percentile for the concurrent blood Pb measurements in that dataset is 2.5 μg/dL, and the mean is 9.7 μg/dL (73 FR 66978). The four different functi ons are either based directly on the lognormal model described in Lanphear et al (2005), or they are derived fr om data presented in that study. 43 The four functions are presented in Figure 3-4 and compared in Tabl e 3-9 with regard to total IQ loss and incremental IQ loss (IQ loss per μg/dL blood Pb) across a range of concurrent blood Pb levels. A brief description of each of the functions is also here:

 Log-linear with cutpoint: log-linear functi on derived from the pooled analysis applied down to 1 μg/dL (concurrent blood Pb metric ) with no IQ loss projected below that exposure level.

 Log-linear with low-exposure linearization: log-linear function applied down to 1 μg/dL (concurrent blood Pb metric) with linearization of the slope at that point which is used to project IQ loss down to the origin.

 Dual linear – stratified at 10 μg/dL: func tion developed by fitting a two-piece linear function stratified at 10 μg/dL (peak blood Pb concentration) to the log-linear function developed from the pooled analysis.

 Dual linear-stratified at 7.5 μg/dL: as above, but based on stratification of the two-piece function at 7.5 μg/dL (peak blood Pb concentration).

42 Risk estimates were also developed for lifetime average PbB levels using concentration-response functions derived from the Lanphear et al (2005) analysis for lifetime average PbB leve ls. Estimates based on the concurrent PbB metric are given primary emphasis, consistent with advice from CASAC (Henderson, 2007b).

43 The two log-linear C-R functions rely on the loglinear model in Lanphear et al (2005). The two dual linear C-R functions rely on the linear models reported in Lanphear et al (2005) for concurrent blood Pb in four groupings of children based on whether peak blood Pb levels were below or at/above 10 or 7.5 μg/dL. In order to utilize the linear models in the REA, we considered the rela tionship between peak and concurrent blood Pb levels in the pooled dataset, as well as in the cohort comprising the bulk of the low blood Pb subsets. In both cases, the difference was approximately a factor of two (2007 REA, section 5.3.1.1). The “dual linear –stratified at 10 μg/dL” function applies the Lanphear et al (200 5) linear coefficient for children with peak blood Pb below 10 μg/dL to REA concurrent blood Pb estimates below 5 ug/dL and the linear coefficient for children with peak blood Pb at or above 10 μg/dL to REA concurrent blood Pb estimates at or above 5 μg/dL (Figure 3-4). The “dual linear –stratified at 7.5 μg/dL” function applies the Lanphear et al (2005) linear co efficient for children with peak blood Pb below 7.5μg/dL to REA concurrent blood Pb estimates below 3.75 μg/dL and the linear coefficient for children with peak blood Pb at or above 7.5 μg/dL to REA concurrent bl ood Pb estimates at or above 3.75 μg/dL.3-53 Figure 3-4. Comparison of four concentration-respons e functions used in risk assessment.

Table 3-9. Comparison of total and incremental IQ loss estimates for blood Pb below 10 μg/dL based on the four concentration-response functions.

Performance Metric Concentration-Response Function Log-linear with cutpoint Log-linear with low-exposure 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

Of the four C-R functions provided above, we have the greatest overall confidence in risk estimates generated using the lo g-linear with low-exposure linear ization (LLL) function because this function (a) is nonlinear, describing greater response per unit blood Pb at lower blood Pb levels consistent with multiple studies, (b) is based on fitting a function to the entire pooled dataset (and hence uses all of th e data in describing response ac ross the range of exposures), (c) is supported by sensitivity analyses showing the model coefficients to be robust (Lanphear et al., 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 linearization3-54 2005), and (d) provides an approach for predicting IQ loss at the lowest exposures simulated in the assessment (which for some simulated children yield blood Pb levels below those studied). Risk estimates generated using the other three C-R functions are also presented to provide perspective on the impact of uncertainty in this key modeling step. For additional detail on the rationale for placing greater emphasis on the LLL function, see section 4.2.1 of the 2007 Pb Staff Paper (USEPA, 2007b). As noted in section 3.2 above, since the comple tion of the ISA in the current review, two errors have been identified with the pooled data set analyzed by Lanphear et al (2005) (Kirrane and Patel, 2014). A recent publication and EPA have separately recalcu lated the statistics and mathematical models of Lanphear et al (2005) using the corrected pooled dataset (Kirrane and Patel, 2014). While th e conclusions drawn from these coe fficients, including the finding of a steeper slope at lower (as compared to highe r) blood Pb concentrations are unaffected, the magnitude of the loglinear and linear regressi on coefficients are somewhat lower based on the corrections. For example, the loglinear model coefficient used for the LLL function, which we focused on in the last review and also focus on here, changed only negligibly from -2.7 to -2.65 when recalculated using the corrected pooled datase t (Kirrane and Patel, 2014). As a result, the
risk estimates for this function described below and presented in Tables 3-10 and 3-11 would be expected to be very similar although slightly lo wer if derived using th e recalculated loglinear
model coefficient for the corrected dataset. 44, 45 Two categories of risk metrics were genera ted for each of the location-specific 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). Greater emphasis has been placed on the median IQ loss estimates due to increased confidence in these estimates relative to the higher percentile estimates, as noted in section 3.4.7.

44 Since the loglinear model coefficient calculated from the corrected dataset is unchanged at two significant figures from that original reported, any change to the risk estimates would be very small and, particularly in light of other uncertainties in the analysis, does not materially affect staff’s consideration of the results.

45 We also note that risk estimates for the other thr ee C-R functions would also be expected to change as a result of corrections to two of the linear model coefficients (Kirrane and Patel, 2014), such that the upper end of the risk estimates range presented parenthetically in Tables 3-10 and 3-11 for all four functions would also be expected to be somewhat lower (the upper end is generally based on estimates from the dual linear-stratified at 7.5 μg/dL, peak, function). As was the case in the last review, the ranges reflecting a ll four functions are not a focus in this review.3-55  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 generalized (local) urban case study, onl y the first type of risk metric, population risk percentiles, was developed because a specif ic location with associated demographic data was not modeled. In summarizing risk estimates from the 2007 REA in this document, we have focused on the first category of risk metric a nd,specifically, on the median IQ loss estimates.

3.4.3.3.2 Air Quality Scenarios Reflecting the Current Standard

As the 2007 REA did not include an air quality scenario simulated to just meet the standard selected by the 2008 decision, 46 we have considered two appr oaches for identifying risk estimates pertaining to conditions just meeting the current Pb standard (set in 2008) for our purposes in this review. We first reviewed all the scenarios analy zed in the 2007 REA and recognize the similarity to the current standard of the then-current condit ions scenario for the Chicago case study. Accordingly, we consider th e risk estimates for that scenario for our purposes in this review of considering risk asso ciated with the current standard (see section 3.4.5 below). Additionally, in recognition of the va riation among specific locations and urban areas with regard to air quality pa tterns and exposed population, we have also newly developed estimates for an air quality scenario just meeti ng the current Pb NAAQS in the context of the generalized (local) urban case study to augment th e risk information available in this current review. The newly developed estimates were de rived based on interpolation from the risk estimates available for scenarios previously asse ssed for the generalized (l ocal) urban case study. Such interpolated estimates we re only developed for the genera lized urban case study due to its use of a single exposure zone which greatly simplified the me thod employed, thus contributing relatively lesser uncertainty from the interpolation step. 47 In newly developing estimates for the current standard in the gene ralized (local) urban case study, the general approach we followed wa s to identify the two alternative standard

46 The 2008 decision on the level for the revised NAAQS was based primarily on consideration of the evidence-based air-related IQ loss fram ework. Although the specific level, av eraging time and form chosen for the new standard were not among the air quality scenarios that had been simulated in that review, the risk estimates available for the range of simulated scenarios were concluded to be roughly consistent with and generally supportive of the evidence-based air-related IQ loss estim ates (73 FR 67006; see section 4.1.1 below).

47 We did not complete interpolation of risk estimates for the current standard for the other case studies (i.e., the primary Pb smelter and location-specific urba n case studies) because those case studies utilized a more complex, spatially-differentiated and population-based appr oach for which precludes application of the simple linear interpolation approach described, without introduction of substantial added uncertainty. The simplicity of the generalized (local) urban study area, however, with its single exposure zone, is amenable to the linear interpolation of risk described here.3-56 scenarios simulated in the 2007 REA which repres ented air quality conditions bracketing those for the current standard and then linearly interpol ate an estimate of risk for the current standard based on the slope created from the two bracketing estimates. In representing air quality conditions for these purposes, we focused on the annual average air Pb concentration estimates used as IEUBK model inputs for the various air quality scenarios. An annual average concentration estimate to represent the current standard was identified in a manner consistent with that employed in the 2007 REA for this cas e study (see section 3.4.3.2 above) with the use of currently available monitoring data for relationships between air quality metrics for representation of the current sta ndard. By this method, the air qua lity scenario for the current standard (0.15 μg/m 3 , as a not-to-be-exceeded 3-month average) was found to be bracketed by
the scenarios for alternat ive standards of 0.20 μg/m 3 (maximum calendar quarter average) and 0.20 μg/m 3 (maximum monthly average). A risk estim ate for the current standard was then derived using the slope relating general ur ban case study IQ loss to annual average Pb concentration used for those two air quality scenar ios. We used this interpolation approach to develop median risk estimates for the current sta ndard based on each of the four C-R functions. Details on the method for the interpolation approach are provided in Appendix 3A. The interpolated median estimates of risk for the cu rrent standard for the ge neralized (local) urban case study are provided be low in Table 3-9.

3.4.4 Challenges in Characterizing Air-related Exposure and Risk

In estimating the portion of total (all-pathway ) blood Pb and IQ loss attributable to airrelated pathways, we faced a variety of challeng es. Although we parsed total estimates into those for diet/drinking water and tw o air-related categories, referred to as “recent air” and “past air”, significant limitations in our modeling tools and data resu lted in an inability to parse specific risk estimates into specific pathways. Although Pb in diet and drinking water sources may include Pb derived from Pb in the ambien t air (as well as Pb fr om nonair sources), limitations precluded explicit mode ling of the contribution from ai r pathways to these exposure pathways, such that the air-related compone nt of these exposures was not estimated. 48 As a result we utilized the estimates from recent and past air categories to create bounds within which we consider air-related risk to fall, as illust rated in Figure 3-5 and described further below.

48 Further, although paint is not an air-related source of Pb exposure, for this analysis, may be reflected somewhat in estimates developed for the “past air” category, due to modeling co nstraints. Fore example, technical limitations of the indoor dust Pb modeling may contribute to paint-related Pb in the “past air” component of indoor dust Pb and limitations in the available data and modeling may contribute to paint-related Pb in estimates of soil Pb.3-57 Figure 3-5. Parsing of air-related risk estimates.

Those Pb exposure pathways tied most directly to ambient air, which consequently have the potential to respond relatively more quickly to changes in air Pb (i.e., inhalation and ingestion of indoor dust Pb derived from the 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. Additionally, while we recognized the potential for these other air-rela ted exposures to be affected (over some time frame) by an adjustment to the Pb NAAQS, lim itations in our date a nd tools precluded our simulation of that relationship with air Pb levels. Among the limitations affecting our estimates for the air-relate d categories is the apportionment of nonair pathways. For exampl e, while conceptually indoor Pb paint
contributions to indoor dust Pb would be cons idered background and included in a “background” category for this assessment, due to technical li mitations related to i ndoor dust Pb modeling, dust from Pb paint was included as part of "other" ind oor dust Pb (i.e., as part of past air exposure). The inclusion of indoor paint Pb as a component of "other" indoor dust Pb (and consequently as a component of the “past air” category) represents a source of potential high bias in our prediction of exposure and risk as sociated with the “pas t air” category because indoor paint Pb is a nonair Pb source. At the same time, Pb in ambient air does contribute to the drinking water 

### “Recent air”

Total Pb risk = recent air pathways + past air pathways + other pathways, including nonair pathways

• 2007 REA simulated just meeting alte rnative NAAQS by changing recent air exposures. • Although no changes were simulated for past air exposures or to diet and drinking water pathways, changes to the NAAQS were expected to also influence those exposure pathways to some extent.

 Air-related risk estimated to fall within range bounded by estimates of recent air and recent air + past air. Ambient air

• newly emitted lead • resuspension of historically emitted and deposited lead • historically emitted Pb (still in home and/or still available for contact in external soil/dust)

• paint • Diet

• Drinking water Indoor dust 

### “Past air” Indoor dust (other)

Outdoor soil

• newly emitted Pb •historically emitted Pb

• nonair contributions3-58 and diet exposure pathways and is likely a s ubstantial contribution to diet. We could not separate the air contribution from the nonair contributions in the dr inking water and diet pathways. As a result, our ri sk estimate for the drinking wate r/diet category of pathways includes some air-related risk representing a source of potential low bias in our predictions of
air-related risk. Further, we note that in simulating 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 fr om the previous review did not simulate decreases in “past air” exposure path ways (e.g., reductions in outdoor soil Pb levels following reduction in ambient air Pb levels and a subsequent decr ease in exposure through incidental soil ingestion and th e contribution of outdoor soil to indoor dust). These exposures
were held constant across all ai r quality scenarios. This m odeling/data limitation, accordingly, precluded estimates for this category from re flecting any impact of changes in air quality conditions and thus any impacts of the alternative standard levels simulated. In summary, because of limitations in th e assessment design, data and modeling tools, our risk estimates for the “past air” category in th e last review include both risks that are truly air-related and potentially, some nonair risk. Because we could not sharply separate Pb linked to
ambient air from Pb from othe r (nonair) sources, some of the three categories of risk are
underestimated and others overestimated. On balan ce, we believe this lim itation leads to a slight
overestimate of the risks in the “past air” category. At the same time, as discussed above, the "recent air" category does not fully represent the ri sk associated with all air-related pathways. Thus, we considered the risk at tributable to air-related exposure pathways to be bounded on the low end by the risk estimated for the “recent ai r” category and on the upper end by the risk estimated for the “recent air” plus “past air” ca tegories. With regard to the latter, we are additionally cognizant of the mode ling and data limitations which reduce the extent to which the upper end of these bounds reflects impacts of alternative air quality conditions simulated.

3.4.5 Risk Estimates

This section summarizes air-related risk estim ates generated for the previous review and also risk estimates that have been newly derived in this review by interpolation from the previous review estimates for the current standard (see section 3.4.3.3.2 above). Included in this summary is consideration of the following question:3-59  What is the nature and magnitude of air-related risks remaining upon just meeting the current Pb standard? The air-related risk quantifie d in the 2007 REA is for IQ loss associated with Pb exposure. As discussed in section 3.2 above, the evidence in the last review, as well as in the current review, supports identification of neurocognitive effects in young children as a particularly sensitive endpoint fo r the exposure circumstances releva nt to this review and which addresses the important at-risk population, young children. With this support in the evidence for quantification, the risk assessment quantified decr ements in IQ, an established indicator of neurocognitive function. With rega rd to the nature of the risks, in addition to recognizing the role of IQ as an indicator of an array of ne urocognitive function impacts, we additionally take note of the evidence regarding implications of neurocognitive impacts in young children with regard to potential future impacts as the ch ildren age, as recognized in section 3.2 above. In presenting risk estimates here, we focus on the median estimates of air-related IQ loss for each case study. Estimates of air-related risk ar e substantially more uncertain for extremes of the risk distribution, such as the 95 th percentile. Those estimates and estimates for other risk metrics, including population incidence for IQ loss at those case studies with population enumeration, are available elsewhere (2007 REA, s ections 4.2 and 5.3.2). In this section, Table 3-10 presents air-related IQ lo ss estimates derived in the 2007 REA for the full set of case studies. Table 3-11 provides a subset of these risk estimates for the generalized (local) urban case study in addition to estimates for air quality cond itions just meeting the current standard, derived by interpolation. A number of details, listed he re, should be kept in mind when reviewing the estimates presented in Tables 3-9 and 3-10.

 The risk estimates represent IQ loss associated with air-r elated Pb exposure for the median child (exposure is modeled through age seven years).

 Our estimation of risk attributable to air- related exposure pathways is approximate, as described in sections 3.4.4 and 3.4.7. We consid er the air-related risk to fall within the ranges presented, bounded on the low end by esti mates for the pathways categorized as “recent air” and on the upper end by the sum of the estimates for both the “recent” and “past air” pathways. 49

 The bolded range of risk estimates is derive d using the C-R function in which we have the highest overall confiden ce (the log-linear with low- exposure linearization – see section 3.4.3.3.1). The wider range of risk estim ates presented within the parentheses in both tables reflects the application of all four C-R functions (see discussion in section 3.4.3.3.1) to exposure estimates for the “recent” and “recent” plus “pas t” air categories.

49 The third category of pathways for which risk wa s estimated in the 2007 REA comprised diet and drinking water pathways. As other (nonair) sources of Pb can be appreciable contributors of Pb to these pathways, this category is referred to as “background” in the 2007 REA.3-60 Consequently, this range of risk estimates reflects both uncertainty in estimation of airrelated exposures as well as uncertainty in the C-R function for IQ loss in children.

Table 3-10. Estimates of air-related risk from 2007 risk assessment.

Air Quality Scenario Just meeting specified maximum quarterly/monthly average ( μ g/m 3 ) Median air-related IQ loss A
Generalized (local) urban case study Primary Pb smelter (subarea) case study B, C Location-specific urban case studies

Cleveland Chicago Los Angeles

Alternative Standards Scenarios
1.5, max quarterly D (previous NAAQS) 3.5 - 4.8 (1.5 - 7.7) < 6 <(3.2 - 9.4) 2.8 - 3.9 E (0.6 - 4.6) 3.4 - 4.7 E (1.4 - 7.4) 2.7 - 4.2 E (1.1 - 6.2)
0.5, max monthly 1.9 - 3.6 < 4.5 0.6 - 2.9 F F (0.7 - 4.8) <(2.1 - 7.7) (0.2 - 3.9) 0.2, max quarterly 1.5 – 3.4 (0.5 – 4.3) <3.8 <(1.5 – 5.6) 0.43 – 2.8 (0.1 – 3.3) F F

0.2, max monthly 1.2 - 3.2 < 3.7 0.6 - 2.8 0.6 - 2.9 0.7 - 2.9 G (0.4 - 4.0) <(1.2 - 5.1) (0.1 - 3.2) (0.3 - 3.6) (0.2 - 3.5)
0.05, max monthly 0.5 - 2.8 < 2.8 0.1 - 2.6 0.2 - 2.6 0.3 - 2.7 (0.2 - 3.3) <(0.9 - 3.4) (<0.1 - 3.1) (0.1 - 3.2) (0.1 - 3.2)
0.02, max monthly 0.3 - 2.6 < 2.9 <0.1 - 2.6 0.1 - 2.6 0.1 - 2.6 (0.1 - 3.1) <(0.9 - 3.3) (<0.1 - 3.0) (<0.1 - 3.1) (<0.1 - 3.1) Then-current (2003-2005) Conditions

0.36, max quarterly 0.7 – 2.9 (0.2 – 3.6) 0.14, max quarterly 0.6 – 2.9 (0.3 – 3.5) 0.09, max quarterly 0.7 – 2.9 (0.2 – 3.5) A - Air-related risk is bracketed by “recent air” (lower bound of presented range) and “recent” plus “past air” (upper bound o f presented range) (see section 3.4.4). Boldface estimates are generated using the C-R function in which we have the highest overall confidence (the log-linear with low-exposure linearization). Values in par entheses reflect the range of estimates associated with all four concentration-response f unctions (see discussion in section 3.4.3.3.1). B – In the case of the primary Pb smelter case study, only recent plus past air estimates are available. C – Median air-related IQ loss estimates for the primary Pb smelte r (full study area) range from <1.7 to <2.9 points, with no consistent pattern across simulated NAAQS levels. This lack of a pattern reflects inclusion of a large fraction of the study population with relatively low ambient air impacts such that there is lower variation (at the population median) across standar d levels (see section 4.2 of the Risk Assessment, Volume 1). D – This corresponds to roughly 0.7 - 1.0 μ g/m 3 maximum monthly mean, across the urban case studies E - A “roll-up” was performed so that the highest monitor in the study area is increased to just meet this level. F – A “roll-up” to this level was not performed. G – A “roll-up” to this level was not performed; these estimate s are based on current conditions in this area (0.17 max monthly ).

The Information in this table is drawn from the 2007 REA, Table 5-9.3-61 Table 3-11. Estimates of air-related risk for the generalized (local) urban case study, including interpolated estimates for current standard.

Air Quality Scenario Just meeting specified metric ( μ g/m 3 ) Median Air-related IQ Loss A for Generalized (local) Urban Case Study Maximum Quarterly Average D Maximum Monthly Average Maximum 3-month Average 1.5 (previous NAAQS) 3.5 - 4.8 (1.5 - 7.7)

0.5 1.9 - 3.6 (0.7 - 4.8) 0.2 1.5 – 3.4 (0.5 – 4.3) 0.15 B (current NAAQS) 1.5 – 3.4 (0.5 – 4.3)
0.2 1.2 - 3.2 (0.4 - 4.0)

0.05 0.5 - 2.8 (0.2 - 3.3)
0.02 0.3 - 2.6 (0.1 - 3.1) A - Air-related risk is bracketed by “recent air” (lower bound of presented range) and “recent” plus “past air” (upper bound of pres ented range) (see section 3.4.4 for additional detail on these categories). Boldface estimates are generated using the C-R function in which we have the highest overall confi dence (the log-linear with low-exposure linearization). Values in parentheses reflect the range of estimates associated with all four concentration-response func tions (see discussion in section 3.4.3.3.1). Values in parentheses reflect the range of estimates associated with all four concentrationresponse functions. B – Risk estimates interpolated - see text.

Key observations regarding thes e air-related risk estimates across the array of air quality scenarios include the following:

All Case Studies

 Relative to the previous Pb NAAQS, substantia l reduction in estimates of air-related risk is demonstrated across the full set of potential alternative standards simulated (Table 3- 10). This is particularly th e case for the lower bound (the recent air estimates) which reflects only the pathways simulated to re spond to changes in air concentrations associated with different air quality scenarios. Generalized (local) Urban Case Study

 As described above, the general urban case st udy provides risk estimates for a single group of children residing in a single area wh ere air concentrations throughout area are near the level of the standard being simulated. In this case study, air-related median IQ3-62 loss, based on the higher confidence C-R func tion (bold), ranged from roughly 2 to 4 IQ points for the 0.5 μg/m 3 , maximum monthly average scen ario, to <1 to roughly 3 IQ points for the 0.02 μg/m 3 , maximum monthly average scenario. These ranges are expanded somewhat with consideration of the full range of C-R functions considered in the analysis. Location-specific Case Studies

 Compared to the other case studies, the air-re lated risk estimates for the location-specific urban case studies are lower because of the br oader range of air-related exposures and the distribution of the population within the study areas. For example, the majority of the populations in each of the location-sp ecific case studies reside in areas with ambient air Pb levels well below each standard assessed, particular ly for standard levels above 0.05 μg/m 3 , as a maximum monthly average. Conse quently, risk estimates for these case studies indicate little re sponse to alternative stan dard levels above 0.05μg/m 3 maximum monthly average (as shown in Table 3-10).

 For the primary Pb smelter subarea, only an upper bound on risk attributable to airrelated exposures is provided due to uncertain ties associated with the dust Pb model used for this case study. 50 For all air quality scenarios, the population median recent plus past air risk estimate is generally similar to or slightly higher than thos e for the general urban case study, likely due to differences in the indoor dust models used for the two case studies (discussed in the 2007 REA, sections 3.1.4).

Key observations regarding air- related risk estimates for the current standard include the following :

 The median air-related IQ loss estimate for then-current conditions in the Chicago study area, which just met a level of 0.14 μg/m 3 as a maximum calendar quarter average, falls somewhere within the lower and upper bounds of 0.6 and 2.9 points IQ loss, respectively (Table 3-10).

 The median air-related IQ loss estimate for th e current standard in the Generalized (local) Urban Case Study, newly derived by inte rpolation from 2007 REA results, falls somewhere within the lower and upper bounds of 1.5 and 3.4 points IQ loss, respectively (Table 3-11). This estimate is derived by in terpolation between the estimates for the 0.2 μg/m 3 maximum quarterly and 0.2 μg/m 3 maximum monthly averag e scenarios that were derived in 2007 REA. The newly interpolated estimate is essentia lly the same as the estimate for 0.2 μg/m 3 maximum quarterly average scenario for this case study.

 Based on results from the last review fo r a location-specific urban study area and on those newly derived in this review based on interpolation from 2007 REA results, median air-related IQ loss for the cu rrent standard is estimated, with rounding, to generally fall above a rough lower bound of 1 point IQ lo ss and below a rough upper bound of 3 points IQ loss.

50 The regression model used for estimating dust Pb concentrations in the primary Pb smelter case study does not lend itself to partitioning the recent air Pb from other contributions. Accordingly, this partitioning was not done for this case study (2007 REA, sections 2.4.3 and 3.1.4.2).3-63 3.4.6 Treatment of Variability

This section discusses the de gree to which the design of th e previous risk assessment reflected consideration for key sources of variab ility associated with the scenarios evaluated (e.g., IQ loss in children associated with ambient Pb in various residential settings). In so doing, we address the following question.

 How are key sources of variability treated in the assessment?

Key sources of variability associated with the risk assessment include:

 Variation in ambient air Pb level s among U.S. urban residential areas: The locationspecific urban study areas were chosen to provide coverage for diverse residential populations in U.S. urban areas with relativ ely elevated ambient air Pb levels (as characterized using monitoring). We believe th at the three cities included in those case studies capture the variability in spatial patte rns of ambient air Pb concentrations within and across such areas reasonably well. In addition, the generalized (local) urban case study provides coverage for a re sidential population exposed in a localized area with air concentrations somewhat near the standard being evaluated, provi ding coverage for a higher-end population risk scenario where a s ubset of urban childre n are exposed without any spatial gradient in ambient air Pb levels.

 Variation in the spatial dist ribution of children within an urban area and assignment of ambient air Pb exposure: Exposure of populations within the three loca tion-specific urban study areas was characterized to the U. S. Census block group level. Each block group was associated ambient air Pb exposure based on proximity to the monitor nearest to block group centroid (2007 RE A, section 5.2.2). While ther e is uncertainty associated with these exposures (populat ion weighted through use of census block groups) - for example, we did not consider time spent by ch ildren away from their residential block group - we believe that this approach provi des reasonable coverage for the potential pattern of interaction between resident children located in these urban study areas and the associated spatial gradients of ambient air Pb levels.

 Variation among children in factors other t han media concentrations that influence Blood Pb levels: The inputs to the blood Pb model we re central tendency estimates foreach exposure zone within each study area (pathway-specific estimates for centraltendency child). The IEUBK model then ge nerated blood Pb levels for that centraltendency child within each exposure zone. Th ese central-tendency blood Pb levels were then combined with a GSD reflecting vari ability in blood Pb levels for young children (at/near age 7 years) to gene rate a distribution of total blood Pb for a group of children within each exposure zone in a given case study under the specific air quality scenario. We have reasonable confidence that this mode ling approach captures variability in total Pb exposure (and consequently total blood Pb levels) for children modeled for a given study area. As noted in secti on 3.4.7 below, however, there is uncertainty associated with parsing individual pathway cont ributions to total blood Pb le vels (and consequently to3-64 total Pb-attributable risk). This is particularly true for high-end population percentile estimates of IQ loss.

 Inter-individual variability in IQ loss related to Pb exposure: The use of C-R functions based on a pooled analysis (Lanphear et al., 2005) which combined study populations from a number of different epidemiological st udies of IQ loss in children likely provides reasonable coverage for variation across child ren regarding IQ loss attributable to Pb exposure. Furthermore, our estimation of risk based on several C-R functions provides further coverage for that variability, as we ll as also addressing uncertainty in the specification of that C-R functional form (see section 3.4.7 below).

3.4.7 Characterizing Uncertainty

Although the risk assessment utilized a numbe r of innovative modeling elements in order to generate representative estima tes of risk for the various stu dy area populations, like all risk models there was uncertainty associated with the model a nd its output.

 What are the important uncertainties associated with any risk/exposure estimates? One overarching area of uncertainty concer ns the precision of our estimation of the neurocognitive risk (as represented by IQ loss) associated with ambient air Pb. For example, because of the evidence for a nonlinear respon se of blood Pb to Pb exposure and also for nonlinearity in the C–R relationship for Pb-associ ated IQ loss, the assessment first estimated
blood Pb levels and associated risk for total Pb exposure (i.e., including Pb from air-related and nonair exposure pathways) and then separated out estimates for pathways of interest. We separated out the estimates of to tal (all-pathway) blood Pb and IQ loss into three categories that included two air-related categories (“past” and “recen t”), in addition to a third category for diet and drinking water. However, significant limitati ons in our modeling tools affected our ability to develop precise estimates for air-related expos ure pathways. As recognized in section 3.4.4 above, we believe these limitations led to a slight overestimation of the risks for the past air category and to an under-representation of air-related pathways for the recent air category. Thus, we characterized the risk attributable to air-related exposure pa thways to be bounded by the estimates developed for the past air category and the sum of estimates for the recent air and past air categories. For air quality scenarios other than those for the previous NAAQS, this upper bound is recognized as having a potential upward bias with re gard to its reflection of the simulated air quality conditions because modeli ng and data limitations precluded simulation of
the influence of lower air Pb concentrations on the outdoor dust and soil exposure pathways, as
noted in section 3.4.4 above. Additional limitations, assumptions and uncertain ties, recognized in various ways in the assessment and presentation of re sults, along with a concise char acterization of their expected impact on results, are listed below. The list be gins with factors rela ted to design of the3-65 assessment or of the case studies, followed by those related to estimation of Pb concentrations in ambient air, indoor dust, outdoor soil/dust, a nd blood, and estimation of Pb-related IQ loss.

 Temporal Aspects: During the 7-year exposure period, media concentrations remain fixed and the simulated child resides at th e same residence (although exposure factors, including behavioral and physiological paramete rs, are adjusted to match the aging of the child). While these aspects of simulation intr oduce uncertainty into the risk estimates, it is not clear whether there is a directional bias. For example, failure to consider population mobility during the simulation period could bias the overall risk distribution upwards unless children move to or from a residentia l location with higher Pb exposure, in which case this would not be the case.

 Generalized (local) Urban Case Study: The design for this case study employs assumptions regarding uniformity that are reasonable in the c ontext of a general description of a small neighborhood populat ion but would contribute significant uncertainty to extrapolation of these estimates to a specific urban lo cation, particularly a relatively large one. Thus, the risk estim ates for this case study, while generally representative of an urban re sidential population exposed to the specified ambient air Pb levels, cannot be readily rela ted to a specific large urban population. As long as these important caveats are considered in interp reting the risk estimates (i.e., these risk estimates likely represent a re latively small portion of the re sident child population in any given city just meeting specific air qualit y conditions), then the potential error of extrapolating these results to a larger child population can be avoided. An additional area of uncertainty is with regard to the represen tation of variability in air quality. Given the relatively greater variability common in area s of high Pb concentrations, the approach used to reflect variability ma y bias the estimates high, althou gh there is uncertainty with regard to the representative ness of the monitoring dataset used to characterize this.

 Location-specific Urban Case Studies: Limitations in the spa tial density of ambient air monitors in the three metropolitan areas si mulated limit our charac terization of spatial gradients of ambient air Pb levels in these case studies. While this factor introduces uncertainty into the risk estimates for this category of case study, it is not clear whether there is a directional bias.

 Air Quality Simulation: The proportional roll-up and roll -down procedures used in some case studies to simulate air quality conditi ons just meeting the previous NAAQS and alternative NAAQS, respectivel y, assume proportional changes in air concentrations across those case study areas to create those air quality scenarios. The EPA recognizes the uncertainty with our simulation of higher ai r Pb concentrations that would just meet the previous (1978) NAAQS in the urban loca tion-specific case studie s, as well as the uncertainty in simulation of conditions associ ated with the implementation of emissions reduction actions to meet a lower standard. Th ere is the potential that the use of the proportional approach for adjusting monitor valu es introduced a degree of high bias into estimates of risk reduction. This could resu lt if we find that urban areas can target specific Pb sources impacting individual m onitors, thereby avoidi ng the need for more generalized reduction strategies resulting in a uniform pa ttern of reduction across all monitors in an urban area. It is important to point out, however, that the generalized urban case study is not affected by this poten tial bias, since, give n the single exposure3-66 zone involved, the single ambient air Pb level is fixed to reflect meeting the standard being considered (i.e., no spatia l gradient is simulated in the small, localized residential area being modeled).

 Outdoor Soil/Dust Pb Concentrations: Limitations in datasets on Pb levels in surface soil/dust Pb in urban areas and in our ability to simulate the impact of reduced air Pb levels related to lowering the NAAQS contribute uncertainty to air-related risk estimates. In this case, it is likely that we have low bi ased our estimates of risk reduction associated with alternative (lower) Pb NAAQS levels , since we have not simulated potential changes in soil Pb related to changes in ambient air Pb.

 Indoor 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. Although our modeling of indoor dust does link changes in ambient air Pb to changes in i ndoor dust Pb (via air exchanges and indoor deposition onto surfaces), the modeling does not include a link betw een ambient air Pb, outdoor soil Pb and subsequent changes in the level of Pb carried (o r “tracked”) into the house. This could introduce low bias into our total estimates of air-related Pb exposure and risk.

 Interindividual Variabil ity in Blood Pb Levels: Uncertainty related to population variability in blood Pb levels (i.e., interindivi dual variability in factors other than media concentration that influence blood Pb) and li mitations in modeling of this introduces significant uncertainty into blood Pb and IQ loss estimates for the 95th percen tile of the population. We are not aware of any systematic bias introduced into the analysis from this source of uncertainty.

 Pathway Apportionment for Higher Percentile Blood Pb and risks: Limitations, primarily in data, prevented us from char acterizing the degree of correlation among highend Pb exposures for the various pathways (e.g., the degree to which an individual experiencing high drinking water Pb exposur e would also experience high Pb paint exposure and high ambient air- related Pb exposure). Our inability to characterize potential correlations between exposure pathwa ys (particularly at the higher percentile exposure levels) limited our ability to (a) e ffectively model high-end Pb risk and (b) apportion that risk between di fferent exposure pathways, in cluding ambient air-related pathways.

 IQ Loss Concentration-response Functions: Specification of the quantitative relationship between blood Pb level and IQ loss is subjec t to greater uncertainty at lower blood Pb levels (e.g., particularly below 2.5 μg/dL concur rent blood Pb). However, we believe that by considering four different models (whi ch each treat the res ponse at low blood Pb levels in a different manner), we have comp leted a reasonable characterization of this source of uncertainty and its impact on risk es timates. Given comparison of risk estimates generated using the four models, it would appe ar that this source of uncertainty has a potentially significant impact on risk.3-67 3.4.8 Updated Interpretation of Risk Estimates

As summarized in prior sections, a range of information gaps and areas of uncertainty
were associated with the information availabl e in the last review. In the REA Planning Document, staff considered the degree to which information newly available since the last Pb NAAQS review might address specific uncertaintie s associated with the 2007 REA, such that an updated risk model might be developed with th e potential to provide new exposure and risk estimates substantially different 51 from estimates generated in 2007 (USEPA, 2011). Staff concluded that the newly availa ble information did not provide the means by which to develop an updated or enhanced risk model that would subs tantially improve the utility of risk estimates in informing the Pb NAAQS review. Specifically it was concluded that none of the primary sources of uncertainty identified to have the greatest impact on risk estimates would be substantially reduced through the use of newly available information (USEPA, 2011). Our ongoing review of the newly av ailable information leads us to conclude at this time, that the key observations regarding air-related Pb risk modeled for the set of standard levels covered in the 2007 REA, as well as the risk esti mates interpolated for th e current standard (as discussed in section 3.4.5) are no t significantly affected by the new information. Our overall characterization of uncertainty and variability associated with those estimates (as described above in sections 3.4.6 and 3.4.7) is not appreciabl y affected by new information. As recognized at the time of the last review, exposure and ri sk modeling conducted for this analysis was complex and subject to significant uncertainties due to limitations in the data, and models, among other aspects. Further, limitations in the assessment design, da ta and modeling tools handicapped us from sharply separating Pb linked to ambient air from Pb that is not air related. In summary, the estimates of risk attributab le to air-related exposures, with which we recognize a variety of sources of uncertainty, are considered to be approximate, falling within upper and lower bounds, roughly estimated as 3 and 1 IQ points, which over- and underestimate risk, respectively. In scenarios for more restri ctive air quality conditions than those associated with the previous Pb standard, substantial reduct ions in air-related risk were demonstrated. Focusing on the results for the ge neralized (local) urban case study, the interpolated estimates for the scenario representing the current standard are very sim ilar to estimates for the two 0.2 μg/m 3 scenarios (maximum monthl y and quarterly averages) simulated in the 2007 REA 52 and are

51 In this context, “substantially different” has been intended to mean that the degree of uncertainty is substantially reduced, or bias is addressed, such that the new risk estimates could convey a different message regarding the magnitude of public health impacts associat ed with the current or potential alternative standards.

52 There is uncertainty associated with judging differe nces between the current st andard and these potential alternative standards due to the difference in air quality data sets used to estimate air concentration variability of the 2007 REA estimates versus the interpolated risk estimate.3-68 appreciably lower than those associated with the previous standard. In characterizing the magnitude of air-related risk as sociated with the current standard, we focus on median estimates, for which we have appreciably greater confiden ce than estimates for outer ends of risk distribution (see section 3.4.7) and on risks derived using the C- R function in which we have greatest confidence (see sections 3.4.3.3.1 and 3.4.7). The risk results for the current standard
estimated in the last review for one of the location-specific urban study area populations and those newly derived in this review using interpolation of the estim ates from the last review for the generalized (local) urban cas e study, which is recognized to re flect a generalized high end of air-related exposure for localized populations, provide approxim ate bounds for air-related risk,
with attendant uncertainti es described above.

3.5 REFERENCES

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Lagerkvist, BJ; Ekesrydh, S; Englyst, V; Nordberg, GF; Soderberg, HA; Wiklund, DE. (1996). Increased blood lead and decreased calcium levels during pregnancy: A prospective study of Swedish women living near a smelter. Am J Public Health 86: 1247-1252.3-71 Lanphear, BP; Roghmann, KJ. (1997). Pathways of lead exposure in urban children. Environ Res 74: 67-73.

Lanphear, BP; Matte, TD; Rogers, J; Clickner, RP; Dietz, B; Bornschein, RL; Succop, P; Mahaffey, KR; Dixon, S; Galke, W; Rabinowitz, M; Farfel, M; Rohde, C; Schwartz, J; Ashley, P; Jacobs, DE. (1998). The contribution of lead-contaminated house dust and residential soil to children's blood lead levels: A pooled analysis of 12 epidemiologic studies. Environ Res 79: 51-68. http://dx.doi.org/10.1006/enrs.1998.3859

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Lanphear, B. P.; Hornung, R.; Khoury, J.; Yolton, K.; Baghurst, P.; Bellinger, D. C.; Canfield, R. L.; Dietrich, K. N.; Bornschein, R.; Greene, T.; Rothenberg, S. J. ; Needleman, H. L.; Schnaas, L.; Wasserman, G.; Graziano, J.; Roberts, R. (2005) Low-level enviro nmental lead exposure and children's intellectual function: an international pooled analysis. Environ. Health Perspect. 113: 894-899.

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### 4 REVIEW OF THE PRIMAR Y STANDARD FOR LEAD

This chapter presents staff conclusions rega rding the primary Pb standard. These staff conclusions are guided by consid eration of key polic y-relevant questions and based on the assessment and integrative synthesis of informa tion presented in the ISA and by staff analyses and evaluations presented in ch apters 2 and 3 herein. The ev aluations and staff conclusions presented in this chapter have also been developed with consideration of CASAC advice and public comment on the external review draft of this document. These evaluations and staff
conclusions will inform the Administrator’s decisi ons on whether to retain or revise the existing primary standard for Pb. Following an introductory section on the ge neral approach for reviewing the primary standard (section 4.1), including a summary of considerations in th e last review, the discussion in this chapter focuses on the central issue of whet her the information available in this review supports or calls into question the adequacy of the current primary standard. Building on the responses to specific policy-rel evant questions on th e scientific evidence and exposure-risk information in chapter 3 above, presentation in sec tion 4.2 is also organized into consideration of key policy-relevant questions framing evidence-b ased and exposure/risk-based considerations. The policy-relevant questions in this document are based on t hose included in the IRP (IRP, section 3.1). In section 4.3, sta ff conclusions are developed. Section 4.4 presents a brief overview of key uncertainties and areas for future research.

4.1 APPROACH Staff’s approach in this revi ew of the current primary sta ndard takes into consideration the approaches used in the last Pb NAAQS review addressing ke y policy-relevant questions in light of currently available scient ific and technical information. The past and current approaches described below are both based, most fundamenta lly, on using EPA’s assessment of the current
scientific evidence and a ssociated quantitative analyses to inform the Administrator’s judgment regarding a primary standard for Pb that protects public health with an adequate margin of safety. In drawing conclusions for consideration with re gard to the primary sta ndard, we note that the final decision on the adequacy of the current st andard is largely a public health policy judgment to be made by the Administrator. The Administ rator’s final decision must draw upon scientific information and analyses about health effect s, population exposure and risks, as well as judgments about how to consider the range and ma gnitude of uncertainties that are inherent in the scientific evidence and analyses. Our appr oach to informing these judgments, discussed more fully below, is based on the recognition that the available health eff ects evidence generally reflects a continuum, consisting of levels at which scientists genera lly agree that health effects4-2 are likely to occur, through lower levels at which the likelihood and magnitude of the response become increasingly uncertain. This approach is consistent with the requirements of the NAAQS provisions of the Act and with how the EP A and the courts have hi storically interpreted the Act. These provisions require the Administra tor to establish primary standards that, in the judgment of the Administrator, are requisite to pr otect public health with an adequate margin of safety. In so doing, the Administ rator seeks to establish standard s that are neither more nor less stringent than necessary for this purpose. The Ac t does not require that pr imary standards be set at a zero-risk level, but rather at a level that avoids unacceptable risks to public health including the health of sensitive groups. 1 The four basic elements of the NAAQS (indicator, averaging time, level, and form) are considered collectivel y in evaluating the health protection afforded by
the current standard. The following subsections include background in formation on the approach used in the previous review of the standard (section 4.1.1) and a discussion of the approach for the current review (section 4.1.2).

4.1.1 Approach Used in the Last Review

The last review of the NAAQS for Pb was completed in 2008 (73 FR 66964). In consideration of the much-expanded health effect s evidence on neurocognitive effects of Pb in children available at that time, the EPA substa ntially revised the prim ary standard from 1.5 μg/m 3 , as a not-to-be exceeded average concentra tion over a calendar quart er, to a level of 0.15 μg/m 3 , as a not-to-be-exceeded rolling 3-month average concentration. The 2008 decision to revise the primary standard was based on the extensive body of scientif ic evidence published over almost three decades, from the time the standard was originally set in 1978 through 2005- 2006. The 2008 decision considered the body of evidence as assessed in the 2006 CD (USEPA, 2006) as well as the 2007 Staff Paper assessment of the policy-relevant information contained in the CD and the quantitative risk/exposure assessment (USEPA, 2007a, 2007b), the advice and recommendations of CASAC (Henderson 2007a , 2007b, 2008a, 2008b), and public comment. While recognizing that Pb has been demonstr ated to exert “a broad array of deleterious effects on multiple organ systems”, the review fo cused on the effects most pertinent to ambient air exposures, which given ambient air Pb reducti ons over the past 30 years are those associated with relatively lower exposures and associated blood Pb levels (73 FR 66975). In so doing, the

1 The at-risk population groups identified in a NAAQS review may include low income or minority groups. Where low income/minority groups are among the at-ris k populations, the rulemaking decision will be based on providing protection for these and other at-risk populations and lifestages (e.g., children, older adults, persons with pre-existing heart and lung disease). To the extent that low income/minority groups are not among the at-risk populations identified in the ISA, a decision based on prov iding protection of the at-risk lifestages and populations would be expected to provide protection for the low income/minority groups.4-3 EPA recognized the general consensus that the developing nervous system in children is among,
if not the most sensitive health endpoint associated with Pb e xposures. Thus, primary attention was given to consideration of nervous syst em effects, including neurocognitive and neurobehavioral effects, in chil dren (73 FR 66976). The body of ev idence included associations of such effects in study populati ons of variously-aged children w ith mean blood Pb levels below 10 μg/dL, extending from 8 down to 2 μg/dL (73 FR 66976). The public health implications of effects of air-related Pb on cognitive function (e.g., IQ) in young children were given particular
focus in the review.

