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

External Review DraftThis page is intentionally blank.EPA-452/P-13-001 January 2013



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

External Review Draft

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

This draft document has been reviewed by the Office of Air Quality Planning and Standards (OAQPS), U.S. Envi ronmental Protection Agency (EPA), and approved for publication. This OAQPS Policy Assessment contains preliminary conclusions of the staff of the OAQPS and does not necessarily refl ect the views of the Agency. Mention of trade names or commercial products is not intended to constitu te endorsement or recommendation for use.ACKNOWLEDGMENTS

This draft 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. Deir dre Murphy. Dr. Karen Martin has managed the project. For the chapter on th e health effects evidence and exposure/risk information, the principal authors include Dr. De irdre Murphy and Dr. Zach Pekar, and Dr. Murphy served as the principal author for the chapter on the primary Pb standard. For the chapters on welfare effects evidence and exposure/risk information and the s econdary Pb standard, th e principal author is Ms. Ginger Tennant. The principal author on th e section discussing ambient air monitoring is
Mr. Kevin Cavender. Contributors of emissions information and air quality analyses are Mr. Marc Houyoux, Mr. Josh Drukenbrod, Dr. Halil Cakir and Mr. Mark Schmidt. Staff from other EPA offices, including the Office of Research and Development and th e Office of General Counsel, also provided valuable comments and contributions.This page is intentionally blankJanuary 2013 Draft – Do Not Quote or Cite i 

### 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
1.3 SCOPE OF CURRENT REVIEW: FA TE AND MULTIMEDIA PATHWAYS OF AMBIENT AIR LEAD .......................................................................................... 1-9
1.3.1 Environmental Distribution and Exposure Pathways......................................... 1-10 1.3.1.1 Human Exposure Pathways ....................................................................... 1-11 1.3.1.2 Ecosystem Exposure Pathways ................................................................. 1-12 1.3.2 Considerations Related to Historically Emitted Lead ........................................ 1-13
1.4 GENERAL ORGANIZATION OF THE DOCUMENT ........................................... 1-15
1.5 REFERENCES .......................................................................................................... 1-16

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 or Released 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 ..................................................................... 2-20 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 ............................................................ 2-32January 2013 Draft – Do Not Quote or Cite ii 2.3.1 Atmospheric Deposition ..................................................................................... 2-32 2.3.2 Terrestrial Media ................................................................................................ 2-33 2.3.2.1 Indoor Household Dust ............................................................................. 2-34 2.3.2.2 Outdoor Dust in Areas of Human Activity ............................................... 2-34 2.3.2.3 Soil ............................................................................................................ 2-36 2.3.2.4 Biota .......................................................................................................... 2-38 2.3.3 Aquatic Media .................................................................................................... 2-38 2.3.3.1 Surface Waters .......................................................................................... 2-38 2.3.3.2 Sediments .................................................................................................. 2-39
2.4 REFERENCES .......................................................................................................... 2-40

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............................................................................................ 3-14
3.3 PUBLIC HEALTH IMPLICATIONS AND AT-RISK POPULATIONS ................ 3-27
3.4 EXPOSURE AND RISK ........................................................................................... 3-36
3.4.1 Conceptual Model for Air-Related Lead Exposure and Risk ............................ 3-37 3.4.2 Case Studies ....................................................................................................... 3-39 3.4.3 Analysis Approach ............................................................................................. 3-41 3.4.3.1 Estimating Exposure ................................................................................. 3-43 3.4.3.2 Air Quality Scenarios Include d in 2007 Assessment ................................ 3-46 3.4.3.3 Methods for Deriving Risk Estimates ....................................................... 3-48 3.4.3.3.1 Full Risk Model in 2007 REA .............................................................. 3-49 3.4.3.3.2 Air Quality Scenarios Re flecting the Current Standard ........................ 3-51 3.4.4 Challenges in Characterizing Air- related Exposure and Risk ............................ 3-53 3.4.5 Risk Estimates .................................................................................................... 3-55 3.4.6 Treatment of Variability ..................................................................................... 3-60 3.4.7 Characterizing Uncertainty ................................................................................ 3-61 3.4.8 Updated Interpretation of Risk Estimates .......................................................... 3-64
3.5 REFERENCES .......................................................................................................... 3-66

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 Conclusion Regarding the Need for Revision ............................................. 4-3 4.1.1.2 Conclusions on Elements of Revised Standard ........................................... 4-5
4.1.2 Approach for the Current Review ...................................................................... 4-10
4.2 ADEQUACY OF THE CURRENT STANDARD .................................................... 4-13
4.2.1 Evidence-based Considerations .......................................................................... 4-13 4.2.2 Exposure/Risk-based Considerations ................................................................. 4-21
4.3 PRELIMINARY STAFF CONCLUSIONS ON THE PRIMARY STANDARD ..... 4-25
4.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND DATA COLLECTION .............................................................................................. 4-33 4.5 REFERENCES .......................................................................................................... 4-36January 2013 Draft – Do Not Quote or Cite iii 5 WELFARE EFFECTS AND RISK/RISK INFORMATION ......................................... 5-1

5.1 WELFARE EFFECTS INFORMATION ................................................................... 5-1
5.2 EXPOSURE AND RISK INFORMATION ............................................................. 5-13
5.2.1 Screening Assessment from Last Review ......................................................... 5-14 5.2.2 Screening Assessment Results and Interpretation ............................................. 5-17
5.3 REFERENCES .......................................................................................................... 5-22

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

6.3 PRELIMINARY STAFF CONCLUSI ONS ON THE SECONDARY
STANDARD ............................................................................................................. 6-10

6.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND
DATA COLLECTION ............................................................................................. 6-12

6.5 REFERENCES ......................................................................................................... 6-14

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-1January 2013 Draft – Do Not Quote or Cite iv LIST OF FIGURES

Figure 1-1. Pathways of human and ecosystem exposur e to lead from ambient air. ................. 1-11 Figure 2-1. Temporal trend in air emissions: 1970-2010. ............................................................ 2-3 Figure 2-2. Geographic distribution of facilities estimat ed to emit at least 0.50 tpy in 2008. ... 2-11 Figure 2-3. Map of Pb-TSP Monitoring Sites in Curre nt Pb NAAQS Monito ring Network. ... 2-15 Figure 2-4. Map of sites near airports for which one year of 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). .................... 2-18 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: 2000-2010 (92 sites). .......................... 2-24 Figure 2-9. Airborne Pb -TSP concentrations (3-m onth average) at fi ve sites near roadways: 1979-2010. ............................................................................................ 2-25 Figure 2-10. Pb-TSP maximum 3-mont h means (215 sites), 2009-2011. ................................. 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, 2009-2011. .................................................... 2-29 Figure 2-12. Distribution of annual mean concentrations of Pb-TSP, Pb-PM 10 and Pb-PM 2.5 at different site types, 2009-2011. .......................................................................... 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, 2009-2011. .................................................... 2-31 Figure 2-14. Temporal trend in sediment concen tration from core samples in 12 lakes at eight National Park s 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 lead. ...................................................... 3-38 Figure 3-3. Overview of analysis approach. .............................................................................. 3-42 Figure 3-4. Comparison of four concentra tion-response functions used in risk assessment. .... 3-50 Figure 3-5. Parsing of air-related risk estimates. ....................................................................... 3-53 Figure 4-1. Overview of approach for review of current primary standard. .............................. 4-12 Figure 5-1. Analytical approach for screening-level assessment in the last review (2006 REA, Exhibit 2-6) ......................................................................................... 5-16 Figure 6-1. Overview of approach for review of current secondary standard. ............................ 6-4January 2013 Draft – Do Not Quote or Cite v LIST OF TABLES

Table 2-1. U.S. lead emissions by source categories estimated to emit at least 4 tpy. ............... 2-4 Table 2-2. Facilities estimated to emit at least 0.50 tpy in 2008. ............................................. 2-10 Table 2-3. Dry deposition of lead in large metropo litan areas and in a smelter town. ............. 2-36

Table 3-1. Empirically derived air-to-blood ratios fo r populations inclusive of children. ....... 3-12 Table 3-2. Associations with neurocognitive function m easures in analyses with child study group blood lead levels <5 μg/dL. .......................................................................... 3-21 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. .................... 3-26 Table 3-4. Number of children aged 5 and under in areas of elevated ambient Pb concentrations relative to the NAAQS. ................................................................... 3-34 Table 3-5. Population size near larger sour ces of lead emissions. ........................................... 3-35 Table 3-6. Types of population exposures assessed. ................................................................ 3-40 Table 3-7. Summary of approaches used to estima te case study media concentrations. .......... 3-44 Table 3-8. Air quality scenarios assessed. ................................................................................ 3-48 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. .............................. 3-50 Table 3-10. Estimates of air-related risk fr om 2007 risk assessment. ........................................ 3-57 Table 3-11. Estimates of air-related risk for th e generalized (local) urban case study, including interpolated estima tes for current standard. ............................................ 3-58This page is intentionally blankJanuary 2013 ES-1 Draft - Do Not Quote or Cite 

### EXECUTIVE SUMMARY 1 2 This draft Policy Assessment (PA) has been prepared by staff in the Environmental 3 Protection Agency’s (EPA) Office of Air Qualit y Planning and Standards (OAQPS) as part of 4 the Agency’s ongoing review of the primary (h ealth-based) and seconda ry (welfare-based) 5 national ambient air quality sta ndards (NAAQS) for lead (Pb). It presents analyses and 6 preliminary staff conclusions regarding the policy im plications of the key sc ientific and technical 7
information that informs this review. The final PA is intended to “bridge the gap” between the 8
relevant scientific ev idence and technical information and the judgments required of the EPA 9 Administrator in determining whether to retain or revise the current stan dards. Development of 10
the PA is also intended to facilitate advi ce and recommendations on the standards to the 11 Administrator from an independe nt scientific review committee, the Clean Air Scientific 12 Advisory Committee (CASAC), as provi ded for in the Clean Air Act (CAA). 13 Staff analyses in this draft PA are based on the scientific assessment presented in the 14
third draft Integrated Science Assessment for Pb (ISA) prepared for this review by the EPA’s 15 Office of Research and Developmen t (ORD) as well as scientific and technical assessments from 16 prior Pb NAAQS reviews. Such assessments in clude quantitative human health and ecological 17 risk and exposure assessments (REAs) developed in the last review as ne w health and ecological 18
REAs were not warranted based on staff’s and CASAC’s consideration of the evidence newly 19 available in this review with regard to risk and exposure assessment. In considering the 20
scientific evidence and other technical information available in this review , emphasis is given to 21
consideration of the extent to which the evidence newly available since th e last review alters 22
conclusions drawn in the last revi ew with regard to health and we lfare effects of Pb, the exposure 23 levels at which they occur and the associated at-risk populations and ecological receptors or 24
ecosystems. 25 The overarching questions in this review, as in all NAAQS reviews, regard the support 26 provided by the currently availabl e scientific evidence and exposure/risk-based information for 27 the adequacy of the current standards and the extent to which the scientific evidence and 28 technical information provides supp ort for concluding that consider ation of alternative standards 29 may be appropriate. The analyses presented in th is draft PA to address such questions lead to 30 preliminary staff conclusions that it is appropria te to consider retaini ng the current primary and 31 secondary standards without revision; accordingly, no potential alternative standards have been 32 identified by staff for consideration in th is review. Comments and recommendations from 33 CASAC, and public comments, based on review of this draft PA, will inform final staff 34 conclusions and the presentation of information in the final PA. 35January 2013 ES-2 Draft - Do Not Quote or Cite Current Lead NAAQS and Scope of Review 1
The NAAQS for Pb was initially set in 1978. Review of the 1978 NAAQS for Pb, 2 completed in October 2008, resulted in substant ial revision based on the large body of evidence 3 accumulated over the intervening three decades. In terms of the basic elements of the NAAQS, 4
the level of the primary standard was lowered by an order of magnitude from 1.5 μg/m 3 to 0.15 5 μg/m 3 and the averaging time was revised to a rolling three-m onth period (from a period based 6 on calendar quarters) with a maximum (not-to-be exceeded) form , evaluated over a 3-year 7 period. The indicator of Pb in total suspended particles (Pb-TSP) was retained, reflecting the 8 evidence that Pb particles of all sizes pose health risks. The s econdary standard was revised to 9 be identical in all respects to the revised primary standard. 10 The multimedia and persistent nature of Pb c ontributes complexities to the review of the 11 Pb NAAQS unlike issues addressed in other NAAQS reviews. Air-related Pb distributes from 12 air to other media, including i ndoor and outdoor dusts, soil, food, drinking water, as well as 13 surface water and sediments. As a result, revi ew of the Pb NAAQS considers the protection 14 provided against the health and environmental e ffects of air-related Pb associated both with 15 exposures to Pb in ambient air and with exposures to Pb that makes its way from ambient air into 16 other media. Additional complexity derives from the recognition that exposure to Pb also results 17 from nonair sources, including Pb in paint, tap wa ter affected by plumbing containing Pb, lead18 tainted products, as well as surface water discharg es and runoff from industrial sites. Such 19 nonair sources contribute to the total burden of Pb in the human body and in the environment, 20 making it much more difficult to assess independently the health and welfare effects attributable 21 to air-related Pb that are the focus of the NAAQS. Further, the persistence of Pb in the human 22 body and the environment is another important cons ideration in assessing the adequacy of the 23 current Pb standards. In so doing, staff is mi ndful of the history of the greater and more 24 widespread atmospheric emissions that occurred in previous y ears (e.g., under the previous Pb 25 standard, and prior to establishmen t of any Pb NAAQS) and that cont ributed to the Pb that exists 26 in human populations and ecosystems today. Like wise, staff also recogni zes the role of nonair 27 sources of Pb, now and in the past, that also cont ribute to the Pb that ex ists in human populations 28 and ecosystems today. As in the last Pb NAAQS review, this backdrop of environmental Pb 29 exposure, and its impact on the populations and ecosystems which may be the subjects of the 30 currently available scientific evidence, complicat es our consideration of the health and welfare 31 protection afforded by the current NAAQS. 32January 2013 ES-3 Draft - Do Not Quote or Cite Characterization of Ambient Air Lead 1