4.1.1.1 Approach Regarding the Need for Revision

The conclusions reached by the Administrator in the last review were based primarily on the scientific evidence, with the risk- and exposure-based in formation providing support for various aspects of the decision. In reaching his conclusion on the adequacy of the then-current standard, which was set in 1978, the Administrator placed prim ary consideration on the large body of scientific evidence av ailable in the review incl uding significant new evidence concerning effects at blood Pb concentrations substantially below those identified when the standard was initially set (73 FR 66987; 43 FR 46246) . Given particular a ttention was the robust
evidence of neurotoxic effects of Pb exposure in children, rec ognizing: (1) that while blood Pb levels in U.S. children had decreased notably si nce the late 1970s, newer epidemiological studies had investigated and reported as sociations of effects on the ne urodevelopment of children with those more recent lower blood Pb levels and (2 ) that the toxicological evidence included extensive experimental laboratory animal eviden ce substantiating well the plausibility of the epidemiological findings observed in human ch ildren and expanding our understanding of likely mechanisms underlying the neurotoxic effects (7 3 FR 66987). Additionally, within the range of blood Pb levels investigated in the available evidence base, a threshold level for neurocognitive effects was not identified (73 FR 66984; 2006 CD, p. 8-67). Further, the evidence indicated a steeper dose-response relationshi p for effects on cognitive func tion at those lower blood Pb levels than at higher blood Pb levels that were more common in the past, “indicating the potential for greater incremental impact associat ed with exposure at these lower levels” (73 FR 66987). As at the time when the standard was in itially set in 1978, the health effects evidence and exposure/risk assessment av ailable in the last review s upported the conclusion that airrelated Pb exposure pathways contribute to bloo d Pb levels in young children by inhalation and ingestion (73 FR 66987). The available information in the last review al so indicated, however,
that the air-to-blood ratio was lik ely larger than the air-to-blood ratio (of 2 μg/dL blood Pb to 1 μg/m 3 air Pb) estimated when the standa rd was initially set (73 FR 66987).4-4 In the Administrator’s decision on the adequ acy of the 1978 standar d, the Administrator considered the evidence using a very specifically defined framework, referred to as an air-related IQ loss evidence-based framework. This framew ork integrates evidence for the relationship between Pb in air and Pb in young children’s bl ood with evidence for the relationship between Pb in young children’s blood and IQ loss (73 FR 77987) , as described in more detail in section 4.1.1.2 below. This evidence-based approach co nsiders air-related effects on neurocognitive function (using the quantitative metric of IQ loss) associated with exposure in those areas with elevated air concentrations equal to potential al ternative levels for the Pb standard. Thus, the conceptual context for the framework is that it provides estimates of ai r-related IQ loss for a subset of the population of U.S. children (i.e., th e subset living in close proximity to air Pb
sources that contribute to elevat ed air Pb concentrations that equal the current level of the standard). This is the subset expected to expe rience air-related Pb exposures at the high end of
the national distribution of such exposures, not at the average. This is the case since when a standard of a particular level is just met at a monitor sited to record the highest source-oriented concentration in an area, the la rge majority of children in th e larger surrounding area would likely experience exposures to concen trations well below that level. The two primary inputs to the evidence-base d air-related IQ loss fr amework are air-toblood ratios and C-R functions for the relations hip between blood Pb and IQ response in young children. Additionally taken into consideration in applying and drawing conclusions from the
framework were the uncertainties inherent in these inputs. App lication of the framework also entailed consideration of an appropriate level of protection from air-related IQ loss to be used in conjunction with the framework. In simplest te rms, the framework provides for estimation of a mean air-related IQ decrement for young children in the high end of the national distribution of air-related exposures by focusing on children exposed to air-rela ted Pb in those areas with
elevated air Pb concentrations equal to specific potential standard levels. The framework estimates of mean air-related IQ loss are derive d through multiplication of the following factors: standard level (μg/m 3 ), air-to-blood ratio in term s of μg/dL blood Pb per μg/m 3 air concentration and slope for the C-R function in terms of points IQ decrement per μg/dL blood Pb. Based on the application of the air-related IQ loss framework to the evidence, the Administrator concluded that, for exposures projected for air Pb concentrati ons at the level of the 1978 standard, the quantitative estimates of IQ loss associated with air-related Pb indicated risk of a magnitude that in his judgment was significant from a public health pe rspective, and that the evidence-based framework supported a conclusion that the 1978 standard did not protect public health with an adequate margin of safety ( 73 FR 77987). The Administ rator further concluded
that the evidence indicated the n eed for a substantially lower standard level to provide increased public health protection, especially for at-risk gr oups (most notably children ), against an array of4-5 effects, most importantly including effects on th e developing nervous syst em (73 FR 77987). In addition to giving primary consideration to the much expanded evidence base since the standard was set, the Administrator also took into consideration the expos ure/risk assessments. In so doing, he observed that, while ta king into consideration thei r inherent uncertainties and limitations, the quantitative estimates of IQ loss a ssociated with air-related Pb in air quality scenarios just meeting the then-current standard also indicated risk of a magnitude that in his judgment was significant from a public health pers pective. Thus, the Administrator concluded the exposure/risk estimates provi ded additional support to the evid ence-based conclusion that the standard needed revision (73 FR 66987).

4.1.1.2 Approach Regarding Elements of Revised Standard

In considering appropriate revisions to the prior standard in the review completed in 2008, each of the four basic elements of the NAAQS (indicator, averaging time, form and level)
was evaluated. The rationale for decisions on those elements is summarized below. With regard to indicator, consideration was given to replacing Pb-TSP with Pb-PM 10

. The EPA recognized, however, that Pb in all pa rticle sizes co ntributes to Pb in blood and associated health effects, addi tionally noting that the difference in particulate Pb captured by
TSP and PM 10 monitors may be on the order of a factor of two in some areas (73 FR 66991). Further, the Administrator recognized uncer tainty with regard to whether a Pb-PM 10 -based
standard would also effec tively control ultra-coarse 2 Pb particles, which may have a greater presence in areas near sources where Pb c oncentrations are highest (73 FR 66991). The
Administrator decided to retain Pb-TSP as the indicator to provide sufficient public health protection from the range of partic le sizes of ambient air Pb, incl uding ultra-coarse particles (73 FR 66991). Additionally, a role was provided for Pb-PM 10 in the monitoring required for a PbTSP standard (73 FR 66991) based on the conclusion that use of Pb-PM 10 measurements at sites not influenced by sources of ultr a-coarse Pb, and where Pb concentrations are well below the standard, would take advantage of the increased precision of these measurements and decreased spatial variation of Pb-PM 10 concentrations, without raising the same conc erns over a lack of protection against health risks from all partic ulate Pb emitted to the ambient air that support retention of Pb-TSP as the indicator ( versus revision to Pb-PM 10 ) (73 FR 66991). Accordingly,
allowance was made for the use of Pb-PM 10 monitoring for Pb NAAQS attainment purposes in certain limited circumstances, at non-source-oriented sites, where the Pb concentrations are

2 The term ultra-coarse is used to refer to particles collected by a TSP sampler but not by a PM 10 sampler. This terminology is consistent with the traditional usag e of ‘‘fine’’ to refer to particles collected by a PM 2.5 sampler, and ‘‘coarse’’ to refer to particles collected by a PM 10 sampler but not by a PM 2.5 sampler, recognizing that there will be some overlap in the particle sizes in the three types of collected material.4-6 expected to be substantially belo w the standard and ultra-coarse pa rticles are not expected to be present (73 FR 66991). With regard to averaging time and form for the revised standard, consideration was given to a monthly averaging time, w ith a form of second maximum, and a 3-month calendar quarter averaging time, with not-to-be exceeded forms. While the Administrator recognized that there were some factors that might im ply support for a period as short as a month for averaging time, he also noted other factors supporting use of a longer time. He additionally took note of the complexity inherent in this consideration for the primary Pb standard, which is greater than in the case of other criteria pollutants due to the multimedia nature of Pb and its multiple pathways of human exposure. In this situation for Pb, the Administrator emphasized the importance of considering all of the relevant factors, both those pertaining to the human physiological response to changes in Pb exposures and those pertaini ng to the response of air-related Pb exposure pathways to changes in airborne Pb, in an integrated ma nner. With regard to the human physiological response to changes in Pb exposures, the evidence discussed in the CD indicated that children’s blood Pb levels respond quickly to increased Pb exposures, such that an abrupt increase in Pb uptake results in increased blood Pb levels. C ontributing to this res ponse is the absorption through the lungs and the gastro intestinal tract and the rapi d distribution, once absorbed, throughout the body. With regard to the relationship between ai rborne Pb and children’s blood Pb, evidence collected during the time of lead ed gasoline usage when airborne Pb was a prominent Pb exposure pathway across the popula tion indicated children’s blood Pb to respond to changes in airborne Pb over a month’s time lag. The phase-out of on-road leaded gasoline, however, has resulted in change d circumstances with regard to children’s exposure pathways, with accompanying temporal implications. Acco rdingly, EPA considered the limited evidence indicating the more numerous f actors influencing ingestion (ver sus inhalation) pathways, which were considered likely to lessen the impact of month-to-month variat ions in airborne Pb
concentrations on levels of air-r elated Pb in children’s blood. Such factors were considered likely to lead to response times (e.g., for the response of blood to air Pb via these pathways) extending longer than a month ( 73 FR 66996). The Administrator also recognized limitations and uncertainties in the evidence including the limited available evidence specific to the consideration of the particular duration of sustained ai rborne Pb levels having the potential to
contribute to the adverse health effects identified as most relevant to this review, as well as variability in the response time of indoor dust Pb loading to ambi ent airborne Pb. Based on these various considerations, the Administrator conclu ded that the information provided support for an averaging time no longer than a 3-month period.4-7 With regard to a three-month averaging tim e, the EPA recognized that a rolling threemonth averaging time can provide (e.g., compared to a block calendar qua rter) control on monthto-month variability in air Pb concentrations and in associat ed exposures (73 FR 66996). The rolling three-month average eliminates the possib ility for two consecutive “high” months falling in two separate calendar quarters to be considered independently (perhaps being mitigated by “low” months falling in each of the same calenda r quarters). Rather, in the rolling 3-month approach, the same month would c ontribute to three different 3- month periods through separate combinations with three different pairs of mont hs, thus providing a more complete consideration of air quality during that month and the 3-month periods in which it fa lls. The Administrator additionally concluded it appropriate to modify the method by which the 3-month average metric is derived, to be the average of three monthly av erage concentrations, as compared to the thencurrent practice by which the average was derive d across the full dataset for a quarter without equally weighting each month within the quarter . Thus, in consideration of the uncertainty associated with the evidence pertinent to av eraging time discussed above, the Administrator noted that the two changes in form for the st andard (to a rolling 3- month average and to providing equal weighting to each month in deri ving the 3-month average) both afford greater weight to each individual month than did the ca lendar quarter form of the 1978 standard, tending to control both the likelihood that any month will exceed the level of the standard and the magnitude of any such exceedance. Based on this integrated consider ation of the range of relevant factors, the averaging time was revised to a rolling three-month period wi th a maximum (not-to- be-exceeded) form, evaluated over a three-year period. As compared to the previous aver aging time and form of calendar quarter (not-to-be exceeded ), this revision was considered to be more scientifically appropriate and more health prot ective (73 FR 77996). The rolling average gives equal weight to all three-month periods, and the new calculati on method gives equal weight to each month within each three-month period (73 FR 77996). Further, the rolling av erage yields 12 threemonth averages each year to be compared to th e NAAQS versus four averages in each year for the block calendar quarters pertaining to the previous standard (73 FR 77996). Lastly, based on the body of scientific eviden ce and information available, as well as CASAC recommendations and public comment, the Administrator decided on a standard level that, in combination with the specified choice of indicator, averaging time, and form, he judged requisite to protect public health, including the health of sensitive groups, with an adequate margin of safety (73 FR 67006). In reaching th e decision on level for the revised standard, the Administrator considered as a useful guide th e evidence-based framework developed in that
review. As described in s ection 4.1.1.1 above, that framework integrates evidence for the relationship between Pb in air and Pb in chil dren’s blood and the rela tionship between Pb in4-8 children’s blood and IQ loss. Application of th e air-related IQ loss evidence-based framework was recognized, however, to provide “no evidence- or risk-based bright line that indicates a single appropriate level” for the standard (73 FR 67006). Rather, the framework was seen as a useful guide for consideration of h ealth risks from exposure to ambien t levels of Pb in the air, in the context of a specified averaging time and form , with regard to the Administrator’s decision on a level for a revised NAAQS that provides public health protection that is sufficient but not more than necessary unde r the Act (73 FR 67004). As noted above, use of the evidence-based air-related IQ loss framework to inform
selection of a standard level i nvolved consideration of the evid ence with regard to two input parameters. The two input parameters are an air-to-blood ratio and a C-R function for population IQ response associated with blood Pb level (73 FR 67004). The evidence at the time of the last review indicated a broad range of air-to-bl ood ratio estimates, each with limitations and
associated uncertainties. Based on the then-availa ble evidence, the Administrator concluded that 1:5 to 1:10 represented a reasonabl e range to consider and identif ied 1:7 as a generally central value on which to focus (73 FR 67004). With regard to C-R functions, in li ght of the evidence of nonlinearity and of steeper slope s at lower blood Pb levels, the Administrator concluded it was appropriate to focus on C-R analys es based on blood Pb levels th at most closely reflected the then-current population of children in the U.S., 3 recognizing EPA’s identi fication of four such analyses and giving weight to the central estimate or median of the resultant C-R functions (73 FR 67003, Table 3; 73 FR 67004). The four study groups from which C-R functions were drawn in 2008, and the associated C-R slopes, are summarized in Table 3-3 above. 4 The median estimate of -1.75 IQ points decrement per μg/dL wa s selected for use with the framework. With the framework, as summarized in section 4.1.1.1 a bove, potential alternativ e standard levels (μg/m 3 ) are multiplied by estimates of air-t o-blood ratio (μg/dL blood Pb per μg/m 3 air Pb) and the median slope for the C-R function (points IQ decrement per μg/dL blood Pb), yielding
estimates of a mean air-related IQ decrement for a specific su bset of young children (i.e., those children exposed to air-related Pb in areas with el evated air Pb concentrations equal to specified alternative levels). As such, the application ofthe framework yields estimates for the mean airrelated IQ decrements of the s ubset of children expected to e xperience air-related Pb exposures

3 The geometric mean blood Pb level for U.S. children aged five years and below, reported for NHANES in 2003-04 (the most recent years for which such an estimate was available at the time of the 2008 decision) was 1.8 μg/dL and the 5 th and 95 th percentiles were 0.7 μg/dL and 5.1 μg/dL, respectively (73 FR 67002).

4 One of these four is from the analysis of the lowest blood Pb subset of the pooled international study by Lanphear et al., (2005). The nonlinear model developed from the full pooled dataset is the basis of the C-R functions used in the 2007 REA (see section 3.4.3.3 above), in which risk was estimated over a large range of blood Pb levels. Given the narrower focus of the evidence-based framework on IQ response at the end of studied blood Pb levels (closer to U.S. mean level), the C-R functions in Table 3-3 are from linear analyses (each from separate publications) for the study group subsets with blood Pb levels closest to mean for children in the U.S. today.4-9 at the high end of the distribution of such exposures. The associated mean IQ loss estimate is the average for this highly exposed subset and is not the average air-related IQ loss projected for the entire U.S. population of children. Uncertainties and limitations were r ecognized in the use of
the framework and in the resu ltant estimates (73 FR 67000). In considering the use of the evidence-based air-related IQ loss framework to inform his judgment as to the appropriate degree of public h ealth protection that should be afforded by the NAAQS to provide requisite protection against risk of neurocognitive effects in sensitive populations, such as IQ loss in children, the Ad ministrator recognized in the 2008 review that there were no commonly accepted guidelines or crit eria within the public health community that would provide a clear basis for such a judgm ent. During the 2008 review, CASAC commented regarding the significance from a public health pe rspective of a 1-2 point IQ loss in the entire population of children and, along with some co mmenters, emphasized that the NAAQS should prevent air-related IQ loss of a significant magnitude , such as on the order of 1-2 IQ points, in all but a small percentile of the population. Similarl y, the Administrator stated that “ideally airrelated (as well as other) exposures to environmental Pb would be reduced to the point that no IQ impact in children would occur” (73 FR 66998). The Administrator further recognized that, in the case of setting a NAAQS, he was required to make a judgment as to what degree of protection is requisite to protec t public health with an adequate margin of safety (73 FR66998). The NAAQS must be sufficient but not more stringe nt than necessary to achieve that result, and the Act does not require a zero-risk standard (73 FR 66998). The Administrator additionally recognized that the evidence-ba sed air-related IQ loss framewor k did not provide estimates pertaining to the U.S. population of children as a whole. Rather, the framework provides estimates (with associated uncertainties and lim itations) for the mean of a subset of that population, the subset of children assumed to be exposed to the level of the standard. As described in the final decision “[t]he framewor k in effect focuses on the sensitive subpopulation that is the group of children living near sources a nd more likely to be exposed at the level of the standard” (73 FR 67000). As further noted in the final decision (73 FR 67000): EPA is unable to quantify the pe rcentile of the U.S. popula tion of children that corresponds to the mean of this sensi tive subpopulation. Nor is EPA confident in its ability to develop quantified estimates of air-related IQ loss for higher percentiles than the mean of this sub population. EPA expects that the mean of this subpopulation represents a high, but not quantifiable, per centile of the U.S. population of children. As a result, EPA expects that a standard based on consideration of this framework would provide the same or greater protection from estimated air-related IQ loss for a high, albeit unquantifiable, percentage of the entire population of U.S. children. In reaching a judgment as to the appropria te degree of protection, the Administrator
considered advice and recommendations from CA SAC and public comments and recognized the4-10 uncertainties in the health effects evidence and re lated information as well as the role of, and context for, a selected air-related IQ loss in the application of the framework, as described above. Based on these considerations, the Administrator id entified an air-related IQ loss of 2 points for use with the framework, as a tool for considering the evidence with regard to the level for the standard (73 FR 67005). In so doing, the Admini strator was not determin ing that such an IQ decrement value was appropriate in other contexts (73 FR 67005). Given the various
uncertainties associated with the framework and th e scientific evidence base, and the focus of the framework on the sensitive subpopula tion of children that are more highly exposed to air-related Pb, a standard level selected in this way, in combination with the selected averaging time and form, was expected to significantly reduce and lim it for a high percentage of U.S. children the risk of experiencing an air-relate d IQ loss of that magnitude ( 73 FR 67005). At the standard level of 0.15 μg/m 3 , with the combination of the generally central estimate of air-to-blood ratio
of 1:7 and the median of the four C-R functions (-1.75 IQ point decrement per μg/dL blood Pb), the framework estimates of air-related IQ loss were below 2 IQ points (73 FR 67005, Table 4). In reaching the decision in 2008 on level for th e revised standard, th e Administrator also considered the results of the qua ntitative risk assessment to provide a useful perspective on risk from air-related Pb. In light of important uncer tainties and limitations for purposes of evaluating potential standard levels, however, the Administ rator placed less weight on the risk estimates
than on the evidence-based assessment. Ne vertheless, in recognition of the general comparability of quantitative risk estimates for th e case studies considered most conceptually similar to the scenario represented by the evid ence-based framework, he judged the quantitative risk estimates to be “roughly consistent with and generally supportive” of the evidence-based framework estimates (73 FR 67006).
Based on consideration of the entire body of evidence and in formation available in the review, as well as the recommendations of CASAC and public comments, the Administrator decided that a level for the pr imary Pb standard of 0.15 μg/m 3 , in combination with the specified choice of indicator, averaging time and form was requisite to protect pub lic health, including the health of sensitive groups, with an adequate margin of safety (73 FR 67006). In reaching
decisions on level as well as the other elements of the revise d standard, the Ad ministrator took note of the complexity associated with consid eration of health effects caused by different
ambient air concentrations of Pb and with uncertainties with rega rd to the relationships between air concentrations, exposures, and health effects For example, selection of a maximum, not to be exceeded, form in conjunction with a rolling 3-month averaging time over a 3-year span was expected to have the effect th at the at-risk population of child ren would be exposed below the standard most of the time (73 FR 67005). Th e Administrator additi onally considered the provision of an adequate margin of safety in making decisions on each of the elements of the4-11 standard, including, for example “selection of TSP as the indicator and the re jection of the use of
PM 10 scaling factors; selection of a maximum, not to be exceeded form, in conjunction with a 3- month averaging time that employs a rolling aver age, with the requirement that each month in the 3-month period be weighted equally (rather th an being averaged by individual data) and that a 3-year span be used for comparison to the st andard; and the use of a range of inputs for the evidence-based framework, that includes a focu s on higher air-to-blood ratios than the lowest ratio considered to be supportable, and steeper rather than shallowe r C-R functions, and the
consideration of these in puts in selection of 0.15 μ g/m 3 as the level of th e standard” (73 FR 67007). He additionally noted that a standard with this level would reduce the risk of a variety of health effects associated with exposure to Pb, including effects indicated in the epidemiological studies at lower blood Pb levels, particularly including neurological effects in children, and the potential for cardiovascular a nd renal effects in adults ( 73 FR 67006). The Administrator additionally considered higher a nd lower levels for the standar d, concluding that a level of 0.15 μg/m 3 provides for a standard that is neither more or less stringent than necessary for this purpose, recognizing that the Clea n Air Act does not require that primary standards be set at a zero-risk level, but rather at a level that reduces risk sufficientl y so as to protect public health with an adequate margin of safety (73 FR 67007). For example, the Administrator additionally considered potential public health protecti on provided by standard levels above 0.15 μg/m 3

, which he concluded were insufficient to protect pub lic health with an adequa te margin of safety.
The Administrator also noted that in light of all of the evidence, including the evidence-based framework, the degree of public health protectio n likely afforded by standard levels below 0.15 μg/m 3 would be greater than what is necessary to protect public safe ty with an adequate margin of safety. The Administrator concluded, based on review of all of the evid ence (including the evidence-based framework), that when taken as a whole the selected standard, including the indicator, averaging time, form, and level, would be “sufficient but not more than necessary to protect public health, including the health of sensitive subpopulations, with an adequate margin of safety” (73 FR 67007).

4.1.2 Approach for the Current Review

To evaluate whether it is appropriate to consider reta ining the current primary Pb standard, or whether considerati on of revision is appropriate, we have adopted an approach in this review that builds upon the general approach used in the last review and reflects the broader body of evidence and information now available. As summarized above, the Administrator’s decisions in the prior review were based on an integration of information on health effects4-12 associated with exposure to Pb, relationships between ambient air Pb and blood Pb; expert judgments on the adversity and public health si gnificance of key health effects; and policy judgments as to when the standard is requisite to protect public h ealth with an adequate margin of safety. These considerations were informed by air quality and relate d analyses, quantitative exposure and risk assessments, and qualitative assessment of impacts that could not be quantified. In conducting this assessment, we draw on the current evid ence and quantitative assessments of exposure pertaining to the public health risk of Pb in ambient air. In considering the scientific and technical information, we consider both the information available at the time of the last review and information newly available since the last review, including the current ISA (USEPA, 2012), as well as the quantitative exposure/ risk assessments from the last review that estimated Pb-related IQ decrements associated w ith different air quality conditions in simulated at-risk populations in multiple case studies (U SEPA, 2007a). Figure 4-1 illustrates the basic construct of our two part appro ach in developing conclusions re garding options appropriate for
the Administrator to consider in this review with regard to the adequacy of the current standard and, as appropriate, potential alte rnate standards. In the boxe s of Figure 4-1, the range of questions considered in chapter 3 above and se ction 4.2 below is represented by a summary of policy-relevant questions that frame our c onsideration of the scientific evidence and exposure/risk information.4-13 Figure 4-1. Overview of approach for review of current primary standard. Evidence-based Considerations

 Does currently available evidence and related uncertainties strengthen or call into question prior conclusions?

 Evidence of health effect s not previously identified or at lower exposures?

 Newly identified at-risk populations?

 Changed understanding of air-to-blood relationships?

 Effects at lower air-related exposures then previously understood or in conditions that would have likely met current standards?  Does newly available information call into question any of the basic elements of standard? Risk-based Considerations

 Nature, magnitude and importance of estimated exposures and risks associated with just meeting the current standard?  Uncertainties in th e exposure and risk estimates?

Consideration of Potential Alternative Standards

Elements of Potential Alternate Standards  Indicator  Averaging Time  Form  Level Consider Retaining Current Standard

YES NO Adequacy of Current Standard

Does information call into question the adequacy of current standard?

Potential Alternative Standards for Consideration4-14 4.2 ADEQUACY OF THE CURRENT STANDARD In considering the adequ acy of the current Pb standa rd, the overarching question we
consider is:

 Does the currently available scientific evidence- and exposure/risk-based information, as reflected in the ISA a nd REA, support or call into question the adequacy of the protection afforded by the current Pb standard? In considering the scientific and technical information, we gi ve our attention to both the
information available at the time of the last revi ew and information newly available since the last review, including most particularly that which has been critically analyzed and characterized in the ISA. In chapter 3 above, at tention was given to addressing specific questions on key aspects of this information. To assist us in interpreti ng the currently available scientific evidence and results of quantitative exposure/ri sk analyses to address the over arching question here, we draw on discussions in chapter 3 above in our cons ideration of broader or more policy-related questions, posed within sections 4.2.1 and 4.2.2 below. For the purposes of this PA, staff has dr awn from EPA’s assessment and integrated synthesis of the scientific evidence presente d in the ISA and on the quantitative exposure and risk information, based on the 2007 REA (USEPA , 2007a), described in section 3.4 above. The evidence-based discussions presented in this chapter draw upon evidence from epidemiological studies and experimental animal studies evaluating health effects related to exposures to Pb, as discussed in the ISA. The exposure/risk-based discussions have drawn from the quantitative health risk analyses for Pb performed in the la st Pb NAAQS review in light of the currently available evidence (2007 REA, REA Planning Docu ment). Together the evidence-based and
risk-based considerations inform our conclusions related to the adequacy of the current primary
standard for Pb.

4.2.1 Evidence-based Considerations

In considering the evidence with regard to th e issue of adequacy of the current standard, we address several questions that build on the information summarized in chapter 3 to more broadly address the extent to which the current evidence base supports the adequacy of the public health protection afforded by the current primary standard. The first question addresses our integrated consideration of the health eff ects evidence, in light of aspects described in chapter 3. The second question focuses on our consid eration of associated areas of uncertainty. The third question then integrates our considerat ion of the prior two questions with a focus on the standard, including each of the four elements.4-15  To what extent has new information al tered the scientific support for the occurrence of health effects as a result of multimedia exposure associated with levels of Pb occurring in the ambient air?
The current evidence continue s to support our conclusions from the previous review regarding key aspects of the health effects evidence for Pb and the health effects of multimedia exposure associated with levels of Pb occurring in ambient air in the U.S. Our conclusions in this regard are based on considerat ion of the assessment of the curr ently available evidence in the ISA, particularly with regard to key aspects summ arized in chapter 3 of this PA, in light of the
assessment of the evidence in the last review as described in the 2006 CD and summarized in the notice of final rulemaking (73 FR 66964). Key aspects of these conclusions are summarized
below. As at the time of the last review, blood Pb continues to be the predominant biomarker employed to assess exposure and health risk of Pb (ISA, chapters 3 and 4), as discussed in section 3.1 above. This widely accepted role of blood Pb in assessing exposure and risk is illustrated by its established use in programs to prevent both occupational Pb poisoning and childhood Pb poisoning, with the latter program , implemented by the CDC, recently issuing updated guidance on blood Pb measurement interp retation (CDC, 2012). As in the past, the
current evidence continues to indicate the clos e linkage of blood Pb levels in young children to their body burden; this linkage is associated with the ongoing bone remodeling during that lifestage (ISA, section 3.3.5). This tight linkage plays a role in the somewhat rapid response of children’s blood Pb to changes in exposure (p articularly to exposure increases), which contributes to its usefulness as an exposur e biomarker (ISA, sections 3.2.2, 3.3.5, and 3.3.5.1). Additionally, the weight of ev idence documenting relationships between children’s blood Pb and health effects, most particularly those on th e nervous and hematological systems (e.g., ISA, sections 4.3 and 4.7), speaks to its usefulness in assessing health risk. As in the last review, the evidence on air-to -blood relationships av ailable today continues to be comprised of studies based on an a rray of circumstances and population groups (of different age ranges), analyzed by a variety of techniques, which together contribute to appreciable variability in the asso ciated quantitative estimates and uncertainty with regard to the relationships existing in the U.S. today. Accordin gly, our interpretation of this evidence base, as discussed in section 3.1 above, al so includes consideration of f actors that may be influencing various study estimates, both with regard to their usefulness for our general purpose of quantitatively characterizing rela tionships between Pb in ambient air and air-related Pb in children’s blood and with regard to their pe rtinence more specifical ly to conditions and populations in the U.S. today. In so doing, we note that the current evidence, while including
two additional studies not available at the time of the last review, is not much changed from that4-16 available in the last review. The range of estimat es that can be derived from the full dataset is broad and not changed by the inclusion of the newl y available estimates. Further, we recognize significant uncertainties regarding the air Pb to air-related blood Pb relationship for the current
conditions where concentrations of Pb in both ambient air and children’s blood are substantially lower than they have been in the past. In cons idering the strengths, lim itations and uncertainties associated with the full dataset, the currently available evidence appears to continue to support a range of estimates for our purposes that is generally consistent with the range given weight in the last review, 1:5 to 1:10 (ISA, section 3.7.4 and Table 3-12; 73 FR 67001-2, 67004). We additionally note that the generally central estimate of 1:7 identified for this range in the last
review is consistent with the study involving blood Pb for pre-school children and air Pb conditions near a large source of Pb to ambient air with concentr ations near (and/or previously above) the level of the current Pb st andard (ISA, section 3.5.1; Hilts, 2003). 5 In so noting, we also recognize the general overlap of such circum stances with those repr esented by the evidencebased, air-related IQ loss framework, 6 for which air-to-blood ratio is a key input. In characterizing the range of air-to- blood ratio estimates, we recognize uncertainty inherent in such estimates as well as the variation in currently available estimates result ing from a variety of factors, including differences in the populations examined, as we ll as in the Pb sources or exposure pathways addressed in thos e study analyses (ISA, section 3.7.4).
The scientific evidence conti nues to recognize a broad array of health effects on multiple organ systems or biological pro cesses related to blood Pb, includi ng Pb in blood prenatally (ISA, section 1.6). The currently available evid ence continues to suppor t identification of neurocognitive effects in young child ren as the most sensitive endpoint associated with blood Pb concentrations (ISA, section 1.6.1), which as an integrated index of exposure reflects the aggregate exposure to all sources of Pb through multiple pathways (inhalation and ingestion).
Evidence continues to indicate that neuroc ognitive effects in young children may not be reversible and may have effect s that persist into adulthood (I SA, section 1.9.6). Thus, as discussed in section 3.2 above, we continue to consider the eviden ce of Pb effects at the low end of the studied blood Pb levels (closest to those co mmon in the U.S. today) to be strongest and of greatest concern for effects on th e nervous system, most particul arly those on cognitive function
in children. As in the last review, evidence on risk fact ors continues to support the identification of young children as an important at-risk population for Pb health effects (ISA, section 5.4). The

5 The older study by Hayes et al (1994) during time of leaded gasoline indicated a generally similar ratio of 1:8, although the blood Pb levels in th at study were much higher than those in the study by Hilts (2003). Among the studies focused on this age group, the latter study includes blood Pb levels closest to those in U.S. today.

6 Concentrations near air sources are higher than those at more distant sites (as described in section 2.2.2); it is near-source locations where there is the potential for concentrations at or near the current standard.4-17 current evidence also continues to indicate important roles as factors that increase risk of leadrelated health effects for the following: nutriti onal factors, such as iron and calcium intake; elevated blood Pb levels; and prox imity to sources of Pb exposure, such as industrial releases or buildings with old, deteriorating, leaded paint. Further, some races or ethnic groups continue to
demonstrate increased blood Pb levels relative to others, which may be related to these and other factors (ISA, sections 5.1, 5.2 and 5.4). With regard to our understanding of the rela tionship between exposur e or blood Pb levels in young children and neurocognitive effects, the evid ence in this review, as in the last, does not establish a threshold blood Pb level for neurocognitive effects in young children (ISA, sections 1.9.4 and 4.3.12). The lowest blood Pb levels at which associations with neurocognitive impacts have been observed in pre-school and school age children continue to range down below 5 μg/dL, with the lowest group levels that have b een associated with such effects ranging down to 2 μg/dL (ISA, sections 1.6.1 and 4.3.15.1). Additionally, as in the last review, there is evidence that the relationship of young child ren’s blood Pb with neurocognitiv e impacts, such as IQ, is nonlinear across a wide range of blood Pb, with gr eater incremental impacts at lower vs. higher blood Pb levels (ISA, sections 1.9.4 and 4.3.12). Accord ingly, as in the last review, we continue to focus our interest on C-R relationships from study groups with blood Pb levels closest to those in children in the U.S. today, which are genera lly lower than epidemiological study groups. The currently available evidence does not identify additional C-R slopes for study groups of young children (e.g., < 7 years) with mean blood Pb leve ls below that of groups identified in the last review, 2.9 – 3.8 μg/dL, as discussed in secti on 3.2 above (ISA, section 4.3.12). Thus, the blood Pb concentration - IQ response f unctions or slopes identified in this review for epidemiological study groups of young children with mean blood Pb leve ls closest to that of children in the U.S. today include the same set recogni zed at the time of the last revi ew (see Table 3-3 above), the median of which is 1.75 points decrement per μg/dL blood Pb (73 FR, 67003).

 To what extent have important uncertaint ies identified in the last review been reduced and/or have new uncertainties emerged? In our consideration of the evidence, as su mmarized in discussing the previous question and in chapter 3 above, we have not identified any new uncertain ties as emerging since the last review. However, we continue to recognize import ant uncertainties identifi ed in the last review that remain today. Importantly, given our focus in this review , as in the last review, on neurocognitive impacts associated with Pb e xposure in early childhood, we recognize remaining uncertainties in our understanding of the C-R rela tionship of neurocognitive impacts, such as IQ decrements, with blood Pb level in young children, particularly across the range of blood Pb levels common in the U.S. today. With rega rd to C-R relationships for IQ, the evidence
available in this review does not include studies that appreciab ly extend the range of blood Pb4-18 levels studied beyond those availa ble in the last review. As in the last review, the early childhood (e.g., 2 to 6 or 7 years of age) blood Pb levels for which associations with IQ response have been reported continue to extend at the low end of the range to study group mean blood Pb levels of 2.9 to 3.8 μg/dL (e.g., 73 FR 67003, Tabl e 3). The lack of studies considering concentration-response relationships for Pb effect s on IQ at lower blood Pb levels contributes to uncertainty regarding the quantitative relati onship between blood Pb and IQ response in populations with mean blood Pb le vels closer to the most recen tly available mean for children aged one to five years of age (e.g., 1.17 μg/d L in 2009-2010 [ISA, p. 3-85]). The studies at the blood Pb levels studied, as summarized in se ction 3.2 above, continue to indicate higher C-R slopes in these groups with lower blood Pb leve ls than in study groups with higher blood Pb levels (ISA, section 4.3.12). Further, we recognize important uncertainti es in our understanding of the relationship
between ambient air Pb concentrations and air- related Pb in children’s blood. The evidence newly available in this review ha s not reduced such key uncertainties. As in the last review, airto-blood ratios based on the available evidence con tinue to vary, with our conclusions based on the current evidence generally consistent with the range of 1:5 to 1:10 given emphasis in the last review (73 FR 67002; ISA, section 3.7.4). There c ontinues to be uncertainty regarding the extent to which this range represents the relationship between ambient air Pb and Pb in children’s blood (derived from the full set of air-related exposure pathways) and with regard to its reflection of exposures associated with ambient air Pb levels common in the U.S. today and to circumstances reflecting just meeting the current Pb standard (ISA, section 3.7.4). We note additionally the significant uncertainty remaining with regard to th e temporal relationships of ambient Pb levels and associated exposure with occurrence of a health effect (73 FR 67005).

 To what extent does newly available info rmation support or call into question any of the basic elements of the current Pb standard? We address this question for each of the elemen ts of the standard in light of the health
effects evidence and other relevant information ava ilable in this review. As an initial matter, however, we recognize the weight of the scientif ic evidence available in this review that continues to support our focus on effects on the nervous system of young children, specifically neurocognitive decrements, as the most sensitive endpoint. Consistent with the evidence available in the last review, the currently available evidence conti nues to indicate that a standard that provides requisite public he alth protection against the occurre nce of such effects in at-risk populations would also provide th e requisite public health protec tion against the full array of health effects of Pb. Accordingly, the discus sion of the elements below is framed by that background.4-19 Indicator The indicator for the current Pb standard is Pb-TSP. Key considerations in retaining this
indicator in the last review are summarized in section 4.1.1.2 above. Exposure to Pb in all sizes of particles passing thro ugh ambient air can contribute to Pb in blood and associated health effects by a wide array of exposure pathways (IS A, section 3.1). These pathways include the ingestion route, as well as inha lation (ISA, section 3.1), and a wide array of particle sizes play a role in these pathways (ISA, section 3.1.1.1). As at the time of the last re view, we continue to recognize the variability of the Pb-TSP FRM in its capture of ai rborne Pb particles (see section 2.2.1.3.1 above). As in the last review, we also note that an alternative appr oach for collection of a conceptually comparable range of particle size s, including ultra-coarse particles, is not yet available, although we take note of activities und erway that may remedy that situation in the future, as referenced in section 2.2.1.3.1 above. Additionally, the limited available information regarding relationships between Pb-TSP and Pb in other size fractions indicates appreciable variation in this relationship, par ticularly near sources of Pb em issions where concentrations and potential exposures are greatest. Thus, the inform ation available in this review does not address previously identified limitations and uncertaintie s for the current indicat or. Nor does the newly available information identify addition al limitations or uncertainties.
The evidence available in this review continue s to indicate the role of a range of air Pb particle sizes in contri buting to Pb exposure (e.g., ISA, sec tion 3.1.1.1) that contri butes to Pb in blood and associated health effects. For example, the evidence indicates larger particle sizes for Pb that occurs in soil and house dust and may be ingested as compared to Pb particles commonly occurring in the atmosphere and the size fraction of the latter th at may be inhaled (ISA, section 3.1.1.1). Taken together the evidence currently av ailable reinforces the appropriateness of an
indicator for the Pb standard that reflects a wide range of airborne Pb particles. Averaging time and form The averaging time and form of the standard were revised in the la st Pb NAAQS review,
based on considerations summarized in section 4.1.1.2 above. The current standard is a not-tobe-exceeded rolling three-month average (CFR 50.16), derived from three monthly averages
calculated in accordance with the current data handling procedures (CFR, Appendix R to Part 50). The form is a maximum, evaluated within a three-year period (CFR 50.16). As at the time of the last review, evidence cont inues to support the importance of periods on the order of three months and the prominent role of deposition- related exposure pathways, with uncertainty associated with characterization of precise tim e periods associating ambient air Pb with airrelated health effects. Relevant factors c ontinue to be those pe rtaining to the human physiological response to changes in Pb exposures and those pertaining to the response of airrelated Pb exposure pathways to changes in airb orne Pb. The newly avai lable evidence in this4-20 review does not appreciably improve our understa nding of the period of time in which air Pb
concentrations would lead to the he alth effects most at issue in th is review. Thus, there continue
to be limitations in the evidence to inform our consideration of these elements of the standard and associated uncertainty. However, there is no newly available information that calls into question this element of the current Pb standard.
Level The level of the current standard is 0.15 μg/m 3 (CFR 50.16). As described in section 4.1.1 above, this level was selected in 2008 with consideration of, among other factors, an evidence-based air-related IQ loss framework, fo r which there are two primary inputs: air-toblood ratios and C-R functions for blood Pb – IQ response in young children. Additionally taken
into consideration were the uncer tainties inherent in these inputs. Application of the framework
also entailed consideration of a magnitude of air-related IQ loss, which as further described in section 4.1.1.2 above, is used in conjunction with this specific framework in light of the framework context, limitations and uncertainties . Additionally, selecti on of a level for the standard in 2008 was made in conj unction with decisions on indica tor, averaging time and form. As an initial matter, we consider the extent to which the evidence-based, air-related IQ
loss framework which informed the Administrator’s decision in the last review is supported by the currently available evidence and information. In so doing, we recognize the support provided by the currently available evidence for the key conc lusions drawn in the last review with regard to health effects of greatest c oncern, at-risk populations, the influe nce of Pb in ambient air on Pb
in children’s blood and the association betw een children’s blood Pb and decrements in neurocognitive function (e.g., IQ). We additi onally note the complexity associated with interpreting the scientific evidence with regard to specific levels of Pb in ambient air, given the focus of the evidence on blood Pb as the key biom arker of children’s aggregate exposure. The need to make such interpretations in the face of the associated complex ity supported use of the
evidence-based framework in the last review. In considering the currently available evidence for the same purposes in this review, we conclude that the evidence-based framework continues to provide a useful tool for consider ation of the evidence w ith regard to the level of the standard. We next turn to consideration of the primary inputs to the framework: air-to-blood ratios and C-R functions for blood Pb – IQ response in young children. With regard to the former, the limited newly available information assessed in the ISA and discussed in section 3.1 above, is generally consistent with the information in this area that was available at the time of the last review. We additionally recogni ze the variability and uncertainty associated with quantitative
air-to-blood ratios based on this in formation, as also existed in the last review. As in the last review, we recognize that factor s contributing to the variabil ity and uncertainty of these estimates are varied and include aspects of the study populations (e.g., age and Pb exposure4-21 pathways) and the study circumstances (e.g., length of study period and vari ations in sources of Pb exposure during the study period). We note that the full range of estimates associated with
the available evidence is wide and consider it appropriate to give emphasis to estimates pertaining to circumstances closest to those in the U.S. today with regard to ambient air Pb and
children’s blood Pb concentrati ons, while recognizing the limita tions associated with the available information with regard to this emphasis. With that in mind, we consider the currently available evidence to continue to support the rang e of estimates concluded in the last review to be most appropriate for the current population of young children in the U.S., in light of the multiple air-related exposure pathways by which children are exposed, in addition to inhalation of ambient air, and of the levels of air and bl ood Pb common today. Identification of this range
also included consideration of the limitations associated with the available information and inherent uncertainties. This range of air-to-blood ratios included 1:10 at th e upper end and 1:5 at the lower end. We further recogni ze that the limited evidence fo r air Pb and children’s blood Pb
concentrations closest to those in U.S. today continues to prov ide support for the Administrator’s emphasis in the 2008 decision on the rela tively central estimate of 1:7. With regard to the second input to the ev idence-based framework, C-R functions for the relationship of young children’s bloo d Pb with neurocognitive impacts (e.g., IQ decrements), we consider several aspects of the evidence. First, as discussed in section 3.2 above, the currently available information continues to provide evidence that this C-R relationship is nonlinear across the range of blood Pb levels from the higher concen trations more prevalent in the past to lower concentrations more common today. Thus, we conti nue to consider it partic ularly appropriate to
focus on the evidence from studies with blood Pb le vels closest to those of today’s population,
which in the last review included studies with study group mean blood Pb levels ranging roughly from 3 to 4 μg/dL in children aged 24 months to 7 years (Table 3-3 above). As discussed in sections 3.2 above, this is also consistent with the evidence currently avai lable for this age group of young children, and the currently available evidence does not include additional C-R slopes for incremental neurocognitive decrement with blood Pb levels at or below this range. In considering whether this set of functions continues to be well supported by the evidence, as assessed in the ISA (ISA, section 4.3.2), we note the somewhat wide range in slopes encompassed by these study groups, while also noting the stability of the median. For example, omission of any of the four slope s considered in the last review does not appreciably change the median (e.g., the median would change from - 1.75 IQ points per μg/dL blood Pb to -1.71 or - 1.79). Thus, we conclude that wh ile differing judgments might be ma de with regard to inclusion of each of the four study groups, these estimates ar e generally supported by the current review of
the evidence in the ISA. Furthe r, the stability of the median to modifications to this limited
dataset lead us to conclude that the currently availabl e evidence continues to support4-22 consideration of -1.75 IQ points per μg/dL blood Pb as a well-founded and stable estimate for purposes of describing the neurocognitive impact quantitatively on this age group of U.S.
children. In summary, in considering the evidence a nd information available in this review pertaining to the level of the current Pb standar d, we note that the evidence available in this review, as summarized in the ISA, continues to support the air-related IQ loss evidence-based framework, with the inputs that were used in th e last review. These include estimates of air-toblood ratios ranging from 1:5 to 1:10, with a gene rally central estimate of 1:7. Additionally, the
C-R functions most relevant to blood Pb levels in U.S. children today continue to be provided by the set of four analyses consider ed in the last review for whic h the median estimate is -1.75 IQ points per μg/dL Pb in young children’s blood. Thus , we observe that the evidence available in this review has changed little if at all with regard to the aspect s given weight in the conclusion on
level for the new standard in the last review and would not appear to call into question any of the basic elements of the standard. In so doing, we additionally recognize that the overall decision on adequacy of the current standard is a public health policy judgment by the Administrator; we
discuss considerations that inform su ch judgments in section 4.3 below.