Emissions to ambient air and associated air Pb concentrations have declined substantially 2 over the past several decades. The most dramatic reductions in Pb emissions occurred prior to 3 1990 in the transportation sector due to the removal of Pb from gasoline. Lead emissions were 4 further reduced substantially between 1990 and 2008, with significant reductions occurring in the 5 metals industries at least in pa rt as a result of national emissions standards for hazardous air 6 pollutants. Additional reductions in stationa ry source emissions are also anticipated from 7 regulations which have been promulgate d since 2008 under Section 112 of the CAA. 8 As at the time of the last review, the major ity of Pb emissions nationally is associated 9
with combustion of leaded avia tion gasoline by piston-driven airc raft. The largest sources on a 10 local scale are generally associated with metals in dustries. As a result of revisions to monitoring 11 regulations stemming from the la st Pb NAAQS review, Pb NAAQS monitors are required near 12 the largest Pb emissions sources, as well as in sites distant from such s ources in large population 13 areas. Ambient air Pb monitoring data available t hus far from this expanded network continue to 14 illustrate the source-related aspect of airborne Pb, with highest concentrations near large sources 15
and lowest in areas removed from sources. In addition, Pb monitoring data are also being 16 collected over at least a one-year period near a set of airports iden tified as most likely to have 17
elevated Pb concentrations due to leaded aviation gasoline usage. These data will inform future 18 airport monitoring activities, as well as an ongoing investigation into Pb emissions from piston19 engine aircraft under Section 231 of the Clean Air Act, separate from this Pb NAAQS review. 20 Lead occurs in ambient air in particulate form and, with characteristics and spatial 21 patterns influenced by a number of factors, depo sits from air to surfaces in natural and human22 made environments. By this deposition process and subsequent transfer processes, ambient air 23 Pb is distributed into multiple human exposure pathways and environmental media in aquatic 24 and terrestrial ecosystems. In areas remove d from large air emissi ons sources, currently 25
available information on Pb concentrations in nonair media includes numerous examples of 26
declines in surface concentrations reflective of the reductions in deposition over the past several 27 decades. In areas near large ai r sources where emissions reductions have occurred, only very 28 limited information is available, such as for re ductions in air and surf ace dust concentrations, 29
with even less information available on trends for other media such as surface soils. 30

Health Effects and Review of the Primary Standard 31 Lead has long been recognized to exert a broad array of deleterious effects on multiple 32 organ systems as described in the ISA for this re view and consistent with conclusions of prior 33
scientific assessments. Over the three decades from the time the standard was initially set in 34 1978 through its revision with the NAAQS re view completed in 2008, the evidence base 35January 2013 ES-4 Draft - Do Not Quote or Cite expanded considerably in a number of areas, incl uding with regard to e ffects on neurocognitive 1 function in young children at in creasingly lower blood Pb levels. These effects formed the 2 primary basis for the 2008 revisions to the primar y standard. The current standard was set most 3 specifically to provide appropriate public health protection from th e effects of air-related Pb on 4 cognitive function (e.g., IQ loss) in young children. In so doing, the standard was judged to 5 provide the requisite public hea lth protection from the full arra y of health effects of Pb, 6 consistent with the CAA requirement that th e primary standard, in the judgment of the 7 Administrator, based on the latest scientific knowle dge, is requisite to protect public health with 8 an adequate margin of safety. 9 The health effects evidence newly available in this review, as critically assessed in the 10 ISA in conjunction with the full body of evidence, reaffirms conclusions on the broad array of 11 effects recognized for Pb in the last review. Furt her, staff observes the ge neral consistency of the 12
current evidence with the evidence available in th e last review, particularly with regard to key 13 aspects of the evidence on which the current stan dard is based. These ke y aspects include those 14 regarding the relationships between air Pb concen trations and the associated Pb in the blood of 15 young children (i.e., air-to-blood ratios) as well as between total blood Pb levels and effects on 16 neurocognitive function (i.e., concentration-resp onse (C-R) functions for IQ loss). Factors 17 characterizing these two relationshi ps are the key inputs to the fr amework developed in the last 18
review to translate the available evidence into a basis for considering a primary Pb standard that 19 would be requisite to protect agai nst this and other Pb-related hea lth endpoints. This framework 20 is again considered in light of the current avai lable evidence. This Pb NAAQS review, like any 21 NAAQS review, requires public health policy judg ments. The public health policy judgments 22 for this review include the public health signifi cance of a given magnitude of IQ loss in a small 23 subset of highly exposed children (i.e., those likely to experience air-related Pb exposures at the 24 level of the standard), as well as how to cons ider the nature and magn itude of the array of 25
uncertainties that are inherent in the evidence an d in the application of this specific framework. 26 In also considering the quantitative risk es timates associated with the current standard, 27
based on the risk assessment conducted in the la st review, staff observe s that these estimates 28
indicate a level of risk that is roughly consiste nt with and generally s upportive of conclusions 29
drawn from the evidence usi ng the evidence-based air-rela ted IQ loss framework. Staff 30 additionally recognizes the complexity of the mo deling done as part of that assessment and the 31
substantial limitations and uncertaintie s in the resulting risk estimates. 32 Based on the above considerations, staff pr eliminarily concludes that the currently 33 available information supports a primary standard as protective as the curre nt standard and that it 34 is appropriate to consider reta ining the current sta ndard without revision. In so doing, staff 35 additionally notes that the final decision on the adequacy of the current standard is largely a 36January 2013 ES-5 Draft - Do Not Quote or Cite public health policy judgment to be made by the Administrator, draw ing upon the scientific 1 information as well as judgments about how to co nsider the range and magnitude of uncertainties 2
that are inherent in the scientific evidence a nd technical analyses. In this context, staff 3 recognizes that the uncertainties and limitations associated with the many aspects of the 4 relationship between air Pb concen trations and blood Pb levels and associated health effects are 5 amplified with consideration of increasingly lower air concentrati ons. In staff’s view, based on 6 the current evidence there is appreciable uncer tainty associated with drawing conclusions 7 regarding whether there would be re ductions in risk to public health from alternative lower levels 8 as compared to the level of the current standar d. Thus, staff concludes that the basis for any 9
consideration of alternative lowe r standard levels would reflect different public health policy 10 judgments as to the appropriate approach for weighing uncertainties in the evidence and for 11 providing requisite protecti on of public health with an adequate margin of safety. Accordingly, 12 and in light of the preliminary staff conclusion that it is appropriate to consider the current 13 standard to be adequate, this document does not identify potential alternative standards for 14
consideration in this review. 15

Welfare Effects and Review of the Secondary Standard 16

Consideration of the welfare effects evidence and screening-level risk information in the 17 last review (completed in 2008) led to the c onclusion that there was a potential for adverse 18
welfare effects occurrin g under the then-current Pb standard (set in 1978), although there were 19 insufficient data to provide a qua ntitative basis for set ting a secondary standard different from 20 the primary standard. Accordingly, the secondary standard was substantially revised to be 21 identical in all respects to the newly revised primary standard. 22 In assessing the currently available scientif ic evidence and the exposure/risk information 23 with regard to support for the ad equacy of the protection afforded by the current standard, staff 24 observes the general consistency of the current ev idence with that availabl e in the last review, 25 including the substantial limitations in the current evidence that complicate conclusions 26 regarding the potential for Pb emissions under the cu rrent, much lower standa rd to contribute to 27 welfare effects. Thus, based on the staff analys is, framed by key policy-relevant questions for 28 the review, staff preliminarily concludes that consideration should be given to retaining the 29 current standard, without revi sion, and this document does not identify potential alternative 30
standards for consideration in this review. 31
32January 2013 Draft – Do Not Quote or Cite 1-1 

### 1 INTRODUCTION 1

1.1 PURPOSE 2 The U.S. Environmental Protection Agency (EPA) is presently conducting a review of 3 the primary (health-based) and secondary (welfare -based) national ambient air quality standards 4 (NAAQS) for lead (Pb). The ove rall plan and schedule for this review were presented in the 5 Integrated Review Plan for the National Ambient Air Qualit y Standards for Lead (IRP; USEPA, 6 2011a). The IRP also identified key policy-relevant issu es to be addressed in this review and 7 discussed the key documents that generally in form NAAQS reviews, including an Integrated 8 Science Assessment (ISA), Risk and Exposure Assessments (REAs), and a Policy Assessment 9 (PA). The PA presents a staff evaluation of th e policy implications of the key scientific and 10
technical information in the ISA and REAs for EPA’s consideration. 1 The PA generally 11 provides a transparent evaluation and staff conclusi ons regarding policy cons iderations related to 12 reaching judgments about the adequacy of the curr ent standards, and, if revision is considered, 13 what revisions may be a ppropriate to consider. 14 When final, the PA is intended to help “bri dge the gap” between the Agency’s scientific 15 assessments presented in the ISA and REAs , and the judgments required of the EPA 16 Administrator in determining whether it is appr opriate to retain or revise the NAAQS. In 17 evaluating the adequacy of the current standard and whether it is appropriate to consider 18 alternative standards, the PA focuses on informati on that is most pertinent to evaluating the basic 19 elements of the NAAQS: indicator, 2 averaging time, form, 3 and level. These elements, which 20 together serve to define each standard, must be considered collectively in evaluating the health 21 and welfare protection afforded by the Pb standa rds. The PA integrates and interprets the 22
information from the ISA and REAs to fr ame policy options for consideration by the 23 Administrator. In so doing, the PA recognizes th at the selection of a specific approach to 24 reaching final decisions on primary and seconda ry NAAQS will reflect the judgments of the 25
Administrator. 26

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 PM 2.5 NAAQS is the 3- year average of the we ighted annual mean PM 2.5 concentrations, while the form of the 8-hour CO NAAQS is the second-highest 8-hour average in a year.January 2013 Draft – Do Not Quote or Cite 1-2 The development of the PA is also intended to facilitate advice to the Agency and 1
recommendations to the Administrator from an independent scientific review committee, the 2 Clean Air Scientific Advisory Committee (CASAC), as provided for in the Clean Air Act. As 3 discussed below in section 1.2.1, the CASAC is to advise not only on the Agency’s assessment 4 of the relevant scientific information, but also on the adequacy of the existing standards, and to 5 make recommendations as to any revisions of th e standards that may be appropriate. The EPA 6
facilitates CASAC advice and recommendations , as well as public input and comment, by 7 requesting CASAC review and public commen t on one or more drafts of the PA. 8 The decision whether to prepare one or mo re drafts of the PA is influenced by 9 preliminary staff conclusions and associated CASAC advice and public comment, among other 10 factors. Typically, a second draft PA has been pr epared in cases where the available information 11 calls into question the adequacy of the current standard and analyses of potential alternative 12 standards are developed taking in to consideration CASAC advice and public comment. In such 13 cases, a second draft PA includes preliminary staf f conclusions regarding potential alternative 14 standards and undergoes CASAC review and public comment prior to preparation of the final 15 PA. When such analyses are not undertake n, a second draft PA may not be warranted. 16 In this draft PA for this review of the Pb NAAQS, we consider the scientific and 17
technical information available in this review as assessed in the third draft Integrated Science 18 Assessment for Lead (henceforth referred to as the IS A [USEPA, 2012a]), prepared by EPA’s 19
National Center for Environmental Assessmen t (NCEA), and the quantitative human exposure 20 and health risk and screening-level ecological risk assessments performed in the last review. As 21 discussed below in section 1.2.3, upon considerati on of the evidence newly available in this 22 review with regard to risk a nd exposure assessment, staff concl uded that new health and welfare 23 REAs were not warranted. Accordingly, the quantit ative risk information considered in this PA 24 is drawn from the quantitative human exposure a nd health risk and screening-level ecological 25 risk assessments performed in the last review (the 2007 Health Risk Assessment Report or 2007 26 REA [USEPA, 2007a] and the 2006 sc reening-level Ecol ogical Risk Assessment or 2006 REA 27 [ICF, 2006]), and is interpreted in the context of newly available evidence in this review. 28 The evaluation and preliminary staff conclusions presented in this draft PA for the Pb 29 NAAQS have been informed by comments and advi ce received from CASAC in their reviews of 30 the other draft Agency documents prepared t hus far in this NAAQS review. Review and 31 comments from CASAC, and public comment, on this draft PA will inform the final evaluation 32
and staff conclusions in the final PA. 33 Beyond informing the EPA Administrato r and facilitating the advice and 34 recommendations of CASAC and the public, the PA is also intended to be a useful reference to 35 all parties interested in the Pb NAAQS review. In these roles, it is intended to serve as a single 36January 2013 Draft – Do Not Quote or Cite 1-3 source of the most policy-relevant information th at informs the Agency’s review of the lead 1 NAAQS, and it is written to be unde rstandable to a broad audience. 2

1.2 BACKGROUND 3

1.2.1 Legislative Requirements 4 Two sections of the Clean Air Act (CAA or the Act) govern the establishment and 5 revision of the NAAQS. Section 108 (42 U.S.C. section 7408) directs the Administrator to 6 identify and list certain air pollutants and then to issue air quality criteria for those pollutants. 7
The Administrator is to list thos e air pollutants that in her “judgm ent, cause or contribute to air 8 pollution which may reasonably be anticipated to endanger public health or welfare;” “the 9 presence of which in the ambient air results fr om numerous or diverse mobile or stationary 10 sources;” and “for which . . . [the Administrator] plans to issue air quality criteria...” Air quality 11
criteria are intended to “accurately reflect the la test scientific knowledge useful in indicating the 12 kind and extent of all identifiable effects on pub lic health or welfare which may be expected 13 from the presence of [a] pollutant in the ambien t air . . .” 42 U.S.C. § 7408(b). Section 109 (42 14 U.S.C. 7409) directs the Admini strator to propose and promulga te “primary” and “secondary” 15 NAAQS for pollutants for which air quality crite ria are issued. Secti on 109(b)(1) defines a 16 primary standard as one “the attainment and maintenance of which in the judgment of the 17 Administrator, based on such criter ia and allowing an adequate margin of safety, are requisite to 18 protect the public health.” 4 A secondary standard, as defined in section 109(b)(2), must “specify 19 a level of air quality the attainment and ma intenance of which, in the judgment of the 20 Administrator, based on such crit eria, is requisite to protect the public welfare from any known 21 or anticipated adverse effects asso ciated with the presence of [the ] pollutant in the ambient air.” 5 22 The requirement that primary standards provi de an adequate margin of safety was 23
intended to address uncertainties associated with inconclusive scientific and technical 24
information available at the time of standard set ting. It was also intende d to provide a reasonable 25 degree of protection against hazards that research has not yet identified. See Lead Industries 26
Association v. EPA , 647 F.2d 1130, 1154 (D.C. Cir 1980), cert. denied , 449 U.S. 1042 (1980); 27
American Petroleum Institute v. Costle , 665 F.2d 1176, 1186 (D.C. Cir. 1981), cert. denied , 455 28

4 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).