4.2.2 Exposure/Risk-based Considerations

Our consideration of the issue of adequacy of public health protection provided by the current standard is also informed by the quantita tive exposure/risk asse ssment completed in the last review, augmented as described in section 3.4 above. We have organized the discussion that follows around two questions to assist us in in terpreting the results of the assessment of case studies simulated to meet several different air qu ality conditions, including those just meeting the
current standard.

 What is the level of confidence associat ed with estimates of air-related risk generated for simulations just meeting the current Pb standard? As an initial matter, we recognize the signifi cant limitations and complexity associated with the risk/exposure assessmen t for Pb that are far beyond those associated with similar assessments typically performed for other criteria pollutants. In completing the assessment we were constrained by significant limitations with rega rd to data and tools particular to the problem at hand. Further, the multimedia and persistent nature of Pb and the role of multiple exposure pathways contribute significant additional complexity to the assessment as compared to other assessments that focus only on the inhalation path way. As a result, our estimates of air-related exposure and risk are approximate, presente d as upper and lower bounds within which we consider air-related risk likely to fall. We ba se our description of overall confidence in this
characterization of air-related ri sk on our consideration of the ove rall design of the analysis (as4-23 described in section 3.4 above), the degree to which key sources of variability are reflected in the design of the analysis, and our characteri zation of key sources of uncertainty. In considering the degree to which key sources of variability (discussed in section 3.4.6 above) are reflected in the design of the analys is, we note the following aspects addressed by the
risk assessment.

 Variation in distributions of potential urban residential exposure and risk across U.S. urban residential areas. This is addressed by the inclus ion of three different (locationspecific) urban study areas that reflect a di verse set of urban areas in the U.S.

 Representation of a more highly exposed subset of urban residents potentially exposed at the level of the standard. This is addressed by the incl usion of the generalized (local) urban study area.

 Variation in residential exposure to ambient air Pb within an urban area. This is addressed through the partitio ning of the location-specific study areas into exposure zones to provide some representation of sp atial gradients in ambient air Pb and their interaction with population dist ribution and demographics. This was done in a somewhat more precise manner in the primary Pb smelter case study, which relied on dispersion modeling to describe gradient s, as compared with the ma nual assignment of gradients related to air concentration differe nces among monitors in an area.

 Inter-individual variability in blood Pb levels. This is addressed though the use of empirically-derived GSDs to develop blood Pb distribution for the child population in each exposure zone, with GSDs selected pa rticular to each case study population.

 Inter-individual variability in IQ response to blood Pb. This is addressed through the use of C-R functions for IQ loss based on a pool ed analysis reflecti ng studies of diverse populations. We also considered key sources of uncerta inty (discussed in section 3.4.7 above), in particular those affecting the pr ecision of the air-related risk estimates, as mentioned above. Associated sources of uncertainty include our inability to simulate changes in air-related Pb as a function of changes in ambient air Pb in exposur e pathways other than th ose involving inhalation of ambient air and ingestion of indoor dust. Th is contributes to the pos itive bias of the upper
bound for the air-related risk estimates. We add itionally recognize the si gnificant uncertainty associated with estimating upper pe rcentiles of the distribution of air-related blood Pb concentration estimates (and associated IQ lo ss estimates) due to limitations in available information. Lastly, we recognize the uncertain ty associated with application of the C-R
function at the lower blood Pb levels in the dist ribution; this relates to the limited representation of blood Pb levels of this magnitude in the da taset from which the C-R function is derived. In the quantitative risk information available in this review, we ha ve air-related risk estimates for simulations just meeting the current standard from one of the location-specific urban case studies (Chicago) and fr om the generalized (local) urba n case study. With regard to4-24 the latter, we note its simplified design that does not include multiple exposure zones, thus reducing the dimensions simulated. We have a r easonable degree of confidence in aspects of the generalized (local) urban case study for the specific situation we consider it to represent (i.e., a temporal pattern of air Pb concentrations that ju st meets the level of the standard), and when the
associated estimates are characterized as approximate, within upper and lower bounds (as described in section 3.4.4 above), while also reco gnizing considerable asso ciated uncertainty.

 To what extent are the air-related risk s remaining upon just meeting the current Pb standard important from a public health perspective? In considering public health importance of estim ated air-related risks, we consider here the nature and magnitude of such estimated risk s (and attendant uncertain ties), including such impacts on the affected population, and we addi tionally consider the size of the affected population. Based on the evidence available in the la st review and consistent with that available today, the quantitative risk estimates developed in the 2007 REA and augmented slightly in this review are for decrements in IQ, an estab lished indicator of neur ocognitive function. In considering these estimates, we recognize that although some neurocognitive effects may be transient, some effects may persist into adulthoo d, affecting success later in life (ISA, sections 1.9.5 and 4.3.14). We additionally recognize the poten tial population impacts of small changes in population mean values of metrics such as IQ, presumi ng a uniform manifestation of leadrelated decrement across the range of population IQ (ISA, section 1.9.1), as noted in section 3.3
above. Exposures and risks associated with air-re lated Pb under several different air quality
conditions were estimated in the 2007 REA. As summarized in section 3.4 above, limitations in our modeling tools and data affected our ability to develop precise estimates for air-related exposure pathways and contributed uncertainties. The results are approximate estimates which we describe through the use of rough upper a nd lower bounds within which we estimate airrelated risk to fall. We have recognized a number of uncertainties in the underlying risk estimates from the 2007 REA and in the interpolation approach employed in the new analyses for this review. We have characterized the magn itude of air-related risk associated with the
current standard with a focus on median estim ates, for which we have appreciably greater
confidence than estimates for outer ends of ri sk distribution (see section 3.4.7) and on risks derived using the C-R function in which we ha ve greatest confidence (s ee sections 3.4.3.3.1 and 3.4.7). These risk estimates include estimates fr om the last review for one of the locationspecific urban study area populations as well as estimates newly de rived in this review based on interpolation from 2007 REA results for the ge neralized (local) urban case study, which is recognized to reflect a generalized high end of air-related exposure for localized populations. Taken together, these results for just meeting the current standa rd include a high-end localized4-25 risk estimate for air-related Pb of a magnitude generally bounded by roug hly 1 and 3 points IQ loss, with attendant uncertainties, and with appr eciably lower risks with increasing distance from the highest exposure locations In considering the importance of such risk from a public health perspective, we also consider the size of at-risk populations represen ted by the REA case studies. As discussed in section 3.4 above, the generalized (l ocal) urban case study is consid ered to represent a localized urban population exposed near th e level of the standard, such as a very small, compact neighborhood near a source contributing to air Pb c oncentrations just meeting the standard. This case study provides representation in the risk assessment for such small populations at the upper end of the gradient in ambient ai r concentrations expected to o ccur near sources; thus estimates for this case study reflect exposures nearest the standard being evaluated. While we do not have precise estimates of the number of young children living in such area s of the U.S. today, we have information that informs our understanding of thei r magnitude. For example, as discussed in section 3.3 above (Table 3-4), we estimate th ere to be approximately 2,400 children, aged 5 years and younger, residing within 0.5 km of a monitor with ai r Pb concentrations above the
current standard. We further observe several additional monitors with maximum 3-month Pb
concentrations that fall below but within 10% of the current standard level (as noted in section 3.3 above); an estimated 265 young children reside near these monitors. Thus, together we estimate some 2700 children, aged 5 years and younge r, living in localized areas with elevated
air Pb concentrations that ar e above or near the current st andard. Based on the 2010 census estimates of approximately 24.3 million children in the U.S. aged five years or younger, this represents approximately one hundredth of one percent of this age group in the U.S. 7 This indicates the size of the popul ation of young children of this age living in areas in close proximity to areas where air Pb concentrations may be above or near the current standard approximately a hundredth of one percent of the full population of correspondingly aged
children. 8

7 While these estimates pertain to the age group of children aged 5 years and younger, we additionally note that a focus on an alternative age range, such as inclusive of slightly older children (e.g., through age 7), while increasing the number for children living in such locations, would not be expected to appreciably change the percentage of the full U.S. age group that the subset repres ents. Further, to the extent some of the source-oriented monitors required by the 2010 monitoring regulation summarized in section 2.2.1.1 above were not yet represented in the analysis of monitoring data summarized in Table 3-4 above and might report su ch elevated concentrations, consideration of the analysis summarized in Table 3-5 indicates the potential for only small changes in the percentage of the full age group represented by the subs et (e.g., potential for less than an additional 0.01%).

8 This estimate includes children in areas where r ecent information indicates the standard is exceeded because areas not in attainment with the standard are required to attain the st andard as expeditiously as practicable, but no later than five years after designation. Accordingly, these areas are for present pu rposes treated as areas withair Pb concentrations just meeting the current standard and are included for purposes of identifying the size of the atrisk population residing in areas likely to have air Pb concentrations near the current standard.4-26 In summary, we recognize substantial uncerta inty inherent in the REA estimates of airrelated risk associated with local ized conditions just meeting the current standard, which we have characterized as approximate and falling near or somewhat above the rough lower bound of 1 and below the rough upper bound of 3 IQ points. 9 This approximate estimate of risk for children living in such areas is generally overlapping with and consistent with the evidence-based airrelated IQ loss estimates summari zed in section 4.2.1 above. With regard to the importance of the estimated risks from a public health perspec tive, we note, based on the currently available monitoring and census data, the estimated size of the population at risk in such areas to be approximately 2700 young children, representing s lightly more than one one hundredth of a percent of the full population of similarly aged children. In considering the exposure/risk estimates during the last review , the Administrator t ook note of the important uncertainties and
limitations associated with thes e assessments and, while placing less weight on the assessment estimates, he recognized the qua ntitative risk estimates to be “roughly consistent with and generally supportive” of t hose estimated by the evid ence-based framework. In our consideration
of the risk estimates considered in the last review, as well as the estimates for the current standard that have been newly developed in th is review for the genera lized (local) urban case study (see section 3.4.3.3.2), we agree with the prev ious characterization. As would be expected by the use of interpolation, the newly derived es timates are consistent with the estimates for similar air quality scenarios that we re available in the last review.

4.2.3 CASAC Advice

In our consideration of the adequacy of the current standard, in a ddition to the evidenceand risk/exposure-based informa tion discussed above, we have al so considered the advice and recommendations of CASAC, based on their revi ew of the ISA, the REA Planning Document, and the earlier draft of this document, as well as comments from the public on the earlier draft of
this document. A limited number of public comments have b een received on this review to date, including comments focused on the draft IRP, the draft REA Planni ng Document or the draft PA. Of the three commenters that addressed adequacy of the current primary Pb standard, two are in agreement with staff conclusions in the draft PA. A third expressed the vi ew that the standard

9 We note that the value of the upper bound is influenced by risk associated with exposure pathways that were not varied with alternative standard levels, a modeling limitation with the potential to contribute to overestimation of the upper bound with air quality scenarios involving air Pb levels below current conditions for the study area (see sections 3.4.4 and 3.4.7 above).4-27 should be revised to be more restrictive given the evidence of Pb effects in populations with mean blood Pb levels below 10 μg/dL. 10 In their comments on the draft PA, the CASA C Pb Panel concurred with staff’s overall preliminary conclusions that it is appropriate to consider retaining the cu rrent primary standard without revision, stating that “the current scientific lite rature does not support a revision to the Primary Lead (Pb) National Ambient Air Qu ality Standard (NAAQS) ” (Frey, 2013). They further noted that “[a]lthough the current review in corporates a substantia l body of new scientific literature, the new literature doe s not justify a revision to the standards because it does not significantly reduce substant ial data gaps and uncertainties (e .g., air-blood Pb relationship at low levels; sources contributing to current population blood Pb levels, especially in children; the relationship between Pb and childhood neurocog nitive function at current population exposure levels; the relationship between ambient ai r Pb and outdoor dust and surface soil Pb concentrations)”. In recognition of these lim itations in the available information, the CASAC provided recommendations on research to address these data gaps and uncertainties so as to inform future Pb NAAQS reviews (Frey, 2013). The CASAC comments indicated agreements with key aspects of staff’s consideration of the exposure/risk information a nd currently available evidence in this review (Frey, 2013, Consensus Response to Charge Questions, p. 7). The use of exposure/risk information from the previous Pb NAAQS review appears appropriate given the absence of si gnificant new information that could fundamentally change the inte rpretation of the exposure/ risk information. This interpretation is reasonable given th at information supporting the current standard is largely unchanged since the current standard was issued. The CASAC agrees that the adverse impact of low levels of Pb exposure on neurocognitive function and development in children remains the most sensitive health endpoint, and that a primary Pb NAAQS designed to protect against that effect will offer satisfactory protecti on against the many other health impacts associated with Pb exposure. The CASAC concurs with the draft PA t hat the scientific fi ndings pertaining to air-to-blood Pb ratios and the C-R re lationships between blood Pb and childhood IQ decrements that formed the basis of the current Pb NAAQS remain valid and are consistent with current data. The CASAC concurred with the appropriateness of the application of the evidence-based framework from the last Pb NAAQS review. With regard to the key inputs to that framework, CASAC concluded that “[t]he new literature pub lished since the previ ous review provides

10 All written comments submitted to the Agency will be av ailable in the docket for this rulemaking, as will be transcripts of the public meetings held in conjunction wi th CASAC’s review of the earlier draft of this document, of the REA Planning Document and of drafts of the ISA.4-28 further support for the health effect conclusions presented in that review ” and that the studies newly available in this review “do not fundamentally alter th e uncertainties for air-to-blood ratios or C-R functions for IQ decrements in young children (Frey, 2013, Consensus Response to Charge Questions, p. 6).
The comments from CASAC took note of the un certainties that remain in this review,
which contribute to the uncertainties associated with drawing conclusions regarding air-related exposures and associated health risk at or be low the level of the current standard (Frey, 2013, Consensus Response to Charge Questions, p. 6). This draft PA is constrained by the absence of new observational and experimental data that addre ss, at least in part, limitations and uncertainties in the evidence that was present at the ti me of the last update of the Pb NAAQS. Until evidence is available to assess Pb exposure and health risks related to air Pb levels reflecting the current standar d, a substantive refinement and update of the PA will not be possible. The obvious uncertainty underlying evaluation of this PA is whether lowering the standard w ould (or would not) impact exposure and thus risk. The CASAC agrees with the EPA conclusion that “there is appreciable uncertainty associated w ith drawing conclusions re garding whether there would be reductions in blood Pb levels from alte rnative lower levels as compared to the level of the current standard.”

4.3 STAFF CONCLUSIONS ON THE PRIMARY STANDARD This section describes staff conclusions rega rding adequacy of the current primary Pb
standard. These conclusions are based on consid erations described abov e and in the discussion below regarding the currently available scientific evidence summarized in the ISA and prior CDs and the risk and exposure information drawn from the 2007 REA. Further, these staff
conclusions have taken into account advice from CASAC and pub lic comment on the draft PA and preliminary staff conclusions. Taking into consideration the discussions res ponding to specific ques tions above in this and the prior chapter, this section addre sses the following overar ching policy question.

 Does the currently available scientific evidence- and exposure/risk-based information, as reflected in the ISA a nd REA, support or call into question the adequacy of the protection afforded by the current Pb standard? Our response to this question takes into c onsideration the discussions responding to the specific policy-relevant questions in prior sections of this document (see sections 3.1-3.4, 4.2.1, and 4.2.2). In so doing, we focus first on consid eration of the evidence, including that newly available in this review, and th e extent to which it alters ke y conclusions suppor ting the current
standard. We then turn to consideration of th e quantitative risk estimates drawn from the 2007
REA and associated limitations and uncertainties. We additiona lly consider the public health policy judgments and judgments about the uncertain ties inherent in the scientific evidence and4-29 quantitative analyses that are i nherent in decisions on the adequacy of the current primary Pb
standard. We first recognize the complexity involved in considering the adequ acy of protection in the case of the primary Pb standard, which di ffers substantially from that involved in consideration of the NAAQS for ot her pollutants. Unlike the case for Pb, the other pollutants for which NAAQS are set involve only inhalation e xposure pathways, a relatively simpler context. 11 In addition, generally an important component of the scientific evidence base considered in reviewing the adequacy of NAAQS for other pollutants is the availability of studies that have investigated associations betw een current concentrations of the pollutant in ambient air (including in circumstances where the current st andard is met) and th e occurrence of health effects judged plausibly relate d to ambient air exposure to th e NAAQS pollutant. While such studies, targeting locations near air Pb sources such as smelters, were available at the time the Pb NAAQS was initially set in 1978, and to a much more limited degree at the time of the last review, such studies of health effects under air quality conditi ons near those reflecting the
current standard are not available in this review . Rather, the evidence ba se that supports our
conclusions in this review includes most prominently epid emiological studies reporting associations of blood Pb levels in U.S. populatio ns, including the partic ularly at-risk population of young children with health eff ects judged plausibly related to Pb exposures. Support for our conclusions regarding the plausibili ty for ambient air Pb to play a role in such findings derives, in part, from studies linking Pb in ambient air w ith the occurrence of health effects. However, such studies (dating from the past or from other countries) involv e ambient air Pb concentrations many times greater than those that would meet th e current standard. T hus, in considering the adequacy of the current Pb standard, rather th an considering studies th at have investigated current concentrations of Pb in ambient air (inc luding in locations where the current standard is met) and the occurrence of health effects, we primarily consider the evidence for, and risk estimated from, models based upon key relationships, such as those between ambient air Pb, Pb exposure, blood Pb and health effects. This evidence, with its asso ciated limitations and uncertainties, contributes to our conclusions re garding a relationship between ambient air Pb
conditions under the current st andard and health effects. In considering the currently available eviden ce, staff gives great weight to the longstanding body of evidence on the hea lth effects of Pb, augmented in some aspects since the last review, which continues to support identificatio n of neurocognitive effects in young children as

11 As described in sections 1.3 and 3.1 above, exposure to Pb from ambient air, unlike exposures for other NAAQS pollutants, involves both ingestion and inhalation ex posure pathways. As an additional complication, other (nonair) sources of Pb also contribute to these pathways, pa rticularly to ingestion exposure pathways. In the case of Pb, the internal biomarker, blood Pb, is an indicator of exposure across different pathways and routes (as discussed in section 3.1 above).4-30 the most sensitive endpoint associated with Pb exposure, as discussed in sections 3.2 and 3.3
above. The evidence continues to indicate that a standard that provides protection from neurocognitive effects in young child ren additionally provides protec tion for other health effects of Pb, such as cardiovascular eff ects later in life. Application of the evidence-ba sed, air-related IQ loss framework, developed in the last review, continues to provide a useful approach for considering and integrating the evidence on relati onships between Pb in ambient air and Pb in children’s blood and risks of neurocognitive effects (IQ loss). The currently available evidence base, while somewhat expanded since the last re view, is not appreciabl y expanded or supportive of appreciably different conclusions with regard to air-to-blood ratios (section 3.1 above) or C-R functions for neurocognitive decrements (section 3.2 above) in young children. As in the last review, uncertainties remain in our understanding of important aspects of ambient air Pb exposure and associated health e ffects. For example, important uncertainties remain, both with regard to air-to-blood ratios that refl ect the relationship between
concentrations of Pb in ambien t air and air-related Pb in children’s blood, and with regard to estimates of the slope of the C-R function for neurocognitive impacts (IQ lo ss) at lower blood Pb levels. With regard to the former, we note pa rticularly the limitations associated with the available studies and gaps in the evidence base with regard to studies that have investigated such quantitative relationships under c onditions pertaining to the current standard (e.g., in localized
areas near air Pb sources where the standard is me t in the U.S. today). Further, in considering our reliance on the evidence in performing qua ntitative modeling of exposure and risk we additionally note important uncerta inties associated with relati onships between ambient air Pb and outdoor soil/dust Pb and indoor dust Pb that pa rticularly affect our quantitative estimates of
air-related risk under conditions of lower ambient air Pb concen trations and lower blood Pb levels (73 FR 66981). These critical exposure path ways are also inherent in the evidence-based air-related IQ loss framework, encompassed within the estimates of air-to-blood ratios. Thus, we recognize uncertainties related to our understanding of these and other processes that also contribute uncertainty to our appl ication of the evidence-based framework. We consider this uncertainty to be greater with a pplication of the framework for levels below the current standard given the weaker linkage with exis ting evidence, as noted below. We additionally take note of th e role of public health policy judgments in considering the evidence-based framework and the exposure/risk information to inform the Administrator’s
decision in 2008 to set the cu rrent standard, as summarized in section 4.1.1.2 above. We recognize that public health policy judgments al ways play an important role in each NAAQS review for each pollutant. One type of public he alth policy judgment focu ses on how to consider the nature and magnitude of the ar ray of uncertainties that are inherent in the scientific evidence and analyses. These judgments are traditionally made with a recognition that our understanding4-31 of the relationships between the presence of a pollutant in ambient air and associated health effects is based on a broad body of information encompassing not only more established aspects of the evidence but also aspects in which there ma y be substantial uncertain ty. In the case of the Pb NAAQS review, we recognize increased uncertainty in char acterizing the relationship of effects on IQ with blood Pb levels below thos e represented in the evidence base. We also recognize increased uncerta inty in projecting the magnitude of blood Pb response to ambient air
Pb concentrations at and below the level of th e current standard. We recognize this increased uncertainty particularly in light of the multiple f actors that play a role in such a projection (e.g., meteorology, atmospheric dispersion and deposit ion, human physiology and behavior), for each of which we recognize attendant uncertainties. Collectively, these aspects of the evidence and associated uncertainties contribute to a recogn ition that for Pb, as for other pollutants, the available health effects evidence generally reflec ts a continuum, consisting of levels at which scientists generally agree that h ealth effects are likely to occur, through lower levels at which the likelihood and magnitude of the response become increasingly uncertain. Reviews may also require judgments as to the point at which health effects become important from a public health perspective. In the case of Pb, such a judgment includes consideration of the public health significance of one to two poin ts IQ loss in at -risk populations, such as young children, in light of associated uncertainties. This type of judgment also includes consideration of the IQ loss estimates yielde d by the air-related IQ loss evidence-based framework for specific combinations of standard level, air-to-blood ra tio and C-R function. With regard to public health significance of one to two points IQ loss in young children, staff gives weight to the comments of CASAC and some public commenters in the last review which recognized such a magnitude of IQ loss to be of public health si gnificance and recommended that a very high percentage of the population be protected from such a magnitude of IQ loss (73 FR 67000). 12 With this objective in mind, we consider the extent to which th e air-related IQ loss
evidence-based framework informs consideratio n of standards that might be concluded to provide such a level of protection. In so doi ng, we first recognize that the IQ loss estimates produced with the evidence-based framework do not correspond to a specif ic quantitative public health policy goal for air-related IQ loss that woul d be acceptable or unacceptable for the entire population of children in the U.S. Rather, the conceptual c ontext for the evidence-based framework is that it provides estimates for the mean air-related IQ loss of a subset of the population of U.S. children (i.e., the subset livi ng in close proximity to air Pb sources that

12 Our focus on IQ, as noted in section 3.3 above, refl ects recognition of IQ being a well established, widely recognized and rigorously standardized measure of neuroc ognitive function, as well as a global measure reflecting the integration of numerous processes (ISA, section 4.3.2; 2006 CD, sections 6.2.2 and 8.4.2). Use of IQ in this framework is thus considered to appropriately also reflect neurocognitive effects more generally.4-32 contributed to elevated air Pb con centrations that equal the current le vel of the standard). This is the subset expected to experi ence air-related Pb exposures at the high end of the national distribution of such exposures. The associated mean IQ loss estimate is the average for this highly exposed subset and is not the average air-related IQ loss projected for the entire U.S. population of children. Further, we recognize uncer tainties associated with those estimates,
which increase with estimates associated with successively lower standard levels. For the current standard level of 0.15 μg/m 3 , an air-to-blood ratio estimate of 7 μg/dL per μg/m 3 (which we note as reasonably representative of the range supported by the evidence) and a C-R slope of -1.75 IQ points per μg/dL, the IQ loss estimate using the evidence-based framework is 1.8 points. 13 As noted above, this value is c onsidered to be an estimate, with attendant uncertainties, of mean ai r-related IQ loss of a subset of the population of U.S. children in the high end of the exposure distribution for air-related Pb. 14 As noted in section 4.2.2 above, our current information on numbers of young childre n living near monitors above or within 10%
of the current Pb standard indicates the size of this population subset to be on the order of 2700 children aged 5 years or younger, which would correspond to approximately one hundredth of one percent of the U.S. populati on of children of this age (estimated at approximately 24 million in 2010 census). A primary objective of the monito ring network for Pb is to identify and monitor
sites of maximum concentration in areas antic ipated to be at risk of exceeding the NAAQS. While we acknowledge the possibility that the monitoring data thus far available may not identify every occurrence of elevated Pb concen trations, the size of such a population subset can
still be concluded to fall well below one tenth of one percent of the full population of children aged 5 years or younger in the U.S. today. Thus , we conclude that the current evidence, as considered within the conceptual and quantitative context of the evidence-based framework, and current air monitoring information indicates that the current standard would be expected to achieve the public health policy goal recommen ded by CASAC in the last Pb NAAQS review that IQ loss on the order of one to two IQ points be “prevented in all but a small percentile of the population” (73 FR 67000). In drawing conclusions from application of th e evidence-based framework with regard to adequacy of the current standard, we further recognize the degree to which IQ loss estimates

13 Using an air-to-blood ratio estimate of 8 μg/dL per μg/m 3 yields a similar, but just slightly higher IQ loss estimate (of approximately 2 IQ points).

14 In giving weight to consideration of the evidence within the context of the air-related IQ loss evidencebased framework, we note that the air-related IQ loss estim ated by the framework is for the mean of the population subset described above. Given the lack of data on the distribution of the air-related portion of blood Pb and on the extent to which distributions of air-related blood Pb levels might differ or correlate with total blood Pb that may be more greatly influenced by other (nonair) Pb exposure pa thways, estimates are not ava ilable that would correspond to upper percentiles of the IQ loss distribution for this population subset. Any such estimates would have substantial associated uncertainty.4-33 drawn from the air-rela ted IQ loss evidence-based framework reflect mean blood Pb levels below those represented in the currently available evidence for young children. For example, in the case of the current standard level of 0.15 μg/m 3 , multiplication by the air-to-blood ratio of 7 yields a mean air-related blood Pb level of 1.05 μg/d L, which is half the le vel of the lowest blood Pb subgroup of pre-school children in which ne urocognitive effects have been observed (Table 3-2 above; Miranda et al., 2009) and well below the means of subgroups for which continuous CR functions have been estimated (Table 3-3 above). 15 Such an extension below the lowest studied levels may be viewed as appropriate give n the lack of identified blood Pb level threshold in the current evidence base for neurocognitive effects and the need for the NAAQS to provide a margin of safety. 16 We note, however, that the framew ork IQ loss estimates for still lower potential standard levels represen t still greater extrapolations from the current evidence base with corresponding increased uncertainty. In recognition of the role of public health policy judgments in drawing conclusions as to adequacy of the Pb NAAQS, we consider the av ailability of new information or new commonly accepted guidelines or criteria with in the public health community with regard to the public health significance of specific IQ decrements in exposed, at-risk populations that might inform public health policy judgments on the appropriate degree of public health protection that should be afforded to protect against risk of su ch neurocognitive effects in at-risk populations, 17 such as children living near air Pb sources. As an init ial matter, we note that no such new information, guidelines or criteria ar e described in the ISA. In further considering the occurrence of any new actions by public health agencies that might indicate the availability of new information,

15 We recognize that children also have Pb in their blood derived from other (nonair) sources. The evidence-based air-related IQ loss fram ework is used, however, to estimate IQ loss attributable to air-related Pb because the NAAQS is intended to protect against risks from ambient air-rela ted Pb. While children also have Pb in their blood derived from other (nonair) sources, the evidence indicates that the neurocognitive risk per increment of blood Pb is greater for children with the lowest blood Pb le vels, as noted in section 3.2 above. Since the evidence indicates Pb exposure to pose the greatest risk on an in cremental basis at lower blood Pb levels, the focus on estimating IQ loss attributable solely to air-related lead (i.e., assuming the presence of no other blood Pb) is a conservative approach, the use of which contributes to the margin of safety provided by the standard.

16 As noted in section 1.2.1 above, the requirement th at primary standards include an adequate margin of safety was intended to address uncertainties associated w ith inconclusive scientific and technical information available at the time of standard setting. It was also intended to provide a reasonable degree of protection against hazards that research has not yet identif ied. Both kinds of uncertainties are co mponents of the risk associated with pollution at levels below those at which human health effe cts can be said to occur with reasonable scientific certainty. Thus, in selecting primary standards that includ es an adequate margin of safety, the Administrator is seeking not only to prevent pollutant levels that have been demonstrated to be harmful but also to prevent lower pollutant levels that may pose an unacceptable risk of harm, ev en if the risk is not precisely identified as to nature or degree. The CAA does not require that primary standards be set at a zero-ris k level or at bac kground concentration levels, but rather at a level that reduces risk sufficiently so as to protect public health with an adequate margin of safety.

17 The term at-risk populations is used here, rather th en the phrase “sensitive populations” used in the last review. In using the term at-risk, we intend the same meaning as has traditionally been intended for the term “sensitive” consistent with discu ssion in section 1.2.1 above.4-34 guidelines or criteria for interp reting public health signi ficance of such effects, we note that the
CDC has revised the blood Pb level used to prioritize young children for whom they recommend particular follow-up health-protective actio ns, as summarized in section 3.1 above. 18 The CDC decision, while emphasizing the critical importa nce of primary prevention of Pb exposure, provides no new guidelines or criter ia with regard to the significance of specific IQ decrements or judgments on appropriate public health protec tion from risk of neurocognitive effects, and
their consideration of the evidence base at the time of their decision does not substantively differ from that presented in the ISA (CDC, 2012). T hus, we are aware of no new information or new commonly accepted guidelines or criteria within the public health community for interpreting public health significance of neurocognitive effects in the context of a decision on adequacy of
the current Pb standard. With respect to exposure/risk-based consider ations, we recognize th e complexity of the REA modeling analyses and the associated limitati ons and uncertainties. We additionally note the differences among the case studies included in the REA and the extent to which they inform our understanding of different aspects of the risk associated with ai r-related Pb in the U.S. For example, the location-specific case studies indica te the distribution of population risk in urban areas with differing types of Pb sources and gradie nts in air Pb concentrations as well as in population density, while the generalized urban (l ocal) case study indicates the magnitude of airrelated risk associated with those specific loca lized circumstances where air concentrations just meet the Pb standard (regardless of source type ). We agree with conclusions drawn in the 2008 review that the quantitative risk estimates, with a focus on those for the generalized (local) urban case study, are “roughly consistent with and ge nerally supportive” of estimates from the evidence-based air-related IQ loss framework ( 73 FR 67006). We further take note of the increasing uncertainty recognized for air quality scenarios involving air Pb concentrations increasingly below the current c onditions for each case study, recognizing that such uncertainty is due in part to modeling limitations deriving fr om uncertainty regardi ng relationships between
ambient air Pb and outdoor soil/dust Pb and i ndoor dust Pb (as noted in section 3.4 above).
Based on the above considerations and with consideration of advice from CASAC, we reach the conclusion that the current body of evid ence, in combination with the exposure/risk information, supports a primary standard as pr otective as the current standard. Further consideration of the evidence and exposure/risk information available in this review and its attendant uncertainties and limitations, advice from CASAC and consideration of the availability of other information that might also inform pub lic health policy judgments by the Administrator,
leads us to reach the additional conclusion that it is appropriate to consider retaining the current

18 Uses identified for the CDC reference level include is the identification of “ high-risk childhood populations and geographic areas most in need of primary prevention” (CDC, 2012).4-35 standard without revision. We base these conc lusions on consideration of the health effects evidence, including consideration of this evidence in the cont ext of the evidence-based, airrelated IQ loss framework, and in combination with the exposure/ri sk information (chapter 3 and sections 4.2.1 and 4.2.2 above) and the uncertain ties attendant with bot h. In so doing, we recognize the complexities and limitations in the evidence base in reaching conclusions regarding the magnitude of risk associated with the current standard, as well as the increasing uncertainty of risk estimates for lower air Pb concentrations. Based on these considerations, these conclusions also recognize what may be considered reasonable judgments on the public health implications of the blood Pb levels and ri sk estimated for air-related Pb under the current standard, including the public hea lth significance of the Pb effect s being considered, as well as aspects of the use of the evidence-based framewor k that may be considered to contribute to the margin of safety. In reaching these conclusions, we additionally note that different public health policy judgments could lead to different conclusions regarding the extent to which the current standard provides protection of public health with an adeq uate margin of safety. Such public health policy judgments include those rela ted to the appropriate degree of public health protection that should be afforded to protect against risk of ne urocognitive effects in at-risk populations, such as IQ loss in young children, as well as with regard to the approp riate weight to be given to differing aspects of the evidence and exposure/ri sk information, and how to consider their associated uncertainties. For example, different judgments might give gr eater weight to more uncertain aspects of the evidence or reflect a differi ng view with regard to margin of safety. As noted in section 4.1 above, in establishing primary standard s under the Act that, in the Administrator’s judgment, are requi site to protect public health with an adequate margin of safety, the Administrator seeks to establish standard s that are neither more nor less stringent than necessary for this purpose. The Act does not requ ire that primary standards be set at a zero-risk level, but rather at a level that avoids unacceptable risks to public health, ev en if the risk is not precisely identified as to nature or degree. The requirement that primary standards provide an adequate margin of safety was intended to addr ess uncertainties associated with inconclusive
scientific and technical informati on available at the time of standard setting. It was also intended to provide a reasonable degree of protection from hazards that research has not yet identified. In this context, we recognize that the uncertainties and limitations associated with the many aspects of the estimated relationships between air Pb concentrations and blood Pb levels and associated health effects are amplified with consideration of increasingly lower air
concentrations. We believe th e current evidence supports the conclusion that the current standard is requisite to protect publ ic health with an adequate marg in of safety. In staff’s view, with which CASAC has agreed (Frey, 2013, p. 6) based on the current evidence, there is4-36 appreciable uncertainty associated with drawi ng conclusions regarding whether there would be reductions in blood Pb levels and risk to public health from alternativ e lower levels of the standard as compared to the level of the current standard. Thus, we conc lude that the basis for any consideration of alternative lower standard le vels would reflect different public health policy judgments as to the appropriate approach for weighing uncertainties in the evidence and for providing requisite protection of public health with an adequate margin of safety. In summary, the newly available health effects evidence, critically assessed in the ISA as part of the full body of evidence, reaffirms conc lusions on the broad arra y of effects recognized for Pb in the last review. Further, we observe the general consistency of the current evidence
with the evidence available in th e last review with regard to key aspects on which the current standard is based, including those particular to the evidence-based framework developed in the last review. We additionally observe that quantit ative risk estimates asso ciated with the current standard, based on the risk assessment performed in the last review, indicate a level of risk generally consistent with conc lusions drawn from the evidence using the evidence-based framework. In so doing, we also recognize the li mitations and uncertainties associated with the currently available information. These consider ations and the advice fr om CASAC provide the
basis for the staff conclusion that consideration should be given to retaining the current standard, without revision. In light of this conclusion, we have not identified any potential alternative
standards for consideration in this review.

4.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND DATA COLLECTION

In this section, we highlight key uncertainties associated w ith reviewing a nd establishing NAAQS for Pb. Such key uncertainties and areas for future health-related research, model development, and data gathering are outlined below. In some cases, research in these areas can go beyond aiding standard setting to aiding in the development of more efficient and effective control strategies. We note, however, that a full set of research recommendations to meet standards implementation and strategy developmen t needs is beyond the scope of this discussion. Rather, listed below are key uncertainties and res earch questions and data gaps that have been thus far highlighted in this review of the health-based primary standard.

 A critical aspect of our cons ideration of the evidence and th e quantitative risk assessment in this review is our understanding of the C-R relationship between blood Pb levels in young children and neurodevelopmental effects, sp ecifically IQ decrement. An important area of uncertainty in the Pb NAAQS review concerns interpreta tion of neurocognitive impact risks and the shape of the C-R relationship at blood Pb levels similar to and below those common in today’s U.S. young child population. Accordingly, additional epidemiological research involving substant ially sized populations with mean blood Pb levels closer to those comm on in today’s population of young children, particularly those4-37 less affected by higher Pb exposures ear lier in childhood, would help to reduce uncertainty in our estimates of IQ decrement associated with these lower blood Pb levels and, accordingly, in characterizing Pb health effects.

 Key uncertainties with regard to other aspect s of the health effects evidence include the following.

 There remains uncertainty in the eviden ce base with regard to the exposure circumstances (pre- and postnatal timi ng, duration, magnitude and frequency) eliciting effects in older children and adu lts. Effects of particular focus include effects on the nervous system later in life, cardiovascular function, and delayed onset of puberty.

 Alzheimer’s-like pathology has been re ported in aged laboratory animals (nonhuman primates and rodents) exposed to Pb early in life. Uncertainty remains, however, regarding the relationships of such pathology with altered function or behavior.

 Epidemiological studies i ndicate detrimental effects of Pb on sperm production and quality, often in occupa tional cohorts. Uncertaint y remains regarding these effects in otherwise healt hy cohorts without occupati onal Pb exposure or other underlying medical conditions.

 An additional area of uncertainty is that related to the inverse association observed in some studies between low blood Pb and renal function.

 A key consideration in the Pb NAAQS review concerns the relati onship between air Pb concentrations and blood Pb levels, most particularly those in young children. Our quantitative estimation of blood Pb levels in response to various exposure circumstances, including air-related exposure pathways associated with current ambient air Pb concentrations, would benefit from research into this relationship.

 Information is limited with regard to th e temporal aspects of the relationship between ambient air Pb and levels of air-related Pb in blood in young children, and our understanding of the factors influe ncing this relationship is incomplete, particularly in the Pb exposure circ umstances common in the U.S. today.

 Important aspects of (or influence on) the air-to-blood relationship include the relationships (1) between ambient air Pb and outdoor dust and surface soil Pb concentrations and (2) between ambient air Pb and indoor dust Pb. Additional information would help to reduce uncer tainty in our understanding of these relationships and in models and methods used to characterize these pathways in future reviews. Specific mechanistic as pects for indoor dust modeling include air exchange rates, home cleaning frequency and efficiency, among other factors. The impact of changes in ambient air Pb on Pb in indoor dust, outdoor dust and soil, including the temporal dynamics of these relationships, and variations for different environments, are important aspects of the Pb NAAQS review, yet current information on multiple aspects of these pathways is limited.

 There is appreciable uncerta inty regarding the magnitude of the contribution of air-related Pb to diet. Additional information is needed regarding sources of Pb to4-38 the diet of different age groups of the U. S. population, including particularly those sources that relate to curren t ambient air Pb, as well as those related to the legacy of historic ambient air Pb emissions.

 Information is lacking on toxicokinetic s of Pb during adolescence which could inform interpretation of epidemiological studies of relati onships between blood Pb and health effects in this lifestage.

 Future quantitative blood Pb modeling would benefit from additional research into several aspects of population blood Pb levels, including contributing exposure pathways. Examples include:

 Interindividual variability in blood Pb levels and methods for characterizing interindividual variability, including consideration of both empirical and mechanistic methods;

 Apportionment of blood Pb levels with re gard to exposure pathway contributions, with particular focus on understanding e xposure pathways and sources that cause the more elevated blood Pb levels among children today, as well as those related to ambient air Pb; and

 Blood Pb model performance evaluati ons, with emphasis on applications pertaining to blood Pb response to ambient air-related pathways and responses to changes in exposures for those pathways.

 An understanding of the spatial gradient of am bient air Pb concentrations and associated particle sizes in urban resident ial areas, as well as near Pb sources, is an important aspect to our implementation of the NAAQS for Pb and a key element in assessing exposure and risk. Additional research in this area is needed. Current limitations in this area additionally contribute uncertainty to characterization of ambient air Pb levels in the risk assessment and the resulting exposure a nd risk estimates. Research in the characterization of spatial variation in am bient air Pb concentrations in different environments and related to di fferent air sources would help to reduce this uncertainty. The potential for systematic trends in the relationship between ambient air Pb concentrations and distribution of urban residential population s is of interest. Example locations of interest include neighborhoods downwind of airpor ts with substantial leaded aviation gasoline usage, as well as those in th e vicinity of older roads with a substantial historical use of leaded ga soline, including inner city ne ighborhoods (with and without substantial reconstruction).

 Another area of uncertainty relates to our understanding of concentrations of relatively larger airborne particles carrying Pb that oc cur in areas near sour ces and where exposure
may occur.4-39 4.5 REFERENCES

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Henderson, R. (2008a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of the Advance Notice of Proposed Rulemaking (ANPR) for the NAAQS for lead. January 22, 2008.

Henderson, R. (2008b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of the Notice of Proposed Rulemaking for the NAAQS for lead. July 18, 2008.

Hilts, S. R. (2003) Effect of smelter emission reductions on children's blood lead levels. Sci. Total Environ. 303: 51- 58.

Lanphear, B. P.; Hornung, R.; Khoury, J.; Yolton, K.; Baghurst, P.; Bellinger, D. C.; Canfield, R. L.; Dietrich, K. N.; Bornschein, R.; Greene, T.; Rothenberg, S. J. ; Needleman, H. L.; Schnaas, L.; Wasserman, G.; Graziano, J.; Roberts, R. (2005) Low-level enviro nmental lead exposure and children's intellectual function: an international pooled analysis. Environ. Health Perspect. 113: 894-899.

Téllez-Rojo, M. M.; Bellinger, D. C.; Arroyo-Quiroz, C.; Lamadrid-Figuero a, H.; Mercado-García, A.; SchnaasArrieta, L.; Wright, R. O.; Hernández-Avila, M.; Hu, H. (2006) Longitudinal associations between blood lead concentrations < 10 μ g/dL and neurobehavioral development in environmentally-exposed children in Mexico City. Pediatrics 118: e323-e330.

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U.S. Environmental Protection Agency. (2013) Integrated Science Assessment for Lead. Washington, DC, EPA/600/R-10/075F. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_isa.html5-1 

### 5 WELFARE EFFECTS AND EXPOSURE/RISK INFORMATION

This chapter presents key aspects of the cu rrent evidence of Pb-related welfare effects and presents exposure and risk information from th e last review in the co ntext of the currently
available information. Staff has drawn from th e EPA’s synthesis of th e scientific evidence presented in the Integrated Science Assessment for Lead (USEPA, 2013; henceforth referred to as the ISA) and the 2006 Air Quality Criteria Document for Lead (USEPA, 2006a; henceforth referred to as the 2006 CD) and from the screenin g level risk assessment performed in the last
review and described in Lead Human Exposure and Health Ri sk Assessments and Ecological Risk Assessment for Sel ected Areas. Pilot Phase (documented in ICF International, 2006; henceforth referred to as the 2006 REA). This ch apter is organized into two sections regarding the currently available welfare effects eviden ce (section 5.1) and the exposure and risk information (section 5.2) interpreted in light of cu rrently available evidence. Presentation within these sections is organized to address key polic y-relevant questions for this review concerning the evidence and exposure/risk informati on, building upon the questions included in the Integrated Review Plan (IRP, section 3.2).