5 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.”January 2013 Draft – Do Not Quote or Cite 1-4 U.S. 1034 (1982); American Farm Bureau Federation v. EPA, 559 F. 3d 512, 533 (D.C. Cir. 1 2009); Association of Battery Recyclers v. EPA , 604 F. 3d 613, 617-18 (D.C. Cir. 2010). Both 2 kinds of uncertainties are components of the risk associated with pollution at levels below those 3
at which human health effects can be said to occu r with reasonable scientific certainty. Thus, in 4 selecting primary standards that provide an adeq uate margin of safety, the Administrator is 5 seeking not only to prevent pollution levels that ha ve been demonstrated to be harmful but also 6 to prevent lower pollutant levels that may pose an unacceptable risk of harm, even if the risk is 7 not precisely identified as to nature or degree. The CAA does not require the Administrator to 8 establish a primary NAAQS at a zero-risk leve l or at background concentration levels, see Lead 9
Industries v. EPA , 647 F.2d at 1156 n.51, but rather at a level that reduces risk sufficiently so as 10 to protect public health with an adequate margin of safety. 11 In addressing the requirement for an adequate margin of safety, the EPA considers such 12 factors as the nature and severity of the health effects involved, th e size of sensitive population(s) 13 at risk, and the kind and degree of the uncertainties that must be addressed. The selection of any 14 particular approach to providing an adequate marg in of safety is a policy choice left specifically 15 to the Administrator’s judgment. See Lead Industries Association v. EPA , 647 F.2d at 1161-62; 16 Whitman v. American Trucking Associations , 531 U.S. 457, 495 (2001). 17 In setting primary and secondary standards that are “requisite” to protect public health 18 and welfare, respectively, as provi ded in section 109(b), EPA’s task is to establish standards that 19 are neither more nor less stringe nt than necessary for these purposes. In so doing, the EPA may 20 not consider the costs of implementing the standards. See generally, Whitman v. American 21 Trucking Associations , 531 U.S. 457, 465-472, 475-76 (2001). Likewise, “[a]ttainability and 22 technological feasibility are not relevant considerations in the promulgation of national ambient 23 air quality standards.” American Petroleum Institute v. Costle , 665 F. 2d at 1185. 24 Section 109(d)(1) requires that “not later than Decemb er 31, 1980, and at 5-year 25 intervals thereafter, the Admini strator shall complete a thor ough review of the criteria 26 published under section 108 and th e national ambient air quality st andards . . . and shall make 27
such revisions in such criteri a and standards and promulgate such new standards as may be 28 appropriate . . . .” Section 109(d)(2) requires th at an independent scie ntific review committee 29 “shall complete a review of th e criteria . . . and the national primary and secondary ambient air 30 quality standards . . . and sha ll recommend to the Administrato r any new . . . standards and 31 revisions of existing criteria and standards as ma y be appropriate . . . .” Since the early 1980's, 32January 2013 Draft – Do Not Quote or Cite 1-5 this independent review function has been pe rformed by the Clean Air Scientific Advisory 1 Committee (CASAC). 6 2

1.2.2 History of Lead NAAQS Reviews 3 Unlike pollutants such as particulate matter and carbon monoxide, ai r quality criteria had 4
not been issued for Pb as of the enactment of the Clean Air Act of 1970, which first set forth the 5 requirement to set national ambient air quality st andards based on air quality criteria. In the 6 years just after enactment of the CAA, the EPA did not intend to issue air quality criteria for Pb, 7 and accordingly had not listed Pb under Section 108 of the Act. The EPA had determined to 8 control Pb air pollution through regu lations to phase-out use of Pb additives in gasoline and the 9 EPA viewed those controls, and possibly additional federal controls, as the best approach to 10 controlling Pb emissions (See 41 FR 14921 (April 8, 1976 ). However, the decision not to list Pb 11 under Section 108 was challenged by environmen tal and public health groups and the U.S. 12
District Court for the Southern Di strict of New York concluded th at the EPA was required to list 13 Pb under Section 108. (Natural Resources Defe nse Council v. EPA, 411 F. Supp. 864 21 [S.D. 14 N.Y. 1976], aff’d, 545 F.2d 320 [2d Cir. 1978]). 15 Accordingly, on April 8, 1976, the EPA published a notice in the Federal Register that 16
Pb had been listed under Section 108 as a cr iteria pollutant (41 FR 14921) and on October 5, 17 1978, the EPA promulgated primary and secondar y NAAQS for Pb under Section 109 of the Act 18 (43 FR 46246). Both primary and secondary standa rds were set at a level of 1.5 micrograms per 19 cubic meter ( μ g/m 3 ), measured as Pb in total suspended particles (Pb-TSP), not to be exceeded 20 by the maximum arithmetic mean concentrati on averaged over a calendar quarter. These 21 standards were based on the 1977 Air Qu ality Criteria for Lead (USEPA, 1977). 22
The first review of the Pb standards was initiated in the mid-1980s. The scientific 23
assessment for that review is described in th e 1986 Air Quality Criteria for Lead (USEPA, 24 1986a), the associated Addendum (USEPA, 1986b) and the 1990 Supplement (USEPA, 1990a). 25 As part of the review, the Ag ency designed and performed human exposure and health risk 26 analyses (USEPA, 1989), the results of which were presented in a 1990 Staff Paper (USEPA, 27 1990b). Based on the scientific assessment and the human exposure and hea lth risk analyses, the 28 1990 Staff Paper presented recommendations for consideration by the Ad ministrator (USEPA, 29 1990b). After consideration of the documents de veloped during the review and the significantly 30 changed circumstances since Pb was listed in 1976, the Agency did not propose any revisions to 31 the 1978 Pb NAAQS. In a parallel effort, the Agency developed the broad, multi-program, 32 multimedia, integrated U.S. Strategy for Reducing Lead Exposure (USEPA, 1991). As part of 33

6 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

.January 2013 Draft – Do Not Quote or Cite 1-6 implementing this strategy, the Agency focused efforts primarily on regulatory and remedial 1 clean-up actions aimed at reducing Pb exposures from a variety of nonair sources judged to pose 2 more extensive public health ri sks to U.S. populations, as well as on actions to reduce Pb 3 emissions to air, such as bringing more ar eas into compliance with the existing Pb NAAQS 4 (USEPA, 1991). 5 The most recent review of the Pb air quali ty criteria and standards was initiated in 6 November 2004 (69 FR 64926) and the Agency’s plans for preparation of the Air Quality 7 Criteria Document and conduct of the NAAQS revi ew were presented in documents completed 8 in 2005 and early 2006 (USE PA, 2005; USEPA 2006a). 7 The schedule for completion of the 9 review was governed by a judicial order in Missouri Coalition for the Environment v. EPA (No. 10 4:04CV00660 ERW, Sept. 14, 2005; and amended on April 29, 2008 and July 1, 2008), which 11 specified a schedule for the review of duration substantially shorter than five years. 12
The scientific assessment for the review is described in the 2006 Air Quality Criteria for 13
Lead (USEPA, 2006b; henceforth referred to as the 2006 CD), multiple drafts of which received 14 review by CASAC and the public. The EPA also conducted human exposure and health risk 15 assessments and a pilot ecological risk assessment for the review, after consultation with 16 CASAC and receiving public comment on a draft an alysis plan (USEPA, 2006c). Drafts of these 17 quantitative assessments were reviewed by CASA C and the public. The pilot ecological risk 18 assessment was released in December 2006 (ICF, 2006) and the final health risk assessment 19 report was released in November 2007 (USEPA , 2007a). The policy assessment based on both 20 of these assessments, air quality analyses and key evidence from the AQCD was presented in the 21 Staff Paper (USEPA, 2007b), a draft of which al so received CASAC and public review. The 22 final Staff Paper presented OAQPS staff’s evalua tion of the public hea lth and welfare policy 23 implications of the key studies and scientific information contai ned in the Criteria Document and 24 presented and interpreted results from the quant itative risk/exposure anal yses conducted for this 25
review. Based on this evaluati on, the Staff Paper presented OAQ PS staff recommendations that 26 the Administrator give consideration to subs tantially revising the primary and secondary 27 standards to a range of le vels at or below 0.2 μg/m 3

. 28 Immediately subsequent to completion of th e Staff Paper, the EPA issued an advance 29 notice of proposed rulemaking (ANPR) that was signed by the Administrator on December 5, 30 2007 (72 FR 71488). 8 CASAC provided advice and recomme ndations to the Administrator with 31 regard to the Pb NAAQS based on its review of the ANPR and the previously released final Staff 32

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

8 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 policy assessment prepared by OAQPS staff (previously termed the OAQPS Staff Paper).January 2013 Draft – Do Not Quote or Cite 1-7 Paper and risk assessment reports. The proposed decision on revisions to the Pb NAAQS was 1 signed on May 1, 2008 and published in the Federal Register on May 20, 2008 (73 FR 29184). 2 Members of the public provided bot h written and, at two public hear ings, oral comments and the 3 CASAC Pb Panel also provided advice and reco mmendations to the Administrator based on its 4 review of the proposal notice. The final de cision on revisions to th e Pb NAAQS was signed on 5 October 15, 2008 and published in the Federal Re gister on November 12, 2008 (73 FR 66964). 6
The November 2008 notice described EPA’s decision to revise the primary and 7 secondary NAAQS for Pb, as discussed more fully in section 4.1.1 below. In consideration of 8 the much-expanded health effects evidence on neur ocognitive effects of Pb in children, the EPA 9 substantially revised the primary standard from a level of 1.5 μg/m 3 to a level of 0.15 μg/m 3

. 10 The averaging time was revised to a rolling th ree-month period with a maximum (not-to-be11 exceeded) form, evaluated over a three-year pe riod. The indicator of Pb-TSP was retained, 12 reflecting the evidence that Pb pa rticles of all sizes pose health risks. The secondary standard 13
was revised to be identical in all re spects to the revise d primary standards. 9 Revisions to the 14 NAAQS were accompanied by revisions to the da ta handling procedures, the treatment of 15 exceptional events and the ambient air monito ring and reporting requirements, as well as 16 emissions inventory re porting requirements. 10 One aspect of the new data handling requirements 17
is the allowance for the use of Pb-PM 10 monitoring for Pb NAAQS attainment purposes in 18
certain limited circumstances at non-source-oriented sites. Su bsequent to the 2008 rulemaking, 19
additional revisions were made to the monitoring network requiremen ts as described in chapter 2 20
below. 21

1.2.3 Current Lead NAAQS Review 22 On February 26, 2010, the EPA formally initiate d its current review of the air quality 23 criteria and standards for Pb, requesting the submission of recent scientific information on 24 specified topics (75 FR 8934). Soon after this, the EPA held a science policy workshop to 25 discuss the policy-relevant science, which info rmed identification of key policy issues and 26 questions to frame the review of the Pb NA AQS (75 FR 20843). Drawing from the workshop 27 discussions, the EPA developed the draft IR P (USEPA, 2011c). The draft IRP was made 28
available in late March 2011 for consultation w ith the CASAC Pb Review Panel and for public 29 comment (76 FR 20347). This document was discussed by the Panel via a publicly accessible 30

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

10 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).January 2013 Draft – Do Not Quote or Cite 1-8 teleconference consultation on May 5, 2011 (76 FR 21346; Frey, 2011a). The final IRP, 1 developed in consideration of CASAC advice a nd public comment, was released in November, 2 2011 (USEPA, 2011a; 76 FR 76972). 3 In developing the ISA for this review, the EPA held a workshop in December 2010 to 4
discuss with invited scientific e xperts preliminary draft materials and released the first external 5
review draft of the document for CASAC re view and public comment on May 6, 2011 (USEPA, 6 2011d; 76 FR 26284; 76 FR 36120). The CASAC Pb Review Panel met at a public meeting on 7 July 20, 2011 to review the draft ISA (76 FR 36120). The CASAC provided comments in a 8 December 9, 2011 letter to the EP A Administrator (Frey and Samet, 2011). The second external 9
review draft ISA was released for CASAC re view and public comment in February 2012 10 (USEPA, 2012b, 77 FR 5247) and was the subject of a public meeting on April 10-11, 2012 (77 11 FR 14783). The CASAC provided comments in a July 20, 2012 letter (Samet and Frey, 2012). 12
The third external review draft was releas ed for CASAC review and public comment in 13 November 2012 (USEPA, 2012a, 77 FR 70776). That doc ument, together with this draft Policy 14 Assessment, will be the subject of a public meeting on February 5-6, 2013 (78 FR 938). The 15 final ISA is targeted for release in late spring 2013. 16 As described in the IRP, the EPA develope d and released for CASAC review and public 17 comment in June 2011 an REA Planning Do cument (USEPA, 2011b; 76 FR 58509). This 18 document presented a critical evaluation of the information related to Pb human and ecological 19 exposure and risk (e.g., data, modeling approaches) newly available in this review, with a focus 20
on consideration of the extent to which new or substantially revised REAs for health and 21 ecological risk are warranted by th e newly available evidence. Eval uation of the newly available 22 information with regard to designing and impl ementing health and ecological REAs for this 23 review led us to conclude that the currently available information did not provide a basis for 24 developing new quantitative risk and exposure assessments that would have substantially 25 improved utility for informing the Agency’s cons ideration of health and welfare effects and 26 evaluation of the adequacy of the current prim ary and secondary standa rds, respectively (REA 27 Planning Document, sections 2.3 and 3.3, respec tively). The CASAC Pb Panel provided 28
consultative advice on that docum ent and its conclusions at a public meeting on July 21, 2011 29 (76 FR 36120; Frey, 2011b). Based on their co nsideration of the REA Planning Document 30 analysis, the CASAC Pb Review Panel generally concurred with the conclusion that a new REA 31 was not warranted in this review (Frey, 2011b). In consideration of the conclusions reached in 32 the REA Planning Document and CASAC’s cons ultative advice, the EPA has not developed 33 REAs for health and ecological risk for this review. Accordingly, this Policy Assessment 34 considers the risk assessment findings from the last review with regard to any appropriate further 35 interpretation in light of the evidence newly available in this review. 36January 2013 Draft – Do Not Quote or Cite 1-9 This draft Policy Assessment is being released for public comment and review by 1 CASAC. Advice from CASAC and public comments received on this draft will be considered in 2 preparing the final PA. 3

1.3 SCOPE OF CURRENT REVIEW: FATE AND MULTIMEDIA PATHWAYS OF 4 AMBIENT AIR LEAD 5 The multimedia and persistent nature of Pb c ontributes complexities to the review of the 6 Pb NAAQS unlike issues addr essed in other NAAQS reviews. 11 As described in section 1.1, 7 NAAQS are established to protect public health with an adequate margin of safety, and public 8
welfare from known or an ticipated adverse effects, from ai r pollutants (substances emitted to 9 ambient air). Since Pb distributes from air to other media and is persistent, our review of the 10 NAAQS for Pb considers the pr otection provided against such effects associated both with 11 exposures to Pb in ambient air and with exposur es to Pb that makes its way into other media 12 from ambient air. Additionally, in assessing the adequacy of protection afforded by the current 13 NAAQS, we are mindful of the history of th e greater and more widespread atmospheric 14 emissions that occurred in pr evious years (e.g., under 1978 NAAQS, and prior to establishment 15 of any Pb NAAQS) and that contributed to the Pb that exists in human populations and 16 ecosystems today. Likewise, we also recognize the role of other, nonair sources of Pb now and 17 in the past that also contribut e to the Pb that exists in hum an populations and ecosystems today. 18 As in the last Pb NAAQS review, this backdrop of environmental Pb exposure, and its impact on 19 the populations and ecosystems which may be the s ubjects of the currently available scientific 20 evidence, complicates our consideration of the health and welfare protection afforded by the 21 current NAAQS. In the first section below, we summarize the environmental pathways of 22 human and ecosystem exposures to Pb emitted to ambient air and associated complexities. The 23 subsequent section briefly discusses the role of historically emitted Pb in our consideration of the 24 adequacy of the current NAAQS for Pb. 25

1.3.1 Environmental Distribution and Exposure Pathways 26 Lead emitted to ambient air is transported thr ough the air and is also distributed to other 27 media through the process of deposition, which ma y occur in dry conditions or in association 28 with precipitation, as summarized further in section 2.3 below (ISA, section 3.7.2). Once 29 deposited, the fate of Pb is influenced by the type of surface onto which the particles deposit and 30 by the type and activity level of transport processes in that location. Prec ipitation and other 31

11 Some aspects of the review of the secondary standard for oxides of nitrogen and sulfur, which involved consideration of pollutant tran sport and fate in nonair media with a focus on impacts to aquatic ecosystems, have some similarity to considerations for Pb, while the Pb review also differs in other important aspects.January 2013 Draft – Do Not Quote or Cite 1-10 natural, as well as human-influen ced, processes contribute to the fate of such particles, which 1 affects the likelihood of subseque nt human and ecological exposur es, e.g., tracking into nearby 2 houses or transport with surface runoff into near by water bodies (ISA, sections 3.3 and 4.1). For 3 example, Pb particles deposited onto impervious surfaces, such as roadway, sidewalk or other 4 urban surfaces, may be more available for human contact while they remain on such surfaces or 5 are transferred to other human environments, su ch as on clothing or through resuspension and 6 infiltration (ISA, section 4.1.1.1). Deposited Pb can also be transported (by direct deposition or 7 stormwater runoff) to water bodies and into asso ciated sediments, which may provide a storage 8 function for Pb in aquatic ecosystems (ISA, sections 3.3.2 and 7.2.1). Lead deposited in 9 terrestrial ecosystems can also be incorporated into soil matri ces (ISA, sections 3.3.3 and 7.2.1). 10 Figure 1-1 illustrates, in summary fashi on, the pathways by which Pb emitted into 11
ambient air can be distributed in the envir onment and contribute to human and ecosystem 12 exposures. As shown in this figure, the multimedia distribution of Pb emitted into ambient air 13 (air-related Pb) contributes to multiple air-related pathways of human and ecosystem exposure 14 (ISA, sections 4.1.1 and 4.7.1). 12 As illustrated in Figure 1-1, air-related pathways may involve 15 media other than air. Additionally, as recognized by the figure and discussed more completely in 16 the subsections below, Pb that has not passe d through ambient air (nonair Pb) may complicate 17 our consideration of ambient air Pb exposures. Fu rther, the persistence of Pb poses an additional 18 complication, also discussed below, with regard to consideration of exposures associated with 19
current Pb emissions. 20
21

12 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 final Risk Assessment Report (USEPA, 2007).January 2013 Draft – Do Not Quote or Cite 1-11 1

Figure 1-1. Pathways of human and ecosystem exposure to lead from ambient air. 2

3

1.3.1.1 Human Exposure Pathways 4 Air-related Pb exposure pathways for human s include inhalation of ambient air or 5 ingestion of food, water or other materials, includ ing dust and soil, that have been contaminated 6 through a pathway involving Pb deposition from am bient air (ISA, section 4.1.1.1). Ambient air 7 inhalation pathways include both inhalation of ai r outdoors and inhalation of ambient air that has 8
infiltrated into indoor en vironments. The air-related ingestio n pathways occur as a result of Pb 9 passing through the ambient air, be ing distributed to other envir onmental media and contributing 10 to human exposures via contact with and ingestion of indoor and outdoor dusts, outdoor soil, 11 food and drinking water. 12 Lead currently occurring in nonair media ma y also derive from sources other than 13 ambient air (nonair Pb sources), as summarized further in section 2.3 be low (ISA, section 4.7.1). 14 For example, Pb in dust inside some houses or ou tdoors in some urban areas may derive from the 15 

### 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 pat hw

ay s i g nifi ca n ce

v

a ri es wi t h l ocat i o

n- a n d

r

ecepto r-

spec ifi c

f

acto r s

. 

### * * *

* * Human Exposures (Inhalation and Ingestion)January 2013 Draft – Do Not Quote or Cite 1-12 common past usage of leaded paint, while Pb in drinking water may derive from the use of 1 leaded pipe or solder in dr inking water distribution systems (ISA, section 4.1.3.3). We also 2 recognize the history of much greater air emissions of Pb in the past , such as that associated with 3 leaded gasoline usage and highe r industrial emissions (as summ arized in section 2.1.1 below) 4
which have also contributed to Pb curre ntly occurring in other (nonair) media. 5 The relative importance of different pathways of human exposure to Pb, as well as the 6
relative contributions from Pb resulting from recent and historic air emissions and from nonair 7 sources, vary across the U.S. population as a result of both extrinsic factor s, such as a home’s 8 proximity to industrial Pb sources or its history of leaded paint us age, and intrinsic factors, such 9 as a person’s age and nutr itional status (ISA, secti ons 6.1, 6.2, 6.2.1, 6.2.5 and 6.2.6). For 10 example, a predominant Pb exposure pathway for very young children is the incidental ingestion 11 of indoor dust by hand-to-mouth activity (ISA, s ection 4.1.1.1). For adults, diet may be the 12 primary Pb exposure pathway (2006 CD, section 3.4) . Similarly, the relative importance of air13
related and nonair-related Pb al so varies with the relative magnitudes of exposure by those 14 pathways, which may vary with different circumst ances. For example, relative contributions to a 15 child’s total Pb exposure from air-related expos ure pathways compared to other (nonair) Pb 16 exposures depend on many factors, including ambien t air concentrations and air deposition in the 17 area where the child resides (as well as in the area from which th e child’s food derives), as well 18 as access to other sources of Pb exposure such as Pb paint, tap water affected by plumbing 19 containing Pb, and lead-tainted pr oducts. Studies indica te that in the absence of paint-related 20 exposures, Pb from other sources such as n earby stationary sources of Pb emissions may 21 dominate a child’s Pb exposures (ISA, sec tions 4.1 and 4.1.3.2; 2006 CD, section 3.2.3). In 22 other cases, such as children living in older housi ng with peeling paint or where renovations have 23 occurred, the dominant source of Pb exposure may be dust from lead paint used in the house in 24 the past. Depending on Pb levels in a home’s tap water, drinking water can sometimes be a 25 significant source. Lead exposure may also be the result of a mixture of contributions from 26 multiple sources, with no one source dominating. Our understanding of the relative contribution 27 of air-related Pb to ingestion exposure pathways is limited by the paucity of studies that parse 28 ingestion exposure pathways with regard to air- related and nonair Pb. Our understanding of the 29
relative contribution of ai r-related Pb associated with histor ical emissions and that from recent 30 emissions is similarly limited. 31

1.3.1.2 Ecosystem Exposure Pathways 32
The distribution of Pb from ambient air to ot her environmental media also influences the 33 exposure pathways in terrestrial and aquatic eco systems. Exposure of terrestrial animals and 34 vegetation to air-related Pb can occur by contact with ambient air or by contact with soil, water 35January 2013 Draft – Do Not Quote or Cite 1-13 or food items that have been contaminated by Pb from ambient air (ISA, section 7.2). Transport 1 of Pb into aquatic systems similarly provides for exposure of biota in those systems, and 2 exposures may vary among systems as a result of differences in sources and levels of 3 contamination, as well as characteristics of the sy stems themselves. In addition to Pb contributed 4 by current atmospheric deposition, Pb may occur in aquatic systems as a result of nonair sources 5 such as industrial discharges or mine-related drainage, of historical air Pb emissions (e.g., 6 contributing to deposition to a wa ter body or via runoff from soils ne ar historical ai r sources) or 7 combinations of different types of sources (e.g., resuspension of sediments contaminated by 8 urban runoff and surface water discharges). 9 The persistence of Pb contribu tes an important temporal aspe ct to lead’s environmental 10 pathways, and the time (or lag) associated with re alization of the impact of air Pb concentrations 11 on concentrations in other media can vary with the media (e.g., ISA, section 7.2.2). For example, 12 human exposure pathways most di rectly involving Pb in ambient air and exchanges of ambient 13 air with indoor air can respond more quickly wh ile pathways involving exposure to Pb deposited 14 from ambient air into the environment (e.g., diet ) generally respond more slowly. An additional 15 influence on the response time for nonair media is the environmental presence of Pb associated 16 with past, generally higher, air concentrations . For example, after a reduction in air Pb 17 concentrations, the time needed for sediment or surface soil concentrations to indicate a response 18 to reduced air Pb concentrations might be expected to be longer in areas of more substantial past 19 contamination than in areas with lesser pa st contamination. Thus, considering the Pb 20 concentrations occurring in nonair media as a result of air quality conditions that meet the 21 current NAAQS is a complexity of this review, as it also was, although to a lesser degree, with 22 regard to the prior standard in the last review. 23

1.3.2 Considerations Related to Historically Emitted Lead 24 In reviews of NAAQS, the overarching consider ation of each review is first focused on 25 the general question as to whet her the currently available info rmation supports or calls into 26 question the adequacy of the current standard(s). In addressing that consideration for the 27 NAAQS for Pb, our focus is on Pb emitted to am bient air under conditions meeting the current 28 standard and its potential to cause health or welfare effects as a result of e xposures to Pb in air or 29
in other media. We frame the focus in this way, which differs from that for NAAQS reviews 30 involving other pollutants, in consideration of the persistence of Pb in the environment over time, 31
a characteristic which does not affect reviews of other NAAQS. In considering the case for Pb, 32 however, we recognize that, because of its persis tence, both recent and past Pb emissions to 33 ambient air contribute to current Pb exposures (via multiple exposure pathways, as summarized 34 in section 1.4.1 above). And we r ecognize that past Pb emissions in many situations were well in 35January 2013 Draft – Do Not Quote or Cite 1-14 excess of the current Pb standar d. Yet our task in this and every NAAQS review is focused on 1 assessing the adequacy of the current standard. 2 Lead emissions, and air concentrations, were hi gher in the past, and most substantially so 3 during the time of leaded gasoline usage, as su mmarized in sections 2.1 and 2.2 below. Nonair 4 sources of Pb to human exposure and the environm ent, an additional complicating feature of Pb 5 NAAQS reviews, were also much higher in the pa st. These air and non air sources contributed 6 to historical human and environmental exposures. Because of the persistence of Pb, historical 7 exposures associated both with air-r elated and nonair-relat ed sources, have contributed Pb that is 8 now stored within older humans and ecosystems. For example, concentrations of Pb in the bone 9 and blood of older members of the U.S. population, who lived during the time of widespread air 10 emissions associated with leaded gasoline us age (as well as higher industrial emissions) under 11 the previous Pb NAAQS or prior to establishm ent of any Pb NAAQS, are greater than what 12 would result from air quality conditions allowe d by the current, more restrictive NAAQS. 13 Epidemiological studies of thes e populations, in which this expos ure history is represented by 14 current bone or blood Pb concentrations, contribute to the overall eviden ce base regarding lead15 related health effects (as discu ssed in chapter 3 below). Such studies of these historically 16 exposed populations, however, are generally less informative in judging the adequacy of the 17 current primary standard (as discu ssed in chapter 3 below). This is in contrast to epidemiological 18 studies of very young populations with much shor ter and more recent exposure histories (also 19 discussed in chapter 3). 20 The current distribution of Pb in U.S. ecosyst ems also reflects the widespread and greater 21 air emissions that occurred in the past, under th e prior Pb NAAQS and prio r to establishment of 22 any Pb NAAQS. 13 We lack information on whether adve rse effects could be anticipated from 23 the Pb in terrestrial and aquatic ecosystems that results from air quality conditions allowed by the 24 current, more restrictive NAAQS. As is discu ssed in section 2.3 below, media in ecosystems 25 across the U.S. are still recovering from the pa st period of higher atmospheric emissions, and 26 their responses (e.g., in terms of temporal change in media concentrations) differ with the extent 27 of contamination in individual sy stems as well as with ecosystem-specific characteristics. Thus, 28 the time required for these ecosystem media to “e quilibrate” or come to a “steady-state” that 29 reflects the influence of the current NAAQS (e stablished in 2008) will also vary, and the 30 resulting “steady-state” media concentrations for the range of U.S. ecosystems are unknown. 31 Evidence of effects pertaining to th e concentrations associated with the past, higher emissions (as 32 well as from nonair sources), while informa tive to our understanding of welfare effects 33 associated with environmental Pb generally, do es not directly inform our consideration of 34

13 The current distribution of Pb in U.S. ecosyst ems also reflects histor ical nonair releases.January 2013 Draft – Do Not Quote or Cite 1-15 welfare effects that might be anticipated under th e current secondary standard and thus may be 1 generally less informative in judging the adequacy of the current standard. 2