5.1 WELFARE EFFECTS INFORMATION
Lead has been demonstrated to have harm ful effects on reproduction and development, growth, and survival in many species as described in the assessment of the evidence available in
this review and consistent with the conclusions drawn in the last review (ISA, section 1.7; 2006 CD). A number of studies on ecolo gical effects of Pb are newly available in this review and are critically assessed in the ISA as part of the full body of evid ence. The full body of currently available evidence reaffirms conclusions on the array of effects recognized for Pb in the last review (ISA, section 1.7). In so doing, in the context of pollutant exposures considered relevant, 1 the ISA determines 2 that causal 3 or likely causal 4 relationships exist in both freshwater

1 With regard to consideration of pollutant exposures for studies included in the ISA, the ISA states the following (ISA, pp. lx-lxi). In drawing judgments regarding causality for the criteria air pollutants, the ISA focuses on evidence of effects in the range of relevant pollutant exposures or doses, and not on determination of causality at any dose. Emphasis is placed on evidence of eff ects at doses (e.g., blood Pb concentration) or exposures (e.g., air concentrations) that are re levant to, or somewhat above, those currently experienced by the population. The extent to which studies of higher concentrations are considered varies by pollutant and major outcome category, but generally includes those with doses or exposures in the range of one to two orders of magnitude abo ve current or ambient conditions. Studies that use higher doses or exposures may also be considered to the extent that they provide useful information to inform understanding of mode of action, interspecies differences, or factors that may increase risk of effects for a population. Thus, a causality determination is based on weight of evidence evaluation for health, ecological or welfare effects, focusing on the evidence from exposures or doses generally ranging from current levels to one or two orders of magnitude above current levels.5-2 and terrestrial ecosystems for Pb with effects on reproduction and development in vertebrates and invertebrates; growth in plants and inve rtebrates; and survival in vertebrates and invertebrates (ISA, table 1-3). Although c onsiderable uncertainties are recognized in generalizing effects observed under particular, smal l-scale conditions, up to the ecosystem level of biological organization, the ISA determines that the cumulative evidence reported for Pb effects at higher levels of bi ological organization and for the above described population-level endpoints is sufficient to concl ude that a causal relationship is likely to exist between Pb exposures and community and ecosyst em-level effects in freshwater and terrestrial systems (ISA, section 1.7.3.7). The ISA also presents evidence for saltwater ecosystems, concluding that current evidence is inadequate to make causa lity determinations for most population-level responses, as well as community and ecosystem effects, while finding the evidence to be suggestive linking Pb and effects on reproduction a nd development in marine invertebrates (ISA, Table 1-3, section 6.3.12 and section 6.4.21).
Based on the extensive assessmen t of the full body of evidence available in this review, the major conclusions drawn by the ISA regarding ecological effects of Pb include the following (ISA, Executive Summary, p. xcvi).
With regard to the ecological effect s of Pb, uptake of Pb into fauna and subsequent effects on reproduction, growth and survival are established and are further supported by more recent evidence. These may lead to effects at the population, community, and ecosystem level of biological organization. In both terrestrial and aquatic organisms, gradien ts in response are observed with increasing concentration of Pb and some st udies report effects w ithin the range of Pb detected in environmental media over the last several decades. Specifically, observations from controlled studies on reproduction, growth, and survival in sensitive freshwater invertebrates are well- characterized at concentrations at or near Pb concentrations occasionally en countered in U.S. fresh surface waters.... However, in natural environments, modifyi ng factors affect Pb bioavailability and toxicity and there are cons iderable uncertainties asso ciated with generalizing effects observed in controlled studies to effects at higher l evels of biological organization. Furthermore, available studies on community and ecosystem-level

2 Since the last Pb NAAQS review, the ISAs which have replaced CDs in documenting each review of the scientific evidence (or air quality criteria) employ a systematic framework for weighing the evidence and describing associated conclusions with regard to causality, using esta blished descriptors (“causal” relationship with relevant exposure, “likely” to be causal, evidence is “suggestive” of causality, “inadequate” evidence to infer causality, “not likely”) (ISA, Preamble).
3 In determining that a causal relationship exists for Pb with specific ecological effects, EPA has concluded that “[e]vidence is sufficient to conclude that there is a causal relationship with relevant pollutant exposures (i.e., doses or exposures generally within one to two orders of magnitude of current levels)” (ISA, p. lxii)

4 In determining a likely causal relationship exists for Pb with specific eco logical effects, EPA has concluded that “[e]vidence is sufficient to conclude that there is a likely causal relationship with relevant pollutant exposures ... important uncertai nties remain” (ISA, p. lxii).5-3 effects are usually from contaminated ar eas where Pb concentrations are much higher than typically encountered in th e environment. The contribution of atmospheric Pb to specific sites is not clear and the conn ection between air concentration of Pb and ecosystem exposure continues to be poorly characterized. Furthermore, the level at which Pb elicits a specific effect is difficult to establish in te rrestrial and aquatic systems, due to the influence of other environmental variables (e.g., pH, organic matter) on both Pb bioavailability and toxicity, and also to s ubstantial species differences in Pb sensitivity.

As in prior reviews of the Pb NAAQS, this review is focused on those effects most pertinent to ambient air Pb exposures. Given th e reductions in ambient air Pb concentrations over the past decades, these effect s are generally those associated with the lowest levels of Pb exposure that have been evalua ted. Additionally, we recognize th e limitations on our ability to draw conclusions about environmental exposures from ecological studies of organism-level effects, as most studies were conducted in labor atory settings which may not accurately represent field conditions or the multiple variables that govern exposure.
Our consideration of welfare effects eviden ce in this review is framed by key policyrelevant questions drawn from t hose included in the IRP. In the following sections, we discuss the pathways by which Pb exposure occurs in ecos ystems, the mechanisms that distribute Pb in the environment and the bioavailability of Pb in different ecosystems. Understanding the movement of Pb in the environment is importa nt to understanding expos ure and bioavailability and, thus, informs the subsequent discussion of the effects of Pb on terrestrial and aquatic ecosystems. Finally, we discuss the association of ambient air Pb with effects and the important role a “critical loads” approach 5 might play in assessing the overall ability of ecosystems to recover from past Pb exposures and the degr ee to which newly deposited Pb may affect ecosystem function and recovery.

 To what extent has the newly available evidence altered our understanding of the movement and accumulation of air-depo sited Pb through ecosystems over time? The extensive history of Pb uses in deve loped countries coupled with atmospheric transport processes has left a legacy of Pb in ecosystems globally (e.g., 1977 CD, section 6.3.1). Records of U.S. atmospheric emissions of Pb in the twentieth and late nineteenth centuries have been documented in sediment cores, as noted in section 2.3 above (ISA, section 2.6.2; Landers et

5 As discussed further in subsequent text of this section, the phrase “critical loads” is generally used to describe loading (i.e. addition of a pollutant) to a system that can occur without caus ing a critical impact, e.g., deposition rates of air pollutants that current knowledg e indicates will not cause lo ng-term adverse effects to ecosystem structure and function. A criti cal loads analysis approach takes in to account what is known about the release of a specific chemical into the environment, its distribution and cycling within and across ecosystems and each ecosystem's sensitivity to the chemical (ISA, section 6.1.3).5-4 al., 2010). Once deposited, Pb can be transpor ted by stormwater runoff or resuspension to catchments and nearby waterbodies or stored in soil layers in forested areas, its further movement influenced by soil or sediment comp osition and chemistry and physical processes.
Some new studies are available that provide additional informa tion, briefly summarized below, on Pb cycling, flux and retention within terrestri al and aquatic systems. This new information does not fundamentally change our understanding fr om the last review of Pb movement through or accumulation in ecosystems over time but rath er improves our understanding of some of the underlying processes and mechanisms in soil, water and sediment. There is little new information, however, on fate and transport in ecos ystems specifically rela ted to air-derived Pb (ISA, section 2.3). There is limited newly availa ble information with regard to the timing of ecosystem recovery from historic atmospheric deposition of Pb. Overall, recent studies in terrestrial ecosyst ems provide deposition data consistent with deposition fluxes reported in the 2006 CD, and demonstrate consistently that atmospheric deposition of Pb has decreased since the phase-out of leaded on-road gasoline, as described in section 2.3.2.2 above (ISA, section 2.3.3). Follo w-up studies in several locations at high
elevation sites indicate little cha nge in soil Pb concentrations si nce the phase-out of leaded onroad gasoline in surface soils, consistent with the high retention reportedly associated with reduced microbial activity at lowe r temperatures associated with high elevation sites. However,
amounts of Pb in the surface soils at some lower altitude sites we re reduced over the same time period in the same study (ISA, section 2.3.3). New studies in the ISA also enhance our understanding of Pb sequestration in forest soils by providing a dditional information on the role
of leaf litter as a Pb reservoir in some situ ations and the effect of litter decomposition on Pb distribution (ISA, section 2.3.3). Recent research on Pb transport in aqua tic systems has provided a large body of observations confirming that such transport is dominated by colloids rich in iron and organic material (ISA, section 2.3.2). Recent research on Pb flux in sediments provides greater detail on resuspension processes than was available in the 2006 CD, including research on resuspended Pb largely associated with organi c material or iron and manganese particles and research on the important role played by anoxic or depleted oxygen environments in Pb cycling in aquatic systems. This newer research is consistent with prior evidence in indicating that appreciable resuspension and release from sediments largely o ccurs during discrete even ts related to storms. It has also confirmed that resuspension is an important process that strongly influences the
lifetime of Pb in bodies of wa ter. Finally, there have been advances in understanding and modeling of Pb partitioning between organic mate rial and sediment in aquatic environments (ISA, section 2.7.2).5-5 In summary, the newly available evidence builds on our understanding of some specific aspects of processes involved in the movement and accumulation of Pb through ecosystems over time. The new information, however, does not s ubstantially alter our overall understanding of the fate and transport of Pb in ecosystems or provide a broad quantitativ e understanding of U.S. ecosystem responses to atmospheric Pb deposition.

 Does the newly available evidence furt her inform our understanding of the bioavailability of Pb in different types of ecosystems and organisms? As discussed in the ISA, bioavailability of Pb is an important component of understanding the effects Pb is likely to have on organisms a nd ecosystems (ISA, section 6.3.3).
It is the amount of Pb that can interact within the organism that leads to toxicity, and there are many factors which govern this interaction (ISA, sections 6.2 .1 and 6.3.3; USEPA, 2007a). The bioavailability of metals vari es widely depending on the physi cal, chemical, and biological conditions under which an organism is exposed (USEPA, 2007a). In both aquatic and terrestrial systems, a primary factor influencing the bioavailab ility of Pb, as well as its fate and tranport is solubility (ISA, p. 6-63). Additionally important characteristics that affect bioavailability are (1) chemical form or species, (2) particle size, (3) lability, and (4) source. The bioavailability of a metal is also dependent upon th e fraction of metal that is bi oaccessible. The bioaccessible
fraction of a metal is the portion (fraction or percentage) of environmentally available metal that actually interacts at the organism ’s contact surface and is poten tially available for absorption or adsorption by the organism (USEPA, 2007a; ISA, section 6.3.3). Studies newly available since the last Pb NAAQS review provide additional insight into factors that influence the bioavailability of Pb to specific organisms (ISA, section 6.3.3). In general, this evidence, briefly summarized below, is supportive of previ ous conclusions and does not identify significant new variables from thos e identified previously. Section 6.3.3 of the ISA provides a detailed discussion of bioavailability in terrestrial systems. With regard to aquatic systems, a detailed discussion of bioavailability in freshwater systems is provided in sections 6.4.3 and 6.4.4 of the ISA, and section 6.4.14 of the ISA discusses bioavaila bility in saltwater systems. In terrestrial systems, the amount of bioavailab le Pb present determines the impact of soil Pb to a much greater extent than does the to tal amount present (ISA, section 6.3.11). In such ecosystems, Pb is deposited either directly onto plant surfaces or onto soil where it can bind with organic matter or dissolve in pore water. 6 The Pb dissolved in pore water is particularly bioavailable to organisms in th e soil and thereby influences the impact of soil Pb on terrestrial ecosystems to a much greater extent than the total amount of Pb pres ent (ISA, section 6.3.11).

6 The term “pore water” refers to the water occupy ing the spaces among the grains of sediment or soil.5-6 Several soil characteristics control the amount of Pb that is dissolv ed in pore water, and the ISA presents evidence that has advanced scientific understanding of some of these variables (ISA, section 6.4.21). Studies have s hown that the two most importa nt determinants of both Pb solubility and toxicity in soils are pH and cation exchange cap acity (ISA, section 2.6.1). Also, evidence newly available in this review has conf irmed the important influence of organic matter on Pb sequestration, leading to re latively longer retention in so ils with higher organic matter content (ISA, section 2.6.1). When soils are amended with soluble metals, aging, both under natural conditions and simulated through leaching, redu ces the bioavailability of Pb to plants and soil organisms (ISA, sections 6.3.2, 6.3.9 and 6.3.11; USEPA, 2007a). In general, soils with higher organic matter content have the capacity for greater retention of Pb in the soil matrix and lesser availability of Pb for release into pore wa ter. Reduction in soil organic material, such as through decomposition, can contribute to subsequent increased availability of Pb (ISA, section 6.3.9; 2006 CD, section 6.1.5). In aquatic systems as in terrestrial systems, the amount of Pb bioavailable to organisms is a better predictor of effect on organisms than the overall amount of Pb in the system. Once atmospherically derived Pb enters surface water bodi es through deposition or runoff, its fate and bioavailability are influenced by many water qua lity characteristics, such as pH, suspended solids levels and organic content (ISA, section 6.4.2). In sediments, bioavailability of Pb to sediment-dwelling organisms may be influenced by the presence of other metals, sulfides, iron oxides and manganese oxides and also by physical disturbance (ISA, se ction 2.6.2). For many aquatic organisms Pb dissolved in the water colu mn can be the primary exposure route, while for others sediment ingestion is significant (ISA, section 2.6.2). As recognized in the 2006 CD and further supported in the ISA, th ere is a body of evidence showing that uptake and elimination of Pb vary widely among aquatic species. Although in freshwater systems the presence of humic acid in dissolved organic material (DOM) is considered to reduce the bioavailable fr action of metals in the water column, there is evidence presented in the ISA that DOM does not have the same effect on free Pb ion concentration and toxicity in seawater (ISA, se ction 6.4.2). For example, the ISA discusses two new studies, performed in artificial seawater systems, that suggest that in saltwat er, the presence of DOM increases (rather than decreases) upta ke of Pb by mussel gill structures, potentially through the alteration of membrane permeability (ISA, section 6.4.2.4). These studies also investigated the individual role s of some DOM components. Th is recent evidence supports the
conclusion from the last review that factors that modify bioava ilability of Pb in saltwater
environments are not identical to those in freshwater systems (ISA, section 6.4.14). The newly available evidence about bioavailab ility from experimental systems, briefly summarized above, builds on our fundamental understa nding of Pb bioavailabi lity in aquatic and5-7 terrestrial systems and species from the last review. Bioavailability remains an important consideration in Pb toxicity and a significant source of uncertainty in relating ambient Pb and
adverse effects.

 Does the current evidence alter our conc lusions from the previous review regarding the ecological effects associated with exposure to Pb? Does the newly available evidence indicate new exposure levels at which ecological systems or receptors are expected to experience effects?
There is a substantial amount of new evidence in this review regarding the ecological
effects of Pb on individual terre strial and aquatic species. On th e whole, this evidence supports previous conclusions that Pb has effects on gr owth, reproduction and survival, and that under
some conditions these effects can be adverse to organisms and ecosystems. The ISA provides evidence of effects in additional species, and in a few cases, at lower exposures than reported in the previous review, but does not substantia lly alter our understanding of the ecological endpoints affected by Pb from the previous review. Looking beyond organism-level evidence, the evidence of adversity in natural systems remains sparse due to the difficulty in determining the effects of confounding factors such as co-occurring metals or system characteristics that influence bioavailability of Pb in field studies. The following is a brief comparison of the newly
available evidence to evidence c onsidered in the 2006 review.
Terrestrial Ecosystems
The evidence available in the last review indicated a range of biological effects of Pb on terrestrial organisms that varied with type of organism and life st age, duration of exposure, form of Pb, and soil characteristics. New res earch since the 2006 CD has broadened our understanding of the evidence of damage to photos ynthetic ability in plants exposed to Pb and provided additional evidence of oxidative stress in response to Pb exposure (ISA, section 6.3.4). For example, reactive oxygen species have been found to increase in plant tissue grown in Pbcontaminated soil, and, with increasing Pb expos ure, the plant tissue responded with increased antioxidant activity (ISA, section 6.3.4). In addition, recent studies have reported reduced growth of plants with increased Pb concentration in soil in some experiments, as well as evidence of genotoxicity, decrea sed germination, and pollen st erility (ISA, section 6.3.4). In terrestrial invertebrates, previous CDs have reported adverse effects of Pb on neurological and reproductive endpoints. Recently published studies have further explored the potential for neurotoxic action of Pb, albeit under artificial liquid media conditions (ISA, section 6.3.4.2). Increased mortality was f ound in recent studies of earthworms at
concentrations similar to those in studies re viewed previously, with additional evidence indicating the strong dependence of effects on soil characteristics including pH, cation exchange capacity, and aging (ISA, section 6.3.4.2). There is also newly available evidence for adverse5-8 effects in terrestrial snails and arthropods exposed through soil or diet (ISA, section 6.3.4.2). The effects vary with species and exposure cond itions, and they include diminished growth and fecundity, endocrine and reproductive a nomalies, and body deformities. Increasing concentration of Pb in the expos ure medium generally resulted in increased effects within each study, but the relationship between concentration and effects is hi ghly variable between studies, even when the same medium, e.g. soil, was use d. Current evidence suggests that soil aging and pH are important modifiers of Pb toxici ty in these studies (ISA, section 6.3.11). In terrestrial vertebrates, some new evidence is available for effects of Pb on amphibians and reptiles as well as birds. 7 Effects reported in reptiles and amphibians include decreased white blood cell counts, decreased testis weight, a nd behavioral anomalies (ISA, section 6.3.4.3). However, depending on various fact ors, studies report large differe nces in effects in different species at the same concentrati on of Pb in soil, and effects we re generally smaller when fieldcollected soils were used. In some birds, recen t studies have found maternal elevated blood Pb
level to be associated with d ecreased hatching success, smaller cl utch size, high corticosteroid level, and abnormal behavior in offspring. Stud ies on some species show little or no effect of
elevated blood Pb level. Effect s of dietary exposure have been studied in several mammalian species, with cognitive, endocri ne, immunological, and growth effe cts observed (ISA, section 6.3.11) in some studies. Experimental evidence of organism-level eff ects presented in the ISA demonstrates that increased exposure to Pb is genera lly associated with increases in observed effects in terrestrial species (ISA, section 6.3.11). It also demonstrates that many factors, including the form of Pb and various soil physiochemical properties, influe nce the Pb concentration-response relationship (ISA, section 6.3.11). Further, resu lts from amended soil exposure s generally do not reflect the important effect of environmental aging on bioava ilability and associated toxicity of such soil Pb amendments and therefore make interpreta tion of the results in an ecosystem context difficult. Given that in natural settings, these modifying factors are highly variable, the ISA notes that without quantitatively accounti ng for these factors, laboratory-derived “characterizations of exposure-resp onse relationships would likely not be transferable outside of experimental settings” (ISA, section 1.7.1). Newly available soil invertebrate studies of multiple Pb concentrations in different soil sy stems also provide inconsistent results with respect to exposure-response relationships (ISA, sections 1.7.1 and 6.3.5). In consideration of these results, the ISA notes that “laboratory-am ended artificial soils provide a poor model for predicting the toxicity of Pb-contaminated field soils, becau se aging and leaching processes,

7 Elevated blood and tissue concentr ations of Pb reported in avian species in some areas have been indicated to be a result of nonair pathways, including ingestion of lead-containing materials such as paint chips in urban areas and Pb ammunition fragments in othe r areas (ISA, sections 6.3.3.3 and 6.3.4.3).5-9 along with variations in physio chemical proterties ... influen ce metal bioavailability” (ISA, section 6.3.5) As reported in both the ISA and the 2006 CD , direct evidence for community- and ecosystem-level effects comes from locations near sources of Pb to the environment, where Pb concentrations are much higher than typically observed environmental co ncentrations and often derive from multiple sources to multiple media (e.g. soil, water, air). Impacts of Pb on terrestrial ecosystems near smelters, mines, and other indu strial sources have been studied for several decades (ISA, section 6.3.12.7). Atmospheric em issions of Pb from smelting and other
industrial activities ar e commonly accompanied by other trac e metals (e.g., Zn, Cu, Cd) and
SO 2 that may cause toxic effects independently or in concert with Pb. Those impacts have been shown to include decreases in species diversity and changes in floral and faunal community composition in locations with histories of substa ntial Pb emissions affect ing air concentrations that were likely well in exceedance of the current NAAQS, (e.g., 1977 CD, section 8.8; 1986 CD, section 8.1.1.3; 2006 CD, p. 7-15). Interpretati on of ecosystem-level field studies with regard to ambient Pb levels associated with ecosystem and community effects is complicated by these confounding factors and the inherent variab ility in natural system s (ISA, section 6.3.12.7).
Limited new evidence of effects of Pb at the community scale has been reported. This
evidence includes several studies of the ameliorative effects of mycorrhizal fungi on plant growth with Pb exposure as well as recently published research on soil microbial communities, which have been shown to be impacted by Pb in both composition and activity (ISA, sections 1.7.1 and 6.3.6). Many recent studies have been c onducted using mixtures of metals, which have attempted to separate the effects of indi vidual metals when possi ble. In studies that included only Pb, or where effects of Pb c ould be separated, soil microbial activity was generally diminished with increased Pb concentr ation and was shown in some of those cases to recover with time (ISA, section 6.3.6). In studi es involving heavily contaminated soils from historic smelters, mining sites, or natural Pb deposits, microbial species and genotype composition were consistently altered after Pb exposure, and findings indicate that those alterations were long-las ting or permanent (ISA, section 6.3.6, pg 6-120).
A recent review has examined differences in species sensitivity, using blood Pb level in birds and mammals as an exposure index rath er than external dose (ISA, section 6.3.9.1; Buekers et al., 2009). In this analysis, varia tion across organisms was lower with the blood Pb index compared to use of media concentration, a nd variation of Pb absorption from the diet of the organism largely accounted for the variation s een in the blood Pb. The analysis also suggests a larger variation in sensitivity across avian species tested compared to mammalian species with regard to the association between blood Pb con centration and toxicity (ISA, section 6.3.9.1).5-10 Overall, recent studies cited in this review support previous conclu sions about the effects of Pb on terrestrial ecosystems, namely that incr easing soil Pb concentrations in areas of Pb contamination (e.g. mining sites and industrial s ites) can cause decrea ses in microorganism abundance, diversity, and function. Previous reviews have also reported on effects on bird and plant communities (2006 CD, section AX7.1.3). Th e shifts in bacteria l species and fungal diversity have been observed near long-establis hed sources of Pb contamination (ISA, section 6.3.12.7). Most recent evidence for Pb toxicity to te rrestrial plants, invert ebrates and vertebrates is from single-species assays in laboratory st udies which do not capture the complexity of bioavailability and other modifier s of effect in natural systems (ISA, section 6.3.12.7). Further, models that might account for modifiers of bi oavailability have proven difficult to develop (ISA, p. 6-16).

Freshwater Ecosystems Studies newly available in this review a ddress trophic transfer of Pb in freshwater ecosystems (ISA, section 6.4.4.4). Evidence su mmarized in the 2006 CD indicated that
measured concentrations of Pb in the tissues of aquatic organisms were generally higher in algae and benthic organisms than in higher troph ic-level consumers, i ndicating that Pb was bioconcentrated but not biomagnified (ISA, sec tion 1.7.2). Some recent studi es indicate transfer of Pb in aquatic food webs; while other recent studi es that have traced Pb in freshwater aquatic food webs have found, similar to the 2006 CD findi ngs, that Pb concentration decreases with increasing trophic level (biodilutio n) (ISA, sections 1.7.2 and 6.4.4.4). Evidence presented in the ISA further suppor ts the findings of past CDs that Pb in freshwater can be highly toxic to aquatic organisms, with toxici ty varying with species and life stage, duration of exposure, form of Pb, a nd water quality charac teristics. The 2006 CD identified evidence of adverse growth effects on several species of fres hwater algae from Pb exposure (2006 CD, Section 7.2.4). The ISA desc ribes several new studies which expand the list of algal species for which these adverse e ffects have been identified (ISA, section 6.4.5.1). For vascular plants, the ISA describes additi onal evidence that oxidative damage, decreased photosynthesis and reduced growth occur with elevated Pb exposure (ISA, section 6.4.5.2). Since the 2006 CD, there is some additional evidence for Pb effects on cellular processes in aquatic invertebrates. Recent studies of reproductive and developmental effects of Pb augment similar findings in the 2006 CD and add additional species information on reproductive endpoints for rotifers and freshwater snails as well as multig enerational effects of Pb in mosquito larvae (ISA, section 6.4.5.2). In the 2006 CD, study concentrations cited at which effects were observed in various aquatic in vertebrates reflected an expansive range from
5 μ g/L (for acute toxicity to Pb nitrate in a test system at a hardness of 18 mg/L calcium carbonate) to greater than 8000 μg/L (for acute toxicity to Pb chloride at a hardness of 280-3005-11 mg/L calcium carbonate) (ISA, p.1-45; 2006 CD, Ta ble AX7-2.4.1). Recent studies cited in the ISA provide additional evidence of effects fr om chronic exposures. These findings are generally consistent with those of the previous review and reflect the variability of Pb toxicity under different environmental conditions and in species with varying sensitivity. Evidence of effects in aquatic vertebrates pr esented in the ISA reite rates the findings of reproductive, behavioral, and gr owth effects stated in prev ious CDs. Some additional mechanisms of Pb toxicity in the gill and the rena l system of fish have been elucidated since the 2006 CD as well as the identification of potentia l new molecular targets for Pb neurotoxicity (ISA, section 1.7.2). As in terrestrial organisms, evidence presen ted in the ISA and prior CDs demonstrates the toxicity of Pb in aquatic ecosystems and the ro le of many factors, incl uding Pb speciation and various water chemistry properties, in modify ing toxicity (ISA, section 1.7.2). Since the 2006 CD, additional evidence for community and ecosystem level effects of Pb is available, primarily
in microcosm studies or field studies with other metals present (ISA, section 6.4.11). Such evidence described in previous CDs includes al teration of predator-prey dynamics, species richness, species composition, and biodiversity. New studies availa ble in this review provide evidence in additional habitats for these community and ecological-scale eff ects, specifically in aquatic plant communities and sediment-associat ed communities at both acute and chronic exposures involving concentrations similar to th ose previously reported (ISA, section 6.4.7). In many cases it is difficult to characterize the na ture and magnitude of effects and to quantify relationships between ambient con centrations of Pb and ecosystem response due to existence of multiple ecosystem-level stressors, variability in field conditions, and differences in Pb bioavailability (ISA, sections 1.7.3.7 and 6.4.7) . Additionally, the degree to which air
concentrations have contributed to such eff ects in freshwater ecosystems is largely unknown.
Saltwater Ecosystems As assessed in the ISA, the evidence for sa ltwater species and eco systems is generally inadequate to draw conclusions regarding the eff ect of Pb (ISA, Tables 1-3 and II). The extent of newly available evidence in the context of prior available evidence is summarized here. With regard to evidence in marine plants, re cently available eviden ce on the toxicity of Pb to marine algae augments the 2006 CD findi ngs of variation in sensitivity across marine species. Recent studies on Pb exposure include reports of growth inhi bition and oxidative stress in a few additional species of marine algae (ISA, section 6.4.15). Recent literature provides little new ev idence of endpoints or effects in marine invertebrates beyond those reported in the 2006 CD. For example, some recent studies strengthen the evidence of Pb effects on enzymes and antioxidant activity in marine
invertebrates and have identified an additional behavioral endpoint (i.e., valve closing speed in5-12 juveniles of a marine scallop affected by 20 da ys exposure to 40-400 μg/L Pb nitrate) from those discussed previously (ISA, section 6.4.15.2). Also, as noted in the 2006 CD and supported by new studies reviewed in the ISA, Pb expos ure negatively affects th e growth of marine invertebrates (ISA, section 6.4.15.2). Recent studie s also identify several species exhibiting particularly low sensitivity to hi gh acute exposures (ISA, section 6.4.15.2).
Little new evidence is available of Pb effects on marine fish and mammals for reproductive, growth and survival endpoints that are particularly relevant to the population level of biological organization and higher (ISA, sectio n 6.4.15). Evidence for effects at higher levels of biological organization in salt water habitats is primarily suppor ted by observations in a small
number of microcosm and field studies where shifts in nematode community structure are the most commonly observed effects of Pb in e xperimentally contaminated sediments (ISA, sections 6.4.17 and Table 6-6). These types of studies were presented in the 2006 CD, and while there are new studies presented in th e ISA, they primarily expand the types of communities (seagrass and amphipods) for which data exist but reach similar conclusions about community structure as the 2006 CD. However, there is no evidence of adverse effects in
saltwater environments associated with current ambient air Pb concentrations, and linkages between any level of ambient air deposition and effects are unknown in all but a few organisms. New studies on organism-level effects from Pb in saltwater ecosystems (ISA, section 6.4.15) provide little evidence to inform our understanding of linkages between atmospheric concentrations, ambient exposures in saltwater systems and such effects or our conclusions regarding the likelihood of adverse effects under conditions a ssociated with the current NAAQS for Pb. Nor does the currently available eviden ce indicate significantly different exposure levels from the previous review at which eco logical systems or rece ptors are expected to experience effects.

 To what extent is there new informat ion that informs our understanding of critical loads of Pb, including criti cal loads in sensitive ecosystems? Critical loads analyses are a me thod that facilitates the assessment of ecosystem impacts as a result of pollutant loading which may ar ise from multiple pathways. A critical loads analysis approach can take into account what is known about the release of a specific chemical into the environment, its distri bution and cycling within (and, as appropriate, across) ecosystems and each ecosystem's sensitivity to the chemical (ISA, section 6.1.3). Thus, this approach provides a conceptual framework for linking a tmospheric deposition to environmental media concentration target values rela ted to ecological endpoints associ ated with impairment (termed “critical limits”). Given the pot ential relevance to considera tion of the secondary NAAQS for Pb, research in this area has been asse ssed in the current ISA and the 2006 CD.5-13 The following generally accepted definition for a critical load of atmospheric pollutant deposition was developed from a pair of inte rnational workshops in the late 1980s (USEPA, 2008).
A quantitative estimate of an exposure to one or more pollutants below which significant harmful effects on specified se nsitive elements of the environment do not occur according to present knowledge.
As critical loads estimates reflect the current state of knowledge and policy priorities, as well as scientific and science pol icy judgments pertaining to the c ontext for their use, there is no single “definitive” critical load fo r a natural resource. The state of scientific knowledge in this area can change in reflection of new informati on in various areas including, for example, new information about dose-response relationships; more comprehensive and detailed characterization of ecosystem resources (e.g., impr oved maps, inventories and survey datasets); more detailed information on pollutant concentr ations (e.g., continuing ti me-series monitoring); and improved numerical models of pollutant fate and transport and ecosystem response. Science policy judgments reflect their context (e.g., goal for protection) as well as th e state of scientific knowledge and consideration of its attendant strengths, limitations and uncertainties. Additionally inherent in critical loads analyses, due to their predictive nature, are a variety of assumptions, which may be relatively more or less numerous depending on the extent of knowledge on environmental processes for a particular application.
Some of the earliest uses of cr itical loads analyses date to consideration of the evidence for air pollutant deposition impacts on acidificati on of sensitive lake systems (2006 CD, section 7.3.2). Accordingly, the integrated science assessment of the ev idence for the air pollutants nitrogen oxides (NOx) and sulfur oxides (SOx) desc ribed in detail the critical loads concept and the substantial evidence base pertaining to its ap plication in considera tion of acidification and eutrophication of aquatic ecosyst ems (USEPA, 2008). In this case, the substantia l evidence of these ecosystem effects and the role of NOx/S Ox atmospheric deposition was assessed (USEPA, 2008), and multiple alternative biological indica tors, critical biological responses, chemical indicators, and critical chemical limits were presented that could be used to determine appropriate critical loads for a quatic and terrestrial ecosystems with regard to acidification and eutrophication (e.g., USEPA, 2008, Table 3-1, sec tions 3.2 and 3.3 and Annexes B, C and D). A comparable evidence base does not exist with regard to impacts of air deposition of Pb on ecosystems. Nonetheless, the potential exists for critical loads to be an especially powerful tool allowing us to assess Pb atmospheric input into an eco system (e.g., deposition) and the potential ecological impairment resulting from that input. Critical load an alyses are dependent on data relating pollutant release into an ecosystem (or multiple connected systems) from various sources with an understanding of the ecosystem concentrations lik ely to result in significant5-14 harmful effects. In the context of Pb, a persistent, naturally occurring material, the bioavailability and mobility are influenced by multiple ecosystem characteristics; the data types for such analysis are numerous and may in clude information in the following areas:

 Pathways and rates by which Pb is released into ecosystems;

 Current Pb presence within and among ecosystems, 8 including spatial distribution, bioavailability and mobility;

 Fate and transport processes, within a nd among ecosystem components, as well as associated rates and factors influencing them;

 Forms and concentrations of Pb in ecosy stem exposure media that likely result in critical ecosystem effects (e.g., concentrations that might relate to critical limits). Additional information pertaining to the cons ideration of critical loads analyses in the context of ambient air standard setting for Pb includes factors that influence the transport and spatial pattern of deposition of airborne Pb, such as part icle size (ISA, section 2.3.1). During the last review, the 2006 CD assessed th e available informati on on critical loads for Pb (2006 CD, section 7.3). This informati on included publications on methods and example applications, primarily in Europe, specific to the bedrock geology, soil types, vegetation, and historical deposition trends in each European country (2006 CD, p. E-24), with no analyses available for U.S. locations (2006 CD, sections 7.3.4-7.3.6). 9 As a result, the 2006 CD concluded that “[c]onsiderable research is neces sary before critical load estimates can be formulated for ecosystems extant in the United St ates” (2006 CD, p. E-24). More generally, the 2006 CD identified the largest sources of uncertainty to include: deri vation of the critical limit, Pb speciation, and soil runoff as an input to a quatic ecosystems (2006 CD, p. 7-45). Overarching
conclusions reached included th e following (2006 CD, p. 7-46).
... At this time, the methods and models commonly used for the calculation of critical loads have not been validated fo r Pb. Many of the methods neglect the speciation of Pb when estimating critical limits, the uptake of Pb into plants, and out flux of Pb in drainage water, limiting the utility of current models. Future efforts should focus on fully incorporating the role of Pb speciation into critical load models, and validating the assumptions used by the models.

8 In the case of Pb, in addition to the role of curr ent air-related pathways, its presence in the ecosystem results from larger historical air emi ssions as well as contributions from nonair pathways which may be appreciable in some areas (e.g., industrial discharges to surface wa ters, contaminated waste disposal, drainage from metals mining sites, Pb ammunition near outdoor shooting areas).

9 The work in Europe is largely responsive to developments, beginning in the late 1980s, associated with the consideration of the critical-load concept for a range of air pollutants in future international agreements limiting air pollutant emissions (2006 CD, section 7.3.2). A key impetus for such international cooperation efforts was research in the 1960s and 1970s indicating the role of long-range trans-boundary transport on ecosystems (e.g., sulfur emissions on the European continent contributing to acidification of Scandinavian lakes). Since about 1990, research has been exploring the use of critical loads in Europe for other air pollutants, including metals (2006 CD, section 7.3.2).5-15 Accordingly, the quantitative assessment for the last Pb NAAQS review (ICF, 2006) did not involve critical load analyses. Newly available evidence pertaining to critical loads analysis in this review includes
limited recent research on consideration of bi oavailability in characterizing Pb effect concentrations or indices and on modeling approa ches to incorporate ch emistry effects on Pb speciation and bioavailability (ISA, sections 6.3.7 and 6.4.8). With consideration of this
information and the four critical load analysis studies newly ava ilable in this review (none of which are for U.S. ecosystems), the ISA does not modify the conclusions noted above from the 2006 CD (ISA, sections 6.1.3, 6.3.7 and 6.4.8). In summa ry, the new information in this review does not appreciably change our evidence base or further inform our understanding of critical loads of Pb, including critical loads in sensitive ecosystems.

 To what extent is there information that improves our understanding of the portion of environmental Pb derived from ambient air and the associated effects on sensitive ecosystems?
There is no new evidence since the last review that substantially improves our understanding of the relationship between ambient ai r Pb and measurable ecological effects. As stated in the last review, the ro le of ambient air Pb in contri buting to ecosystem Pb has been declining over the past several decades. It re mains difficult to apportion exposure between air
and other sources to better inform our understandi ng of the potential for ecosystem effects that might be associated with air emissions. As noted in the ISA, “[t]he amoun t of Pb in ecosystems is a result of a number of inputs and it is not currently possible to determine the contribution of atmospherically-derived Pb from total Pb in terre strial, freshwater or saltwater systems” (ISA, section 6.5). Further, considerable uncertainti es also remain in drawing conclusions from
evidence of effects observed under laboratory conditions with regard to effects expected at the ecosystem level in the environment. In many cases it is difficult to characterize the nature and magnitude of effects and to quantify relationshi ps between ambient con centrations of Pb and ecosystem response due to the existence of multipl e stressors, variability in field conditions, and differences in Pb bioavailability at that level of organization (ISA, section 6.5). In summary, the ISA concludes that “[r]ecent information availa ble since the 2006 Pb AQCD, includes additional
field studies in both terrestr ial and aquatic ecosystems, but the connection between air concentration and ecosystem exposure continues to be poorly characterized for Pb and the contribution of atmospheric Pb to specifi c sites is not clear ” (ISA, section 6.5).5-16 5.2 EXPOSURE AND RISK INFORMATION
The risk information available for this revi ew and described here is based primarily on the pilot ecological risk assessmen t developed in the last review of the Pb NAAQS (henceforth referred to as the 2006 REA [ICF, 2006]). This in formation is described within the context of the evidence presented in the ISA that is newly available for this review. As described in the IRP, careful consideration of newly available information in this review led us to conclude that developing a new REA for this revi ew was not warranted. In light of critical limitations and
uncertainties that are still unresolved in the cu rrent evidence, staff concluded that currently available information does not provide the basi s for developing a new quantitative risk and exposure assessment with substantially impr oved utility for informing the Agency’s
consideration of welfare effects and evaluation of the adequacy of the current secondary standard or alternatives (REA Planning Do cument, section 3.3). More specifi callly, we also indicated our conclusion that the information newly available in this review did not provide the means by which to develop an updated or enhanced risk m odel that would substantially improve the utility of risk estimates in informing the current Pb NAAQS review (REA Planning Document, section 3.3). Based on their consideration of the RE A Planning Document, th e CASAC Pb Review Panel generally concurred with the conclusion that a new REA was not warranted in this review (Frey, 2011; Frey, 2013). Accordingly, the informati on described here is drawn primarily from
the 2006 REA. The focus for the risk assessment and associated estimates presented here is on Pb derived from sources emitting Pb to ambient air. While there is some new evidence that improves our understanding of some of the envi ronmental variability affecting the disposition and toxicity of Pb in the environment, the information and methods to support a quantitative assessment of the role of atmospheric Pb in th e U.S are limited. Specific constraints include the limited availability of location-specific data describing a range of U.S. ecosystems and their pertinent environmental characteristics as well as a more complete understanding of bioavailability and its modifier s and data and methods to inform the apportionment of Pb allowed by the current standard and of lead-re lated effects between ai r and non air sources. These data gaps and areas of uncertainty in the current evidence restrict our ability to assess quantitatively the relationship between concentrati ons of Pb in ambient air and terrestrial and/or aquatic systems, and their effect on welfare. As discussed in section 1.3 above, the multimedia and persistent nature of Pb, the role of multiple exposure pathways (illustrated in Figur e 1-1 above), and the contributions of nonair sources of Pb to exposure media all present ch allenges and contribute significant additional complexity to the ecological risk assessment that goes far beyond the situation for similar assessments typically performed for other NAAQ S pollutants (e.g., that focus only on a single5-17 media pathway or for which air is the only signifi cant source). Limitations in the available data
and models affected our characterization of the va rious complexities associated with exposure to ambient air Pb. As a result, the 2006 assessmen t was conducted as a pilot study with a number of simplifying assumptions with regard to th e representativeness of the case studies for ecological exposures and our ability to isolate case studies where air-derived Pb was the only or most significant source. Therefore, this section presents a brief summary of the screening-level ecological risk assessment conducted in 2006 fo r the Pb NAAQS review completed in 2008 and addresses several questions rela ting to the current evidence a nd understanding that may inform
our view of the results of that assessment. Th e discussion here also ta kes into consideration
CASAC recommendations in the last review with regard to interp retation of the screening-level assessment (Henderson, 2007a, b), as well as comments received from the CASAC Pb Panel in the current review, as part of the consulta tion on the REA Planning Document (Frey, 2011).

5.2.1 Screening Assessment from Last Review

The screening-level risk assessment perfor med for the last review was focused on estimating the potential for ecological risks asso ciated with ecosystem exposures to Pb emitted into ambient air (2006 REA, section 7). A natio nal-scale screen was us ed to evaluate surface water and sediment monitoring lo cations across the United States for the potential for ecological impacts that might be associated with atmospheri c deposition of Pb (described in detail in 2006 REA, section 7.1.2). In addition to the natio nal-scale screen (2006 REA, section 3.6), the assessment involved a case study approach, with case studies for areas surrounding a primary Pb smelter (2006 REA, section 3.1) and a secondary Pb smelter (2006 REA, section 3.2), as well as a location near a non-urban roadway (2006 REA, s ection 3.4). An additional case study, focused on consideration of atmospherically derived Pb effects on an ecologically vulnerable ecosystem (Hubbard Brook Experimental Forest), was iden tified (2006 REA, section 3.5). The Hubbard Brook Experimental Forest (HBEF), in the White Mountain National Forest, near North Woodstock, New Hampshire, was selected as a f ourth case study because of its location and its long record of available data on c oncentration trends of Pb in thr ee media (air or deposition from air, soil, and surface water). While no quantitativ e analyses were performed, summary review of
the literature search was incl uded in the assessment report (20 06 REA, Appendix E). For the other three case studies, exposure concentrations of Pb in soil, surface water, and/or sediment
concentrations were estimated from available monitoring data or modeling analysis and then compared to ecological screening benc hmarks (2006 REA, section 7.1).
All three case studies and the national-scale assessment generally cons idered then-current
or recent environmental conditions . In all cases but the primary Pb smelter case study, current air quality conditions were below the then-cur rent NAAQS. Air Pb c oncentrations in the5-18 primary Pb smelter case study exceeded the then -current NAAQS. A comple te discussion of air quality in each of the case studies can be found in section 4 of the 2006 REA. An overview of the approach developed to implement the selected elements of the conceptual model for the ecological risk assessmen t is provided in Figure 5-1. This figure shows the key types of information and models involved in each part of the assessment and how they are related to each other and to the other parts of the analysis. Appendix 5A gives the locations and spatial resolution for each of the case st udies and the national scale screen while summarizing the source of the screening values used or each location and media type. As indicated in Figure 5-1 and Appendix 5A, the specific approach for each case study differed based on the nature of the case study (e.g., type of source, locations of populations) and the sitespecific measurements available.5-19 Figure 5-1. Analytical approach for screening-level eco logical risk assessment in the last review (2006 REA, Exhibit 2-6).5-20 To estimate the potential for ecological risk, modified ecological soil screening levels (Eco-SSLs) derived from t hose developed by EPA’s Supe rfund program (USEPA, 2005a,b), EPA’s recommended ambient water quality crit eria (2006 REA, secti on 7.1) and sediment screening values developed by MacDonald and ot hers (2000, 2003) were us ed, as described in detail in section 7.1.3 of the 2006 REA. A hazard quotient (HQ) was calculated for adverse effects on the survival, growth, and reproduction of exposed ecological receptors to determine the potential for risk to that recep tor. Ecological receptors used in the pilot are discussed in detail in section 7.1 of the 2006 REA. The HQ was calculate d as the ratio of the media concentration to the ecotoxicity screening value. In each case study, HQ values were calculated for each location
where either modeled or measur ed media concentrations were available. Separate soil HQ values were calculated for each ecological recep tor group for which an ecotoxicity screening value has been developed (i.e., birds, mammals, so il invertebrates, and plants), as described in detail in section 7.1.2 of the 2006 REA. HQ values less than or equal to 1.0 were concluded to suggest that Pb concentrations in a specific medium were unlikel y to pose significant risks to ecological receptors, while HQ values greater than 1.0 indicated a potential for adverse effects.