1.4 GENERAL ORGANIZATION OF THE DOCUMENT 3 Following this introductory chapter, this documen t is organized into th ree main parts: the 4 characterization of ambient Pb; le ad-related health effects and the primary Pb NAAQS; and lead5 related welfare effects and the secondary Pb NAAQS. The characterization of ambient Pb is 6 presented in Chapter 2 and includes information on Pb properties in ambient air, current Pb 7 emissions and air quality patterns, historic trends, and background levels. Chapter 2 also 8 describes the Pb NAAQS surveillance and other Pb monitoring networks. In recognition of the 9
multimedia nature of Pb and the distribution into other media of Pb emitted into the air, Chapter 10 2 also includes information on Pb in media other than air including outdoor dust, soil, surface 11 water and sediment. This chapter provides a fr ame of reference for exposure and risk-related 12 considerations and subsequent discussion of the Pb NAAQS. 13 Chapters 3 and 4 comprise the second main part of this document, dealing with human 14 health and the primary standard. These chapte rs are organized around a series of questions, 15 drawn from the IRP, that address the key policy-re levant issues related to the primary standard. 16 Chapter 3 presents an overview of key policy-relevanthealth effects evidence and major health17 related conclusions from the ISA; an examination of issues related to the quantitative assessment 18 of health risks; key results from quantitativ e assessments together with a discussion of 19 uncertainty and variability in th e results; and discussion of the pub lic health implications of the 20 evidence and exposure/risk information. In this draft PA, chapter 4 includes staff’s preliminary 21 consideration of the scientific evidence and exposure/risk information related to the primary 22 standard and associated preliminary conclusi ons on the adequacy of the current primary 23
standard. 24 Chapters 5 and 6 comprise the third main pa rt of this document. These chapters are 25 similarly organized around a series of questions , drawn from the IRP, that address the key 26 policy-relevant issues re lated to the secondary standard. Chapter 5 presents an overview of 27
welfare effects evidence related to these key policy-relevant i ssues and major welfare effects 28 related conclusions from the ISA; an examina tion of issues related to the screening level 29 ecological risk assessment; and key results from the risk assessment together with a discussion of 30 uncertainty and variability in th e results; and discussion of the pub lic welfare implications of the 31 quantitative assessment with regard to the curr ent standard. The final chapter, chapter 6, 32 includes staff’s preliminary conclusions relate d to the adequacy of the current secondary 33
standard. 34January 2013 Draft – Do Not Quote or Cite 1-16 1.5 REFERENCES 1

Frey, H.C. (2011a) Letter from Dr. H. Christopher Frey , Chair, Clean Air Scientif ic Advisory Committee Lead 2 Review Panel, to Administrator Lisa P. Jackson. Re : Consultation on EPA’s Draft Integrated Review Plan 3 for the National Ambient Air Quality Standards for Lead. May 25, 2011. 4

Frey, H.C. (2011b) Letter from Dr. H. Christopher Frey , Chair, Clean Air Scientif ic Advisory Committee Lead 5 Review Panel, to Administrator Lisa P. Jackson. Re: Consultation on EPA’s Review of the National 6 Ambient Air Quality Standards for Lead: Risk and Exposure Assessment Planning Document. October 14, 7 2011. 8

Frey, H.C. and Samet, J.M. (2011) Letter from Drs. H. Christopher Frey, Chair, Clean Air Scientific Advisory 9 Committee Lead Review Panel, and Jonathan M. Samet, Chair, Clean Air Scien tific Advisory Committee, 10 to Administrator Lisa P. Jackson. Re: CASAC Re view of the EPA’s Integrat ed Science Assessment for 11 Lead (First External Review Dr aft – May 2011). December 9, 2011. 12

ICF International. (2006) Lead Human Exposure and Hea lth Risk Assessments and Ec ological Risk Assessment for 13 Selected Areas. Pilot Phase. Draft Technical Report. Prepared for the U.S. EP A's Office of Air Quality 14 Planning and Standards, Research Triangle Park, NC. December. 15

Jackson, L. (2009) Memorandum from Administrator Lisa Jackson, Subject: Development of regulations and 16 policies. September 11, 2009. Available at: 17 http://www.epa.gov/ttn/naaqs/pdfs/N AAQSReviewProcessMemo52109.pdf 18

Samet, J.M. and Frey, H.C. (2012) Letter from Drs. Jona than M. Samet, Chair, Clean Air Scientific Advisory 19 Committee and H. Christopher Frey, Ch air, Clean Air Scientific Adviso ry Committee Lead Review Panel, 20 to Administrator Lisa P. Jackson. Re: CASAC Re view of the EPA’s Integrat ed Science Assessment for 21 Lead (Second External Review Draft – February 2012). July 20, 2012. 22

U.S. Environmental Protection Agency. (1977) Air quality criteria for lead. Research Triangle Park, NC: Health 23 Effects Research Laboratory, Criteria and Special Studies Office; EPA report no. EPA-600/8-77-017. 24 Available from: NTIS, Springfield, VA; PB-280411. 25

U.S. Environmental Protection Agency. (1986a) Air quality criteria for lead. Research Tr iangle Park, NC: Office of 26 Health and Environmental Assessment, Environmental Criteria and Assessment Office; EPA report no. 27 EPA-600/8-83/028aF-dF. 4v. Available from: NTIS, Springfield, VA; PB87-142378. 28

U.S. Environmental Protection Agency. (1986b) Lead effe cts on cardiovascular functi on, early development, and 29 stature: an addendum to U.S. EPA Air Quality Criteri a for Lead (1986). In: Air quality criteria for lead, v. 30 1. Research Triangle Park, NC: Office of Health an d Environmental Assessment, Environmental Criteria 31 and Assessment Office; pp. A1-A67; EPA report no. EPA-600/8-83/028aF. Available from: NTIS, 32 Springfield, VA; PB87-142378. 33

U.S. Environmental Protection Agency. (1989) Review of the national ambient air quality standards for lead: 34 Exposure analysis methodology and validation: OAQPS staff report. Research Triangle Park, NC: Office of 35 Air Quality Planning and Standards; report no. EPA-450/2-89/011. Available on the web: 36 http://www.epa.gov/ttn/naaqs/standards/pb/data/rnaaqsl_eamv.pdf 37

U.S. Environmental Protection Agency. (1990a) Air quality criteria for lead: supplement to the 1986 addendum. 38 Research Triangle Park, NC: Office of Health and Environmental Assessment, Environmental Criteria and 39 Assessment Office; report no. EPA/600/8-89/049F. Available from: NTIS, Springfield, VA; PB91-138420. 40

U.S. Environmental Protection Agency. (1990b) Review of the national ambient air quality standards for lead: 41 assessment of scientific and technical information: OAQPS staff paper. Research Triangle Park, NC: Office 42January 2013 Draft – Do Not Quote or Cite 1-17 of Air Quality Planning and Standards; report no. EPA-450/2-89/022. Available from: NTIS, Springfield, 1 VA; PB91-206185. Available on the web: http://www.epa.gov/ttn/naaqs/standards/pb/data/rnaaqsl_asti.pdf 2

U.S. Environmental Protection Agency. (1991) U.S. EPA Strategy for Reducing Lead Exposure. Available from 3 U.S. EPA Headquarters Library/Washington, D.C. (Library Code EJBD; Item Call Number: EAP 4 100/1991.6; OCLC Number 2 346675). http://www.ep a.gov/ttn/naaqs/standa rds/pb/s_pb_pr.html 5

U.S. Environmental Protection Agency. (2005) Project Work Plan for Revised Air Quality Criteria for Lead. 6 CASAC Review Draft. National Center for Enviro nmental Assessment, Research Triangle Park, NC. 7 NCEA-R-1465. Available at: http://www.epa .gov/ttn/naaqs/standards/pb/s_pb_cr_pd.html 8

U.S. Environmental Protection Agency. (2006a) Plan for Re view of the National Ambient Air Quality Standards for 9 Lead. Office of Air Quality Planning and Standard s, Research Triangle Park, NC. Available at: 10 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_pd.html 11

U.S. Environmental Protection Agency. (2006b) Air Quality Criteria for Lead. Washington, DC, EPA/600/R12 5/144aF. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr.html 13

U.S. Environmental Protection Agency. (2006c) Analysis Plan for Human Health and Ecological Risk Assessment 14 for the Review of the Lead National Ambient Air Quality Standards. Office of Air Quality Planning and 15 Standards, Research Triangle Park, NC. Available at: 16 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_pd.html 17

U.S. Environmental Protection Agency. (2007a) Lead: Huma n Exposure and Health Risk Assessments for Selected 18 Case Studies, Volume I. Human Exposure and Hea lth Risk Assessments – Full-Scale and Volume II. 19 Appendices. Office of Air Quality Planning and Stan dards, Research Triangle Park, NC. EPA-452/R-07- 20 014a and EPA-452/R-07-014b. http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_td.html 21

U.S. Environmental Protection Agency. (2007b) Review of the National Ambient Air Quality Standards for Lead: 22 Policy Assessment of Scientific an d Technical Information, OAQPS St aff Paper. Office of Air Quality 23 Planning and Standards, Research Triangle Park, NC. EPA-452/R-07-013. Available at: 24 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_sp.html 25

U.S. Environmental Protection Agency. (2011a) Integrat ed Review Plan for the National Ambient Air Quality 26 Standards for Lead. Research Triangle, NC. EPA-452/R-11-008. Available online at: 27 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html 28

U.S. Environmental Protection Agency. (2011b) Review of the National Ambient Air Quality Standards for Lead: 29 Risk and Exposure Assessment Planning Document. Office of Air Quality Planning and Standards, 30 Research Triangle Park, NC. EP A/452/P-11-003. Available at: 31 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_pd.html 32

U.S. Environmental Protection Agency. (2011c) Integrat ed Review Plan for the National Ambient Air Quality 33 Standards for Lead. External Review Draft. Research Triangle, NC. EP A-452/D-11-001. Available online 34 at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html 35

U.S. Environmental Protection Agency. (2011d) Integrated Science Assessment for Lead (First External Review 36 Draft). Washington, DC, EPA/600/R-10/075A. Available online at: 37 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html 38

U.S. Environmental Protection Agency. (2012a) Integrated Science Assessment for Lead (Third External Review 39 Draft). Washington, DC, EPA/600/R-10/075C. Available online at: 40 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_isa.html 41January 2013 Draft – Do Not Quote or Cite 1-18 U.S. Environmental Protection Agency. (2012b) Integrated Science Assessment for Lead (Second External Review 1 Draft). Washington, DC, EPA/600/R-10/075B. Available online at: 2 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html 3January 2013 Draft – Do Not Quote or Cite 2-1 

### 2 AMBIENT AIR LEAD 1

The focus for this Pb NAAQS review is on Pb derived from those sources emitting Pb to 2
ambient air. As noted in sect ion 1.3, air emissions contribute to concentrations in multiple 3
environmental media and the role of the nonair medi a is enhanced by the pers istent nature of Pb. 4 Consequently this chapter discusses our curren t understanding of Pb in ambient air and of 5
ambient air-related Pb in other media. 6 Lead emitted to the air is predominantly in pa rticulate form, with the particles occurring 7 in various sizes (ISA, section 3.3.1). While in some limited circumst ances associated with 8 incomplete combustion of leaded gasoline, Pb may be emitted in gaseous form, atmospheric 9 conditions readily contribute to condensation into particles (ISA, section 3.2). Once emitted, Pb 10 can be transported long or shor t distances depending on their si ze, which influences the amount 11 of time spent in the aerosol phase. Consistent with previous eviden ce, recent research on 12 particulate matter with mass median diam eter of 2.5 and of 10 micrometers (PM 2.5 and PM 10 ) 13 confirms the transport of airborne Pb apprecia ble distances from its sources. For example, 14 samples collected at altitude over the Pacific Oc ean, as well as the seas onal pattern of Pb-PM 2.5 15
at rural sites in the western U.S. indicate tran sport of Pb from sources in Asia, although such 16
sources have been estimated to contribute less than 1 ng/m 3 to western U.S. Pb concentrations 17 (ISA, section 3.3.1; Murphy et al., 2007). As a ge nerality, larger particle s tend to deposit more 18 quickly, within shorter distances from emissions poi nts, while smaller particles remain in aerosol 19 phase and travel longer distan ces before depositing (ISA, sec tion 2.2.1). As summarized in 20 section 2.2.2 below, airborne c oncentrations of Pb near sour ces are much higher, and the 21 representation of larger particles generally greater, than at sites not directly influenced by 22

sources. 23 In this chapter, we discuss the current in formation on ambient Pb regarding sources and 24 emissions (section 2.1), current ambient air m onitoring methods and networks and associated 25 measurements (section 2.2) and th e contribution of ambi ent air Pb to Pb in other media (section 26 2.3). 27

2.1 SOURCES AND EMISSIONS TO AMBIENT AIR 28 In this section we describe the most recently available information on sources and 29
emissions of Pb into the ambient air. The sect ion does not provide a comprehensive list of all 30 sources of Pb, nor does it provide estimates of emission rates or emission factors for all source 31 categories. Rather, the discussion here is intended to identify the larger source categories, either 32 on a national or local scale, and generally descri be their emissions and distribution within the 33
U.S. 34January 2013 Draft – Do Not Quote or Cite 2-2 The primary data source for this discussion is the National Emissions Inventory (NEI) for 1
2008 1 . The NEI is a comprehensive and detailed es timate of air emissions of both criteria and 2 hazardous air pollutants from air em issions sources. The NEI is generally prepared every three 3 years by the EPA based primarily upon emission estimates and emission model inputs provided 4 by state, local, and tribal air agencies for sour ces in their jurisdictions, and supplemented by data 5 developed by the EPA. Some of these esti mates are required by regulation while some are 6 voluntarily reported. For example, states are required to report Pb emissions from facilities 7 emitting more than 5 tons of Pb per year (tpy) and from facilities emitting greater than threshold 8 amounts for other criteria pollutants (e.g., 100 tp y of particulate matter or volatile organic 9 compounds; CFR 51, subpart A). Estimates of Pb emissions presented in this document (and in 10 the ISA) are drawn from the 2008 NEI version 3. 2 As a result of various Clean Air Act 11 requirements, emissions standards implemented since 2008 for a number of source categories 12 represented in the NEI are project ed to result in considerably lo wer emissions at the current time 13
or in the near future. 14 The following sections present information relative to 2008 Pb emissions on a national 15 and local scale. Lead is emitted from a wide variety of source types, some of which are small 16 individually but for which the cumulative emissions are large, and some for which the opposite is 17 true. For example, a source category may be composed of many sma ll (i.e., low-emitting) 18 sources or of just a few very large (high-emitting) sources. Temporal trends in the national totals 19 of Pb emissions are presented in Section 2.1.1. Information about the emissions source types or 20 categories that are large on a national scale as of 2008 is presented in Section 2.1.2, while 21 information on the sources that are large at th e local scale is presen ted in Section 2.1.3. 22 Additional information on data sources for, limita tions of and our confidence in the information 23 summarized here is described in Appendix 2A. 24

2.1.1 Temporal Trends on a National Scale 25 Figure 2-1 shows the substantial downward trend in Pb emissions that has occurred over 26 the past several decades. The most dramatic re ductions in Pb emissions occurred prior to 1990 27 in the transportation sector due to the removal of Pb from gaso line. Lead emissions were further 28 reduced substantially between 1990 and 2008, with si gnificant reductions occurring in the metals 29 industries at least in pa rt as a result of national emissions st andards for hazardous air pollutants. 30
31

1 http://www.epa.gov/ttn/chief/net/2008inventory.html
2 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.January 2013 Draft – Do Not Quote or Cite 2-3 1 2 3 4 5 6 7

8

Figure 2-1. Temporal trend in air emissions: 1970-2010. 9

10

2.1.2 Sources and Emissions on National Scale - 2008 11 As indicated in Figure 2-1, the largest source sector emitting Pb into the atmosphere on a 12 national scale is aviation gasolin e usage by piston engine driven aircraft. The next largest 13 nationally is metal working and mining. Considering the national estimates at a more detailed 14 scale, the largest source categories emitting Pb in to the atmosphere on a national scale, after 15 emissions from aircraft operating on leaded fuel, are boilers and process heaters (fuel 16 combustion) which, while individually are generally small sources, are large when aggregated 17 nationally (Table 2-1). The next largest categories are various metals industries, including lead18 specific industries (Table 2-1). Together these and other sources were estimated to emit just 19 under a thousand tpy of Pb in the U.S. in 2008. 20January 2013 Draft – Do Not Quote or Cite 2-4 Table 2-1. U.S. lead emissions by source categorie s estimated to emit at least 4 tpy. 1

Source Category Description 2008 Emissions (tons)
ALL CATEGORIES A 950 Aircraft operating on leaded fuel B 550 Industrial/Commercial/Institutional Boilers & Process Heaters 64 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 7 Secondary Non-ferrous Metals (other) 7 Primary Non-ferrous Metals (other) 7 Carbon Black 6 Pulp and Paper Production 6 Secondary Copper Smelting 5 Fabricated Metal Products Manufacturing 5 Residential Heating 5 Municipal Waste Incineration 5 Commercial Marine Vessels 5 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 lead 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 is planning to cease the existing smelter operations at this site by April 2014 (DRRC, 2010).January 2013 Draft – Do Not Quote or Cite 2-5 1

2.1.2.1 Stationary Sources 2 Since the last review of the Pb NAAQS, th e EPA has completed a number of regulations 3
which will result in reduced Pb emissions from stationary sources regulated under the Clean Air 4 Act sections 112 and 129. For example, in January 2012, the EPA updated the National 5
Emission Standards for Hazardous Air Pollutants (NESHAP) for Secondary Lead Smelting (77 6 FR 555). These amendments to the original ma ximum achievable control technology standards 7 apply to facilities nationwide that use furnaces to recover lead from lead-bearing scrap, mainly 8 from automobile batteries (15 ex isting facilities, one under construc tion). By the effective date 9 in 2014, this action is estimated to result in a lead emissions reduction of 13.6 tpy across the 10 category (a 68% reduction). Al so, the NESHAP for Primary Lead Smelting was revised in 2011 11 (76 FR 70834) and more than a dozen additional EP A actions taken in the past 5 years, which 12
would not be reflected in the 2008 NEI estimates , will result in Pb emissions reductions 13 (Appendix 2B). 14
15 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.January 2013 Draft – Do Not Quote or Cite 2- 6 2.1.2.2 Mobile Sources 1 Forty years ago, combustion of leaded gasoline wa s the main contributor of Pb to the air. 2 In the early 1970s, the EPA set national regulati ons to gradually reduce the Pb content in 3 gasoline. In 1975, unleaded gasoli ne was introduced for motor vehi cles equipped with catalytic 4
converters. The EPA banned the use of leaded gasoline in highway vehicles after December 5
1995. 6 Lead emissions from piston-engine aircraft operating on leaded fu el are currently the 7 largest source of Pb air emissions on a national scale. Lead is adde d to aviation gasoline 8 (commonly referred to as “avgas”) used in most pi ston-engine aircraft in order to boost octane 9 and prevent engine knock. 3 The most commonly used avgas, 100 Octane Low Lead, contains up 10 to 2.12 grams Pb per gallon (ASTM D 910). The Fe deral Aviation Administration estimates that 11 in 2008, 248 million gallons of avgas were consumed in the U.S. 4 contributing an estimated 550 12 tons of Pb to the air that compri se 57% of the national Pb inventory. 5 Leaded avgas is used at 13 approximately 20,000 airport f acilities in the U.S. 14 The EPA is currently collecting and evaluati ng information regarding emissions and air 15 concentrations of lead resulting from avgas combus tion by piston-engine aircra ft. This is part of 16 an ongoing investigation under section 231 of the Clean Air Act into the potential for these 17
emissions to cause or contribute to air pollution that may reasona bly be anticipated to endanger 18 public health or welfare. This evaluation by the EPA is occurring separate from the NAAQS 19 review. The EPA’s investigation includes subs tantial analytical work. The timeline for 20 completion of this investigation and possible issuance of a final endangerment determination 21 includes completion of necessa ry modeling and monitoring information and other data, 22 development of a proposal which will be publishe d for public comment, review and analysis of 23
comments received and issuance of the final de termination. If the EPA issues a positive 24
determination that Pb emissions from aircraft engines cause or contribute to air pollution that 25 may reasonably be anticipated to endanger public health or welfare, the EPA would then be 26 required to propose and promulgate emissions standa rds to control aircraft engine Pb emissions, 27
and the Federal Aviation Administ ration would be required to prom ulgate regulations addressing 28

3 Lead is not added to jet fuel used in commercial airc raft, military aircraft, or ot her turbine engine aircraft.
4 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.
5 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.pdfJanuary 2013 Draft – Do Not Quote or Cite 2- 7 the fuel used by those aircraft. More info rmation about EPA’s actions is available at 1 www.epa.gov/otaq/aviation.htm. 2 Vehicles used in racing are not regulated by the EPA under the Clean Air Act and can 3 therefore use alkyl-Pb additives to boost octane . The National Association for Stock Car Auto 4 Racing (NASCAR) formed a volunta ry partnership with the EPA with the goal of permanently 5 removing alkyl-Pb from racing fuels used in the racing series now known as the Sprint Cup, the 6 Nationwide Series and the Campi ng World Truck Series. The major NASCAR race series now 7
use unleaded fuels. 8 Due to the presence of Pb as a trace contamin ant in gasoline, diesel fuel and lubricating 9 oil, cars, trucks, and engines operating in nonroa d equipment, marine engines and jet aircraft 10 emit small amounts of Pb (ISA, Section 3.2.2.6). A dditional mobile sources of Pb include brake 11 wear, tire wear, and loss of Pb wheel weights (ISA, Section 3.2.2.6). 12

2.1.2.3 Natural Sources and Long-range Transport 13
Some amount of Pb in the air derives from natural sources, such as volcanoes, sea salt, 14 and windborne soil particles from areas free of an thropogenic activity and so me may also derive 15 from anthropogenic sources of airborne Pb loca ted outside of the U.S. (ISA, section 3.5.5). 16 Emissions estimates for these sources, as well as wild forest fires and biogenic sources have not 17 been developed for the NEI and quantitative estim ates for these processes remain an area of 18 significant uncertainty. Based on several different approaches , the ISA identifies several 19
estimates of the concentration of airborne Pb derived from natural sources. All of the estimates 20 are no higher than 1 nanogram per cubic meter (ng/m 3 ), and range down as low as 0.02 ng/m 3 21 (ISA, section 3.5.5). The data avai lable to derive such an estimate are limited and such a value 22 might be expected to vary geographically with the natural dist ribution of Pb. 23
Another contribution to U.S. ai rborne Pb concentrations is long-range transport such as 24
that associated with ai r masses carrying Pb from sources in Asia, where controls on Pb emissions 25 have lagged those in the U.S. and Canada (ISA, section 3.5.5; Osterberg et al., 2008). The most 26 recent estimates of contributions from Asia, how ever, conclude that the Asian contribution to 27
U.S. airborne Pb concentrations is generally less than 1 ng/m 3 (ISA, section 3.5.5; Murphy, 28 2007; Ewing et al., 2010). 29

2.1.2.4 Previously Deposited or Released Lead 30 Lead-bearing particles that occur on surface so ils or built surfaces as a result of previous 31 or historic deposition can be a s ource of airborne Pb as a result of particle resuspension and may 32 be a significant source of airborne Pb in areas near major sources of Pb emissions. Outdoor dust 33 may be resuspended into the air by wind or hum an-induced mechanical forces, such that the 34 main drivers of particle resuspension are typically mechanical stressors such as vehicular traffic, 35January 2013 Draft – Do Not Quote or Cite 2-8 construction and agricultural operations, and, gene rally to a lesser extent, the wind (ISA, section 1 3.3.1.3; 2006 CD, section 2.3.3). Wind resuspension is often defined in terms of a resuspension 2 rate, which is the fraction of a surface contamin ant released per unit time. Resuspension rates 3 are dependent on many factors, including wind speed, soil/surface moisture, particle sizes, 4 presence of saltating particles and presence of vegetation; typical va lues range over several 5 orders of magnitude (ISA, section 3.3.1.3; 2006 CD, section 2.3.3). Vehicular resuspension 6 results from shearing stress of tires or turbul ence generated by a passing vehicle and can be 7 affected by a number of factors in cluding vehicle size, vehicle spee d, moisture and particle size 8 (ISA, section 3.3.1.3; 2006 CD, section 2.3.3). Add itionally, the amount of material available 9 for resuspension can be influenced by removal pr ocesses such as surface runoff associated with 10 rainfall (ISA, sections 2.2.1, 3.3.2 and 3.3.2.4). Rath er than a continuous process, resuspension 11 may occur as a series of events. Short ep isodes of conditions or factors conducive to 12 resuspension may dominate annual averages of upward flux (2006 CD, p. 2-65). Variability and 13 uncertainty in these factors, and with regard to surface soil/dust composition, affect quantitative 14 emissions estimates for these processes (2006 CD, section 2.3.3). 6 15
Consideration of Pb concentr ations in air and surface soi l/dust in different types of 16 locations also informs our understanding of the re lative importance of resuspension of previously 17 deposited dust particles as an influence on airbor ne Pb concentrations. The relative importance 18 would be expected to vary with site-specifi c circumstances, such as the magnitude of Pb 19 concentrations in the surface dust and air Pb contributions from nearby sources of new Pb 20 emissions, as well as with variation in the for ces that influence particle resuspension. For 21 example, the contribution of resuspension to airb orne concentrations app ears to be greatest in 22 areas of highly contaminated surface dust such as at historically active industrial sites, which 23 may or may not be currently ac tive (ISA, sections 3.3.1.3 and 3.5.3). 24 Emissions from currently active metals i ndustries include those related to current 25 industrial activity and to resuspension of previ ously deposited material (often a component of 26 “fugitive” emissions estimates 7 ). Accordingly, the relative magn itude of air Pb concentrations 27 associated with no longer active i ndustries would be expected to ge nerally be lower than that for 28

6 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.
7 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).January 2013 Draft – Do Not Quote or Cite 2-9 active industries yet greater than that in locations somewh at removed from i ndustrial sources. 1 The limited available data for comparison gene rally confirms this (section 2.2.2.2 below). 2 Lead-bearing particulate matter in other, non-in dustrial, locations of appreciable historic 3 lead contamination, such as in soils or on surfaces in older urban areas or near older 4 transportation corridors ma y, if disturbed, also become suspende d into the air a nd contribute to 5
air Pb concentrations. In olde r transportation corri dors or other locations not influenced by 6 active industries, the significance of resuspension (e.g., in terms of resultant air Pb 7 concentrations) appears to be much less that that associated with active industries or now closed 8 industries with substantial emissions in the past. 8 For example, the available data indicate that 9 current Pb concentrations near roadways are subs tantially lower than those near large, currently 10 active industrial sources (see ISA, section 3.3.1.3 and Figures 2-9 a nd 2-11 below). In general, 11
air Pb concentrations at sites described as not influenced by an active industry are much lower 12
than those near activ e sources (see ISA, section 3.5.1.2 and Figure 2-11 below). 13

2.1.3 Sources and Emissions on Local Scale 14 Based on the 2008 estimates, the highest emissi ons in specific (loc al) situations are 15 different types of metals industries, 23 of wh ich had 2008 estimates greater than or equal to 1.0 16 tpy Pb (Table 2-2). The geogra phic distribution of the facilities summarized in Table 2-2 is 17 presented in Figure 2-2. 18
19

8 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).January 2013 Draft – Do Not Quote or Cite 2-10 Table 2-2. Facilities estimated to em it at least 0.50 tpy in 2008. 1

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 3 2 3.1 - 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 Black Plant 1 1 6.3 Primar y Non-ferrous Metal Smeltin g

/Refinin g

Plant ( not Lead, Aluminum, or Co pp

er

) 1 1 5.4 Mine or Quarry 5 2 1.6 - 3.8 Ethanol Biorefinery 2 2 1.5 - 3.8 Portland Cement Plant 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 Products Plant 1 1 2.3 Foundry, Iron and Steel 3 3 1.1 - 2.3 10 8 Secondary Copper Smelting/Refining Plant 1 1 2.3 Foundry, Non-ferrous 3 2 1.2 - 2.0 1 1 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 1 1 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 Fabricated Metal Products Plant 6 5 Municipal Waste Combustor 3 3 Glass Plant 2 2 Lumber/Sawmill 2 1 Plastic, Resin, or Rubber Products Plant 1 1 Taconite Processing Plant 1 1 Petrochemical Plant 1 1 Bulk Terminal or Bulk Station 1 1
A