5.2.2 Screening Assessment Results and Interpretation

The results for the ecological screening a ssessment for the three case studies and the
national-scale screen for surface wa ter and for sediment indicated a potential for adverse effect from ambient Pb to multiple ecological recepto r groups in terrestrial and aquatic locations. 10 Below are descriptions of the location-specifi c case studies and the national screening assessment, key findings of the risk assessment fo r each, and an interpretati on of the results with regard to past air conditions as well as the current standard (USEPA, 2007b).

 What do the key findings of the 20 06 screening-level a ssessment indicate regarding the likelihood that adverse welf are effects would result from levels of air-related Pb that would meet the current standard? In addressing this question, the findings of the 2006 REA are summarized below.
Primary Pb Smelter Case Study

 The primary Pb smelter case study location is at one of the largest and longestoperating primary Pb smelters in the wo rld (since 1892), the only one currently operating in the U. S. (ICF, 2006). 11

 Concentrations of total Pb in several of the soil and sedime nt locations within the case study were measured in 2000 and exceeded scre ening values, indica ting a potential for adverse effects to terrestrial and sediment-dwelling organisms.

10 It is important to note that the screening values available and used in the assessment lacked adjustment for some critical measures of bioavailability. See uncertainty discussion below.

11 As noted in section 2.1.2 above, this smelter ceased smelting operations at this facility at the end of 2013.5-21  While the contribution to th ese Pb concentrations from air as compared to nonair sources is not quantified, air emissions from this facility are subs tantial (ICF, 2006). In addition, this facility that has been emitting Pb for many decades, including some seven decades prior to establishment of any Pb NAAQS, such that it is likely air concentrations associated with the facil ity were substantial relative to the 1978 NAAQS, which it exceeded at the time of the last review. At the time of the previous review (2006) and also since the adoption of the current standa rd, concentrations monitored near this facil ity exceeded the level of the applicable NAAQS (USEPA 2007b, Appendix 5A and Appendix 2D of this document). Accordingly, this case study is not informative for considering the likelihood of adverse welfare effects related to Pb from air sources under air quali ty conditions associated with meeting the current Pb standard. Secondary Pb Smelter Case Study

 The secondary Pb smelter location falls w ithin the Alabama Coastal Plain in Pike County, Alabama, in an area of disturbed forest s. The industrial faci lity in this case study is much younger than the primary Pb sme lter, becoming active less than ten years prior to the establishment of the 1978 Pb standard.

 Estimates of total Pb concentration in soils (based on fate and transport modeling using 1997-2000 emissions data and data for similar locations measured in a 1995 study) exceeded screening values for plants, birds and mammals, indicating the potential for adverse effects to these groups.

 While the contributions from air-related Pb to the total Pb concentrations modeled in soils at this location are unclear, the facili ty continues to emit Pb, and the county where this facility is located does not meet the current Pb standard (Appendix 2D and 5A). Given the exceedances of the current standard, which likely extend back over 4 to 5 decades, this case study also is not inform ative for considering the likelihood of adverse welfare effects related to Pb fr om air sources under air quality conditions associated with meeting the current Pb standard. Near-Roadway Non-urban Case Study

 This case study comprises two non-urban site s adjacent to established highways for which soil Pb data were available: (1) in Co rpus Christi, Texas (ICF, 2006), and (2) in Atlee, Virginia (ICF, 2006). Measured soil concentration data were used to develop estimates of Pb in soils for each location.

 Estimates of total Pb concentrations taken in 1994 and 1998 in soils in this case study exceeded screening values for plants, birds and mammals, indicating the potential for adverse effect to these groups. These case study locations are highly impacted by past deposition of gasoline Pb. It is unknown whether current conditions at these si tes exceed the current Pb standard, but given evidence from the past of Pb concentrations near highways that ranged above the previous (1978) Pb standard (1986 CD, s ection 7.2.1), conditions at these locations during the time of leaded gasoline very likely exceeded the current standard. Similarly, those conditions likely resulted in Pb deposition associated with leaded gasoline that exceeds that being deposited unde r air quality conditions that would meet the current5-22 Pb standard. Given this legacy, considera tion of the potential for environmental risks from levels of air–related Pb associated w ith meeting the current Pb standard in these locations is highly uncertain. Vulnerable Ecosystem Case Study

 This case study was focused on consideration of information available for the Hubbard Brook Experimental Forest (HBEF) in the White Mountain National Forest near North Woodstock, New Hampshire, which incl uded a long record (from 1976 through 2000) of available data on concentra tion trends of Pb in three media (air or deposition from air, soil, and surface water).

 While no quantitative analyses were performed, a summary review of literature published on HBEF was developed. This li terature indicated: (1) atmospheric Pb inputs do not directly affect stream Pb levels at HBEF because deposited Pb is almost entirely retained in the soil profile; and (2) soil horizon analysis results showed Pb to have become more concentrated at lower so il depths over time, with the soil serving as a Pb sink, appreciably reducing Pb in pore wa ter as it moves through the soil layers to streams (dissolved Pb concentrations were reduced from 5 μg/L to about 5 ng/L from surface soil to streams). Further, the available studies concluded insignificant contribution of dissolved Pb from soils to streams (ICF, 2006, Appendix E). It is unlikely that conditions have changed from the previous conclusions made based on soil data through 2000, and, theref ore, current ambient air concentrations likely do not directly impact stream Pb levels under ai r quality conditions associated with meeting the current standard. National-scale Surface Water and Sediment Screen

 The national-scale screen was performed usi ng a national database of surface water and sediment monitoring data (s ee Appendix 5A; ICF, 2006).

 The screen identified 15 non-mining sites at which at least one surface water dissolved Pb concentration taken be tween 1994 and 2004 exceeded the chronic screening value, indicating a potential for adverse effect if concentrations were persistent over long time periods. The acute screening value was not exceeded at any of these locations.

 Analysis of the sediment concentratio ns for the 15 sites taken from 1991 to 2000 analyzed in the surface water scr een identified a subset for which concentrations exceeded the screening va lue, indicating a potential for adverse effects to sediment dwelling organisms.

 The extent to which past air emissions of Pb have contributed to surface water or sediment Pb concentrations at the locations identified in the screen is unclear. For some of the surface water loca tions, nonair sources likely contributed significantly to the surface water Pb concentrations. For other locations, a lack of nearby nonair sources indicated a potential role for air so urces to contribute to observed surface water Pb concentrations. Additionally, these concentrations may have been influenced by Pb in resuspended sediments and may reflect cont ribution of Pb from erosion of soils with Pb derived from historic as well as current air emissions.5-23 There are multiple sources of uncertainty associated with different aspects of this assessment (discussed in detail in 2006 REA, s ection 7.4). For example, there are significant
limitations and uncertainties associated with conclu sions that can be drawn from the primary Pb smelter case study regarding the impact of atmo spheric deposition under conditions associated with meeting the Pb NAAQS (past or present). Additionally, while cas e study locations were chosen with the objective of including locations fo r which recent Pb data were available and for which Pb exposures might be influenced by ai r-related Pb and not be dominated by nonair sources, there is significant un certainty regarding the extent to which nonair sources and
conditions associated with histor ic emissions (e.g., prior to establishment of past or present Pb NAAQS) have likely contributed to the Pb exposure estimates in some locations. The screening
values available and used in the assessment (e.g., ambient water quality criteria, Eco-SSLs, sediment criteria) lacked adjustment for some critical measures of bioavailability and were sources of uncertainty with regard to potential for ecological risk. There is also uncertainty regarding the extent to which the screening va lues could identify poten tial hazards of Pb for some threatened or endangered species or unus ually sensitive aquati c ecosystems (ICF 2006). Thus, while the assessment results are generally c onsistent with evidence-based observations of the potential influence of Pb on eco logical systems, they are limited with regard to quantitative conclusions and potential hazard or risk associated with the Pb NAAQS, most particularly with regard to the current standard. The Hubbard Br ook case study represents the most applicable case study for current conditions, and based on the previous analysis undertaken in the last review, current ambient ai r concentrations likely do not direc tly impact stream Pb levels under air quality conditions associated wi th meeting the current standard. With data limitations and the difficulties in apportioning Pb in ecosystems, there are no additional known locations in the U.S. that would likely provide addi tional insight into the effects of ambient Pb under the current standard, therefore no additional case study an alyses were undertaken in this review.

 What are the important uncertainties asso ciated with interpreting the prior assessment in light of newly availa ble evidence in this review? In interpreting the results from the 2006 REA, we consider newly available evidence that may inform our interpretation of risk under the cu rrent standard. Factors necessary to alter our interpretation of risk would include new evidence of harm at lower concentrations of Pb, new linkages that enable us to dr aw more explicit conclusions as to the air contribution of environmental exposures, and/or new methods of interpreting confoundi ng factors that were largely uncontrolled in the previ ous risk assessment. In general, however, the key uncertainties
identified in the last review re main today, as described below. With regard to new evidence of harm at lowe r concentrations, it is necessary to consider that the evidence of adversity due specifically to Pb in natural systems is limited, in no small part5-24 because of the difficulty in determining the e ffects of confounding fact ors such as multiple metals and modifying factors infl uencing bioavailability in field studies. Modeling of Pb-related exposure and risk to ecol ogical receptors is subject to a wide array of so urces of both variability and uncertainty. Variability is associated with geographic location, hab itat types, physical and
chemical characteristics of soils and water that influence Pb bioavailability, terrestrial and aquatic community composition. Furthermore Pb upt ake rates by invertebrates, fish, and plants may vary by species and season. Fo r wildlife, variability also is associated with food ingestion rates by species and season, prey selection, and locations of home ranges for foraging relative to the Pb contamination levels (USEPA, 2005b). There are significant difficulties in quantifying the role of air emissions under the current standard, which is significantly lower than the pr evious standard. As recognized in section 1.3.2 above, Pb deposited before the standard wa s enacted remains in soils and sediments, complicating interpretations regarding the impact of the current standard; historic Pb emitted from leaded gasoline usage continues to move slowly through systems along with more recently deposited Pb and Pb derived from non air sources. The results from the location-specific case studies and the surface and sediment screen performe d in the last review are difficult to interpret in light of the current standard and are not la rgely useful in informing our judgments of the potential for adverse effects at levels of deposition meeting the current standard. Under such
constraints it is difficult to a ssess the merit of the risk findi ngs from the previous review.5-25 5.3 REFERENCES
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U.S. Environmental Protection Agency. (2006b) Analysis Plan for Human Health and Ecological Risk Assessment for the Review of the Lead National Ambient Air Quality Standards. Office of Air Quality Planning and Standards, Research Triangle Park, NC. Available at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_pd.html5-26U.S. Environmental Protection Agency. (2007a). Framework for metals risk assessment [EPA Report]. (EPA 120/R07/001). Washington, D.C. Available online at: http://www.epa.gov/raf/metalsframework/index.htm

U.S. Environmental Protection Agency. (2007b). Review of the National Ambient Air Quality Standards for Lead:Policy Assessment of Scientific and Technical Information OAQPS Staff Paper. Washington, DC, EPA452/R-07-013. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr.html

U.S. EPA (Environmental Protection Agency). 2008. Inte grated Science Assessment (IS A) for Oxides of Nitrogen and Sulfur–Ecological Criteria (Final Report). EPA/600/R-08/082F. U.S. Environmental Protection Agency, National Center for Environmental Assessment–RTP Division, Office of Research and Development, Research Triangle Park, NC. Available at http://cfpub.epa.gov/ncea/cfm/r ecordisplay.cfm?deid=201485

. U.S. Environmental Protection Agency. (2013) Integrated Science Assessment for Lead. Washington, DC, EPA/600/R-10/075F. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html6-1 

### 6 REVIEW OF THE SECOND ARY STANDARD FOR LEAD

This chapter presents staff conclusions regard ing the secondary Pb standard. These staff conclusions are guided by consid eration of key polic y-relevant questions and based on the assessment and integrative synthesis of informa tion presented in the ISA and by staff analyses and evaluations presented in ch apters 2 and 5 herein. These ev aluations and staff conclusions
have also taken into consideration CASAC advi ce and public comment on the draft PA and will
inform the Administrator’s decisions on whether to retain or revise the existing secondary
standard for Pb. Following an introductory section on the gene ral approach for reviewing the secondary standard (section 6.1), including a summary of considerations in th e last review, the discussion in this chapter focuses on whether th e information available in this review supports or calls into question the adequacy of the current secondary standard. Building on th e responses to specific policy-relevant questions on the scientific evidence and exposure-risk information in chapter 5, presentation in section 6.2 is al so organized into consideration of key policy-relevant questions framing evidence-based and exposur e/risk-based considerations. The policy-relevant questions
in this document are based on those included in th e IRP (IRP, section 3.2). Staff conclusions are reported in Section 6.3. Section 6.4 presents a brief overview of key uncertainties and areas for
future research.

6.1 APPROACH Staff’s approach for reviewing the current sec ondary standard takes into consideration the approaches used in the last Pb NAAQS revi ew and involves addressi ng key policy-relevant questions in light of currently available scientific and techni cal information. The past and current approaches described below are al l based most fundamentally on using EPA’s
assessment of the current scientific evidence and previous quantitative analyses to inform the Administrator’s judgment with regard to the seco ndary standard for Pb. In drawing conclusions for the Administrator’s consideration with regard to the secondary standard, we note that the final decision on the adequacy of the current s econdary Pb standard is largely a public welfare policy judgment to be made by the Administrator. The Administrator’s fi nal decision must draw upon scientific information and analyses about we lfare effects, exposure and risks, as well as judgments about the appropriate response to the ra nge of uncertainties that are inherent in the scientific evidence and analyses. This approach is consistent with the requirements of the NAAQS provisions of the Clean Air Act. Th ese provisions require the Administrator to establish a secondary standard that, in the judgment of the Administrator, is “requisite to protect the public welfare from any known or anticipated adverse effects asso ciated with the presence of6-2 the pollutant in the ambient air”. In so doing, th e Administrator seeks to establish standards that are neither more nor less stringent than necessary for this purpose.

6.1.1 Approach Used in the Last Review In the last review, completed in 2008, the current secondary st andard for Pb was set equal to the primary standard (73 FR 66964). As su mmarized in section 1.2.2 and described in more detail in section 4.1.1, the primary standard was substantially revise d in the last review based on the much-expanded health effects evidence of neuroc ognitive effects of Pb in children. The level of the revised NAAQS is 0.15 μg/m 3 . The averaging time was also revised to a rolling threemonth period with a maximum (not-to-be-exceede d) form, evaluated over a three-year period. Compared to the previous averaging time of one calendar quarter, this revi sion was considered to be more scientifically appropria te and more protective for human health. The indicator of PbTSP was retained, reflecting the evidence that Pb pa rticles of all sizes pose health risks (73 FR 67007). The 2008 decision considered the body of evidence as assessed in the 2006 CD (USEPA, 2006) as well as the 2007 Staff Paper as sessment of the policy-relevant information contained in the 2006 CD and the screening-le vel ecological risk as sessment (ICF, 2006; USEPA, 2007), the advice and recommendati ons of CASAC (Henderson 2007a, 2007b, 2008a, 2008b), and public comment. In the 2008 review, the Staff Paper conclude d, based on laboratory studies and current
media concentrations in a wide ra nge of locations, that it seemed likely that adverse effects were occurring, particularly near point sources, under the then-current standard (73 FR 67010). Given the limited data on Pb effects in ecosystems, and associated uncertainties, such as those with regard to factors such as the presence of multiple metals and historic environmental burdens, it was at the time, as it is now, necessary to look at evidence of Pb effects on organisms and extrapolate to ecosystem effects. Taking into account the available evidence and current media concentrations in a wide range of locations, the Administrator concluded th at there was potential for adverse effects occurring under the then-curre nt standard; however th ere were insufficient data to provide a quantitative basi s for setting a seconda ry standard different than the primary (73 FR 67011). Therefore, citing a general lack of data that would indicate the appropriate level of Pb in environmental media that may be asso ciated with adverse effects, as well as the comments of the CASAC Pb panel that a significan t change to current air concentrations (e.g., via a significant change to the standard) was likely to have significant be neficial effects on the magnitude of Pb exposures in the environment, the secondary standard was revised to be
consistent with the revised primary standard (73 FR 67011).6-3 6.1.2 Approach for the Current Review In evaluating whether it is appropriate to consider retaining the current secondary Pb standard, or whether considerati on of revision is appropriate, we have adopted an approach in this review that builds on the general approach from the last review and reflects the body of
evidence and information now available. As summ arized above, the Administrator’s decisions in the previous review were based on the conclu sion that there was the potential for adverse ecological effects under th e previous standard. In our appr oach here, we intend to focus on
consideration of the extent to which a broader body of scientific evidence is now available that
would inform decisions on either the potential for adverse effect s to ecosystems under the current standard or the ability to set a more ecologically relevant secondary standard than was feasible in the previous review. In conducti ng this assessment, we draw on the ecological effects evidence presented in detail in the ISA and aspects summarized above in chapter 5, along with the information associated with the screening-leve l risk assessment also summarized above. Figure
6-1 illustrates the basic construc t of our approach in developing conclusions regarding options appropriate for the Administrator to consider in this review with regard to the adequacy of the current secondary NAAQS standard and, as a ppropriate, potential alte rnate standards. In developing conclusions in this review, we have taken into account both evidencebased and risk-based considerations framed by a series of policy-relevant questions. These questions are outlined in the secti ons below and generally discuss the extent to which we are able
to better characterize effects and the likelihood of adverse eff ects in the environment under the current standard. Our approach to considering these questions recognizes that the available welfare effects evidence generally reflects labor atory-based evidence of toxicological effects on specific organisms exposed to concentrations of Pb. It is widely recognized, however, that environmental exposures from atmospherically derived Pb are likely to be lower and/or accompanied by significant confounding and modifyi ng factors (e.g., other metals, acidification), which increases our uncertainty about the like lihood and magnitude of organism and ecosystem

responses.6-4 Figure 6-1. Overview of approach for review of current secondary standard. Evidence-based Considerations

 Does currently available evidence and related uncertainties strengthen or call into question prior conclusions?

 Evidence of welfare effects not previously identified or at lower exposures?

 Newly identified at-risk ecosystems?

 Changed understanding of le ad bioavailability and movement of through ecosystems?

 Effects at lower air-related exposures than previously understood or in conditions that would have likely met current standard? Risk-based Considerations

 Nature, magnitude and importance of screening level risk information?  Uncertainties in the screening level risk assessment?

Consideration of Potential Alternative Standards Consider Retaining Current Standard

YES NO Adequacy of Current Standard

Does information call into question the adequacy of current standard?

Elements of Potential Alternative Standards  Indicator  Averaging Time  Form  Level

Potential Alternative Standards for Consideration6-5 6.2 ADEQUACY OF THE CURRENT STANDARD In considering the ade quacy of the current Pb standa rd, the overarching question we
consider is:

 Does the currently available scientific evidence- and exposure/risk-based information, as reflected in the ISA a nd REA, support or call into question the adequacy of the protection afforded by the current Pb standard?
To assist us in interpreting the currently av ailable scientific evidence and screening-level risk information to address this question, we have focused on a series of more specific questions, posed within sections 6.2.1 and 6.2.2 below. In so doing, we consider both the information
available at the time of the last review and in formation newly available since the last review which has been critically analyzed and characterized in the ISA.

6.2.1 Evidence-based Considerations In considering the welfare effects evidence wi th respect to the ade quacy of the current standard, we consider the array of evidence newly assessed in the ISA with regard to the degree to which this evidence supports conclusions about the effects of Pb in the environment that were
drawn in the last review and th e extent to which it reduces previously recognized areas of uncertainty. Further, we consider the current evidence and associated conclusions about the potential for effects to occur as a result of the much lower ambient Pb concentrations allowed by the current secondary standard (set in 2008) than those allowed by the pr ior standard, which was
the focus of the last review. These considera tions, discussed in the context of the specific questions below, inform our conclusions regardin g the extent to which the evidence supports or calls into question the ade quacy of protection afforded by the current standard.

 To what extent does the available informat ion indicate that Pb-related effects are occurring as a result of multimedia pa thways associated with ambient air conditions that would meet the current standard?

The current evidence continue s to support our conclusions from the previous review regarding key aspects of the eco logical effects evidence for Pb and the effects of exposure associated with levels of Pb occurring in ecologi cal media in the U.S. Our conclusions in this regard are based on consideration of the assessment of the currently available evidence in the ISA, particularly with regard to key aspects summ arized in chapter 5 of this PA, in light of the
assessment of the evidence in the last review as described in the 2006 CD and summarized in the notice of final rulemaking (73 FR 67008). Key asp ects of conclusions drawn in the last review (73 FR 67010) are summarized below.

 There are several difficulties to quantifying the role of recent air emissions of Pb in the
environment:6-6  While the removal of Pb from on-road gasoline and reducti ons in industrial
emissions have resulted in dramatic re ductions in overall deposition rates (2006 CD, pp. AX7-34 and AX7-103), Pb deposited before the 1978 standard, and the relatively lesser amount deposited since, is still present in soils and sediments.

 Historic Pb from gasoline-derived and othe r air emissions as well as nonair sources has produced a legacy of Pb in forest so ils that continues to move slowly through these systems (2006 CD, section AX7.1.4.3).

 The evidence of adversity in natural systems is very sparse due in no small part to the difficulty in determining the effects of c onfounding factors such as multiple metals or factors influencing bioavailability of Pb in field studies (2006 CD, E-19).

 For areas influenced by stationary sources of air Pb that met the st andard considered in
the last review at the time of the last review (although they likely did not throughout their active period), concentr ations of Pb in soil may exceed by many orders of magnitude the concentrations which are c onsidered harmful to laboratory organisms (2006 CD, sections 3.2 and AX7.1.2.3).

 Environmental conditions exist in which Pb-associated adverse effects to aquatic organisms and thereby ecosystems may be an ticipated given experimental results.
While the evidence does not indicate that di ssolved Pb in surface water constitutes a threat to those ecosystems that are not di rectly influenced by point sources, the evidence regarding Pb in sediment is less clea r. Some areas with long term historical deposition of Pb to sediment from a variet y of sources as well as areas influenced by point sources have the potential for adve rse effects to aquatic communities (2006 CD, sections AX7.2.2.2 and AX7.2.4).

The range of effects that Pb can exert on te rrestrial and aquatic organisms indicated by
information available in the current review is summarized in the ISA (ISA, sections 1.7, 6.3 and 6.4) and largely mirror the findings of from th e previous review (summarized above). The integrated synthesis contained in the ISA conveys how effects of Pb can vary with species and life stage, duration of exposure, form of Pb, a nd media characteristics such as soil and water chemistry. A wide range of organism effect s are recognized, includ ing effects on growth, development (particularly of th e neurological system) and repr oductive success (ISA, section 6.3 and 6.4). Lead is recognized to distribute from the air into multiple environmental media, as summarized in section 1.3 above, contributing to multiple exposure pathways for ecological receptors. As discussed in section 5.1 above, many factors affect the bioavailability of Pb to receptors in terrestrial and aqua tic ecosystems, contributing to differences between laboratory-6-7 assessed toxicity and Pb toxicity in these ecosystems, challenging our consideration of environmental impacts of Pb emitted to ambient air. In studies in a variety of ecosystems, adverse ecosystem-level effects (including decreases in species diversity, loss of vegeta tion, changes to community composition, primarily in soil microbes and plants, decreased growth of vegetation, and increase d number of invasive species) have been demonstrated near smelters, mines and other industries that have released substantial amounts of Pb, among other materials, to the environment (ISA, sections 6.3.12 and 6.4.12). As noted in section 5.1 above, however, our ability to characte rize the role of air emissions of Pb in contributing to these effects is complicated because of coincident releases to other media and of other pollutants. Co-releas ed pollutants include a variety of other heavy metals, in addition to sulfur dioxide, which ma y cause toxic effects in themselves and may
interact with Pb in the environm ent, contributing uncertainty to ch aracterization of the role of Pb from ambient air with regard to the reported eff ects. These uncertainties limit our ability to draw conclusions regarding the extent to which Pb-related effects may be associated with ambient air
conditions that would meet the current standard. The role of historically em itted Pb, as discussed in section 1.3.2 above, poses additional complications in addressing this question. The va st majority of Pb in the U.S. environment today, particularly in terrestrial ecosystems, wa s deposited in the past during the use of Pb additives in gasoline (2006 CD, pp. 2-82, AX7- 36 to AX7-38, AX7-98; Johnson et al., 2004), although contributions from industrial activities, including metals industr ies have also been documented ( ISA, section 2.2.2.3, Jackson et al., 2004). The gasoline-derived Pb was emitted in very large quantities (2006 CD, p. AX7-98 and ISA, Figure 2-8) and predominantly in small sized particles which were widely dispersed a nd transported across large distances, within and beyond the U.S. (ISA, section 2.2). As recogni zed in sections 2.3.1 and 2.3.3.2 above, historical records provided by sediment cores in various environments document th e substantially reduced Pb deposition (associated with reduced Pb emi ssions) in many locations (ISA, section 2.2.1). As Pb is persistent in the environment, these substa ntial past environmental re leases are expected to generally dominate current nonair media concentrations. There is limited evidence to relate specific ecosystem effects with current ambient air concentrations of Pb through deposition to terrestrial and aquatic ecosystems and subs equent movement of deposited Pb through the environment (e.g., soil, sediment, water, organism s). The potential for ecosystem effects of Pb from atmospheric sources under conditions meeting the current standard is difficult to assess due to limitations on the availability of information to fully characterize the distribution of Pb from the atmosphere into ecosystems over the long te rm, as well as limitations on information on the bioavailability of atmospherically deposited Pb (as affected by the specific characteristics of the receiving ecosystem). Therefore, while info rmation available since the 2006 CD includes6-8 additional terrestrial and aquati c field studies, “the connection between air concentration and ecosystem exposure and associated potential for welfare effects co ntinues to be poorly characterized for Pb” (ISA, section 6.5). Such a c onnection is even harder to characterize with respect to the current standard than it was in th e last review with respect to the previous, much higher, standard.

 To what extent have important uncertaint ies identified in the last review been reduced and/or have new uncertainties emerged?

In the characterization of effects associated w ith Pb in ambient air for the last review, the areas of largest uncertainty were identified to be associated with our abilities to determine the
extent of lead-related effects in the natural environment and to apportion effects between air and nonair sources, and with the relationship be tween effects and environmental conditions
associated with the standard. While we have so me new evidence with regard to bioavailability and its role in influencing the pot ential for effects in the environment, overall these remain the major sources of uncertainty in our evaluati on of effects and exposure evidence for Pb in ecosystems. Moreover, the impact of these uncer tainties is larger in this review given our current focus on a secondary standard much lowe r than that which was the focus of the last
review. With regard to the extent of lead-related effects in the natural environment, it remains difficult to assess the concentrations at which Pb elicits specific effects in terrestrial and aquatic systems, due to the influence of other envir onmental variables on both Pb bioavailability and toxicity and also due to substa ntial species differences in Pb susceptibility (ISA, sections 6.3.2- 6.3.4 and 6.4.2 -6.4.5). There is little new informati on that would facilitate extrapolation of evidence on individual species, ge nerally from controlled labora tory studies, to conclusions regarding adversity to populations or ecosystems within the natura l environment. For example, in terrestrial systems, evidence reviewed in th e ISA (ISA, sections 6.2.3 and 6.2.4) demonstrates that exposure to Pb is generally associated with negative effects on growth, reproduction and survival in terrestrial ecosyste ms. Many factors, including speci es composition and various soil physiochemical properties, interact strongly with Pb concentration to modify effects. Also, the changes associated with environm ental aging of lead-contaminated material is a particularly important factor in terrestrial systems, where so il is the main route of exposure, however, aging
of lead-contaminated soil is difficult to re produce experimentally (ISA, sections 6.3.9.3 and 6.3.11). Without quantitatively accounting for these factors, laboratory-derived “characterizations of exposure-resp onse relationships would likely not be transferable outside of experimental settings” (ISA, p. 1-42). With regard to the role of air-related Pb, as discussed above and noted in the ISA, “the
connection between air concen tration and ecosystem exposures continues to be poorly6-9 characterized for Pb and the contri bution of atmospheric Pb to speci fic sites is not clear” (ISA, p. 6-264). Thus, the limited evidence and associated uncertainties connecting air concentrations to ecosystem exposures and possible effects, in combination with those that influence Pb bioavailability and ecosystem mobility, are areas pa rticularly limiting the exte nt to which critical loads analyses might otherwise be useful to our a ssessment in this review, as discussed in section 5.1. Thus, the evidence is lacking in quantitativ e relationships between Pb in ambient air and welfare effects, including identification of a specific exposure metric or index (e.g., mathematical formulation of averaging time and c oncentration) by which to consider ambient air Pb concentrations with regard to the potential for adverse effects to public welfare. In the decision in the last review to set the secondary standard equal to the primary standard, EPA similarly recognized a lack of evid ence that related welfare effects to Pb in ambient air and from which differing standard elements (e.g., averagin g time and concentration) might be derived for the secondary standard. 1 These limitations in the evidence base remain in the current review. As in the last review, consideration of th e environmental risks and potential welfare
effects associated with the current standard is complicated by the environmental burden associated with air Pb concentrations, predom inantly in the past, that exceeded both the previously existing standard and the curre nt standard (USEPA, 2007, section 6.4.4.2). For example, a large portion of Pb deposited before th e current standard was enacted is likely still present in soils and sediments, and historic Pb from gasoline (and othe r historic sources) continues to move slowly th rough systems as does Pb derived from current air and nonair sources. As a general matter, the currently availa ble evidence, as assessed in the ISA, does not significantly reduce any of the ar eas of uncertainty described he re which, given the standard considered in the present review (with its much lower level than the previous standard), weigh heavily in our consideration of the adequacy of the current standard.

6.2.2 Exposure/Risk-based Considerations

 To what extent does risk or exposure information indicate that air-related ecosystem exposures important from a pub lic welfare perspective are likely to occur with air Pb levels that just meet the current standard?

The current evidence continues to support our conclusions with regard to interpreting the risk and exposure results from the previous revi ew. Our conclusions in this regard are based on

1 As described in section 6.1.1 above, the EPA concluded in the last review that the then-current secondary standard did not provide requisite protection from effects adverse to public welfare. In considering the appropriate revision, EPA recognized that the Agency lacked the rele vant data to provide a clear quantitative basis for setting a secondary Pb NAAQS that differs from the primary standard, yet recognized that signifi cant beneficial effects were likely to result in terms of reduced magnitude of Pb exposur es in the environment and asso ciated toxicity impacts on ecosystems from a significant change to the level for the seco ndary standard, such as the order-of-magnitude change which was achieved by setting the secondary standard iden tical to the revised primary standard (73 FR 67012).6-10 consideration of the scre ening-level ecological risk assessment results from the previous review
as described in the 2006 REA and summarized in the notice of final rulemaking (73 FR 67009) and in light of the currently available evidence in the ISA. Key aspects of these results in the
context of the current standard are summarized below, drawing from the discussion of the 2006 REA results in section 5.2.2 above, which is based on the information in the 2006 REA (ICF, 2006). Primary Pb Smelter Case Study

 While the contribution to Pb concentrations from air as compared to nonair sources is not quantified, air emissions from this fac ility are substantial (ICF, 2006). Currently, the county where this facility is loca ted exceeds the now-current Pb NAAQS.
Secondary Pb Smelter Case Study

 While the contribution from air deposited Pb to the overall Pb concentrations modeled in soils at this location is unclear, the f acility continues to emit Pb and the county where this facility is located exceeds the now-current Pb NAAQS (Appendices 2D and 5A).
Near Roadway Non-urban Case Study

 These case study locations are highly impacted by past deposition of gasoline Pb. It is unknown whether current conditions at these si tes exceed the now-current Pb standard, but given evidence from the past of Pb con centrations near highways that ranged above the previous (1978) Pb standard (1986 CD, section 7.2.1), conditions at these locations during the time of leaded gasoline very likely exceeded the 1978 standard.
Vulnerable Ecosystem Case Study

 The previous review concluded that atmospheri c Pb inputs do not dir ectly affect stream Pb levels at Hubbard Brook Experimental Forest because deposited Pb is almost entirely retained in the soil profile and that there was “little eviden ce that sites affected primarily by long-range Pb tr ansport [such as this one] ha ve experienced significant effects on ecosystem structure or functi on” (2006 CD, p. AX-98). Further, it is unlikely that conditions have changed from the data through 2000 on which the previous conclusions were based, and, theref ore, current ambient air concentrations likely do not directly impact stream Pb leve ls under air quality conditions associated with meeting the now-current standard.
National-scale Surface Water and Sediment Screen

 The extent to which past air emissions of Pb have contributed to surface water or sediment Pb concentrations at the locations identified in the screen is unclear. For some of the surface water loca tions, nonair sources likely contributed significantly to the surface water Pb concentrations. For other locations, a lack of nearby nonair sources indicated a potential role for air so urces to contribute to observed surface water Pb concentrations. Additionally, these concentrations may have been influenced by Pb6-11 in resuspended sediments and/or reflect contribution of Pb from erosion of soils with Pb derived from historic as well as current air emissions.
Although the available risk a nd exposure information continues to be sufficient to
conclude that the 1978 standard was not providing adequate pr otection to ecosystems, that information, when considered with regard to air-r elated ecosystem exposures likely to occur with air Pb levels that just meet the now-current standard, does not provide evidence that the current secondary standard (set in 2008) is inadequate.

6.2.3 CASAC Advice In our consideration of the adequacy of the cu rrent standards, in a ddition to the evidenceand risk/exposure-based informa tion discussed above, we have al so considered the advice and recommendations of CASAC, based on their review of the ISA and the earlier draft of this document. Comments from the public on earlier drafts of this document did not address the adequacy of the current secondary standard. 2 In their advice and comments conveyed in the c ontext of their review of the draft PA, the CASAC agreed with staff’s preliminary conclusions that the available information since the last
review is not sufficient to wa rrant revision to the secondary standard (Frey, 2013). On this subject, the CASAC letter said the following.
Overall, the CASAC concurs with the EPA t hat the current scientific literature does not support a revision to the Pr imary Lead (Pb) National Ambient Air quality Standard (NAAQS) nor the Secondary Pb NAAQS. The CASAC also recognized the many uncertainties a nd data gaps in the new scientific literature and recommended that research be performed in the future to address these limitations. Given the existing scientific data, the CA SAC concurs with retaining the current secondary standard without revision. However, the CASAC also notes that important research gaps remain. For exa mple questions remain regarding the relevance of the primary standard’s indicato r, level, averaging time, and form for the secondary standard. Other areas for addi tional research to address data gaps and uncertainty include developing a crit ical loads approach for U.S. conditions and a multi-media approach to account for legacy Pb and contributions from different sources. Addressing these gaps may require reconsideration of the secondary standard in future assessments.

2 All written comments submitted to the Agency will be av ailable in the docket for this rulemaking, as will be transcripts of the public meetings held in conjunction wi th CASAC’s review of the earlier draft of this document, of the REA Planning Document and of drafts of the ISA.6-12 6.3 STAFF CONCLUSIONS ON THE SECONDARY STANDARD This section describes staff conclusions rega rding adequacy of the current secondary Pb
standard. These conclusions are based on consid erations described abov e and in the discussion below regarding the currently available scientific evidence summarized in the ISA and prior CDs and the risk and exposure information drawn from the 2006 REA. These conclusions also take into account advice from CASAC and public comment on the draft PA and preliminary
conclusions. Taking into consideration the discussions res ponding to specific ques tions above in this and the prior chapter, this section addre sses the following overar ching policy question:

 Does the currently available scientific evidence- and exposure/risk-based information, as reflected in the ISA a nd REA, support or call into question the adequacy of the protection afforded by the current secondary Pb standard?
With respect to evidence-based considerat ions, the body of eviden ce on the ecological effects of Pb, expanded in some aspects since th e last review, continues to support identification of ecological effects in organisms relating to growth, reproduction, and survival as the most relevant endpoints associated with Pb exposure. In consideration of the appreciable influence of site-specific environmental characteristics on the bi oavailability and toxicity of environmental Pb in our assessment here, we give greater weig ht to studies conducte d under conditions most closely reflecting the natural environment as compared to laboratory-based exposures. The currently available evidence, while somewhat e xpanded since the last review, does not include evidence of significant effects at lower concentr ations or evidence of higher level ecosystem effects beyond those reported in the last review. There continue to be significant difficulties in interpreting effects evidence from laboratory stud ies to the natural environment and linking those
effects to ambient air Pb concentrations. Fu rther, we are aware of no new critical loads information that would inform our interpretation of the public welfare sign ificance of the effects of Pb in various ecosystems (as discussed in section 5.1). In summary, while new research has added to the understanding of Pb biogeochemistry and expanded the list of organisms for which Pb effects have been described, there remains a significant lack of knowledge about the potential for adverse effects on public welfare from ambien t air Pb in the environment and the exposures that occur from such air-derived Pb, pa rticularly under the current standard. With respect to exposure/risk-based consid erations, we recogni ze the complexity of interpreting the previous risk assessment with regard to th e ecological risk of ambient air Pb associated with conditions meeting the curren t standard and the associated limitations and uncertainties of such assessments. For example, the location-specific case studies as well as the
national screen conducted in the last review reflect both current air Pb deposition as well as past
air and nonair source contributi ons. We conclude that whil e the previous assessment is6-13 consistent with and generally supportive of th e evidence-based conclusions about Pb in the environment, the limitations of apportioning Pb between past and presen t air contributions and
between air and nonair sour ces remain significant. In now considering the adequacy of the cu rrent standard in this review, we have considered the ecological and welfare effects ev idence assessed in the ISA and discussed in sections 5.1, 2.3 and 6.2.1 above, as well screening-le vel exposure;/risk information gained from
the 2006 REA discussed in sections 5.2 and 6.2.2 above, and staff judgments on associated implications with regard to public welfare. As summarized, in section 6.2 .1 above, the scientific evidence presented in detail in the ISA, inclusive of that newly available in this review, is not substantively changed, most particularly with regard to our needs in reviewing the current standard, from the information that was available in the last review. The evidence base does not
indicate that the current standa rd is inadequate. Further, our updated consideration of the screening-level risk informa tion from the 2006 REA, as summarized in section 6.2.2 above, additionally does not provide eviden ce that the current secondary st andard is inadequate. Thus, we conclude that the currently available evidence and exposure/ri sk information do not call into question the adequacy of the current standard to provide the requisite protection for public welfare. Accordingly, we reach the conclusion that it is approp riate to consider retaining the current secondary standa rd without revision.

6.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND DATA COLLECTION

In this section, we highlight key uncertainties associated with reviewing the secondary NAAQS for Pb. Such key uncertainties and re commendations for ecosystem-related research, model development, and data gath ering are outlined below. In some cases, research in these areas can go beyond supporting standa rd setting to aiding in the development of more efficient and effective control strategies. We note, however, that a full set of research recommendations to meet standards implementation and strategy development needs is beyond the scope of this discussion. Rather, listed below are key uncertainties and research questions and data gaps that have been thus far highlighted in this review of the welfare-based sec ondary standard for Pb.

 Our understanding of the extent and degree of adverse impact occurring in the environment due to Pb (from atmospheric and other sources) is incomplete and leads to uncertainty in characterizing environmental e ffects of Pb, which is necessary to assess potential associated eff ects on public welfare.

 The available studies on community and ecosystem-level effects are sparse and usually from contaminated areas where Pb concentrations are much higher than typically encountered in th e environment as a result of atmospheric input and are usually co-occurring with elevated concentrations of other pollutants.6-14  Many ecosystem-specific characteristics a ffect bioavailability and associated toxicity, contributing uncerta inty to our interpretati on of study results from laboratory test-systems. For example, the ro le of modifying factors such as soil and water chemistry on Pb toxicity continue s to be a source of uncertainty when determining the degree of adverse impact from Pb. 3

 Evidence regarding relationships between organism-level effects of Pb (e.g., reproduction, growth, and survival) and effects at the populat ion level and higher is lacking especially in natural systems.

 A better understanding of the potential for a dverse effects from Pb in estuarine and marine systems is needed.

 There is appreciable uncertainty in our unders tanding of the current dynamics of Pb in U.S. ecosystems.

 In general, the connection between air c oncentration of Pb and ecosystem exposure continues to be poorly charac terized and is complicated by the legacy of historical inputs both from air and, in some systems, also from other sources.

 There is uncertainty in characterizing the fate and transport of Pb in the environment through air, water, and soil media. This limits our ability to account for the role of past Pb releases in current media concentrations and to link effects to current air contributions.

 An important source of uncertainty in charac terizing the effects of air-related Pb in some U.S. ecosystems is that associated with distinguishing air-related Pb from other sources of Pb. It is difficult to dete rmine the portion of Pb occurring in some ecosystems that derives from the atmosphe re as compared to that from other

sources.

 Development of critical loads informati on for U.S. ecosystems would allow for a much improved understanding of the significan ce of air contributi ons to ecosystems and ecological receptor exposures, as well as that of contribu tions from other sources. Development of a critical loads approac h, with sensitivity analysis, would inform identification of processes critical to eco logical receptor exposu res and toxicity.

 Such critical loads analyses could inform characterization of the variability of response across ecosystems to determine which ecosystems are most sensitive.

 Additional research is needed to provide inputs for deve lopment of critical loads, particularly for a broader range of ecosystem-level endpoints.

 Information is currently lacking to inform id entification of standard elements, such as averaging time and form, specifically re flecting a ecological and public welfare context for ambient air Pb.

3 Further uncertainty accompanies the interpretation of t oxicity data from test systems involving artificial media such as hydroponic system s, agar or culture media.6-15 6.5 REFERENCES

Frey, H.C. (2013) Letter from Dr. H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee and Clean Air Scientific Advisory Committee Lead Review Pane l, to Acting Administrator Bob Perciasepe. Re: CASAC Review of the EPA’s Policy Assessment for Lead (External Review Draft – January 2013). June 4, 2013.

Henderson, R. (2007a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of the 1st Draft Lead Staff Paper and Draft Lead Exposure and Risk Assessments. March 27, 2007.

Henderson, R. (2007b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of the 2nd Draft Lead Human Expo sure and Health Risk Assessments. September 27, 2007.

Henderson, R. (2008a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of the Advance Notice of Proposed Rulemaking (ANPR) for the NAAQS for lead. January 22, 2008.

Henderson, R. (2008b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of the Notice of Proposed Rulemaking for the NAAQS for lead. July 18, 2008.

ICF International. (2006) Lead Human Exposure and Hea lth Risk Assessments and Ec ological Risk Assessment for Selected Areas. Pilot Phase. Draft Technical Report. Prepared for the U.S. EP A's Office of Air Quality Planning and Standards, Research Triangle Park, NC. December.

Jackson, B. P.; Winger, P. V.; Lasier, P. J. (2004) At mospheric lead deposition to Okefenokee Swamp, Georgia, USA. Environ. Pollut. 130: 445-451.

Johnson, C. E.; Petras, R. J.; April, R. H.; Siccama, T. G. (2004) Post-glacial lead dynamics in a forest soil. Water Air Soil Pollut. 4: 579-590.

U.S. Environmental Protection Agency. (2006) Air Quality Criteria for Lead. Referred to as 2006 CD. Washington, DC, EPA/600/R-5/144aF. Available online at: http:// www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr.html

U.S. Environmental Protection Agency. (2007). Review of the National Ambient Air Quality Standards for Lead:Policy Assessment of Scientific and Technical Information OAQPS Staff Paper. Washington, DC, EPA452/R-07-013. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr.html

U.S. Environmental Protection Agency. (2013) Integrated Science Assessment for Lead. Referred to as ISA

. Washington, DC,. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.htmlThis page is intentionally blank

### APPENDICES

Appendix 2A. Recent Regulatory Actions on Stationary Sources of Lead ............................ 2A-1 Appendix 2B. The 2008 NEI: Data Sour ces, Limitations and Confidence ........................... 2B-1 Appendix 2C. Criteria for Air Quality Data Analysis ............................................................ 2C-1 Appendix 2D. Air Quality Data Analysis Summary .............................................................. 2D-1 Appendix 3A. Interpolated Risk Estimates for the Generalized (Local) Urban Case Study .. 3A-1 Appendix 5A. Additional Detail on 2006 Ec ological Screening Assessment ........................ 5A-12A-1 

### APPENDIX 2A

RECENT REGULATORY ACTIONS ON STATIONARY SOURCES OF LEAD

The table below identifies recent actions projec ted to result in reductions in Pb emissions from stationary sources.

Action Source Categories Affected Citation Estimated Pb Emissions Reduction

(tons per

year) Year of Compliance (year in which

reductions estimated to begin)
NESHAP Secondary Lead Smelting 77 FR 555 (1/5/2012) 13.6 2014

NESHAP Primary Lead Smelting 76 FR 70834 (11/15/2011) 10 2013

NESHAP Area Sources: Clay Ceramics Manufacturing, Glass Manufacturing, and Secondary Nonferrous Metals Processing 72 FR 73179 (12/26/2007) Unquantified* 2007, 2009, 2007

NESHAP Area Sources: Electric Arc Furnace Steelmaking Facilities 72 FR 74088 (12/28/2007) Unquantified* 2008 or 2010

NESHAP Iron and Steel Foundries Area Sources 73 FR 225 (1/2/2008) Unquantified* 2010

NESHAP Area Source Standards for Aluminum, Copper, and Other Nonferrous Foundries 74 FR 30366 (6/25/2009) Unquantified* 2011
NESHAP, NSPS Portland Cement Manufacturing Industry 78 FR 10006 (2/12/2013) 6.72 2015
EGES, NSPS Commercial and Industrial Solid Waste Incineration Units 76 FR 9112 (02/07/2013) 2.51 2018

EGES, NSPS Standards of Performance for New Stationary Sources and Emission Guidelines for Existing Sources: Sewage Sludge Incineration Units 76 FR 15372 (3/21/2011) 1.2-1.5 2016

NESHAP Major Sources: Industrial, Commercial, and Institutional Boilers, and Process Heaters 78 FR 7138 (1/31/2013) Unquantified* 2016

EGES, NSPS Standards of Performance for New Stationary Sources and Emissions Guidelines for Existing Sources: Hospital/Medical/Infectious Waste Incinerators 74 FR 51367 (10/6/2009) 0.16 2014

EGES = Emissions Guidelines for Existing Sources NESHAP = National Emission Standards for Hazardous Air Pollutants NSPS = New Source Performance Standards *Unquantified = Reductions in Pb emissions expected from cont rols in response to regulatory action have not been quantified.2B-1 

### APPENDIX 2B

THE 2008 NEI: DATA SOUR CES, LIMITATIONS AND CONFIDENCE

The process of identifying sour ces that emit Pb into the ai r has been ongoing since before the Clean Air Act of 1970. The comprehensivene ss of emission inventories generally, and the NEI, specifically, depends upon knowledge of sour ce types emit Pb, their locations and their operating characteristics, as well as the reporting of this informa tion to the inventory. As noted above, the NEI relies on information that is av ailable from a variety of sources for this information. There are numerous steps, each with its own uncertainties, associated with the development of this information for use in the em issions inventory. First, the categories emitting Pb must be identified. Second, the sources’ pr ocesses and control devices must be known. Third, the activity throughputs and operating schedules of these s ources must be known. Finally,
we must have emission factors to relate em issions to the operati ng throughputs, process conditions and control devices. The proce ss, control device, throughputs and operating schedules are generally available for each sour ce. However, the emission factors represent average emissions for a source type and average emissions may differ significantly from source to source. In some cases, emissions testing pr ovides source-specific information. In others,
emissions factors must be estimated from simila r sources or source categories, or from other
information. More information on emission factor s and the estimation of emissions is found in the introduction to EPA’s Compilation of Air Pollutant Emissions Factors. 1 The Pb emissions information presented in chapter 2 is drawn largely from EPA’s NEI
for 2008. The NEI is based on information submitte d from State, Tribal and local air pollution agencies and data obtained during the prepara tion of technical support information for EPA’s hazardous air pollutant regulatory programs. Data in the 2008 NEI for Pb emissions from the use of leaded aviation gasoline were deve loped by EPA using the Federal Aviation Administration’s operations act ivity data, where available. 2 The data were then reviewed by State, Tribal, and local air pollution agencies. W ith some additions, the information presented in this document is primarily based on version 3 of the NEI for 2008, available on the EPA’s CHIEF website at ( http://www.epa.gov /ttn/chief/net/2008 inventory.html ). The NEI is limited

1 U.S. Environmental Protection Agency. (1996-2011) . AP-42, Compilation of Air Pollutant Emission Factors, 5th Edition. Volume 1: Stationary Point and Area Sources, Chapter 13: Miscellaneous Sources. Available
at: http://www.epa.gov/ttn/chief/ap42/ch13/index.html . Further information on emissi on factors is available at: http://www.epa.gov/ttn/chief/ap42/

2 Eastern Research Group (ERG), 2011a. Project report: Documentation for Aircraft Component of the National Emissions Inventory Methodology, ERG No. 0245.03.402.011, January 27, 2011.2B-2 with regard to Pb emissions estimates for so me sources. For example, we have not yet developed estimates for the NEI of Pb emissions for the miscellaneous categories of on-road emissions (e.g., combustion of fuel with Pb traces, lubricating oil, mechanical wear of vehicle components, etc.) and Pb that may be emitted from wildfires, or for emissions associated with resuspension of Pb residing in roadway dust a nd nearby surface soil in areas not otherwise
associated with industrial f acilities (see section 2.1.2).
The 2008 NEI underwent extensive external review , including a review of the process for developing the inventory which in cludes extensive quality assurance and quality control steps (QA/QC). We provided feedback reports to point source data providers and we posted several versions of the inventory on our website. We also conducted additional QA targeted at facilities with appreciable Pb emissions in previous year s to ensure that 2008 Pb emissions were reported, and we augmented with TRI where facilities w ith annual emissions greater than 0.5 tpy in 2005 were not reported to NEI in 2008 due to Pb emissions reporting thresholds (ftp://ftp.epa.gov/EmisInventor y/20008v2/doc/2008neiv2_issues.xlsx ). Further, there was additional QA/QC conducted for emission inventor y information for facilities that are included in Risk and Technology Re view source categories. 3 As a result we have strong confidence in the quality of the data for these f acilities. In summary, generic limitations to the 2008 NEI include the following.

 Consistency: The 2008 NEI for Pb is a com posite of emissions estimates generated by state and local regulatory agencies, in dustry, and EPA. Because the estimates originated from a variety of sources, as well as for differing purposes, they will in turn vary in quality, whether Pb is reported for particular so urce types, method of reporting compound classes, level of deta il, and geographic coverage.

 Variability in Quality and Accuracy of Em ission Estimation Methods: The accuracy of emission estimation techniques varies with pol lutants and source categories. In some cases, an estimate may be based on a fe w or only one emission measurement at a similar source. The techniques used and qua lity of the estimates will vary between source categories and between area, major, and mobile source sectors. Generally, the more review and scrutiny given to emissi ons data by states and other agencies, the more certainty and accuracy there is in those estimates.

3 The Risk and Technology Review is a combined effort to evaluate both risk and technology as required by the Clean Air Act (CAA) after the application of maximum achievable control technology (MACT) standards. Section 112(f)(2) of the CAA directs EPA to conduct ri sk assessments on each source category subject to MACT standards, and to determine if additional standards are need ed to reduce residual risks. Section 112(d)(6) of the CAA requires EPA to review and revise the MACT standard s, as necessary, taking in to account developments in practices, processes and control tech nologies. For more information: http://www.epa.gov/ttn/atw/rrisk/rtrpg.html

.2C-1 

### APPENDIX 2C
CRITERIA FOR AIR QUALITY DATA ANALYSIS

Criteria for the 2010-2012 data analysis pres ented in Figures 2-10 through 2-13 are as listed below, with abbreviations defined following this list.

 Years utilized were 2010-2012. November and December 2009 data were also used for the rolling 3-month average analysis.

 Data were extracted from EPA’s Ai r Quality System in June of 2013.

 Data for parameter 14129 (Pb-TSP FRM/FEM LC) were used for Pb-TSP analysis; data for parameters 84128 (Pb-PM 2.5 STP) and 88128 (Pb-PM 2.5 LC) were used for PbPM2.5 analysis; and data for parameters 82128 (Pb-PM 10 STP), 85128 (Pb-PM 10 LC), and 85129 (Pb-PM 10 FRM/FEM LC) were used for Pb-PM10 analysis. No adjustment was made to the STP or LC data to make th em more comparable to each other; based on previous analysis, the LC and STP versi ons of same-site-day samples are extremely similar. Collocated data – for same size cut- were combined to a site basis by using the following hierarchy, evaluated each site-d ay: LC FRM/FEM parameter data takes precedence over LC (non-FRM/FEM) paramete r data, and those data take precedence overSTP parameter data; also, within thos e categories, lower POC numbers take precedence over higher POC numbers.

 For maximum rolling 3-month average an alysis, the 2010-2012 databases also encompassed the prior 2 months (i.e., November and December 2009 data): 3 or more observations were needed to make a valid monthly; 3 valid consecutive months were required to make a valid rolling 3-month pe riod; 6 valid rolling 3-month periods were required to make a valid year; and 1, 2, or 3 valid years were requi red to make a valid 3-year metric. Thus, the shortest duration th at could potentially meet these criteria for the maximum 3-month average analysis is 8 months. The 3-year maximum rolling 3- month average metric (by size cut for 2010-2012 ) was identified as the highest valid 3- month average across the valid (1, 2, or 3) years.

 For maximum monthly analysis: 3 or more obs ervations were needed to make a valid monthly; 6 valid months were required to make a valid year; and 1, 2, or 3 valid years were required to make a valid 3-year metr ic. Thus, the shortest duration that could potentially meet these criteria for the maxi mum monthly analysis is 6 months. The 3- year maximum monthly metric (by size cu t for 2010-2012) was identified as the highest valid monthly average across the valid (1, 2, or 3) years.

 For annual average analysis: monthly aver ages were used to construct annual averages,3 or more observations were require d to make a valid; 6 valid months were required to make a valid year (i.e., annual average) and 1, 2, or 3 valid years were required to make a valid annual metric. Thus, the shortest duration that could potentially meet these criteria for the annual average analysis is 6 months. The 3-year annual mean metric (by size cut for 2010-2012) was identified as the average of the 1, 2, or 3 (2010, 2011, and/or 2012) valid annual means.2C-2 Definitions for Abbreviations FEM – Federal equivalent method

FRM – Federal reference method

LC – Local conditions

POC – Parameter occurrence code STP – Standard temperature and pressure

The process for classifying monitors as “sour ce oriented” or “non-s ource-oriented” began with the application of these criteria: (a) a minimum of 0.5 cumulative tons per year of Pb emissions within 1 mile of the monitoring site based on 2008 NEI and/or (b) monitors identified as “source-oriented” within AQS based on the sa me-name Monitoring Objective tag. Next, the Regional monitoring leads reviewed the listings and provided local, and often monitor-specific information and lastly Google Earth and more focused queries were applied. The 14 monitors sited for the airport monito ring study, along with the 3 monitors sited at airports estimated to emit at least 1 tpy were clas sified as source-oriented (airport) sites and the remaining source-oriented sites were classified as source-o riented (non-airport) sites. Among the remaining sites that were not classi fied as “source-oriented”, previous sourceoriented sites were those that had previously been active source sites but for which current information indicated the impacting facility had closed. The particular circumstances related to
the emission sources associated with these nine monitoring sites vary considerably. In some
instances the emission sources have been closed fo r more than a decade and the facility locations have undergone remediation. For other sources, production and clean-up status was not fully
ascertained.
Non-source sites were what was left after making the airport sour ce-oriented, non-airport source-oriented, and previous source-oriented designations.

### APPENDIX 2D

State County Site Maximum 3

- month

mean (μg/m 3 ) Annual average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) Non-airport

sourceoriented (during 2010- 2012) Airport

sourceoriented Previous

sourceoriented

Alabama Limestone 010830005 0.009 0.007 0.012 0 1 0
Alabama Pike 011090003 1.296 0.613 2.262 1 0 0
Alaska A nchorage Municipal i 020200051 0.067 0.054 0.073 0 1 0 Arizona Gila 040071002 0.267 0.131 0.306 1 0 0
Arizona Gila 040078000 0.061 0.030 0.077 1 0 0 Arizona Maricopa 040134018 0.038 0.031 0.049 0 1 0
Arizona Pima 040191028 0.002 0.002 0.003 0 0 0
California Fresno 060190011 0.005 0.004 0.005 0 0 0 California Imperial 060250005 0.026 0.017 0.031 0 0 0 California Los Angeles 060371103 0.013 0.009 0.014 0 0 0 California Los Angeles 060371302 0.015 0.007 0.014 0 0 0 California Los Angeles 060371402 0.061 0.033 0.092 0 1 0 California Los Angeles 060371403 0.110 0.055 0.124 1 0 0 California Los Angeles 060371404 0.108 0.042 0.140 1 0 0 California Los Angeles 060371405 0.450 0.241 0.523 1 0 0 California Los Angeles 060371406 0.072 0.035 0.085 1 0 0 California Los Angeles 060371602 0.013 0.008 0.017 0 0 0 California Los Angeles 060374002 0.009 0.005 0.010 0 0 0 California Los Angeles 060374004 0.010 0.006 0.010 0 0 0 California Los Angeles 060375005 0.006 0.003 0.008 0 0 0
California Riverside 060651003 0.008 0.005 0.010 0 0 0
California Riverside 060658001 0.008 0.006 0.010 0 0 0
California San Bernardino 060711004 0.010 0.006 0.012 0 0 0
California San Bernardino 060719004 0.011 0.007 0.013 0 0 0 California San Diego 060730003 0.006 0.005 0.007 0 0 0 California San Diego 060731020 0.127 0.234 0 1 0 California San Diego 060731021 0.058 0.074 0 1 0
California San Mateo 060812002 0.331 0.255 0.401 0 1 0
California Santa Clara 060852010 0.119 0.090 0.151 0 1 0
California Santa Clara 060852011 0.093 0.070 0.102 0 1 0 Colorado Arapahoe 080050007 0.023 0.014 0.035 0 1 0 Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2010-2012.

2D - 1

### APPENDIX 2D

State County Site Maximum 3

- month

mean (μg/m 3 ) Annual average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) Non-airport

sourceoriented (during 2010- 2012) Airport

sourceoriented Previous

sourceoriented Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2010-2012.

Colorado Denver 080310025 0.010 0.006 0.013 0 0 0
District of Colum b

District of Columbia 110010043 0.004 0.003 0.005 0 0 0 Florida Hillsborough 120570100 0.044 0.025 0.100 1 0 0 Florida Hillsborough 120571066 0.984 0.374 1.959 1 0 0 Florida Hillsborough 120571073 0.423 0.151 0.977 1 0 0 Georgia Bartow 130150003 0.027 0.015 0.039 1 0 0 Georgia DeKalb 130890003 0.004 0.003 0.006 0 0 0 Georgia Muscogee 132150009 0.230 0.128 0.424 1 0 0 Georgia Muscogee 132150010 0.170 0.114 0.234 1 0 0 Georgia Muscogee 132150011 0.071 0.023 0.140 0 0 1
Hawaii Honolulu 150030010 0.001 0.001 0.001 0 0 0
Illinois Cook 170310001 0.024 0.018 0.028 0 0 0
Illinois Cook 170310022 0.047 0.034 0.064 0 0 0
Illinois Cook 170310026 0.034 0.023 0.038 0 0 0
Illinois Cook 170310052 0.024 0.017 0.032 0 0 0
Illinois Cook 170310110 0.294 0.077 0.580 1 0 0
Illinois Cook 170310210 0.053 0.032 0.092 1 0 0
Illinois Cook 170313103 0.041 0.014 0.103 0 0 0
Illinois Cook 170313301 0.027 0.019 0.028 0 0 0
Illinois Cook 170314201 0.011 0.010 0.012 0 0 0
Illinois Cook 170316003 0.042 0.024 0.080 0 0 0
Illinois Macon 171150110 0.199 0.073 0.386 1 0 0
Illinois Madison 171190010 0.416 0.140 0.848 1 0 0
Illinois Madison 171193007 0.036 0.020 0.053 0 0 0
Illinois Peoria 171430037 0.011 0.010 0.013 0 0 0
Illinois Peoria 171430110 0.016 0.012 0.024 1 0 0
Illinois Peoria 171430210 0.015 0.011 0.026 1 0 0
Illinois St. Clair 171630010 0.029 0.020 0.038 0 0 1
Illinois Whiteside 171950110 0.028 0.020 0.040 1 0 0 Illinois Winnebago 172010110 0.063 0.028 0.118 1 0 0
Indiana Delaware 180350009 0.338 0.159 0.476 1 0 0

2D - 2

### APPENDIX 2D

State County Site Maximum 3

- month

mean (μg/m 3 ) Annual average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) Non-airport

sourceoriented (during 2010- 2012) Airport

sourceoriented Previous

sourceoriented Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2010-2012.

Indiana Lake 180890023 0.077 0.031 0.087 1 0 0
Indiana Lake 180890032 0.060 0.023 0.144 1 0 0
Indiana Lake 180890033 0.139 0.055 0.298 1 0 0
Indiana Lake 180892008 0.046 0.020 0.103 0 0 0
Indiana Marion 180970063 0.079 0.028 0.125 1 0 0
Indiana Marion 180970076 0.020 0.010 0.029 1 0 0
Indiana Marion 180970078 0.011 0.006 0.021 0 0 0
Indiana Porter 181270023 0.022 0.013 0.032 1 0 0
Indiana Porter 181270027 0.041 0.027 0.085 1 0 0 Indiana Vanderburgh 181630020 0.006 0.004 0.008 0 0 0
Iowa Pottawattamie 191550011 0.263 0.123 0.282 1 0 0
Iowa Scott 191630015 0.012 0.010 0.024 0 0 0
Kansas Saline 201690004 0.421 0.164 0.488 1 0 0 Kansas Wyandotte 202090021 0.011 0.008 0.012 0 0 0 Kentucky Boyd 210190016 0.004 0.003 0.007 1 0 0 Kentucky Madison 211510003 0.248 0.057 0.281 1 0 0 Kentucky Madison 211510005 1.584 0.703 2.244 1 0 0 Kentucky Russell 212070001 0.063 0.027 0.109 1 0 0 Louisiana East Baton Rouge P a 220330009 0.002 0.002 0.003 0 0 0 Louisiana East Baton Rouge P a 220330014 0.011 0.004 0.027 1 0 0 Louisiana St. John the Baptist P 220950003 0.053 0.025 0.066 1 0 0 Massachusetts Nantucket County 250190001 0.010 0.009 0.020 0 1 0 Michigan Charlevoix 260290011 0.006 0.005 0.010 1 0 0 Michigan Ionia 260670002 0.049 0.071 0.298 1 0 0 Michigan Ionia 260670003 0.284 0.096 0.414 1 0 0 Michigan Kent 260810020 0.008 0.005 0.010 0 0 0 Michigan Oakland 261250013 0.022 0.019 0.027 0 1 0 Michigan Tuscola 261570001 0.034 0.021 0.063 1 0 0 Michigan Wayne 261630001 0.006 0.005 0.007 0 0 0 Michigan Wayne 261630033 0.023 0.012 0.034 0 0 0
Minnesota Anoka 270031002 0.011 0.006 0.012 0 0 0

2D - 3

### APPENDIX 2D

State County Site Maximum 3

- month

mean (μg/m 3 ) Annual average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) Non-airport

sourceoriented (during 2010- 2012) Airport

sourceoriented Previous

sourceoriented Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2010-2012.

Minnesota Anoka 270036020 0.038 0.017 0.078 1 0 0
Minnesota Beltrami 270072303 0.001 0.002 0 0 0
Minnesota Cass 270210001 0.001 0.002 0 0 0
Minnesota Dakota 270370020 0.004 0.004 0.018 0 0 0
Minnesota Dakota 270370465 0.259 0.096 0.568 1 0 0
Minnesota Dakota 270370470 0.002 0.001 0.004 0 0 0 Minnesota Hennepin 270530963 0.004 0.003 0.006 0 0 0 Minnesota Hennepin 270530966 0.005 0.004 0.008 0 0 0 Minnesota Hennepin 270531007 0.004 0.003 0.007 0 0 0
Minnesota Mille Lacs 270953051 0.001 0.000 0.002 0 0 0 Minnesota Ramsey 271230871 0.007 0.005 0.010 0 0 0
Minnesota St. Louis 271377001 0.008 0.002 0.022 0 0 0
Minnesota St. Louis 271377555 0.004 0.003 0.008 0 0 0
Minnesota Stearns 271453053 0.008 0.004 0.012 1 0 0 Minnesota Washington 271630438 0.005 0.003 0.008 0 0 0 Minnesota Washington 271630446 0.001 0.000 0.003 0 0 0
Missouri Iron 290930016 0.882 0.484 1.436 1 0 0
Missouri Iron 290930021 1.147 0.522 1.698 1 0 0
Missouri Iron 290930027 0.083 0.033 0.107 0 0 1
Missouri Iron 290930029 0.115 0.038 0.271 0 0 1
Missouri Iron 290930032 0.354 0.987 1 0 0
Missouri Iron 290930033 0.057 0.026 0.105 1 0 0
Missouri Iron 290930034 0.402 0.241 0.615 1 0 0
Missouri Iron 290939007 0.581 0.392 0.844 1 0 0
Missouri Iron 290939008 0.387 0.209 0.538 1 0 0 Missouri Jasper 290970005 0.019 0.014 0.024 0 0 0
Missouri Jefferson 290990004 1.122 0.888 1.576 1 0 0
Missouri Jefferson 290990005 0.396 0.223 0.498 1 0 0
Missouri Jefferson 290990009 0.191 0.055 0.280 1 0 0
Missouri Jefferson 290990013 0.305 0.135 0.418 1 0 0
Missouri Jefferson 290990020 0.865 0.546 1.233 1 0 0

2D - 4

### APPENDIX 2D

State County Site Maximum 3

- month

mean (μg/m 3 ) Annual average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) Non-airport

sourceoriented (during 2010- 2012) Airport

sourceoriented Previous

sourceoriented Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2010-2012.

Missouri Jefferson 290990022 0.630 0.469 0.861 1 0 0
Missouri Jefferson 290990023 0.563 0.386 0.700 1 0 0
Missouri Jefferson 290990024 0.659 0.340 0.862 1 0 0
Missouri Jefferson 290990025 0.085 0.042 0.134 1 0 0
Missouri Jefferson 290990026 0.080 0.036 0.138 1 0 0
Missouri Jefferson 290990027 0.592 0.454 0.857 1 0 0
Missouri Jefferson 290999001 1.100 0.812 1.558 1 0 0
Missouri Jefferson 290999002 0.431 0.228 0.593 1 0 0
Missouri Jefferson 290999003 0.327 0.175 0.551 1 0 0
Missouri Jefferson 290999004 0.442 0.156 0.545 1 0 0
Missouri Jefferson 290999005 1.432 0.913 2.185 1 0 0
Missouri Jefferson 290999006 0.103 0.049 0.136 1 0 0 Missouri Reynolds 291790001 0.059 0.031 0.087 1 0 0 Missouri Reynolds 291790002 0.068 0.034 0.172 1 0 0 Missouri Reynolds 291790003 0.100 0.027 0.268 1 0 0 Missouri Reynolds 291790034 0.161 0.078 0.297 1 0 0
Missouri St. Francois 291870006 0.132 0.043 0.302 0 0 0
Missouri St. Francois 291870007 0.134 0.053 0.364 0 0 0
Missouri St. Louis 291892003 0.008 0.007 0.009 0 0 0 Missouri St. Louis city 295100085 0.028 0.026 0.045 0 0 0 Nebraska Dodge 310530005 0.139 0.055 0.197 1 0 0 Nebraska Douglas 310550019 0.006 0.005 0.008 0 0 0
Nebraska Nemaha 311270002 0.115 0.034 0.206 1 0 0
Nevada Clark 320030540 0.003 0.004 0 0 0
New Mexico Bernalillo 350010023 0.006 0.003 0.012 0 0 0 New York Orange 360713001 0.101 0.025 0.134 1 0 0 New York Orange 360713002 1.027 0.123 2.821 1 0 0 New York Orange 360713004 0.007 0.005 0.011 1 0 0
New York Suffolk 361030024 0.027 0.017 0.031 0 1 0
Ohio Butler 390170015 0.009 0.006 0.013 0 0 0
Ohio Columbiana 390290019 0.057 0.020 0.136 0 0 0

2D - 5

### APPENDIX 2D

State County Site Maximum 3

- month

mean (μg/m 3 ) Annual average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) Non-airport

sourceoriented (during 2010- 2012) Airport

sourceoriented Previous

sourceoriented Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2010-2012.

Ohio Columbiana 390290020 0.025 0.015 0.035 0 0 0
Ohio Columbiana 390290022 0.044 0.019 0.065 0 0 0 Ohio Cuyahoga 390350038 0.021 0.013 0.026 0 0 0 Ohio Cuyahoga 390350042 0.030 0.013 0.044 0 0 0 Ohio Cuyahoga 390350049 0.531 0.136 0.719 1 0 0 Ohio Cuyahoga 390350060 0.030 0.020 0.035 0 0 0 Ohio Cuyahoga 390350061 0.023 0.015 0.030 0 0 1 Ohio Cuyahoga 390350072 0.035 0.014 0.054 1 0 0
Ohio Franklin 390490025 0.011 0.009 0.016 0 0 0
Ohio Fulton 390510001 0.178 0.070 0.210 1 0 0 Ohio Logan 390910006 0.006 0.004 0.008 0 0 1
Ohio Marion 391010003 0.088 0.041 0.155 1 0 0
Ohio Marion 391010004 0.017 0.013 0.028 1 0 0 Ohio Montgomery 391137001 0.008 0.007 0.012 0 0 0
Ohio Stark 391510017 0.023 0.015 0.032 1 0 0
Ohio Trumbull 391550012 0.011 0.007 0.017 1 0 0 Ohio Washington 391670008 0.007 0.005 0.010 0 0 0 Ohio Washington 391670010 0.008 0.005 0.010 0 0 0
Oklahoma Ottawa 401159006 0.022 0.012 0.049 0 0 0
Oklahoma Ottawa 401159007 0.034 0.018 0.056 0 0 0 Oklahoma Pittsburg 401210416 0.004 0.003 0.006 1 0 0
Oklahoma Tulsa 401431127 0.008 0.006 0.009 0 0 0 Oregon Yamhill 410711702 0.045 0.021 0.078 1 0 0 Pennsylvania Allegheny 420030002 0.016 0.014 0.024 0 0 0 Pennsylvania Allegheny 420030008 0.014 0.008 0.020 0 0 0 Pennsylvania Allegheny 420030070 0.056 0.018 0.110 1 0 0 Pennsylvania Allegheny 420031009 0.138 0.035 0.149 1 0 0 Pennsylvania Beaver 420070006 0.085 0.051 0.198 1 0 0 Pennsylvania Beaver 420070007 0.253 0.166 0.393 1 0 0 Pennsylvania Beaver 420070505 0.151 0.089 0.291 1 0 0 Pennsylvania Berks 420110020 0.509 0.158 1.064 1 0 0

2D - 6

### APPENDIX 2D

State County Site Maximum 3

- month

mean (μg/m 3 ) Annual average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) Non-airport

sourceoriented (during 2010- 2012) Airport

sourceoriented Previous

sourceoriented Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2010-2012.

Pennsylvania Berks 420110021 0.139 0.044 0.319 1 0 0 Pennsylvania Berks 420110022 0.118 0.035 0.261 1 0 0 Pennsylvania Berks 420111717 0.217 0.146 0.285 1 0 0 Pennsylvania Carbon 420250214 0.104 0.321 1 0 0 Pennsylvania Delaware 420450002 0.047 0.028 0.048 0 0 0 Pennsylvania Delaware 420450004 0.047 0.028 0.048 1 0 0 Pennsylvania Franklin 420550002 0.046 0.028 0.047 1 0 0 Pennsylvania Indiana 420630005 0.049 0.025 0.058 1 0 0 Pennsylvania Lancaster 420710009 0.068 0.039 0.093 1 0 0 Pennsylvania Lawrence 420730011 0.023 0.026 0.046 1 0 0 Pennsylvania Luzerne 420790036 0.137 0.054 0.268 1 0 0 Pennsylvania Philadelphia 421010449 0.029 0.021 0.029 0 0 1 Pennsylvania Philadelphia 421011002 0.051 0.030 0.069 0 0 0 Pennsylvania Westmoreland 421290009 0.046 0.023 0.047 1 0 0
South Carolina Charleston 450190003 0.007 0.005 0.013 0 0 0
South Carolina Florence 450418001 0.044 0.013 0.101 1 0 0
South Carolina Florence 450418002 0.015 0.006 0.024 1 0 0
South Carolina Florence 450418003 0.011 0.005 0.013 0 0 0
South Carolina Greenville 450450015 0.006 0.005 0.008 0 0 0
South Carolina Richland 450790007 0.005 0.004 0.007 0 0 0
South Carolina Richland 450790019 0.024 0.011 0.061 0 0 0
Tennessee Knox 470930023 0.165 0.108 0.214 1 0 0
Tennessee Knox 470930027 0.042 0.020 0.078 1 0 0
Tennessee Knox 470931017 0.037 0.018 0.058 1 0 0 Tennessee Shelby 471570075 0.005 0.004 0.005 0 0 0
Tennessee Sullivan 471633001 0.076 0.056 0.107 0 0 1
Tennessee Sullivan 471633002 0.044 0.036 0.052 0 0 1
Tennessee Sullivan 471633003 0.053 0.038 0.056 0 0 1
Tennessee Sullivan 471633004 0.080 0.044 0.124 0 0 1
Texas Cameron 480610006 0.008 0.004 0.018 0 0 0
Texas Collin 480850003 0.371 0.136 0.625 1 0 0

2D - 7

### APPENDIX 2D

State County Site Maximum 3

- month

mean (μg/m 3 ) Annual average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) Non-airport

sourceoriented (during 2010- 2012) Airport

sourceoriented Previous

sourceoriented Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2010-2012.

Texas Collin 480850007 0.199 0.093 0.240 1 0 0
Texas Collin 480850009 0.774 0.388 1.178 1 0 0
Texas Collin 480850029 0.180 0.052 0.335 1 0 0
Texas Dallas 481130069 0.013 0.009 0.022 0 0 0
Texas El Paso 481410002 0.040 0.022 0.087 0 0 0
Texas El Paso 481410033 0.019 0.017 0.023 0 0 0
Texas El Paso 481410037 0.025 0.022 0.032 1 0 0
Texas El Paso 481410055 0.019 0.010 0.032 0 0 0
Texas El Paso 481410058 0.022 0.016 0.022 0 0 0
Texas Harris 482011034 0.008 0.005 0.009 0 0 0
Texas Harris 482011039 0.004 0.003 0.008 0 0 0
Texas Kaufman 482570020 0.104 0.044 0.110 1 0 0
Texas Potter 483750024 0.020 0.007 0.029 1 0 0
Texas Webb 484790016 0.026 0.018 0.035 0 0 0
Utah Salt Lake 490351001 0.057 0.024 0.086 1 0 0 Virginia Amherst 510090007 0.018 0.006 0.016 1 0 0 Virginia Buchanan 510270006 0.014 0.012 0.021 1 0 0 Virginia Henrico 510870014 0.005 0.005 0.024 0 0 0 Virginia Roanoke city 517700011 0.109 0.033 0.272 1 0 0 Washington King 530330029 0.055 0.036 0.087 0 1 0 Washington Snohomish 530610013 0.023 0.013 0.032 0 1 0 West Virginia Cabell 540110006 0.012 0.010 0.013 0 0 0 Wisconsin Sheboygan 551170008 0.152 0.056 0.225 1 0 0
Puerto Rico A recibo Municipio, P u 720130001 0.339 0.171 0.416 1 0 0 Puerto Rico Bayamón Municipio, P 720210010 0.011 0.004 0.027 0 0 0 Puerto Rico Salinas Municipio, Pu 721230002 0.017 0.008 0.042 0 0 0
counts → 236 243 243 121 15 11

2D - 8

### APPENDIX 2D

State County Site Maximum 3-month

mean (μg/m 3 ) Annual
average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) North Carolin a Wake 371830014 0.002 0.002 Georgia DeKalb 130890002 0.002 0.001 0.003 Massachusett s Suffolk 250250002 0.002 0.002 0.003 New Hampsh i Rockingham 330150018 0.002 0.002 0.003 North Carolin a Mecklenburg 371190041 0.002 0.003 Oregon Jackson 410290133 0.003 0.002 0.003 Oregon Jackson 410292129 0.002 0.003 Oregon Lane 410390060 0.002 0.001 0.003 Oregon Lane 410390062 0.002 0.002 0.003 Vermont Chittenden 500070007 0.002 0.001 0.003 Florida Hillsborough 120573002 0.003 0.002 0.004 Florida Pinellas 121030018 0.003 0.002 0.004 Kentucky Henderson 211010014 0.003 0.003 0.004 Nevada Clark 320030540 0.003 0.004 New York Monroe 360551007 0.003 0.003 0.004 Arkansas Pulaski 051190007 0.004 0.003 0.005 California Sacramento 060670006 0.003 0.002 0.005 Delaware New Castle 100032004 0.004 0.003 0.005 District of Co l District of Colum b 110010043 0.004 0.003 0.005 Florida Orange 120951004 0.002 0.005 Idaho Ada 160010010 0.002 0.002 0.005 Massachusett s Suffolk 250250042 0.005 0.003 0.005 Rhode Island Providence 440070022 0.003 0.003 0.005 Washington King 530330080 0.004 0.003 0.005 California Santa Clara 060850005 0.006 0.002 0.006 Florida Pinellas 121030026 0.004 0.002 0.006 Kentucky Fayette 210670012 0.004 0.003 0.006 Kentucky Fayette 210670014 0.005 0.004 0.006 Michigan Wayne 261630001 0.006 0.004 0.006 New Jersey Essex 340130003 0.005 0.003 0.006 Arizona Maricopa 040139997 0.006 0.004 0.007 Ohio Hamilton 390610040 0.005 0.005 0.007 Texas Harris 482011039 0.004 0.002 0.007 Arizona Maricopa 040134009 0.005 0.008 Kentucky Jefferson 211110067 0.006 0.005 0.008 Massachusett s Hampden 250132009 0.006 0.004 0.008 New York Bronx 360050110 0.006 0.006 0.008 Utah Davis 490110004 0.006 0.003 0.009 Table 2D-2. Pb-PM 10 concentrations at urban Pb-PM 10 sites, 2010-2012.

2D - 9

### APPENDIX 2D

State County Site Maximum 3-month

mean (μg/m 3 ) Annual
average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) Table 2D-2. Pb-PM 10 concentrations at urban Pb-PM 10 sites, 2010-2012.

Illinois Cook 170314201 0.006 0.004 0.010 Wisconsin Milwaukee 550790010 0.006 0.010 New York Bronx 360050080 0.008 0.006 0.012 Oregon Multnomah 410510246 0.006 0.004 0.012 Connecticut New Haven 090090027 0.008 0.004 0.013 Maryland Prince George's 240330030 0.008 0.004 0.016 Texas Harris 482011035 0.008 0.005 0.016 Virginia Henrico 510870014 0.007 0.003 0.016 California Los Angeles 060371103 0.013 0.007 0.026 Kentucky Boyd 210190002 0.020 0.013 0.029 California Riverside 060658001 0.013 0.006 0.030 Illinois St. Clair 171639010 0.015 0.031 Missouri St. Louis city 295100085 0.017 0.012 0.032 Michigan Wayne 261630033 0.023 0.011 0.035 Alabama Jefferson 010730023 0.029 0.019 0.040 Mississippi Hinds 280490019 0.074 0.082
counts → 45 54 54

2D - 10

### APPENDIX 2D

state_name county_name SITE Maximum 3-month

mean (μg/m 3 ) Annual
average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) California Kern 060299001 0.001 0.001 0.001 Hawaii Honolulu 150030010 0.001 0.000 0.001 Wyoming Laramie 560210100 0.000 0.000 0.001 California Butte 060070008 0.002 0.002 Colorado Adams 080010006 0.002 0.001 0.002 Florida Broward 120111002 0.001 0.001 0.002 Idaho Ada 160010010 0.001 0.001 0.002 North Carolina Buncombe 370210034 0.001 0.001 0.002 North Carolina Wake 371830014 0.002 0.001 0.002 Oklahoma Oklahoma 401091037 0.001 0.001 0.002 Rhode Island Providence 440071010 0.002 0.002 0.002 South Carolina Charleston 450190049 0.002 0.001 0.002 South Carolina Richland 450790007 0.002 0.001 0.002 Texas Harris 482011039 0.001 0.001 0.002 Vermont Chittenden 500070012 0.002 0.001 0.002 Wisconsin Brown 550090005 0.001 0.001 0.002 Alabama Madison 010890014 0.002 0.001 0.003 Arizona Pima 040191028 0.002 0.001 0.003 California Butte 060070002 0.003 0.002 0.003 California Fresno 060190008 0.002 0.001 0.003 California Ventura 061112002 0.002 0.001 0.003 Colorado Weld 081230008 0.002 0.001 0.003 District of Colum b District of Columbia 110010043 0.002 0.001 0.003 Florida Hillsborough 120573002 0.002 0.001 0.003 Florida Pinellas 121030026 0.002 0.001 0.003 Georgia Clarke 130590001 0.002 0.001 0.003 Georgia DeKalb 130890002 0.002 0.001 0.003 Iowa Linn 191130037 0.002 0.002 0.003 Iowa Polk 191530030 0.002 0.001 0.003 Louisiana East Baton Rouge Parish 220330009 0.003 0.002 0.003 Minnesota Hennepin 270530963 0.002 0.002 0.003 Mississippi Hinds 280490019 0.003 0.001 0.003 Missouri Clay 290470005 0.002 0.001 0.003 Nevada Washoe 320310016 0.002 0.001 0.003 New Jersey Morris 340273001 0.002 0.001 0.003 New York Monroe 360551007 0.002 0.002 0.003 North Carolina Catawba 370350004 0.002 0.002 0.003 Table 2D-3. Pb-PM 2.5 concentrations at urban CSN PM 2.5 sites, 2010-2012.

2D - 11

### APPENDIX 2D

state_name county_name SITE Maximum 3-month

mean (μg/m 3 ) Annual
average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) Table 2D-3. Pb-PM 2.5 concentrations at urban CSN PM 2.5 sites, 2010-2012.

North Carolina Mecklenburg 371190041 0.002 0.001 0.003 North Carolina Rowan 371590021 0.006 0.001 0.003 Oregon Lane 410392013 0.002 0.001 0.003 Pennsylvania Centre 420270100 0.002 0.001 0.003 South Dakota Minnehaha 460990008 0.002 0.001 0.003 Tennessee Roane 471451001 0.002 0.002 0.003 Texas Cameron 480612004 0.002 0.001 0.003 Texas Jefferson 482450021 0.002 0.002 0.003 Texas Travis 484530020 0.002 0.001 0.003 Washington Yakima 530770009 0.002 0.001 0.003 California Fresno 060190011 0.002 0.001 0.004 California Santa Clara 060850005 0.003 0.001 0.004 Colorado Denver 080310025 0.002 0.001 0.004 Georgia Bibb 130210007 0.003 0.001 0.004 Illinois Madison 171199010 0.002 0.004 Indiana Elkhart 180390008 0.003 0.002 0.004 Indiana Vanderburgh 181630021 0.003 0.002 0.004 Maryland Prince George's 240330030 0.002 0.001 0.004 Massachusetts Hampden 250130008 0.003 0.002 0.004 Michigan Wayne 261630001 0.003 0.002 0.004 Nevada Clark 320030540 0.003 0.001 0.004 New Jersey Middlesex 340230006 0.003 0.002 0.004 New Jersey Union 340390004 0.004 0.002 0.004 New Mexico Bernalillo 350010023 0.002 0.001 0.004 New York New York 360610134 0.003 0.002 0.004 North Dakota Cass 380171004 0.002 0.001 0.004 Ohio Franklin 390490081 0.003 0.002 0.004 Ohio Lucas 390950026 0.003 0.002 0.004 Oklahoma Tulsa 401431127 0.003 0.001 0.004 Pennsylvania Adams 420010001 0.002 0.001 0.004 Tennessee Shelby 471570024 0.003 0.002 0.004 Washington Clark 530110013 0.003 0.001 0.004 Arizona Maricopa 040134009 0.004 0.003 0.005 Arizona Maricopa 040139997 0.003 0.002 0.005 California Kern 060290014 0.004 0.001 0.005 California Riverside 060658001 0.003 0.002 0.005 California Sacramento 060670010 0.003 0.002 0.005

2D - 12

### APPENDIX 2D

state_name county_name SITE Maximum 3-month

mean (μg/m 3 ) Annual
average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) Table 2D-3. Pb-PM 2.5 concentrations at urban CSN PM 2.5 sites, 2010-2012.

California San Diego 060730003 0.004 0.002 0.005 California San Diego 060731002 0.004 0.002 0.005 California Tulare 061072002 0.004 0.002 0.005 Delaware New Castle 100032004 0.004 0.002 0.005 Illinois Cook 170314201 0.003 0.002 0.005 Indiana Clark 180190006 0.003 0.002 0.005 Minnesota Olmsted 271095008 0.003 0.001 0.005 New Jersey Essex 340130003 0.003 0.002 0.005 New York Bronx 360050110 0.004 0.003 0.005 North Carolina Davidson 370570002 0.003 0.001 0.005 Pennsylvania Chester 420290100 0.004 0.002 0.005 Pennsylvania Philadelphia 421010055 0.003 0.002 0.005 Tennessee Davidson 470370023 0.003 0.002 0.005 Tennessee Hamilton 470654002 0.003 0.002 0.005 Tennessee Montgomery 471251009 0.003 0.001 0.005 Texas Nueces 483550034 0.003 0.002 0.005 Virginia Henrico 510870014 0.002 0.001 0.005 Washington Snohomish 530611007 0.004 0.001 0.005 West Virginia Kanawha 540390011 0.003 0.002 0.005 California Alameda 060010007 0.005 0.002 0.006 Delaware Kent 100010003 0.003 0.001 0.006 Illinois Cook 170310076 0.004 0.003 0.006 Illinois St. Clair 171630900 0.005 0.003 0.006 Iowa Linn 191130040 0.003 0.002 0.006 Michigan Kent 260810020 0.004 0.002 0.006 Nebraska Douglas 310550019 0.004 0.001 0.006 New York Albany 360010005 0.004 0.002 0.006 Pennsylvania Westmoreland 421290008 0.004 0.003 0.006 Rhode Island Providence 440070022 0.004 0.003 0.006 Tennessee Shelby 471570075 0.003 0.002 0.006 Wisconsin Milwaukee 550790026 0.004 0.003 0.006 Connecticut New Haven 090090027 0.004 0.002 0.007 Indiana Marion 180970078 0.004 0.003 0.007 Kentucky Boyd 210190017 0.005 0.003 0.007 Maryland Baltimore 240053001 0.006 0.002 0.007 Michigan Monroe 261150005 0.005 0.002 0.007 Ohio Summit 391530023 0.005 0.004 0.007

2D - 13

### APPENDIX 2D

state_name county_name SITE Maximum 3-month

mean (μg/m 3 ) Annual
average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) Table 2D-3. Pb-PM 2.5 concentrations at urban CSN PM 2.5 sites, 2010-2012.