- Emissions totals from 2008 National Emissions Inventory, version 3 (January 2013), except in the case of airports for which EPA specific estimates were used. B - This category includes facilities with total emissions estimates greater than or equal to 0.95 tpy. C - This category includes facilities with total emissions estimates greater than or equal to 0.495 and less than 0.95 tpy. D - There is some uncertainty regarding this total emissions estimate for this facility, the only remaining operational primary Pb smelter in the U.S., which is planning to cease the existing smelter o perations at this site by April, 2014 (DRRC, 2010).January 2013 Draft – Do Not Quote or Cite2-111Figure 2-2.Geographic distribution of facilities estimated to emit at least 0.50 tpy in 2008.2* Includes facilities with emissions greater than or equal to 1.0 tpy (after rounding to 1 decimal place).** Includes facilities with emissions greater than or equal to 0.50 tpy (after rounding to 2 decimal places) and less than 1.0 (after rounding to 1 decimal place).Study airports are described in section 2.2 below.January 2013 Draft – Do Not Quote or Cite 2-12 2.2 AMBIENT AIR QUALITY 1 The EPA and state and local agencies have b een measuring Pb in the atmosphere since 2 the 1970s. In response to reduced emissions (see section 2.1), Pb concentrations have decreased 3 dramatically over that period. Currently, the highest concentrat ions occur near some metals 4
industries where some individual locations have concentrations that exceed the NAAQS. This 5
section describes the ambient Pb measurement methods, the sites and networks where these 6 measurements are made, and how the ambient Pb concentrations va ry geographically and 7 temporally. 8

2.2.1 Air Monitoring 9
Ambient air Pb concentrations are measured by five national monitoring networks. The 10
networks include the State a nd Local Air Monitoring Sites (S LAMS) intended for Pb NAAQS 11 surveillance, the PM 2.5 Chemical Speciation Network (CSN ), the Interagency Monitoring of 12 Protected Visual Environments (IMPROVE) networ k, the National Air Toxics Trends Stations 13 (NATTS) network, and the Urban Air Toxics Mon itoring program. All of the data from these 14
networks are accessible via EPA’s Air Quality System (AQS): 15 http://www.epa.gov/ttn/airs/airsaqs/ . In addition to these networks, various environmental 16 organizations have operated other sampling site s yielding data (which may or may not be 17 accessible via AQS) on ambient air concentrations of Pb, often for limited periods and/or for 18 primary purposes other than quantification of Pb itself. The subsections below describe each 19
network and the Pb measurements made at these sites. 20

2.2.1.1 Lead NAAQS Surveillance Network 21 This section describes sample collection, analysis and network aspects for the Pb SLAMS 22 network, the main purpose of which is survei llance of the Pb NAAQS. As such, the EPA 23 regulates how this monitoring is conducted in order to ensure accurate and comparable data for 24 determining compliance with the NAAQS. The code of federal regulations (CFR) at parts 50, 53 25 and 58 specifies required aspects of the ambi ent monitoring program for NAAQS pollutants. 9 In 26 order to be used in NAAQS attainment designat ions, ambient Pb concentration data must be 27 obtained using either the federal reference method (FRM) or a federal equi valent method (FEM). 28 The indicator for the current Pb NAAQS is Pb-TSP. However, in some situations, 10 ambient Pb- 29

9 The federal reference methods (FRMs) for sample coll ection and analysis are specified in 40 CFR part 50, the procedures for approval of FRMs and federal equivalent methods are specified in 40 CFR part 53 and the rules specifying requirements for the planning and operations of the ambient monitoring network are specified in 40 CFR part 58.
10 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 pa rt 58 Appendix D paragraph 2.10.1.2. These conditionsJanuary 2013 Draft – Do Not Quote or Cite 2-13 PM 10 concentrations may be used in judging non attainment. Accordingly, FRMs have been 1
established for Pb-TSP and for Pb-PM 10 . The current FRM for the measurement of Pb-TSP is 2 provided in 40 CFR part 50 Appendix G. This FRM includes sampling using a high-volume 3 TSP sampler that meets the design criteria identi fied in 40 CFR part 50 Appendix B and sample 4 analysis for Pb content using flame atomic absorption. There are 24 FEMs currently approved 5
for Pb-TSP. 11 All 24 FEMs are based on the use of hi gh-volume TSP samplers and a variety of 6 approved equivalent analysis methods. 7
A new FRM for Pb-PM 10 was promulgated as part of the 2008 review. This FRM is 8
based on the PM 10 sampler defined in 40 CFR part 50 Appendix J coupled with x-ray 9 fluorescence (XRF) analysis. In addition, one FEM for Pb-PM 10 has been finalized for the 10 analysis of Pb-PM 10 based on inductively coupled plasma mass spectroscopy (ICP-MS). 11 The current Pb monitoring network desi gn requirements for NAAQS compliance 12 purposes (40 CFR part 58, Appendix D, paragraph 4.5) include two types of monitoring sites – 13 source-oriented monitoring site s and non-source-oriented monito ring sites. Source-oriented 14 monitoring sites are required near sources of air Pb emissions which are exp ected to or have been 15
shown to contribute to ambient air Pb concentr ations in excess of the NAAQS. At a minimum, 16
there must be one source-oriented site locate d to measure the maximum Pb concentration in 17 ambient air resulting from each non-airport Pb so urce estimated to emit 0.50 or more tons of Pb 18 per year and from each airport estimated to emit 1.0 or more tons of Pb per year. 12 The EPA 19 Regional Administrators may require additi onal monitoring beyond the minimum requirements 20 where the likelihood of Pb air qualit y violations is signif icant. Such locations may include those 21 near additional industrial Pb sources, recently cl osed industrial sources and other sources of 22 resuspended Pb dust, as well as airports where piston-engine aircraft em it Pb (40 CFR, part 58, 23 Appendix D, section 4.5(c)). 24 Monitoring agencies are also required, unde r 40 CFR, part 58, Appendix D, to conduct 25 non-source-oriented Pb monitoring at the NCore sites required in Core metropolitan with a 26 population of 500,000 or more. 13 NCore is a new network of mu ltipollutant monitoring stations 27

include where Pb concentrations are not expected to equal or exceed 0.10 micrograms per cubic meter as an 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.
11 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
12 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)).
13 Defined by the US Census Bureau - http://www.c ensus.gov/population/www/metroareas/metroarea.htmlJanuary 2013 Draft – Do Not Quote or Cite 2-14 intended to meet multiple monitoring objectives. The NCore stations are a subset of the state and 1 local air monitoring stations network and are in tended to support long-term trends analysis, 2 model evaluation, health and ecosystem studies, as well as NAAQS compliance. The complete 3 NCore network consists of appr oximately 60 urban and 20 rural st ations, including some existing 4
SLAMS sites that have been modified for add itional measurements. Each state will contain at 5 least one NCore station, and 46 of the states pl us Washington, DC, will have at least one urban 6
station. 7
Either Pb-TSP or Pb-PM 10 monitoring may be performed at these sites. Of 24 NCore 8 sites measuring Pb concentrations, 17 are meas uring Pb in TSP and 7 are measuring Pb in PM 10
. 9 While non-source-oriented monitoring data can be used for purposes of NAAQS attainment 10 designations, a main objective fo r non-source-oriented monitoring is to gather information on 11 neighborhood-scale lead concentrat ions that are typical in urba n areas in order to better 12
understand ambient air-related Pb exposures for populations in these areas. 13
Source-oriented monitors near sources estima ted to emit 1.0 tpy Pb were required to be 14 operational by January 1, 2010, and the remainde r of the newly required source-oriented 15 monitors were required to be operational by December 27, 2011 (75 FR 81126). Currently, 16 approximately 260 Pb-TSP monitors are in opera tion; these are a mixture of source- and non17 source-oriented monitors. Figure 2-3 shows th e geographic distribution of these monitors (in 18 addition to the airport study monitors described below) in the current 14 Pb NAAQS surveillance 19 network, with the Pb-TSP monitors existing at the time of the 2008 rulemaking indicated 20 separately from the newly sited Pb-TSP monitors. 21

14 This figure reflects Pb-TSP monitors in AQS as of September 2012.January 2013 Draft – Do Not Quote or Cite 2-15 1

Figure 2-3. Map of Pb-TSP Monitoring Sites in Current Pb NAAQS Monitoring 2 Network. 15 3

The current regulations also required one year of Pb-TSP monitoring (using FRM or 4 FEM methods) near 15 specific airports in or der to gather additional information on the 5 likelihood of NAAQS exceedances n ear airports due to the combustion of leaded aviation 6 gasoline (75 FR 81126). These airports were se lected based on three criteria: annual Pb 7 inventory between 0.5 ton/year and 1.0 ton/year, ambient air within 150 meters of the location of 8 maximum emissions (e.g., the end of the runway or run-up location), and airport configuration 9 and meteorological scenario that leads to a gr eater frequency of operations from one runway. 10
These characteristics were select ed because they are expected, co llectively, to identify airports 11 with the highest potential to have ambient Pb concentrations approaching or exceeding the Pb 12 NAAQS. Data from this monitoring study will be used to assess the need for additional Pb 13

15 Estimates for source-oriented monitors are base d on Pb emissions estimates in the 2008 National Emissions Inventory.January 2013 Draft – Do Not Quote or Cite 2-1 6 monitoring at airports. These 15 s ites (Figure 2-4) were intended to be operational no later than 1 December 27, 2011, although delays in monitor siting extended the installation of some of these 2
monitors into late 2012. 3

4

Figure 2-4. Map of sites near airports for which one year of monitoring is required. 16 5

6

2.2.1.2 Other Lead Monitoring Networks 7 The NATTS network, designed to monitor c oncentrations of ha zardous air pollutants 8 including lead compounds, incl uded 25 sites measuring Pb-PM 10 as of June 2012. Most of these 9 sites (20) are in urban areas (F igure 2-5). In addition to the NATTS network, states collect Pb10
PM 10 at an additional 28 sites (most as part of the Urban Air Toxics Monitoring program). All 11 collect particulate matter as PM 10 for toxic metals analysis using either a high-volume PM 10 12 sampler or a low volume PM 10 sampler, typically on a 1 in 6 day sampling schedule. Most of 13 these monitoring locations are not measuring using FRM/FEM methods at this time. Lead in the 14

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).January 2013 Draft – Do Not Quote or Cite 2-1 7 collected sample is generally quantified vi a an ICP/MS method. The standard operating 1 procedure for metals by ICP/MS is availabl e at: http://www.epa.gov/ttn/amtic/airtox.html. 2

3

Figure 2-5. Pb-PM 10 monitoring sites. 4

Two networks measure Pb in PM 2.5 , the EPA CSN and the IMPROVE network. The 5 CSN consists of 53 long-term trends sites (co mmonly referred to as the Speciation Trends 6 Network or STN sites) and appr oximately 150 supplemental sites, all operated by state and local 7 monitoring agencies. Most STN sites operate on a 1 in 3 day sampling schedule, while most 8 supplemental sites operate on a 1 in 6 day samp ling schedule. All sites in the CSN network 9
determine Pb concentrations in PM 2.5 samples. Lead is quantified via the XRF method. 17 Data 10 are accessible through AQS. The locations of the CS N are shown in Figure 2-6. Nearly all of the 11 CSN sites are in urban areas, often at the location of highest known PM 2.5 concentrations. The 12 first CSN sites began operation around 2000. 13

17 The standard operating procedure for metals by XRF is available at: http://www.epa.gov/ttnamti1/files/ambient/pm25/spec/xrfsop.pdf.January 2013 Draft – Do Not Quote or Cite 2-18 The IMPROVE network is administered by th e National Park Service, largely with 1 funding by the EPA, on behalf of federal land mana gement agencies and state air agencies that 2
use the data to track trends in rural visibility. Lead in PM 2.5 is quantified via the XRF method, as 3 in the CSN. Data are managed and made accessible mainly through the VIEWS website 4 (http://vista.cira.colostate.edu/vi ews/) but are also available via AQS. Samplers are operated by 5 several different federal, state, and tribal host agencies on the same 1 in 3 day schedule as the 6 STN. In the IMPROVE network, PM 2.5 monitors are placed in “Class I” areas (including 7 National Parks and wilderness areas) and are mostly in rural locations (Fig ure 2-6). The oldest 8 of these sites began operation in 1988, while many others began in the mid 1990s. There are 110 9 formally designated IMPROVE sites, which are locat ed in or near nationa l parks and other Class 10 I visibility areas, virtually all of these being ru ral. Approximately 80 additional sites at various 11 urban and rural locations, requested and funded by various parties, are also informally treated as 12 part of the network. 13

14

Figure 2-6. Pb-PM 2.5 monitoring sites in CSN and IMPROVE networks (2012). 15

16January 2013 Draft – Do Not Quote or Cite 2-19 2.2.1.3 NAAQS Surveillance Monitoring Considerations 1 In this section aspects of th e methods for sampling and analysis of the Pb are reviewed, 2 and the current NAAQS surveillance network of monitoring locations is considered. The 3 methods for sampling and analysis are considered in light of the indicator for the Pb NAAQS, 4 and conclusions regarding the current NAAQS and associated indicator appear in chapter 4. 5 Consideration of the ambient air monitoring ne twork generally informs the interpretation of 6
current data on ambient air concentrations and helps identify whether the monitoring network is 7 adequate to determine compliance with the NAAQS . This section disc usses considerations 8 related to these aspect s of the ambient air m onitoring program for Pb. 18 9

2.2.1.3.1 Sampling Considerations 10 As described in section 2.2.1.1 above, consistentwith the Pb NAAQS indicator being Pb11 TSP, the FRM for Pb, which is required at all so urce-oriented sites, is measurement of Pb-TSP 12 using a high-volume TSP sampler meeting the design criteria specifie d in 40 CFR part 50 13 Appendix B. During the review of the Pb NAAQS completed in 2008, CASAC noted the 14 variability in high-volume TSP sample measuremen ts associated with the effects of wind speed 15
and wind direction on collection effi ciency in their comments regard ing the indicator. However, 16 at the time of the 2008 review, no alternative TSP sampler designs were identified that had an 17 adequate characterization of thei r collection efficiency over a wide range of particle sizes. The 18 existing high-volume sampler was retained as the sampling approach for the Pb-TSP FRM and 19
FEMs. 20 Since promulgation of the 2008 Pb NAAQS, the EPA has initiated an effort to review 21 alternative sampler designs in an effort to de velop a new sampler to replace the current high22 volume Pb-TSP sampler. Efficient collection of particles much larger than 10 μm is 23 considerably more challenging b ecause the greater inertia and hi gher settling velocities of Pb 24 particles hinder their efficient intake by sample rs. The sampling difficulties and the long history 25 of research to develop adequate sampling t echnology for large particles have been thoroughly 26 reviewed (Garland and Nicholson, 1991). Some existing commercia lly available sampler inlets 27 are designed to collect particles larger than 10 μm with greater than 50% efficiency (Kenny et 28 al., 2005), and these inlets can be tested as potential replacemen ts for TSP sampling. However, 29 no alternatives to the FRM TSP sampler have be en identified that have been adequately 30
characterized. 31