Pennsylvania Erie 420490003 0.004 0.002 0.007 Tennessee Knox 470931020 0.006 0.003 0.007 Texas Dallas 481130050 0.005 0.003 0.007 Utah Davis 490110004 0.003 0.002 0.007 Washington King 530330080 0.003 0.001 0.007 West Virginia Kanawha 540391005 0.005 0.002 0.007 West Virginia Marshall 540511002 0.007 0.004 0.007 Alaska Fairbanks North Star Boroug h 020900010 0.005 0.002 0.008 California Solano 060950004 0.006 0.003 0.008 Florida Leon 120730012 0.004 0.002 0.008 Georgia Richmond 132450091 0.004 0.001 0.008 Georgia Walker 132950002 0.005 0.002 0.008 Illinois DuPage 170434002 0.004 0.002 0.008 Kansas Sedgwick 201730010 0.004 0.002 0.008 Kansas Wyandotte 202090021 0.006 0.004 0.008 Oregon Multnomah 410510080 0.005 0.003 0.008 Pennsylvania Washington 421255001 0.005 0.003 0.008 South Carolina Greenville 450450015 0.006 0.002 0.008 Texas Ellis 481390016 0.006 0.003 0.008 Texas El Paso 481410044 0.006 0.003 0.008 Texas Harris 482010024 0.006 0.003 0.008 Washington Pierce 530530029 0.005 0.003 0.008 California Sacramento 060670006 0.004 0.001 0.009 California Stanislaus 060990005 0.005 0.003 0.009 Georgia Floyd 131150003 0.005 0.002 0.009 Louisiana Bossier Parish 220150008 0.006 0.003 0.009 Ohio Hamilton 390610040 0.005 0.002 0.009 Pennsylvania Lancaster 420710007 0.007 0.003 0.009 Pennsylvania York 421330008 0.006 0.002 0.009 New York Queens 360810124 0.005 0.002 0.010 Pennsylvania Lackawanna 420692006 0.006 0.003 0.010 West Virginia Ohio 540690010 0.008 0.005 0.010 Kentucky Fayette 210670012 0.006 0.002 0.011 North Carolina Forsyth 370670022 0.006 0.002 0.011 Ohio Cuyahoga 390350060 0.009 0.006 0.011 Pennsylvania Dauphin 420430401 0.007 0.003 0.011 Pennsylvania Philadelphia 421010004 0.006 0.003 0.011

2D - 14

### APPENDIX 2D

state_name county_name SITE Maximum 3-month

mean (μg/m 3 ) Annual
average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) Table 2D-3. Pb-PM 2.5 concentrations at urban CSN PM 2.5 sites, 2010-2012.

Kentucky Jefferson 211110067 0.007 0.004 0.012 Massachusetts Suffolk 250250042 0.005 0.002 0.012 Ohio Cuyahoga 390350038 0.008 0.004 0.012 Ohio Jefferson 390811001 0.009 0.005 0.012 Ohio Lawrence 390870012 0.009 0.005 0.012 Texas Dallas 481130069 0.007 0.003 0.012 Utah Utah 490494001 0.006 0.002 0.012 Washington King 530330057 0.008 0.004 0.013 Wisconsin Waukesha 551330027 0.010 0.005 0.013 Alabama Montgomery 011011002 0.008 0.003 0.014 Arkansas Pulaski 051190007 0.006 0.002 0.014 California Los Angeles 060371103 0.015 0.002 0.015 Missouri St. Louis city 295100085 0.010 0.006 0.016 New York Erie 360290005 0.012 0.007 0.016 Pennsylvania Berks 420110011 0.013 0.007 0.016 Utah Salt Lake 490353006 0.007 0.002 0.016 Iowa Scott 191630015 0.010 0.005 0.017 Missouri Jefferson 290990019 0.009 0.004 0.017 Ohio Mahoning 390990014 0.012 0.007 0.017 Texas Lubbock 483030325 0.007 0.003 0.017 Indiana Lake 180890022 0.011 0.005 0.018 Pennsylvania Northampton 420950025 0.008 0.003 0.018 Texas El Paso 481410053 0.017 0.006 0.018 Illinois St. Clair 171639010 0.014 0.010 0.019 Minnesota Anoka 270031002 0.012 0.006 0.019 Ohio Stark 391510017 0.012 0.007 0.019 Pennsylvania Philadelphia 421011002 0.012 0.006 0.020 California Alameda 060010011 0.011 0.004 0.021 Pennsylvania Allegheny 420030008 0.016 0.008 0.022 Alabama Jefferson 010732003 0.018 0.006 0.023 Ohio Lorain 390933002 0.012 0.006 0.023 Pennsylvania Cambria 420210011 0.013 0.007 0.023 California Imperial 060250005 0.018 0.012 0.025 Michigan Wayne 261630015 0.012 0.006 0.027 Alabama Russell 011130001 0.016 0.004 0.028 Michigan Wayne 261630033 0.017 0.006 0.028 Georgia Muscogee 132150011 0.014 0.004 0.029

2D - 15

### APPENDIX 2D

state_name county_name SITE Maximum 3-month

mean (μg/m 3 ) Annual
average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) Table 2D-3. Pb-PM 2.5 concentrations at urban CSN PM 2.5 sites, 2010-2012.

Michigan St. Clair 261470005 0.015 0.004 0.030 Illinois Madison 171190024 0.020 0.010 0.032 Washington Pierce 530530031 0.015 0.004 0.032 Ohio Montgomery 391130032 0.014 0.003 0.033 California San Bernardino 060712002 0.037 0.017 0.037 Indiana Lake 180892004 0.022 0.010 0.037 California Orange 060590007 0.042 0.013 0.043 Pennsylvania Allegheny 420030064 0.038 0.018 0.051 Alabama Jefferson 010730023 0.041 0.020 0.063 Illinois Cook 170310057 0.069 0.011 0.199
counts → 193 195 195

2D - 16

### APPENDIX 2D

state_name county_name SITE Maximum 3-month

mean (μg/m 3 ) Annual
average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) Alaska Aleutians East Borough 020130002 0.002 0.001 0.002 Alaska Denali Borough 020680003 0.001 0.000 0.001 Alaska Kenai Peninsula Borough 021220009 0.001 0.000 0.002 Alaska Northwest Arctic Borough 021889000 Alaska Yukon-Koyukuk Census Are a 022909000 0.001 0.000 0.001 Arizona Apache 040018001 0.001 0.001 0.002 Arizona Gila 040070010 0.005 0.003 0.008 Arizona Gila 040078100 0.001 0.001 0.002 Arizona Navajo 040170119 0.001 0.001 0.002 Arkansas Newton 051019000 0.002 0.001 0.003 Arkansas Polk 051130003 0.002 0.001 0.003 California Del Norte 060150002 0.001 0.000 0.001 California Inyo 060270101 0.001 0.001 0.002 California Mariposa 060430003 0.001 0.001 0.002 California Mono 060519000 0.001 0.000 0.001 California Siskiyou 060930005 0.001 0.000 0.001 California Trinity 061059000 0.001 0.001 0.001 Colorado Alamosa 080039000 0.001 0.000 0.002 Colorado Garfield 080450015 0.001 0.002 Colorado Jackson 080579000 0.001 0.000 0.001 Colorado La Plata 080679000 0.001 0.001 0.001 Colorado Montezuma 080839000 0.001 0.001 0.001 Colorado Pitkin 080979000 0.001 0.000 0.001 Colorado Rio Blanco 081039000 Colorado San Juan 081119000 0.001 0.001 0.001 Connecticut Litchfield 090050005 0.002 0.001 0.002 Georgia Charlton 130499000 0.002 0.001 0.002 Hawaii Hawaii 150019000 Hawaii Hawaii 150019001 Hawaii Hawaii 150019002 0.005 0.001 0.010 Idaho Custer 160370002 0.001 0.000 0.001 Idaho Lemhi 160590007 Iowa Montgomery 191370002 0.002 0.002 0.003 Iowa Van Buren 191770006 0.003 0.002 0.004 Iowa Van Buren 191779000 Kansas Brown 200139000 0.003 0.002 0.003 Kansas Chase 200170001 0.002 0.001 0.003 Table 2D-4. Pb-PM 2.5 concentrations at non-urban IMPROVE PM 2.5 sites, 2010-2012.

2D - 17

### APPENDIX 2D

state_name county_name SITE Maximum 3-month

mean (μg/m 3 ) Annual
average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) Table 2D-4. Pb-PM 2.5 concentrations at non-urban IMPROVE PM 2.5 sites, 2010-2012.

Kansas Trego 201950001 0.001 0.001 0.001 Louisiana Winn Parish 221279000 0.001 0.001 0.002 Maine Aroostook 230031020 0.002 0.001 0.004 Maine Hancock 230090103 0.001 0.001 0.002 Maine Washington 230291004 0.001 0.001 0.002 Maryland Garrett 240239000 0.002 0.002 0.003 Massachusetts Dukes 250070001 0.001 0.001 0.002 Michigan Keweenaw 260839000 0.001 0.001 0.002 Michigan Keweenaw 260839001 Michigan Schoolcraft 261539000 0.002 0.001 0.002 Minnesota Lake 270759000 0.001 0.001 0.002 Minnesota Rock 271339000 0.002 0.002 0.003 Minnesota Winona 271699000 0.002 0.002 0.002 Missouri Cedar 290390001 0.002 0.002 0.003 Missouri Stoddard 292070001 0.004 0.003 0.005 Missouri Taney 292130003 0.002 0.002 0.003 Montana Fergus 300279000 0.001 0.001 0.001 Montana Flathead 300299001 0.001 0.000 0.001 Montana Lake 300479000 0.001 0.000 0.001 Montana Lewis and Clark 300499000 0.001 0.000 0.001 Montana Powell 300779000 0.001 0.000 0.001 Montana Ravalli 300819000 0.001 0.000 0.001 Montana Roosevelt 300859000 0.001 0.001 0.001 Montana Rosebud 300870762 0.001 0.000 0.001 Montana Sanders 300899000 0.001 0.000 0.001 Montana Sheridan 300919000 0.001 0.001 0.001 Nebraska Garden 310699000 0.001 0.001 0.001 Nebraska Thomas 311719000 0.001 0.001 0.001 Nebraska Thurston 311739000 Nevada Elko 320079000 0.001 0.000 0.002 Nevada Mineral 320219000 Nevada White Pine 320339000 0.001 0.000 0.001 New Hampshire Coos 330074002 0.001 0.001 0.001 New Mexico Catron 350039000 0.001 0.001 0.001 New Mexico Chaves 350059000 0.001 0.001 0.002 New Mexico Lincoln 350279000 0.001 0.001 0.002 New Mexico Los Alamos 350281002 0.001 0.001 0.002

2D - 18

### APPENDIX 2D

state_name county_name SITE Maximum 3-month

mean (μg/m 3 ) Annual
average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) Table 2D-4. Pb-PM 2.5 concentrations at non-urban IMPROVE PM 2.5 sites, 2010-2012.

New Mexico Rio Arriba 350399000 0.001 0.001 0.002 New Mexico Socorro 350539000 0.001 0.001 0.002 New Mexico Taos 350559000 0.001 0.000 0.001 New York Steuben 361019000 0.002 0.002 North Carolina Avery 370110002 0.001 0.001 0.002 North Carolina Hyde 370959000 0.002 0.001 0.002 North Dakota Billings 380070002 0.001 0.001 0.001 North Dakota Burke 380130004 0.001 0.001 0.001 Ohio Noble 391219000 0.005 0.003 0.008 Oklahoma Adair 400019009 0.002 0.002 0.003 Oklahoma Ellis 400450890 0.001 0.001 0.001 Oklahoma Kay 400719010 0.002 0.001 0.003 Oregon Klamath 410358001 0.001 0.000 0.001 Oregon Union 410610010 0.001 0.000 0.001 Oregon Wallowa 410630002 0.002 0.001 0.003 South Dakota Jackson 460710001 0.001 0.001 0.001 Texas Brewster 480430101 0.002 0.001 0.002 Texas Culberson 481099000 0.001 0.001 0.002 Utah Garfield 490170101 0.001 0.001 0.001 Utah San Juan 490379000 0.001 0.001 0.001 Utah Wayne 490559000 0.001 0.000 0.001 Vermont Bennington 500038001 0.001 0.001 0.002 Virginia Madison 511139000 0.002 0.001 0.002 Virginia Rockbridge 511639000 0.004 0.003 0.006 Washington Clallam 530090013 0.000 0.000 0.001 Washington Clallam 530090014 Washington Clallam 530090020 0.001 0.001 0.002 Washington Kittitas 530370004 0.001 0.001 0.001 Washington Klickitat 530390010 0.002 0.001 0.002 Washington Klickitat 530390011 0.001 0.001 0.001 Washington Lewis 530410007 0.001 0.000 0.001 Washington Okanogan 530470012 0.001 0.000 0.001 West Virginia Tucker 540939000 0.002 0.001 0.002 Wyoming Albany 560019000 Wyoming Campbell 560050123 0.000 0.000 0.001 Wyoming Johnson 560199000 0.001 0.000 0.001 Wyoming Park 560299002 0.001 0.000 0.001

2D - 19

### APPENDIX 2D

state_name county_name SITE Maximum 3-month

mean (μg/m 3 ) Annual
average (μg/m 3 ) Maximum monthly

mean (μg/m 3 ) Table 2D-4. Pb-PM 2.5 concentrations at non-urban IMPROVE PM 2.5 sites, 2010-2012.

Wyoming Sublette 560359000 0.001 0.000 0.001 Wyoming Sublette 560359001 0.001 0.000 0.001 Wyoming Teton 560399000 0.001 0.000 0.001 Virgin Islands St John 780209000 0.001 0.001 0.001
counts → 102 104 104

2D - 20

### APPENDIX 2D

(units are μg/m 3 ) n min Pct1 Pct5 Pct10 Pct25 mean Pct50 Pct75 Pct90 Pct95 Pct99 max

All Pb-TSP sites 235 0.001 0.001 0.004 0.006 0.011 0.1396 0.040 0.132 0.416 0.659 1.296 1.584

Pb-TSP non-airport source-oriented sites 119 0.004 0.004 0.011 0.017 0.045 0.2493 0.109 0.338 0.659 1.100 1.432 1.584
Pb-TSP airport source-oriented sites 13 0.010 0.010 0.010 0.010 0.020 0.0677 0.040 0.070 0.120 0.330 0.330 0.330
Pb-TSP previous source-oriented sites 11 0.006 0.006 0.006 0.023 0.029 0.0554 0.053 0.080 0.083 0.115 0.115 0.115

Pb-TSP not source-oriented sites 93 0.001 0.001 0.002 0.004 0.006 0.0180 0.011 0.024 0.041 0.047 0.134 0.134

Pb-PM10 urban sites 45 0.002 0.002 0.002 0.002 0.003 0.0065 0.005 0.006 0.013 0.020 0.029 0.029

Pb-PM2.5 urban CSN sites 193 0.000 0.001 0.002 0.002 0.002 0.0064 0.004 0.007 0.013 0.017 0.042 0.069

Pb-PM2.5 non-urban IMPROVE sites 102 0.000 0.000 0.001 0.001 0.001 0.0014 0.001 0.002 0.002 0.003 0.005 0.005 Table 2D-5. Distribution of maximum 3-month means, 2010-2012.

2D - 21

### APPENDIX 2D

(units are μg/m 3 ) n min Pct1 Pct5 Pct10 Pct25 mean Pct50 Pct75 Pct90 Pct95 Pct99 max All Pb-TSP sites 242 0.000 0.001 0.003 0.004 0.007 0.0718 0.021 0.055 0.166 0.386 0.812 0.913

Pb-TSP non-airport source-oriented sites 121 0.003 0.003 0.006 0.012 0.024 0.1261 0.044 0.140 0.386 0.522 0.888 0.913 Pb-TSP airport source-oriented sites 15 0.004 0.004 0.004 0.009 0.014 0.0557 0.033 0.071 0.128 0.254 0.254 0.254 Pb-TSP previous source-oriented sites 11 0.004 0.004 0.004 0.015 0.020 0.0298 0.033 0.038 0.044 0.056 0.056 0.056 Pb-TSP not source-oriented sites 96 0.000 0.000 0.001 0.003 0.004 0.0101 0.006 0.014 0.020 0.028 0.053 0.053 Pb-PM10 urban sites 54 0.001 0.001 0.001 0.002 0.002 0.0055 0.003 0.005 0.011 0.015 0.074 0.074 Pb-PM2.5 urban CSN sites 195 0.000 0.000 0.001 0.001 0.001 0.0029 0.002 0.003 0.006 0.008 0.018 0.020 Pb-PM2.5 non-urban IMPROVE sites 104 0.000 0.000 0.000 0.000 0.000 0.0009 0.001 0.001 0.002 0.002 0.003 0.003 Table 2D-6. Distribution of annual means, 2010-2012.

2D - 22

### APPENDIX 2D

(units are μg/m 3 ) n min Pct1 Pct5 Pct10 Pct25 mean Pct50 Pct75 Pct90 Pct95 Pct99 max All Pb-TSP sites 243 0.000 0.000 0.010 0.010 0.020 0.2213 0.060 0.230 0.580 0.990 2.240 2.820

Pb-TSP non-airport source-oriented sites 121 0.010 0.010 0.020 0.030 0.080 0.4012 0.210 0.500 0.990 1.580 2.260 2.820 Pb-TSP airport source-oriented sites 15 0.010 0.010 0.010 0.020 0.030 0.0933 0.070 0.100 0.230 0.400 0.400 0.400 Pb-TSP previous source-oriented sites 11 0.010 0.010 0.010 0.030 0.030 0.0882 0.060 0.120 0.140 0.270 0.270 0.270 Pb-TSP not source-oriented sites 96 0.000 0.000 0.000 0.010 0.010 0.0299 0.010 0.030 0.060 0.100 0.360 0.360 Pb-PM10 urban sites 54 0.000 0.000 0.000 0.000 0.000 0.0109 0.010 0.010 0.030 0.030 0.080 0.080 Pb-PM2.5 urban CSN sites 184 0.000 0.000 0.000 0.000 0.000 0.0098 0.010 0.010 0.020 0.030 0.050 0.200 Pb-PM2.5 non-urban IMPROVE sites 104 0.000 0.000 0.000 0.000 0.000 0.0005 0.000 0.000 0.000 0.000 0.010 0.010 Table 2D-7. Distribution of maximum monthly means, 2010-2012.

2D - 23

### APPENDIX 2D

Table 2D-8. Pb-TSP metric ratios, 2010-2012.

State County Site Maximum 3-month

mean (μg/m 3 ) Annual average (μg/m 3 ) Ratio of max 3-month mean to annual mean Ratio of max 3- month mean to annual mean for

CBSAs > 1M

population

Alabama Limestone 010830005 0.009 0.007 1.2857 Alabama Pike 011090003 1.296 0.613 2.1142 Alaska Anchorage Municipality 020200051 0.067 0.054 1.2407 Arizona Gila 040071002 0.267 0.131 2.0382 Arizona Gila 040078000 0.061 0.030 2.0333 Arizona Maricopa e 040134018 0.038 0.031 1.2258 1.2258 Arizona Pima 040191028 0.002 0.002 1.0000 California Fresno 060190011 0.005 0.004 1.2500 California Imperial 060250005 0.026 0.017 1.5294 California Los Angeles e 060371103 0.013 0.009 1.4444 1.4444 California Los Angeles e 060371302 0.015 0.007 2.1429 2.1429 California Los Angeles e 060371402 0.061 0.033 1.8485 1.8485 California Los Angeles e 060371403 0.110 0.055 2.0000 2.0000 California Los Angeles e 060371404 0.108 0.042 2.5714 2.5714 California Los Angeles e 060371405 0.450 0.241 1.8672 1.8672 California Los Angeles e 060371406 0.072 0.035 2.0571 2.0571 California Los Angeles e 060371602 0.013 0.008 1.6250 1.6250 California Los Angeles e 060374002 0.009 0.005 1.8000 1.8000 California Los Angeles e 060374004 0.010 0.006 1.6667 1.6667 California Los Angeles e 060375005 0.006 0.003 2.0000 2.0000 California Riverside e 060651003 0.008 0.005 1.6000 1.6000 California Riverside e 060658001 0.008 0.006 1.3333 1.3333 California San Bernardino e 060711004 0.010 0.006 1.6667 1.6667 California San Bernardino e 060719004 0.011 0.007 1.5714 1.5714 California San Diego e 060730003 0.006 0.005 1.2000 1.2000 California San Diego e 060731020 0.127 California San Diego e 060731021 0.058 California San Mateo e 060812002 0.331 0.255 1.2980 1.2980 California Santa Clara e 060852010 0.119 0.090 1.3222 1.3222 California Santa Clara e 060852011 0.093 0.070 1.3286 1.3286 Colorado Arapahoe e 080050007 0.023 0.014 1.6429 1.6429 Colorado Denver e 080310025 0.010 0.006 1.6667 1.6667 District of Columbia District of Columbia e 110010043 0.004 0.003 1.3333 1.3333 Florida Hillsborough e 120570100 0.044 0.025 1.7600 1.7600 Florida Hillsborough e 120571066 0.984 0.374 2.6310 2.6310

2D - 24

### APPENDIX 2D

Table 2D-8. Pb-TSP metric ratios, 2010-2012.

State County Site Maximum 3-month

mean (μg/m 3 ) Annual average (μg/m 3 ) Ratio of max 3-month mean to annual mean Ratio of max 3- month mean to annual mean for

CBSAs > 1M

population
Florida Hillsborough e 120571073 0.423 0.151 2.8013 2.8013 Georgia Bartow e 130150003 0.027 0.015 1.8000 1.8000 Georgia DeKalb e 130890003 0.004 0.003 1.3333 1.3333 Georgia Muscogee 132150009 0.230 0.128 1.7969 Georgia Muscogee 132150010 0.170 0.114 1.4912 Georgia Muscogee 132150011 0.071 0.023 3.0870 Hawaii Honolulu 150030010 0.001 0.001 1.0000 Illinois Cook e 170310001 0.024 0.018 1.3333 1.3333 Illinois Cook e 170310022 0.047 0.034 1.3824 1.3824 Illinois Cook e 170310026 0.034 0.023 1.4783 1.4783 Illinois Cook e 170310052 0.024 0.017 1.4118 1.4118 Illinois Cook e 170310110 0.294 0.077 3.8182 3.8182 Illinois Cook e 170310210 0.053 0.032 1.6563 1.6563 Illinois Cook e 170313103 0.041 0.014 2.9286 2.9286 Illinois Cook e 170313301 0.027 0.019 1.4211 1.4211 Illinois Cook e 170314201 0.011 0.010 1.1000 1.1000 Illinois Cook e 170316003 0.042 0.024 1.7500 1.7500 Illinois Macon 171150110 0.199 0.073 2.7260 Illinois Madison e 171190010 0.416 0.140 2.9714 2.9714 Illinois Madison e 171193007 0.036 0.020 1.8000 1.8000 Illinois Peoria 171430037 0.011 0.010 1.1000 Illinois Peoria 171430110 0.016 0.012 1.3333 Illinois Peoria 171430210 0.015 0.011 1.3636 Illinois St. Clair e 171630010 0.029 0.020 1.4500 1.4500 Illinois Whiteside 171950110 0.028 0.020 1.4000 Illinois Winnebago 172010110 0.063 0.028 2.2500 Indiana Delaware 180350009 0.338 0.159 2.1258 Indiana Lake e 180890023 0.077 0.031 2.4839 2.4839 Indiana Lake e 180890032 0.060 0.023 2.6087 2.6087 Indiana Lake e 180890033 0.139 0.055 2.5273 2.5273 Indiana Lake e 180892008 0.046 0.020 2.3000 2.3000 Indiana Marion e 180970063 0.079 0.028 2.8214 2.8214 Indiana Marion e 180970076 0.020 0.010 2.0000 2.0000 Indiana Marion e 180970078 0.011 0.006 1.8333 1.8333 Indiana Porter e 181270023 0.022 0.013 1.6923 1.6923

2D - 25

### APPENDIX 2D

Table 2D-8. Pb-TSP metric ratios, 2010-2012.

State County Site Maximum 3-month

mean (μg/m 3 ) Annual average (μg/m 3 ) Ratio of max 3-month mean to annual mean Ratio of max 3- month mean to annual mean for

CBSAs > 1M

population

Indiana Porter e 181270027 0.041 0.027 1.5185 1.5185 Indiana Vanderburgh 181630020 0.006 0.004 1.5000 Iowa Pottawattamie 191550011 0.263 0.123 2.1382 Iowa Scott 191630015 0.012 0.010 1.2000 Kansas Saline 201690004 0.421 0.164 2.5671 Kansas Wyandotte e 202090021 0.011 0.008 1.3750 1.3750 Kentucky Boyd 210190016 0.004 0.003 1.3333 Kentucky Madison 211510003 0.248 0.057 4.3509 Kentucky Madison 211510005 1.584 0.703 2.2532 Kentucky Russell 212070001 0.063 0.027 2.3333 Louisiana East Baton Rouge Parish 220330009 0.002 0.002 1.0000 Louisiana East Baton Rouge Parish 220330014 0.011 0.004 2.7500 Louisiana St. John the Baptist Parish e 220950003 0.053 0.025 2.1200 2.1200 Massachusetts Nantucket County 250190001 0.010 0.009 1.1111 Michigan Charlevoix 260290011 0.006 0.005 1.2000 Michigan Ionia 260670002 0.049 0.071 0.6901 Michigan Ionia 260670003 0.284 0.096 2.9583 Michigan Kent 260810020 0.008 0.005 1.6000 Michigan Oakland e 261250013 0.022 0.019 1.1579 1.1579 Michigan Tuscola 261570001 0.034 0.021 1.6190 Michigan Wayne e 261630001 0.006 0.005 1.2000 1.2000 Michigan Wayne e 261630033 0.023 0.012 1.9167 1.9167 Minnesota Anoka e 270031002 0.011 0.006 1.8333 1.8333 Minnesota Anoka e 270036020 0.038 0.017 2.2353 2.2353 Minnesota Beltrami 270072303 0.001 Minnesota Cass 270210001 0.001 Minnesota Dakota e 270370020 0.004 0.004 1.0000 1.0000 Minnesota Dakota e 270370465 0.259 0.096 2.6979 2.6979 Minnesota Dakota e 270370470 0.002 0.001 2.0000 2.0000 Minnesota Hennepin e 270530963 0.004 0.003 1.3333 1.3333 Minnesota Hennepin e 270530966 0.005 0.004 1.2500 1.2500 Minnesota Hennepin e 270531007 0.004 0.003 1.3333 1.3333 Minnesota Mille Lacs e 270953051 0.001 0.000 Minnesota Ramsey e 271230871 0.007 0.005 1.4000 1.4000 Minnesota St. Louis 271377001 0.008 0.002 4.0000

2D - 26

### APPENDIX 2D

Table 2D-8. Pb-TSP metric ratios, 2010-2012.

State County Site Maximum 3-month

mean (μg/m 3 ) Annual average (μg/m 3 ) Ratio of max 3-month mean to annual mean Ratio of max 3- month mean to annual mean for

CBSAs > 1M

population

Minnesota St. Louis 271377555 0.004 0.003 1.3333 Minnesota Stearns 271453053 0.008 0.004 2.0000 Minnesota Washington e 271630438 0.005 0.003 1.6667 1.6667 Minnesota Washington e 271630446 0.001 0.000 Missouri Iron 290930016 0.882 0.484 1.8223 Missouri Iron 290930021 1.147 0.522 2.1973 Missouri Iron 290930027 0.083 0.033 2.5152 Missouri Iron 290930029 0.115 0.038 3.0263 Missouri Iron 290930032 0.354 Missouri Iron 290930033 0.057 0.026 2.1923 Missouri Iron 290930034 0.402 0.241 1.6680 Missouri Iron 290939007 0.581 0.392 1.4821 Missouri Iron 290939008 0.387 0.209 1.8517 Missouri Jasper 290970005 0.019 0.014 1.3571 Missouri Jefferson e 290990004 1.122 0.888 1.2635 1.2635 Missouri Jefferson e 290990005 0.396 0.223 1.7758 1.7758 Missouri Jefferson e 290990009 0.191 0.055 3.4727 3.4727 Missouri Jefferson e 290990013 0.305 0.135 2.2593 2.2593 Missouri Jefferson e 290990020 0.865 0.546 1.5842 1.5842 Missouri Jefferson e 290990022 0.630 0.469 1.3433 1.3433 Missouri Jefferson e 290990023 0.563 0.386 1.4585 1.4585 Missouri Jefferson e 290990024 0.659 0.340 1.9382 1.9382 Missouri Jefferson e 290990025 0.085 0.042 2.0238 2.0238 Missouri Jefferson e 290990026 0.080 0.036 2.2222 2.2222 Missouri Jefferson e 290990027 0.592 0.454 1.3040 1.3040 Missouri Jefferson e 290999001 1.100 0.812 1.3547 1.3547 Missouri Jefferson e 290999002 0.431 0.228 1.8904 1.8904 Missouri Jefferson e 290999003 0.327 0.175 1.8686 1.8686 Missouri Jefferson e 290999004 0.442 0.156 2.8333 2.8333 Missouri Jefferson e 290999005 1.432 0.913 1.5685 1.5685 Missouri Jefferson e 290999006 0.103 0.049 2.1020 2.1020 Missouri Reynolds 291790001 0.059 0.031 1.9032 Missouri Reynolds 291790002 0.068 0.034 2.0000 Missouri Reynolds 291790003 0.100 0.027 3.7037 Missouri Reynolds 291790034 0.161 0.078 2.0641

2D - 27

### APPENDIX 2D

Table 2D-8. Pb-TSP metric ratios, 2010-2012.

State County Site Maximum 3-month

mean (μg/m 3 ) Annual average (μg/m 3 ) Ratio of max 3-month mean to annual mean Ratio of max 3- month mean to annual mean for

CBSAs > 1M

population

Missouri St. Francois 291870006 0.132 0.043 3.0698 Missouri St. Francois 291870007 0.134 0.053 2.5283 Missouri St. Louis e 291892003 0.008 0.007 1.1429 1.1429 Missouri St. Louis city e 295100085 0.028 0.026 1.0769 1.0769 Nebraska Dodge 310530005 0.139 0.055 2.5273 Nebraska Douglas 310550019 0.006 0.005 1.2000 Nebraska Nemaha 311270002 0.115 0.034 3.3824 Nevada Clark e 320030540 0.003 New Mexico Bernalillo 350010023 0.006 0.003 2.0000 New York Orange e 360713001 0.101 0.025 4.0400 4.0400 New York Orange e 360713002 1.027 0.123 8.3496 8.3496 New York Orange e 360713004 0.007 0.005 1.4000 1.4000 New York Suffolk e 361030024 0.027 0.017 1.5882 1.5882 Ohio Butler e 390170015 0.009 0.006 1.5000 1.5000 Ohio Columbiana 390290019 0.057 0.020 2.8500 Ohio Columbiana 390290020 0.025 0.015 1.6667 Ohio Columbiana 390290022 0.044 0.019 2.3158 Ohio Cuyahoga e 390350038 0.021 0.013 1.6154 1.6154 Ohio Cuyahoga e 390350042 0.030 0.013 2.3077 2.3077 Ohio Cuyahoga e 390350049 0.531 0.136 3.9044 3.9044 Ohio Cuyahoga e 390350060 0.030 0.020 1.5000 1.5000 Ohio Cuyahoga e 390350061 0.023 0.015 1.5333 1.5333 Ohio Cuyahoga e 390350072 0.035 0.014 2.5000 2.5000 Ohio Franklin e 390490025 0.011 0.009 1.2222 1.2222 Ohio Fulton 390510001 0.178 0.070 2.5429 Ohio Logan 390910006 0.006 0.004 1.5000 Ohio Marion 391010003 0.088 0.041 2.1463 Ohio Marion 391010004 0.017 0.013 1.3077 Ohio Montgomery 391137001 0.008 0.007 1.1429 Ohio Stark 391510017 0.023 0.015 1.5333 Ohio Trumbull 391550012 0.011 0.007 1.5714 Ohio Washington 391670008 0.007 0.005 1.4000 Ohio Washington 391670010 0.008 0.005 1.6000 Oklahoma Ottawa 401159006 0.022 0.012 1.8333 Oklahoma Ottawa 401159007 0.034 0.018 1.8889

2D - 28

### APPENDIX 2D

Table 2D-8. Pb-TSP metric ratios, 2010-2012.

State County Site Maximum 3-month

mean (μg/m 3 ) Annual average (μg/m 3 ) Ratio of max 3-month mean to annual mean Ratio of max 3- month mean to annual mean for

CBSAs > 1M

population
Oklahoma Pittsburg 401210416 0.004 0.003 1.3333 Oklahoma Tulsa 401431127 0.008 0.006 1.3333 Oregon Yamhill e 410711702 0.045 0.021 2.1429 2.1429 Pennsylvania Allegheny e 420030002 0.016 0.014 1.1429 1.1429 Pennsylvania Allegheny e 420030008 0.014 0.008 1.7500 1.7500 Pennsylvania Allegheny e 420030070 0.056 0.018 3.1111 3.1111 Pennsylvania Allegheny e 420031009 0.138 0.035 3.9429 3.9429 Pennsylvania Beaver e 420070006 0.085 0.051 1.6667 1.6667 Pennsylvania Beaver e 420070007 0.253 0.166 1.5241 1.5241 Pennsylvania Beaver e 420070505 0.151 0.089 1.6966 1.6966 Pennsylvania Berks 420110020 0.509 0.158 3.2215 Pennsylvania Berks 420110021 0.139 0.044 3.1591 Pennsylvania Berks 420110022 0.118 0.035 3.3714 Pennsylvania Berks 420111717 0.217 0.146 1.4863 Pennsylvania Carbon 420250214 0.104 Pennsylvania Delaware e 420450002 0.047 0.028 1.6786 1.6786 Pennsylvania Delaware e 420450004 0.047 0.028 1.6786 1.6786 Pennsylvania Franklin 420550002 0.046 0.028 1.6429 Pennsylvania Indiana 420630005 0.049 0.025 1.9600 Pennsylvania Lancaster 420710009 0.068 0.039 1.7436 Pennsylvania Lawrence 420730011 0.023 0.026 0.8846 Pennsylvania Luzerne 420790036 0.137 0.054 2.5370 Pennsylvania Philadelphia e 421010449 0.029 0.021 1.3810 1.3810 Pennsylvania Philadelphia e 421011002 0.051 0.030 1.7000 1.7000 Pennsylvania Westmoreland e 421290009 0.046 0.023 2.0000 2.0000 South Carolina Charleston 450190003 0.007 0.005 1.4000 South Carolina Florence 450418001 0.044 0.013 3.3846 South Carolina Florence 450418002 0.015 0.006 2.5000 South Carolina Florence 450418003 0.011 0.005 2.2000 South Carolina Greenville 450450015 0.006 0.005 1.2000 South Carolina Richland 450790007 0.005 0.004 1.2500 South Carolina Richland 450790019 0.024 0.011 2.1818
Tennessee Knox 470930023 0.165 0.108 1.5278
Tennessee Knox 470930027 0.042 0.020 2.1000
Tennessee Knox 470931017 0.037 0.018 2.0556

2D - 29

### APPENDIX 2D

Table 2D-8. Pb-TSP metric ratios, 2010-2012.

State County Site Maximum 3-month

mean (μg/m 3 ) Annual average (μg/m 3 ) Ratio of max 3-month mean to annual mean Ratio of max 3- month mean to annual mean for

CBSAs > 1M

population
Tennessee Shelby e 471570075 0.005 0.004 1.2500 1.2500 Tennessee Sullivan 471633001 0.076 0.056 1.3571 Tennessee Sullivan 471633002 0.044 0.036 1.2222 Tennessee Sullivan 471633003 0.053 0.038 1.3947 Tennessee Sullivan 471633004 0.080 0.044 1.8182 Texas Cameron 480610006 0.008 0.004 2.0000 Texas Collin e 480850003 0.371 0.136 2.7279 2.7279 Texas Collin e 480850007 0.199 0.093 2.1398 2.1398 Texas Collin e 480850009 0.774 0.388 1.9948 1.9948 Texas Collin e 480850029 0.180 0.052 3.4615 3.4615 Texas Dallas e 481130069 0.013 0.009 1.4444 1.4444 Texas El Paso 481410002 0.040 0.022 1.8182 Texas El Paso 481410033 0.019 0.017 1.1176 Texas El Paso 481410037 0.025 0.022 1.1364 Texas El Paso 481410055 0.019 0.010 1.9000 Texas El Paso 481410058 0.022 0.016 1.3750 Texas Harris e 482011034 0.008 0.005 1.6000 1.6000 Texas Harris e 482011039 0.004 0.003 1.3333 1.3333 Texas Kaufman e 482570020 0.104 0.044 2.3636 2.3636
Texas Potter 483750024 0.020 0.007 2.8571 Texas Webb 484790016 0.026 0.018 1.4444 Utah Salt Lake e 490351001 0.057 0.024 2.3750 2.3750 Virginia Amherst 510090007 0.018 0.006 3.0000 Virginia Buchanan 510270006 0.014 0.012 1.1667 Virginia Henrico e 510870014 0.005 0.005 1.0000 1.0000 Virginia Roanoke city 517700011 0.109 0.033 3.3030 Washington King e 530330029 0.055 0.036 1.5278 1.5278 Washington Snohomish e 530610013 0.023 0.013 1.7692 1.7692 West Virginia Cabell 540110006 0.012 0.010 1.2000 Wisconsin Sheboygan 551170008 0.152 0.056 2.7143 Puerto Rico Arecibo Municipio, Puerto Rico 720130001 0.339 0.171 1.9825 Puerto Rico Bayamón Municipio, Puerto Rico e 720210010 0.011 0.004 2.7500 2.7500 Puerto Rico Salinas Municipio, Puerto Rico 721230002 0.017 0.008 2.1250

2D - 303A-1 

### APPENDIX 3A

INTERPOLATED RISK ESTIMA TES FOR THE GENERALIZED (LOCAL) URBAN CASE STUDY

This Appendix describes the method used to develop risk estimates for conditions just meeting the current standard (0.15 μg/m 3 , as a maximum 3-month average) for the generalized (local) urban case study. These risk estimates were developed by interpolation from the 2007 REA results for this case study. The general a pproach was to identif y the two alternative
standard scenarios simulated in the 2007 RE A which represented air quality conditions bracketing those for the current st andard and then linearly interpol ate an estimate of risk for the current standard based on the slope created from the two bracketing estimates. In representing air quality conditions for these purposes, we focused on the annua l average air Pb concentration
estimates as that is the metric which had been the IEUBK model inputs fo r the various air quality scenarios (IEUBK does not accept air quality inputs of a temporal scale shorter than a year). 1 An annual average concentration estimate to represen t the current standard was identified in a manner consistent with that employed in the 2007 REA for this case study (see section 3.4.3.2 above, use of 2003-2005 data) with the use of cu rrently available monitoring data (2010-2012) for relationships between air quality metrics for representation of the current standard. By this method, the air quality scenario fo r the current standard (0.15 μg/m 3 , as a not-to-be-exceeded 3- month average) was found to be bracketed by the scenarios for alternativ e standards of 0.5 and 0.20 μg/m 3 (maximum monthly averages). A risk estimate for the current standard was then derived using the slope relating generalized (l ocal) urban case study IQ loss to the annual average Pb concentration used for those two air qu ality scenarios. We us ed this interpolation approach to develop median risk estimates for th e current standard based on each of the four C-R
functions. Details on the method for the in terpolation approach are provided below.
1. Identify an estimate of annual average air Pb concentration to repr esent each air quality scenario. For the alternative s cenarios, this was done in the 2007 REA using the 2003- 2005 Pb-TSP dataset for urban areas of populatio n greater than one million. For analysis

1 Although many different patterns of temporally vary ing air concentration will just meet a given potential alternative standard, the shortest ti me step accommodated by the blood Pb model is a year. Thus, the air Pb concentration inputs to the blood Pb model for each air qu ality scenario are annual average air Pb concentrations. For the generalized (local) urban case study, the national Pb-TSP monitoring dataset wa s analyzed to characterize the distribution of site-specific relationships between metrics reflecting the averaging time and form for the air quality scenarios being assessed (Table 3-8 of this docu ment) and the annual average. The IEUBK annual average input was then derived by multiplying the level for a given air quality scenario by the ratio for the averaging time and form for that air quality scenario. For the location-specific case studies, however, the full temporally varying air Pb concentration dataset for each exposure zone was used to derive the average annual concentration for the IEUBK input.3A-2 of the current standard here, this uses the recent Pb-TSP dataset (2010-2012) for urban areas of population greater than one million. The concentration in terms of the metric being assessed (e.g., maximum 3-month or ca lendar quarter average) was derived per monitoring site, as was the annual average co ncentration and also the ratio of the two (2007 REA, Appendix A; Appendix 2D of this document). From the average of the monitor-specific ratios we derived the annual average estimate. [In the 2007 REA, this was the IEUBK air quality input for each AQ scenario.] With the 2010-2012 data, the average, across monitors in urban areas grea ter than 1 million populat ion, of the ratio of maximum 3-month average to annual average is 1.92 (Appendix 2D in this document).

- This ratio was used to derive an an nual average air Pb-TSP concentration estimate to represent the current st andard scenario (annual value = 0.15 μ g/m 3 * 1/1.92 = 0.078 μ g/m 3 ). The annual average values for the scenarios included in the 2007 REA and also for the current standard scenario considered in this interpolation are shown in Table 3A-1 below.

Table 3A-1. Annual average air Pb-TSP concentratio n estimates for different air quality scenarios.

Air Quality Scenarios

Annual Average Estimate ( μ g/m 3 ) Maximum Quarterly Average D ( μ g/m 3 ) Maximum Monthly Average ( μ g/m 3 ) Maximum 3-month Average ( μ g/m 3 ) 1.5 (previous NAAQS) 0.60
0.5 0.130 0.2 0.08
0.15 0.078*
0.2 0.05 0.05 0.013 0.02 0.005 * Derived as described in step 1 using 2010-2012 air quality dataset.

2. Identify the two “bounding” alternative standar d levels that will be used to derive a slope for the risk interpolati on for the current standard level. Based on comparison of the annual ambient air Pb estimates for each of the 2007 REA air qua lity scenarios and for the current standard we determine which scenarios “bound” the current standard (in terms of the annual average ambient Pb estimate). As Table 3A-1 above shows, the bounding scenarios are the scenarios for ju st meeting maximum monthly average concentrations of 0.5 and 0.2 μg/m 3

.

3. Calculate the slopes of generalized (loc al) urban case study IQ loss per unit annual average Pb estimate for each risk estimate of interest for the two bounding scenarios. This calculation is (IQ Loss Scenario X – IQ Loss Scenario Y )/ (annual average Scenario X – annual
average Scenario Y ). The risk estimates for the 4 di fferent C-R functions and two exposure pathway categories of interest ( Recent Air and Recent + Past Air ), with the derived slopes, are in Table 3A-2.3A-3 Table 3A-2. Risk estimates for bounding air qualit y scenarios and associated slopes.

Risk Estimates for different C-R functions a nd exposure pathway categories Log-linear with low-exposure linearization Dual linear – stratified at 10 μ g/dL peak Log-linear with cutpoint Dual linear - stratified at 7.5 μ g/dL peak Recent

air Recent + past air Recent air Recent + past air Recent air Recent + past air Recent air Recent + past air 0.2 μ g/m 3 , max quarterly average 1.53 3.37 0.54 1.18 0.63 1.38 1.97 4.34

0.2 μ g/m 3 max monthly average 1.21 3.16 0.41 1.08 0.47 1.22 1.53 3.99
Slope * 10.69 7.03 4.10 3.38 5.31 5.28 14.77 11.66
* In terms of points IQ loss per unit annual average air Pb in generalized (local) urban case study (see texts for explanation)

.

4. Derive interpolated risk estimates for the current standard scenario. Using the slopes presented in Table 3A-2 and the lower bounding air quality scenario risk estimates, derive corresponding risk estimat es for the current standard scenario: Risk = lower bounding risk + (incre ment annual average Pb * slope)

Where:

 lower bounding risk = risk for the lower bound air quality scenario (i.e., for 0.2 μg/m 3 maximum monthly average)

 increment annual average Pb is the difference between the annual average estimates for the current standa rd and the lower bounding scenario.

 slope is the value described in Step 4, which differs across the 8 combinations of C-R functions a nd exposure pathway categories. The resulting interpolated risk estim ates are presented in Table 3A-3.

Table 3A-3. Interpolated risk estimates for the current NAAQS scenario for the generalized (local) urban case study.

Risk Estimates for different C-R functions a nd exposure pathway categories Log-linear with low-exposure linearization Dual linear – stratified at 10 μ g/dL peak Log-linear with cutpoint Dual linear - stratified at 7.5 μ g/dL peak Recent

air Recent + past air Recent air Recent + past air Recent air Recent + past air Recent air Recent + past air Interpolated

Estimate* 1.51 3.36 0.53 1.17 0.62 1.37 1.94 4.32

* Points IQ loss in generalized (local) urban case study (see text for explanation).5A-1 APPENDIX 5A

ADDITIONAL DETAIL ON 2006 ECOLOGICAL SCREENING ASSESSMENT

Setting and spatial extent of dataset or modeling analysis Media Screened and Screening Levels Used

Soil Freshwater water column Freshwater Sediment

Primary Smelter Case Study Herculaneum, Missouri: soil and waterbody samples from study area 6 km diameter, centered on point

source Soil screening

values developed based on U.S. EPA Superfund methodology for developing ecological soil screening levels (USEPA, 2005a,b) U.S. EPA freshwater AWQC for aquatic lifeadjusted for sitespecific water hardness Sediment screening values based on MacDonald et al. (2000) sediment quality assessment guidelines

Seconday Smelter Case Study Troy (Pike County), Alabama: soil concentrations in census blocks near facility predicted from dispersion and soil mixing model NA NA

Near Roadway

Non-Urban Case Study Two datasets: Corpus Christi, Texas (within 4 m from road), and Atlee, Virginia (within 2 to 30 m from road)

Vulnerable Ecosystem Case Study Hubbard Brook Experimental Forest, New Hampshire: forest in oblong basin about 8 km long by 5 km wide While no quantitative analyses were performed, summary review of literature search indicated: (1) atmospheric Pb inputs do not directly affect stream Pb levels at HBEF because deposited Pb is almost entirely retained in the soil profile; (2) soil horizon analysis results show Pb has become more concentrated at lower depths over time and that the soil profile serves as a Pb sink, appreciably reducing Pb in porewater as it moves through the soil layers to streams, (3) dissolved Pb concentrations were reduced (5 ppb to about 5 ppt) as Pb moves from the Oa horizon to streams. Studies concluded insignificant contribution of dissolved Pb from soils to streams (less than 0.2 g

· ha ̄1

· yr ̄1). (ICF, 2006, Appendix E)

National Surface Water Screen Surface water bodies in the 47 basin study units from all regions of the United States, covering

approx. 50% of U.S. land base NA U.S. EPA freshwater AWQC for aquatic life adjusted for hardness at site or nearby water body Sediment screening values based on MacDonald et al. (2000) sediment quality assessment guidelines
AWQC= Ambient water quality criteria. NA = Not applicable; medium not part of case study. NOTE: Information here is drawn from ICF, 2006 and EPA, 2007b.

### ATTACHMENT

Clean Air Scientific Advisory Committee Letter (June 4, 2013)UNITED STATES ENVIRONMENTAL PROTECTION AGENCY WASHINGTON D.C. 20460

OFFICE OF THE ADMINISTRATOR SCIENCE ADVISORY BOARD June 4, 2013

EPA

- CASAC

- 1 3

- 005

The Honorable Bob Perciasepe Acting Administrator U.S. Environmental Protection Agency 1200 Pe nnsylvania Avenue, N.W. Washington, D.C. 20460

Subject: CASAC Review of the EPA’s Policy Assessment for the Review of the Lead National Ambient Air Quality Standards (External Review Draft

– January 2013)

Dear Acting Administrator Perciasepe :

The Clean Air Scientific Advisory Committee (CASAC) Lead Review Panel met on February 5

- 6
, 201 3

, to peer review the EPA’s Policy Assessment for the Review of the Lead National Ambient Air Quality Standards (External Review Draft

– January 2013) , hereafter referre d to as the P A

. The CASA C’s consensus responses to the a gency’s charge questions and the i ndividual review comments from the CASAC Lead Review Panel are enclosed . The CASAC’s key points are highlighted below.

Overall, the CASAC concurs with the EPA that t he cu rrent scientific literature does not support a revision to the Primary Lead (Pb) National Ambient Air Quality Standard (NAAQS) nor the Secondary Pb NAAQS. Although the current review incorporates a substantial body of new scientific literature, the

ne w literature does not justify a revision to the standards because it does not significantly reduce substantial data gaps and uncertaint ies (e.g.

, air

- blood Pb relationship at low levels ; sources contributing to current population blood Pb leve ls, especiall y in children; the relationship between Pb and childhood neurocognitive function at current population exposure levels ; the relationship between ambient air Pb and outdoor dust and surface soil Pb concentrations ). Further detail s on these and other researc h needs

are provided in the consensus responses. T he CASAC recommends that research be performed to address these data gaps and uncertainties to inform future Pb NAAQS reviews.

The CASAC has additional comments and recommendations on improving the documen t

. W ith the completion of the recommended revisions outlined below and in the consensus responses, the PA will serve its intended purpose

. A nother CASAC review of the document is not need ed

.

The PA should include a discussion that Pb i s a unique pollutant in many ways. Unlike other criteria air pollutants, Pb is of concern from a multimedia perspective . Millions of tons of Pb are present in the environment from legacy sources . The distribution of this substantial reservoir of Pb is not known

. T hus

, the ext ent of current human exposure from t his legacy cannot be reliably estimated. The PA generally captures the key aspects of the health effects evidence presented in the Integrated Science Assessment , but can be made more concise and cl e ar by providing summar y conclusions2 regarding the health effects evidence at the beginning of the sections. The risk and exposure information from the previous Pb NAAQS review is adequately presented . The CASAC concurs that a new risk and exposure assessment ( REA ) is not needed due the lack of sufficient new scientific information to warrant revision of the prior REA data and methods

. The application of the evidence

- based framework and the use of the health risk and exposure information from the previous Pb NAAQS review seem a ppropriate and provide a sufficient rationale to support retaining the current primary standard without revision . However, there should be more description in the PA of the data and rationale behind the averaging time and form of the current primary standa rd. Additionally, research is needed to address uncertainties and data gaps in the evidence

- based framework and in the health risk and exposure information for future Pb NAAQS reviews.

Given the existing scientific data , t he CASAC concurs with retaining t he current secondary standard without revision

. However, the CASAC also notes that important research gaps remain. For example questions remain regarding the relevance of the primary standard’s indicator, level, averaging time

, and form for the secondary s tandard. Other areas for additional research to address data gaps and uncertainty include developing a critical loads approach for U.S. conditions and a multi

- media approach to account for legacy Pb and contributions from different sources. Addressing thes e gaps may require reconsideration of the secondary standard in future assessments.

The CASAC also wishes to highlight the importance of a separate but related policy issue. The CASAC notes that it has not considered this separate policy issue in providi ng advice on the NAAQS. The decrease in childhood lead poisoning in the United States over the last three decades is a great public health success story. Concurrently, there is a trend of increased relocation of Pb production, recycling, and recovery to ot her nations. One example is the export of spent lead acid batteries (SLAB) to Mexico. As detailed in a report by the Secretariat of the Commission for Environmental Cooperation (CEC), environmental and health protections in the secondary lead industry in o ther countries are not functionally equivalent to those in the United States. The CEC offers recommendations to avoid development of pollution havens and for the United States to work with Mexico and Canada to foster adoption of best practi ces throughout N orth America. The CASAC recognize s the role of the EPA Administrator as a member of the CEC Council and strongly urge s the EPA to carefully consider the recommendations of the CEC report, and to support decisive action that will enable the success of the P b NAAQS in the United States to be a role model for development of best practices internationally that avoid adverse public health impacts abroad. For example, the considerable effort by the EPA to develop the ISA and the PA could be a valuable starting po int for other countries to develop or revise their own ambient standards for lead.3 The CASAC appreciates the oppo rtunity to provide advice a nd looks forward to receiving the EPA’s
response

. Sincerely,

/s igned/

Dr. H. Christopher Frey, Chair Clean Air Scientific Advisory Committee

Enclosuresi NOTICE

This report has been written as part of the activities of the EPA's Clean Air Scientific Advisory Committee (CASAC), a federal advisory committee independently chartered to provide e xtramural scientific information and advice to the Administrator and other officials of the EPA . The CASAC provides balanced, expert assessment of scientific matters related to issues and problems facing the

a gency

. This report has not bee n reviewed for ap proval by the a gency and, hence, the contents of this report do not necessarily represent the views and policies of the EPA, nor of other agencies within the Executive Branch of the federal government

. In addition, any mention of trade names or commercial products does not constitute a recommendation for use . The CASAC reports are posted on the EPA

w ebsite at: http://www.epa.gov/casac

.ii 

### U.S. Environmental Protection Agency Clean Air Scientific Advisory Committee CASAC L ead Review Panel (2010

- 2013)

CHAIR Dr. H. Christopher Frey , Distinguished University Professor, Department of Civil, Construction and Environmental Engineering, College of Engineering, North Carolina State University, Raleigh, NC

OTHER CASAC MEMBER Mr . George A. Allen , Senior Scientist, Northeast States for Coordinated Air Use Management (NESCAUM), Boston, MA

CONSULTANTS Dr. Herbert Allen , Professor Emeritus, Department of Civil and Environmental Engineering, University of Delaware, Newark, DE

Dr. R ichard Canfield , Senior Research Associate, Division of Nutritional Sciences, Cornell University, Ithaca, NY

Dr. Deborah Cory

- Slechta , Professor, Department of Environmental Medicine, School of Medicine and Dentistry, University of Rochester, Rochester, N Y

Dr. Cliff Davidson , Professor, Civil and Environmental Engineering, Syracuse University, Syracuse, NY

Dr. Philip E. Goodrum , Senior Consultant, Cardno ENTRIX, Syracuse, NY

Dr. Sean Hays , President, Summit Toxicology, Allenspark, CO

Dr. Philip Hopke

, Bayard D. Clarkson Distinguished Professor, Department of Chemical and Biomolecular Engineering, Clarkson University, Potsdam, NY

Dr. Chris Johnson , Professor, Department of Civil and Environmental Engineering , Syracuse University, Syracuse, NY

Dr. Susa n Korrick , Assistant Professor of Medicine , Department of Medicine, Brigham and Women's Hospital, Channing Laboratory, Harvard Medical School, Boston, MA

Dr. Michael Kosnett , Associate Clinical Professor, Division of Clinical Pharmacology and Toxicology, Department of Medicine, University of Colorado School of Medicine, Denver, COiii Dr. Roman Lanno , Associate Professor and Associate Chair, Department of Evolution, Ecology, and Organismal Biology, Ohio State University, Columbus, OH

Mr. Richard L. Poirot

, Environmental Analyst, Air Pollution Control Division, Department of Environmental Conservation, Vermont Agency of Natural Resources, Waterbury, VT

Dr. Joel G. Pounds , Laboratory Fellow, Cell Biology & Biochemistry, Biological Sciences Division, Pacific N orthwest National Laboratory, Richland, WA

Dr. Michael Rabinowitz , Geochemist, Marine Biological Laboratory, Newport, RI

Dr. William Stubblefield , Senior Research Professor, Department of Molecular and Environmental Toxicology, Oregon State University, C orvallis, OR

Dr. Ian von Lindern , President, TerraGraphics Environmental Engineering, Inc., Moscow, ID

Dr. Gail Wasserman , Professor of Clinical Psychology in Child Psychiatry, Division of Child and Adolescent Psychiatry, College of Physicians and Surgeo ns, Columbia University, New York, NY

Dr. Michael Weitzman , Professor, Pediatrics; Psychiatry, New York University School of Medicine, New York, NY

SCIENCE ADVISORY BOARD STAFF Mr. Aaron Yeow , Designated Federal Officer, U.S. Environmental Protection A gency, Science Advisory Board (1400R), 1200 Pennsylvania Avenue, NW, Washington, DCiv 

### U.S. Environmental Protection Agency Clean Air Scientific Advisory Committee CASAC

CHAIR Dr. H. Christopher Frey , Distinguished University Professor, Department of Civi l, Construction and Environmental Engineering, College of Engineering, North Carolina State University, Raleigh, NC

MEMBERS Mr. George A. Allen , Senior Scientist, Northeast States for Coordinated Air Use Management (NESCAUM), Boston, MA

Dr. Ana Diez

- Rou x , Professor of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, MI

Dr. Jack Harkema , Professor, Department of Pathobiology, College of Veterinary Medicine, Michigan State University, East Lansing, MI

Dr. Helen Suh , Associate Pro fessor, Bouve School of Health Sciences, Northeastern University, Boston, MA

Dr. Kathleen Weathers , Senior Scientist, Cary Institute of Ecosystem Studies, Millbrook, NY

Dr. Ronald Wyzga , Technical Executive, Air Quality Health and Risk, Electric Power Re search Institute, Palo Alto, CA

SCIENCE ADVISORY BOARD STAFF Dr. Holly Stallworth , Designated Federal Officer, U.S. Environmental Protection Agency, Science Advisory Board (1400R), 1200 Pennsylvania Avenue, NW, Washington, DC1 Consensus Responses to Char ge Questions on EPA’s Policy Assessment for the Review of the Lead National Ambient Air Quality Standards (External Review Draft

– January 2013)

Chapter 1

– Introduction

This chapter provides context for the review, including the background of past rev iews, as well as the scope for the current review. This includes discussion of fate and multimedia pathways of ambient air Pb and other nonair sources of Pb in the environment.

Does the Panel find the introductory and background material, including that p ertaining to previous reviews of the Pb standard and the scope of the current review to be appropriately characterized and clearly communicated?

Chapter 1 of the Policy Assessment ( PA ) is reasonably well characterized and for the most part clearly communi cated, although there are several improvements that should be made (see below). The CASAC

concurs with the EPA that the current scientific evidence does not justify a change to the current Lead (Pb) National Ambient Air Quality Standards ( NAAQS ) , with the caveats stated below

. Chapter 1 should emphasize Pb as a unique pollutant in many ways. Historically, anthropogenic emissions of Pb to the air around the globe exceed ed natural emissions by a huge margin, more than any other trace metal. Natural emission s come from unpolluted soil, seaspray, and other natural sources. R emoval of Pb from gasoline, paint, solder, and other anthropogenic sources constitutes what is arguably the biggest environmental success story for any pollutant to

- date. U nlike other crite ria air pollutants, Pb is of concern from a multimedia perspective; human exposure to Pb comes from inhalation of air and also from ingestion of food, water, and dust. In addition, Pb may be the pollutant with the biggest legacy problem : millions of tons o f Pb are now present in the environment as a result of discharges from years ago

. T he distribution of this huge reservoir of Pb is not known , and thus current human exposure from this legacy cannot reliably be estimated

. What is known , however, is that hum an activities have on average substantially elevated the Pb content of soil at numerous locations around the United S tates , more so than other trace metals process ed in large quantities. Although air Pb levels are much lower because of reduced emissions, s oil Pb can be expected to remain elevated for many years. These unique aspects of Pb, especially the problem of not knowing the distribution of legacy Pb, should be clearly discussed in the PA.

This c hapter conclu des that there is no information published in the last five years justifying reconsideration of the current NAAQS. Although that is true , this conclusion should be conveyed with an assessment of the adequacy of the old information. In particular, there were significant unknowns and uncertainties a ssociated with a lack of information five years ago; those unknowns and uncertainties still remain.

There are no statements in the PA that the Integrated Science Assessment ( ISA ) is limited only to exposures and data sources considered currently relevant to the U

. S

. population , as oppos ed to populations outside of the United S tates

. Furthermore, the literature is considered only to assess how new studies relate to c onclusio ns drawn in the past review, and t hen only to studies in the peer

- reviewed literatur e. This has resulted in an ISA that is dedicated predominately to toxicology, health effects,2 bio kinetics, and causal determinations. These are areas that were data rich in the last review, and continue to produce volumes of new peer

- reviewed information. In contrast, in areas where the least is known and EPA relies on past findings, uncertainty is becoming greater as the existing information becomes outdated

. Additionally, t he current assessment excludes consideration of impacts on populations outside of t he U nited S tates

.

There is considerable discussion dedicated to the reduction of Pb in air and other media in the U nited S tates over the last four decades. Most of the reduction was achieved through the elimination of tetra

ethyl Pb gasoline additives. A nother major component of the reduction was substantial decreases in emissions from primary and secondary smelters, and metals processing industries. In the case of moto r vehicle gasoline

- related emissions, these ceased and other non

- Pb products were subst ituted in commerce. This resulted in decreased Pb emissions and health and environmental effects in both the U nited S tates and globally. Within the U nited S tates, Pb continues to be used as an octane boosting fuel additive for very high octane fuels used i n general aviation for piston engine aircraft. In the case of Pb production and secondary recovery, however, this production and recovery were exported overseas. T here is no mention of the impact of the “avoided emissions” in their new locales.

Thus, over all, there is no reason to change the c urrent airborne Pb standard. However, although ai rborne Pb is far more limited as a problem within the United States

, potential exposure to Pb in other environmental media in the U nited S tates is likely to be more sig nificant. Furthermore, there may be increasing Pb exposures overseas (e.g., as d escribed in CEC, 2013 )

.

There are a few areas that need revision for clarity and accuracy. On page ES

- 1, line 25

, the following
sentence should be added to the end of the para graph: “ This approach was taken to aid in the decision to retain or revise the current standards.” O n page 1

- 13 line 35 , it states: “And we recognize that past Pb emissions in many situations were well in excess of the current Pb standard.” One cannot comp are emissions to an airborne standard. This sentence can be revised to state: “ W e recognize that past Pb emissions in many situations caused airborne Pb concentrations far in excess of the current Pb standard.”

Chapter 2

– Ambient Air Lead

This chapter provides an overvie w of current information on air Pb emissions and monitoring data, consideration of the current air Pb monitoring requirements and an overview of current information on Pb in nonair media.

To what extent does the Panel agree that the mos t relevant information on emissions (section 2.1), air quality (section 2.2.2), and Pb concentrations in other media (section 2.3) is presented, and to what extent is the information presented appropriately characterized and clearly communicated?

With a f ew minor exceptions (see specific individual panel member comments)

, the information on Pb emissions, air quality and concentrations in other media is appropriately characterized and clearly presented. Historical and recent (2008) emissions data are summar ized quantitatively in clear charts and tables, with additional detail on the 2008 National Emissions Inventory ( NEI ) data sources and limitations provided in Appendix 2A. There are also qualitative discussions and an informative Appendix 2B on recent regu latory actions, indicating that current emissions have declined since 2008, with additional reductions pending. However, q uantitative estimates of emissions reductions w ould be3 informative

. To the extent that these or other historical controls of U

. S

. Pb s ource categories have shifted Pb emissions to other countries, it would be informative to include discussion of those displaced emissions.

The information on ambient air concentrations is clearly presented (for sites with 1 to 3 years of valid data for 20 09 to 2011) in maps, charts and in a detailed appendix ( Appendix 2D). More recent measurements from sites (including near airports) initiated since the previous Pb NAAQS review w ould help inform the current Pb NAAQS review, as well as the separate Section 231 av iation gas oline ( “ avgas ” ) review.

Given t he “not to be exceeded” 3

- month rolling average form of the Pb NAAQS , an exceedance could be determined with as few as 3 months of new data

. Therefore, i t would be useful if more recent data are summarized i n the next Pb PA , without being limited to sites with multiple years of valid data.

The information on Pb concentrations in other media is clearly presented. The sections (2.3.2.1 and 2.3.2.2) on indoor and outdoor dust are highly relevant to exposure ass essments and would benefit from some added discussion of how dust Pb concentration, loading, and loading rates are measured. In particular, information relating to the differences in particle sizes in dust samples and ambient air samples would be helpful. More information on changes, if any, over time in t he availability of historically deposited soil Pb for resuspension to the air or for direct uptake through ingestion could help clarify the significance of this potentially important source category.

Wit h regard to information on ambient Pb monitoring (section 2.2.1), to what extent is this information appropriately characterized and clearly communicated?

The information on ambient Pb monitoring is appropriately characterized and clearly communicated. It is understood that the high

- volume ( Hi

- Vol ) Total Suspended Particulates ( TSP ) sampler i s an imperfect historical artifact, and that there is not time for this review cycle of the Pb NAAQS to develop

, fully test

, and deploy alternative samplers that would consistently capture particles (less than and) greater than 10 microns with appropriate collection efficiencies and size ranges under varying wind spee ds and directions. The draft PA notes that the EPA expects a new, improved sampler to be “available for

co nsideration in a future review.” Toward this goal, discussion is needed regarding the desirable cut size characteristics of, and practical constraints on, an alternative sampler. Information from the ISA could be cited here, such as material currently on page 3

- 67 of the 3 rd external draft of the ISA that may be revised for the final ISA regarding discussion of the desirable cut size.

If an alternative low

- volume sampler could be developed with an upper 50% particle cut size in the range of 15 to 20 mi crons, and without the wind speed and direction biases of the Hi

- Vol TSP sampler

, it seems likely that such a sampler would typically capture as much (or occasionally more) Pb as the Hi

Vol TSP sampler

. The CASAC has previously recommended the development of a new air Pb sampler that collects larger particle sizes

, that could improve the quality of sampling in the National Air Toxics Trends Station (NATTS) network , and that could serv e as an Federal Reference Method ( FRM ) or Federal Equivalent Method ( FEM ) for Pb . Filters collected by this sampler also would be amenable to multi

- elemental analyses by lower

- cost analytical methods and could be useful for more accurate and precise assessments of other particulate pollutants with significant coarse mode concent rations, including chemical contaminants ( like hexavalent chromium, silica, and cadmium) and biological components like pollen, fungi

, and endotoxins.4 Chapter 3

– Health Effects and Exposure/Risk Information

This chapt er discusses key policy relevant aspe cts of the health effects evidence and exposure/risk information.

To what extent does the information in sections 3.1 (Internal Disposition and Biomarkers of Exposure and Dose), 3.2 (Nature of Effects) and 3.3 (Public Health Implications and At

- Risk Popu lations) capture and appropriately characterize the key aspects of the evidence assessed and integrated in the ISA?

C hapter 3 of the draft PA generally captures the key aspects of the evidence presented in the ISA ; therefore

, concerns about content stem f rom the content of the ISA and not its condensation in the PA.

Recognizing the degree of condensation needed to summarize the ISA in only a few pages, this format presents a great writing challenge, and the writing in the chapter lack s clarity

. W ordiness should be reduced to directly and efficiently convey the meaning. For example, sentences such as the following could be shortened and recast in a more active voice: “The results from the various case studies assessed, with consideration of the context in which they were derived (e.g., the extent to which the range of air

- related pathways were simulated, and limitations associated with those simulations), and the multiple sources of uncertainty (see section 3.4.7 below) are also informative to our understan ding of air

- to

- blood ratios.” (Please refer to Dr. Canfield’s individual comments for details on the sentences in need of streamlining and clarification.)

In addition, there are a few places where legacy text f rom the previous PA remains, so extraneous wo rds need to be deleted and tenses updated. What needs the most attention is the length and complexity of
some sentences

. To what extent is the newly available evidence on air

- to

- blood ratios appropriately characterized and considered in light of informat ion previously available in past reviews?

The new information on air

- to

- blood ratios is presented in context of previous information and no change in the estimate is justified at this time.

When revising this section (3.1) it would be helpful to first r ead the last (summary paragraph) on page 3

- 14. Those conclusions should be included in the first paragraph of the section and then restated at the end of the section when the reader will be in a position to understand the context.

To what extent is the n ewly available evidence on concentration

- response functions for IQ decrements in young children appropriately characterized and considered in light of information previously available in past reviews?

The newly available evidence is appropriately characte rized. Parametric information could be extracted from these data to produce quantitative results for blood Pb subgroups, but the quality of the data would
not likely provide a useful basis for altering the conclusions reached from the data available prior to 2008.

There is a critical need for more information about effe cts of Pb at levels in the 0

- 5 μ g/dL range. Studies about effects of Pb at these low levels are a future research need.5 With regard to the exposure and risk information, to what extent is th e information drawn from the human exposure and health risk assessment in the last review sufficiently characterized and clearly communicated? To what extent is the information appropriately interpreted in light of the currently available information and f or the purpose of assessing the adequacy of the now current standard?

Information from the last review is well

- characterized and appropriately interpreted , but t he c larity of communication should be improved. Putting the conclusion in the first paragraph of the section was very helpful. The CASAC concurs that a new risk and exposure assessment ( REA ) is not warranted at this time.

Are the limitations and uncertainties in the exposure/risk information appropriately characterized and considered in our inter pretation of the information in the context of this current review?

The l imitations and uncertainties in the exposure/risk information are well characterized. Epidemiological data are inherently limited; there is a lack of data on the effects of Pb exposu re at the levels that are common today and thus concentration

- response ( C

- R ) estimates require extrapolation. Parameter choices for biokinetic models typically require restrictive assumption s

. No single air quality scenario is adequate.

There are specific areas of the chapter that should be revised for clarity:

• Page 3

- 2, Line 15 , referring to distribution of Pb from bone to blood, includes the sentence: “Changes in Pb exposure circumstances also can influence these exchanges, e.g., substantial reductions in exposure levels contribute to increased release of Pb from the bone into the blood (ISA, section 4.3.5).” This sentence should be revised, as it appears to incorrectly characterize the information in section 4.3.5 of the ISA. A reduction in external Pb exposure does not, from a pharmacodynamic standpoint, induce an increase in the release of Pb from bone. In the context of the paragraph, the intended point could be expressed as follows: “When there are substantial reductions in external Pb exposure, the relative contribution of Pb from bone to the concentration of Pb in blood increases.”

• Page 3

- 5, line 29 to Page 3

- 6, line 9: The italicized sentence in this paragraph, reproduced below, should be revised to improve clarity:

“ The response of adult blood P b levels to appreciable changes in exposure circumstances is generally slower than that of blood Pb levels in young children. For example, simulations using biokinetic models indicate that blood Pb levels in adults achieve a new quasi

- steady state within 7 5

- 100 days (approximately 3

- 4 times the blood elimination half

- life) subsequent to abrupt increases in Pb intake (ISA, section 4.3.5.2); similar models indicate a much quicker response of blood Pb levels in children both with regard to abrupt increases and reductions in Pb exposure (ISA, section 4.3.5.1). The response in young children may reflect their much more labile bone pool associated with the rapid turnover of bone mineral in response to their rapid growth rates (ISA, section 4.3.5 ). As a result of t hese physiological processes in young children, their blood Pb levels tend to more quickly reflect changes in their total body burden (associated with their shorter exposure history), and also can reflect changes in recent exposures (ISA, section 4.3.5). ”6 Instead of the italicized sentence above, substitution of a sentence such as the following might enhance clarity: “Because the skeletal compartment of Pb is relatively smaller and subject to more rapid turnover in children compared to adults, the blood P b concentration of children is more reflective of their recent external exposure.”

• Page 3

- 19 lines 23

- 24 : It might be clearer to use the phrase “qualitatively change” rather than “appreciably change” to allow for appreciable strengthening of the previous conclusion but no change of consequence.

• Page 3

- 22 lines 17

- 23: This is a helpful discussion of the problem with unknown earlier exposures in adults and older children. The topic comes up multiple times throughout this document and becomes redundant. May be this should be covered fully (including this as a general critique of cross

- sectional studies), early in the chapter and then simply referred back to when the context warrants.

Chapter 4

– Review of the Primary Standard for Lead

This chap ter describ es the basis for the current primary standard and consideration of the current evidence and exposure/risk

- based information with regard to reaching preliminary staff conclusions about the adequacy of the current standard.

In this chapter, staff applies t he same evidence

- based air

- related IQ loss framework as developed and used in the last review, which has fundamentally two key inputs: an air

- to

- blood ratio and the slope of a concentration

- response (C

- R ) function for IQ decrements in young children.

This draft PA is constrained by the absence of new observational and e xperimental data that address

, at least in part, limitations and uncertainties in the evidence that was present at the time of the last update of the Pb NAAQS. U ntil evidence is available to assess Pb exposure and health risks related to air Pb levels reflecting the current standard, a substantive refinement and update of the PA will not be possible. The obvious uncertainty underlying evaluation of this PA is whether lowering the standard wou ld (or would not) impact exposure and thus risk. The CASAC agrees with the EPA conclusion that “there is appreciable uncertainty associated with drawing conclusions regarding whether there would be reductions in blood Pb levels from alternative lower level s as compared to the level of the current standard.” If lowering the primary standard would lower blood Pb levels amongst the U

. S

. population, then the re would be potential public health benefit s from a lower standard. Research priorities discussed below a re designed to help inform these uncertainties.

To what extent does the Panel agree with application of the evidence

- based framework from the last review, particularly with regard to consideration of the currently available information, and related limita tions and uncertainties, for air

- to

- blood ratios and C

- R functions for IQ decrements in young children?

The application of the evidence

- based framework from the previous Pb NAAQS review seems appropriate . The new literature published since the previous re view provides further support for the health effect co nclusions presented in th at review. Additionally, the new studies do not fundamentally alter the uncertainties for air

- to

- blood ratios or C

- R functions for IQ decrements in young children.7 As previousl y discussed with CASAC, staff concluded that the current information does not warrant development of a new REA in this review. Thus, exposure/risk information was drawn from the REA conducted in the last review.

What are the Panel’s views on staff’s inter pretation of the exposure/risk information, and on staff’s conclusions that the information is generally supportive of conclusions drawn from the evidence

- based framework as to the adequacy of the current standard?

The use of exposure/ risk information fro m the pr evious Pb NAAQS review appears appropriate given the absence of significant new information that could fundamentally change the interpretation of the exposure/risk information

. This interpretation is reasonable given that information supporting the current standard is largely unchanged since the current standard was issued.

The CASAC agrees that the adverse impact of low levels of Pb exposure on neurocognitive function and development in children remains the most sensitive health endpoint, and that a primary Pb NAAQS designed to protect against that effect will offer satisfactory protection against the many other health impacts as sociated with Pb exposure.

The CASAC concurs with the draft PA that the scientific findings pertaining to air

- to

- blood P b ratios and the C

- R relationships between blood Pb and childhood IQ decrements that formed the basis of the
current Pb NAAQS remain valid and are consistent with current data.

In reaching preliminary staff conclusions, staff notes that, like any NAAQS review, this Pb NAAQS review requires public health policy judgments. The public health policy judgments for this review include the public health significance of a given magnitude of IQ loss in a small subset of highly exposed children (i.e., those likely to experience air

- related Pb exposures at the level of the standard), as well as how to consider the nature and magnitude of the array of uncertainties that are inherent in the evidence and in the application of this specific framework.

What are the Pane l’s views on public health policy judgments that inform staff’s preliminary conclusions with regard to the adequacy of current standard and a lack of support for consideration of potential alternative standards?

The PA states repeatedly that no threshold for Pb effects on IQ can be identified. In some respects, the ability to define a threshold may already be a moot issue. Reductions in IQ in children are being reported at blood Pb values as low as 2 μg/dL . In essence, these effects are being reported at t he lowest levels of Pb in blood that can be reliably measured by most laboratories doing such analyses. Child IQ is the Pb

- sensitive health endpoint on which this PA (and the previous one) is based. Thus, the discussion of health policy judgment needs to be carefully considered in light of the far

- reaching public health value of childhood cognitive and neurobehavioral health. For example, the 2012 Centers for Disease Control and Prevention ( CDC ) update of recommendations regarding childhood Pb poisoning

ac knowledge s that there is no blood Pb level in childhood that has been shown to be without deleterious effects. In this context, defining the threshold for "unacceptable risks to public health" or "sufficient public health protection" is difficult. Indeed, such language

- with its implicit use of a threshold approach to a process that presumably has no threshol d

- may no longer be appropriate. Although there is evidence that even very low Pb levels are related to measurable reductions in IQ in children, the extent to which the blood Pb l evels observed in children are linked to ambient air Pb levels below the8 current standard (as opposed to other sources of Pb in the environment) has not been established. Therefore there is not justification for modifying the current standard based on these data at this point in time. However additional research on air to blood Pb at low levels may require reconsideration of this decision in the future.

In the Panel’s view, does the discussion in section 4.3 provide an approp riate and sufficient rationale to support staff’s preliminary conclusion that it is appropriate to consider retaining the current standard (including the indicator, level, averaging time, and form) without revision?

G iven the evidence

- based framework , the discussion in section 4.3 provide s an appropriate and sufficient rationale to support retaining the current standard without revision

. For example, there is discussion in the PA regarding the choice of indicator level

. However, there should be more descri ption of supporting data and rationale behind the recommendation for the averaging time and form of the current standard.

The CASAC concurs that the new science does not support lowering the Pb NAAQS from its current level (0.15 μ g/m 3 ). Additionally, t he CASAC concurs with the caveats provided about the uncertainty in the science behind the NAAQS for Pb

. In particular it appreciates and affirms a key point on page 4

- 28, lines 2

- 3: “We also recognize increased uncertainty in projecting the magnitude of blo od Pb response to ambient air Pb concentrations at and below the level of the current standard

. ” Likewise, the key idea on page 4

- 32, lines 32

- 35 is important, but a clarifying revision is recommended as follows:

Page 4

- 32, lines 3 2

- 35 , current text : “In staff’s view, based on current evidence there is appreciable uncertainty associated with drawing conclusions regarding whether there would be reductions in risk to public health from alternative lower levels as compared to the level of the current standard

. ” This should be re

- written to read “In staff’s view, based on current evidence there is appreciable uncertainty associated with drawing conclusions regarding whether there would be reductions in blood lead levels from alternative lower levels as compared to the level of the current standard

. ”

Does the Panel have any recommendations regarding additional interpretations and conclusions based on the available information that would be appropriate for consideration beyond those discussed in this chapter?

A s noted above, repeated statements about a threshold do not seem warranted given that IQ reductions now occur at the lowest blood Pb levels that can be reliably meas ured in most laboratories. It is for this reason that the Advisory Committee on Childhood L ead Poisoning Prevention recommended to CDC a complete elimination of the phrase ‘level of concern’ and stated that no blood Pb level in children has been shown to be without deleterious effects.

The EPA should encourage development of research programs t o address those limitations and uncertainties in currently available evidence (and exposure/risk information) that are critical to the identification of "sufficiently health protective" air Pb standards in the future.9 There are some areas that need re vision for clarity:

• Page 4

- 34, line 13: The statement should be edited to: “Factors affecting relationships between Pb in ambient air and Pb in blood at low exposures experienced in the general population today”

• Page 4

- 34, lines 19

- 21: This research need is profound, but as written is too vague to be appreciated by the average reader. This research need should be revised to: “Apportionment of blood Pb levels with regard to exposure pathways, with particular focus on understanding exposure pathways and sour ces that cause the more elevated blood Pb levels among children today.”

Research Needs

Several areas of research that could assist in further refinement of the Pb NAAQS include :

1. For the purposes o f policy and decision making, key research priorit ies sho uld be studies t hat elucidate: (1) the air

- blood Pb relationship at low levels ; (2) sources (exposure pathways) contributing to current population blood Pb leve ls, especially in children ; (3) the relationship between Pb and childhood neurocognitive functio n at current population exposure levels ; and (4) the relationship between ambient air Pb and outdoor dust and surface soil Pb concentrations, including the temporal dynamics of that relationshi p

. These research priorities are of particular interest because of the prominent contribution of past (as opposed to recent) Pb emissions to Pb in soil and dust, and the significant contribution of dust and soil matrices to the Pb exposure of children.

2. For the typical American adult not subject to current or past po int sources or occupational Pb
exposure, Pb in the diet is likely to constitute the largest fraction of daily Pb exposure. Therefore, another research need of considerable interest is to determine the source of contemporary dietary Pb , including the indire ct contribution of historical air Pb emissions (i.e. “legacy Pb ”). Further, there remains a need to determine how much of dietary Pb is from legacy and how much can be amenable to interventions.

3. The shape of the C

- R curve for IQ reductions at extremely l ow levels requires further clarification. In addition, studies on more sensitive endpoints in the domain of emotion and behavior regulation are warranted, given that they may yield specific and sensitive measures and thereby assist in defining appropriate intervention strategies for children.

4. There has been a long

- term reliance on the Integrated Exposure Uptake Biokinetic ( IEUBK ) model. However, greater understanding of inter

- individual variability , as quantified in the Geometric Standard Deviation ( GSD ) input parameter , is needed . Information about toxicokinetics during adolescence remains limited

. Th e All Ages Lead Model could be utilized to improve this understanding . There is also the need to know more about gene

- environment interactions, particularly in driving inter

- individual susceptibility and vulnerability.

5. Characterization and better understanding of Pb exposure hotspots/sources will give better representation of significant exposure risks.10 6. Understanding of the impacts of Pb exposures during cri tical developmental windows and their contribution to adverse outcomes; e.g., little is known about the specific effects of prenatal
exposure.

7. The effect of contemporary Pb exposure (i.e.

, that resulting in blood Pb co ncentrations on the order of 5 μ g/dL or lower) on the future risk of hypertension and cardiovascular morbidity and mortality, and on age

- related neurodegeneration, as these could lead to additional information related to most sensitive health outcomes.

8. A further understanding of the role of “reverse causation” in the inverse association observed in some studies between low blood Pb concentration and renal function ( e.g., glomerular filtration rate).

9. The extent to which product substitution, i.e.

, replacement of Pb with less hazardous alterna tive substances in contemporary commerce, may result in reduction of human Pb exposure. The EPA might consider supporting studies on Pb potentially undertaken by programs such as the Toxic Use Reduction Program in Massachusetts, and the Green Chemistry Ini tiative in California.

10. As yet, the extent to which global warming will i nfluence exposure to Pb ( e.g., through soil erosion, resuspension ) has not been evaluated.

Chapter 5

– Welfare Effects and Exposure/Risk Information

This chapter discusses key poli cy relevant aspects of the environmental evidence and exposure/risk information.

Chapter 5 of the PA is a well

- written synthesis of the findings related to ecological effects in the ISA

. The ISA supports the conclusion that recent research has not changed our fundamental understanding of Pb fate, transport and toxicity in the env ironment

. To what extent does the information in section 5.1 (Welfare E ffects Information) capture and

a

ppropriately characterize the key aspects of the evidence assessed and int egrated in the ISA?

Section 5.1 does a good job of summarizing the evidence for ecological effects from the ISA. The general conclusion is that recent research has added depth and nuance to the understanding of the fate and transport of Pb in ecological s ystems, and to the understanding of effects on organisms in terrestrial and aquatic ecosystems, but has not changed the understanding in a way that merits reconsideration of the relationships used to assess risk.

A persistent theme in the ecological effe cts sections of the ISA and this PA document is that it is difficult to isolate the effects of air Pb on ecosystems from other Pb sources, including “legacy” Pb accumulated in soils and sediments. The threat of release of legacy Pb in soils and sediments, whatever the original source, may necessitate a lower secondary air quality standard than would be warranted in the absence of the legacy Pb. With respect to critical loads, it is recommended that Chapter 5 acknowledge the impact on raptors and water fowl of Pb in spent ammunition; these are the ecological11 receptors most heavily exposed to Pb , and thus potentially the most susceptible to the incremental contribution of Pb in air.

With regard to the exposure and risk information in section 5.2 (Exposure and Risk Information), to what extent is the information drawn from the screening

- level risk assessment in the last review sufficiently characterized and clearly communicated? To what extent is the information appropriately interpreted in light of the current ly available information and for the purpose of assessing the adequacy of the current standard?

The results of the 2006 REA are summarized in section 5.2. The summary is concise and clear, both in the explanation of the model employed and in the descripti ons of the case studies used in the assessment.

The interpretation of the results from the 2006 REA is appropriate insofar as it re

- states the conclusions from that document, and there have been no fundamental changes to our understanding of key threshold s or ecological recep tors in the intervening years. Of four terrestrial case studies employed, the results from two (the primary and secondary smelter cases) are judged to be “not informative.” The relevance of a third case study (non

- urban near

- roadway co nditions) is deemed “highly uncertain” due to the presence of legacy Pb in roadside soils. The only terrestrial case study that is deemed relevant is the Hubbard Brook case, where ambient Pb concentrations are far below the current (and proposed) standard. Results from analysis of surface water and sediment data are judged to be inconclusive because of possible non

- air sources to waters and legacy Pb in sediments. Therefore, o verall, four of the five major efforts in the 2006 REA are judged to be of limited or no value for the purposes of this PA

. Given that there is little field research underway on Pb in U.S. ecosystems that are not impacted by point sources, it would appear to be unlikely that data for new REA case studies is forthcoming. A robust critica l loads approach , which is a research priority to support a future review, is needed to fill this gap.

Are the limitations and uncertainties in the exposure/risk information appropriately characterized and considered in our interpretation of the informati on in the context of this current review?

The discussion of limitations and uncertainties is generally good. Issues such as legacy Pb, multi

stressor effects, and lab

- to

- field applicability create considerable uncertainty. The use of conservative screenin g levels in the calculation of hazard quotients is particularly useful be cause the calculated risks

are overstated.

Chapter 6

– Review of the Secondary Standard for Lead

This chapter describes the basis for the current secondary standard and considerati on of the current evidence and exposure/risk

- based information with regard to reaching preliminary staff conclusions about the adequacy of the current standard.

Does the Panel agree with preliminary staff conclusions about the evidence and previous risk

a ssessment in light of current standards as presented in secti on 6.2 (Adequacy of the Current Standard)?12 The preliminary staff conclusions provide a good assessment of the available evidence and the previous risk assessment in light of the current secondar y standard. The CASAC note s , however, the concerns raised in the response to the chapter 5 charge questions regarding the previous risk assessment.

In the Panel’s view, does the discussion in this chapter provide an appropriate and sufficient rationale
t o support preliminary staff conclusions that it is appropriate to consider retaining the current standard (including the indicator, level, averaging time, and form) without revision?

T he discussion provides appropriate and sufficient rationale to support retaining the current secondary standard without revision. A general lack of new data that would indicate the appropriate level of Pb in environmental media that may be associated with adverse effects suggests that the secondary standard should be retained . Questions remain regarding the relevance of the indicator, level, averaging time and form to the secondary standard (ecological context). A multi

- media approach may be necessary to account for legacy Pb and contributions from different sources for a seco ndary standard.

Does the Panel have any recommendations regarding additional interpretations and conclusions based on the available information that would be appropriate for consideration beyond those discussed in this chapter?

The CASAC does not have any recommendations regarding additional interpretations and conclusions beyond what is contained in the chapter . Developing a critical load s approach for U.S. conditions would be an important area for additional research. The discussion of uncertainties a t the end of the chapter is excellent. It should include mention of the use and/or relevance of toxicity data that are generated in test systems that deploy exposures to media other than soil or water for appropriate organisms (e.g., plants in hydroponic s ystems, soil nematodes in agar or culture medium).

Research Needs

Application of a critical loads approach with sensitivity analysis will help to determine which processes are most important in determining Pb exposure to ecological receptors. This would be an integrated, holistic, multi

- media approach that could be used to examine the contributions of current aerial Pb deposition to historical aerial deposition as well as Pb from other sources. Current critical loads models are largely qualitative and emp irical. Mechanistic sub

- models need to be incorporated into the critical loads model to provide an adequate means to predict Pb bioavailability, exposure, and toxicity. This critical loads approach could be integrated to include other aerial pollutants suc h as oxides of nitrogen and oxides of sulfur

.13 Reference

Secretariat of the Commission for Environmental Cooperation (C EC), (2013 ), Hazardous Trade? An E

xaminat ion of US

- generated Spent Lead

- a cid Battery Exports and Secondary Lead R ecycling in Mexico, the United States and Canada , Final Report, 15 April

.United StatesEnvironmental ProtectionAgencyOffice of Air Quality Planning and StandardsHealth and Environmental Impacts DivisionResearch Triangle Park, NCPublication No. EPA-452/R-14-001May 2014