18 The code of federal regulations (CFR) at parts 50, 53 and 58 specifies required aspects of the ambient monitoring program for NAAQS pollutants. The federa l reference methods (FRMs) for sample collection and analysis are specified in 40 CFR part 50, the procedures for approval of FRMs and federal equivalent methods (FEMs) are specified in 40 CFR part 53 and the rules specifying requirements for the planning and operations of the ambient monitoring network are specified in 40 CFR part 58.January 2013 Draft – Do Not Quote or Cite 2-20 The EPA has initiated efforts to characteri ze the collection effici ency of alternative 1 sampler designs through wind tunnel testing as a necessary step towards the development of a 2 new sampler capable of sampling particles larger than PM 10 without the noted wind speed and 3
wind direction biases. In addition to the difficulties in collecti on of particles much larger than 10 4 μm, physical limitations in the abil ity to generate and transport ultra-coarse particles limit the 5 ability to adequately characteri ze the new sampler. These lim itations ultimately limit the upper 6 cut-point of potential samplers to the range of 18-20 micrometers. Following characterization in 7 a wind tunnel, field testing of promising candidates would be re quired to evaluate performance 8 and to make comparisons to the existing Pb-TSP sa mplers. This effort is expected to take 9 several years to complete, and, as such, it is unlik ely that this new sampler will be available in 10 time for consideration during this NAAQS review due to the activities which will need to be 11 completed to adequately characterize its perfor mance both in the laboratory and the field. We 12 expect the new sampler to be available for consid eration in a future review and consequently do 13 not expect to consider new alternatives for sampli ng methods for Pb-TSP as part of this review. 14 In addition to the FRM for Pb-TSP, there is also, as noted in section 2.2.1.1 above, a 15
FRM for Pb-PM 10 , based on the PM 10 sampler defined in 40 CFR part 50 Appendix J coupled 16 with XRF analysis. The Pb-PM 10 measurements may be used as an alternative to Pb-TSP 17
measurements in certain condi tions defined in 40 CFR part 58 Appendix D paragraph 2.10.1.2. 18
These conditions include where Pb concentratio ns are not expected to equal or exceed 0.10 19 micrograms per cubic meter on an arithmetic 3- month mean and where the source of Pb 20 emissions is expected to emit a substa ntial majority of its Pb in the PM 10 size fraction. At this 21 time, we believe the low-volume FRM sampler for Pb-PM 10 to be adequate for this application. 22 Hence, we do not expect to consid er new sampling methods for Pb-PM 10 as part of this review. 23

2.2.1.3.2 Analysis Considerations 24 Due to reduced availability of laborator ies capable of performing flame atomic 25 adsorption analyses and general a dvances in analysis methods, the EPA has initiated an effort to 26 expand FRM analysis methods beyond atomic adsorp tion to include the more modern analysis 27 method, ICP-MS. A consultation with the CASAC Ambient Air Monitoring and Methods 28 Subcommittee was held on September 15, 2010 (Russell and Samet, 2010), and the EPA plans to 29 propose a new FRM for Pb-TSP based on this more modern analysis method in 2013. In 30 addition, the EPA has approved several new FEMs (for ICP-MS and other analysis methods) 31 since the last Pb NAAQS review was completed in 2008. 32 With regard to Pb-PM 10 samples, in addition to the FRM analysis method (XRF), two 33 FEMs have been accepted for Pb-PM 10 analysis since the 2008 Pb NAAQS rulemaking. These 34
methods are based on ICP-MS and are consistent with analysis methods used for the NATTS 35January 2013 Draft – Do Not Quote or Cite 2-21 network. The EPA will continue to cons ider new FEMs for analysis of Pb-PM 10 and Pb-TSP as 1 applications are received, although no ne w FRMs (beyond the Pb-TSP FRM for ICP-MS 2 discussed above) are expected during this NAAQS review. 3

2.2.1.3.3 Network Design Considerations 4 Significant revisions to the Pb network de sign requirements (40 CFR part 58, Appendix 5 D) were made as part of the 2008 Pb NAAQS review and an associ ated revision to the 6 requirements in 2010. As summarized in se ction 2.1.1.1 above, the current Pb monitoring 7 network design requirements (40 CFR part 58, A ppendix D, paragraph 4.5) include two types of 8 monitoring sites – source-oriented monitoring site s and non-source-oriented monitoring sites - as 9 well as the collection of a year of Pb-TSP measurements at 15 sp ecific airports. This section 10 describes the design considerations for the Pb NAAQS surveillance network. 11 Source-Oriented Monitoring. Since the phase out of Pb in on-road gasoline, Pb is 12 widely recognized as a source-oriented air pollutant . As summarized in the ISA, variability in 13 air Pb concentrations is highest in areas including a Pb sour ce, “with high concentrations 14
downwind of the sources and low concentration at areas far from sources” (ISA, p. 3-88). 15
Recent data summarized in section 2.2.2.2 belo w indicates that the highest ambient Pb 16 concentrations are found near large Pb sources, usually metals industries (see, for example, 17 Figures 2-11 through 2-13 below). Analysis of the monitoring network during the last Pb 18 NAAQS review with regard to adequacy of monitoring near su ch sources found that monitors 19 were lacking near many of the larger Pb emissions sources, leading the EPA to conclude that the 20 monitoring network existing at that time was in adequate to determine compliance with the 21 revised Pb NAAQS (73 FR 29262). Findings and conclu sions of that analysis led to revisions of 22 network design requirements fo r source-oriented monitorin g, begun with the 2008 Pb NAAQS 23 rulemaking (73 FR 66964). Additional revisions were completed as part of a reconsideration of 24 the monitoring requirements in December 2010 (75 FR 81126). 25 The current requirements for source-oriented monitoring include placement of monitor 26
sites near sources of air Pb emissions which are e xpected to or have been shown to contribute to 27
ambient air Pb concentrations in excess of th e NAAQS. At a minimum, there must be one 28
source-oriented site located to measure the maxi mum Pb concentration in ambient air resulting 29 from each non-airport Pb source which emits 0.50 or more tons of Pb per year and from each 30 airport which emits 1.0 or more tons of Pb per year. 19 The expansion of the network, including 31 these source-oriented sites, is shown in Figur e 2-3. Comparison of Figure 2-3 (monitors) with 32

19 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).January 2013 Draft – Do Not Quote or Cite 2-22 Figure 2-2 (sources) illust rates the coverage whic h the current monitoring network now provides 1 of large Pb emissions sources. 2
The emissions threshold for source-oriented monitoring sites, 0.50 tpy, was developed 3 based on an analysis intended to estimate the lowest emission ra te that under reasonable worst4 case conditions (e.g., meteorological and emission rele ase conditions that lead to poor dispersion 5
and associated elevations in Pb concentrations) could l ead to Pb concentrations exceeding the Pb 6 NAAQS (Cavender, 2008). This an alysis included three approaches . The first two of the three 7 approaches included a simple scaling of the hist oric 5 tpy emission threshold applied to the old 8 1.5 μg/m 3 Pb NAAQS, and a simplified modeling effort using a screening model. The third 9 approach relied on design values based on Pb monitoring data surrounding large sources (1 tpy 10 or greater) of Pb. At the time of the 2008 re view, complete 3-year design values were only 11 available for 7 source-monitor pairs 12 As more recent data become available, an alysis of the updated and expanded dataset will 13 inform evaluation of the appropriateness of the cu rrent threshold. Since the analysis performed 14 during the 2008 review, over 150 additional source-or iented monitors have been installed that 15 may be useful in such an evaluation. At this time, the new monitors have not collected a 16 complete 3-year dataset, which is needed for the development of complete design values for the 17
new source-oriented monitors

. For monitors installed in res ponse to the 2008 revisions (near 18 sources estimated to emit 1.0 tpy or more of Pb), 3-years of certified data will be available in 19 spring 2013. Three-years of certified data for th e monitors required in the 2010 reconsideration 20 will be available in spring 2015. Accordingly, an alysis of the emissions threshold for source21 oriented monitors may be an appropriate i ssue for consideration in future reviews. 22 One-year Airport Monitoring. In addition to the above source-oriented monitoring 23 requirement, one year of monito ring was required near 15 specific airports in order to gather 24
additional information on the likelihood of N AAQS exceedances near airports due to the 25 combustion of leaded aviation gasoline (75 FR 81126). This airport monitoring study may 26 provide useful information to assess the need for additional Pb monitoring at airports, and 27 appropriate requirements, such as considerati on of the 1.0 tpy emissions threshold and regional 28 administrator authority for siting of source-orie nted monitors at airports (75 FR 81131-81132). 29 This airport monitoring study is currently underway. Given dela ys in monitor siting, monitor 30
installation at some of thes e sites extended into late 2012. Accordingly, the timing for 31 completion of the year of monitoring will vary across the 15 locations, with all of them projected 32 to finish by late 2013. The completed datasets, wh en available and certifie d, will inform EPA’s 33 considerations on next steps with regard to monito ring at airports using le aded aviation gasoline. 34 Also, as described further in section 2.1.2.2above, th e airport monitoring data will also inform 35 EPA’s ongoing investigation in to the potential for lead emissions from piston-engine aircraft to 36January 2013 Draft – Do Not Quote or Cite 2-23 cause or contribute to air pollu tion that may reasonably be antici pated to endange r public health 1 or welfare. This investiga tion is occurring under Section 231 of the Clean Air Act (CAA), 2 separate from the lead NAAQS review. 3 Non-Source-Oriented Monitoring. Monitoring agencies are also required to conduct 4 non-source-oriented monitoring at NCore sites with a population of 500,000 or more, as noted 5
above. 20 Currently, there are 24 NCore sites measuri ng Pb concentrations, with 17 measuring Pb 6 in TSP and 7 measuring Pb in PM 10 . While non-source-oriented monitoring data can be used for 7 designation purposes, an a lternative objective stated for these sites is the collection of data on 8 neighborhood-scale Pb concentrations that are typical in urban ar eas to inform our understanding 9 of ambient air-related Pb exposures for the gene ral population. At this still early stage in data 10 collection at these sites, we have not identified specific gaps or inad equacies. Thus, at this stage, 11 the current requirement for non-source-oriented Pb monitoring appears to be adequate for these 12

purposes. 13
14

20 Defined by the US Census Bureau - http://www.c ensus.gov/population/www/metroareas/metroarea.htmlJanuary 2013 Draft – Do Not Quote or Cite 2-24 2.2.2 Ambient Concentrations 1

2.2.2.1 Temporal Trends 2
Ambient air concentrations of Pb in the U.S. have declined substantially over the past 30 3 years. Figure 2-7 illustrates this decline in terms of site-specific maximum 3-month average 4
concentrations at the se t of 31 monitoring sites that have b een operating across this period. The 5 median of this dataset has declined by more than 90% over the 30-year period, and the average 6 by 89%. Over the past 10 years, a larger datase t of 92 sites operating across that period also 7 indicates a decline, which is on the order of 60% for the average of that dataset (Figure 2-8). 21 8

9
Note: Based on annual maximum 3-month average at 31 sites. 10

Figure 2-7. Temporal trend in Pb -TSP co ncentrations: 1980-2010 (31 sites). 11

12
Note: Based on annual maximum 3-month average at 92 sites. 13

Figure 2-8. Temporal trend in Pb-TSP con centrations: 2000-2010 (92 sites). 14

21 http://www.epa.gov/air/airtrends/lead.htmlJanuary 2013 Draft – Do Not Quote or Cite 2-25 The role of the phase-out of leaded gasoline on declining concentrations is evident from 1 temporal trends in air Pb concentrations near roadways, as illustrated in Figure 2-9 which 2 presents data for five mon itors sited near roadways. 22 These sites additionally indicate the 3 concentrations currently common at such sites, with the maximum 3-month average 4 concentrations at all five sites falling below 0.03 μg/m 3 in the most recent years. 5

6 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). 7
Figure 2-9. Airborne Pb -TSP concentrations (3 -month average) at five sites near 8 roadways: 1979-2010. 9

10

22 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. 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

250250002January 2013 Draft – Do Not Quote or Cite 2-2 6 2.2.2.2 Current Concentrations 1
As a result of revisions to the Pb NAAQS surveillance monitoring requirements 2 (described in section 2.2.1 above), Pb monitoring sites have been in transition over the last few 3 years as indicated by Figure 2-3. For presentation in this do cument, we have focused on the 4 most recent period for which adequately comp lete data are available, 2009-2011, recognizing 5 that the dataset developed for this period includes many but not all of the monitors newly 6 required by the December 2010 regulations. 7 Lead concentrations, in te rms of maximum 3-month aver age Pb-TSP concentration, at 8 monitoring sites active across the U.S. during the period 200 9-2011, and for which sufficient 9 data are available to meet completeness criteri a described in Appendix 2C, are presented in 10 Figure 2-10. 23 Highest concentrations occur in the vi cinity of large metals industries, as 11
discussed in section 2.1.2.1. 24 As can be seen through comparison of Figure 2-10 with Figure 2- 12 3, only limited data (not meeting co mpleteness criteria for the data analysis) are available to date 13 for some of the monitors newly required by the Pb NAAQS monitoring network revisions 14 completed in 2010 (see section 2.2.1.1). 15

23 Criteria for development of the 2009-2011 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.
24 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.January 2013 Draft – Do Not Quote or Cite2-271Figure 2-10.Pb-TSP maximum 3-monthmeans (215 sites), 2009-2011.2January 2013 Draft – Do Not Quote or Cite 2-28 Figures 2-11 through 2-13 illustrate differen ces in Pb-TSP concentrations, in terms of 1 three different metrics (maximum 3-month me an, annual mean, and maximum monthly mean), 2 among sites near and more distant from emissions sources. The Pb-TSP sites indicate the much 3 greater site and temporal variab ility in concentrations at sour ce-oriented and previous source4 oriented sites as compared to non-source-oriented sites. Across the Pb-TSP sites, as would be 5 expected, highest concentrations are observed at the source-o riented sites, followed by the 6 previous source-oriented sites. This is the case for all three metrics analyzed (maximum 3- 7 month mean, maximum monthly mean and annual mean). 8 Figures 2-11 through 2-13 additional indicate distributions of Pb-PM 10 and Pb-PM 2.5 9
concentrations in urban and rural locati ons where they are monitored. The Pb-PM 10 and Pb10
PM 2.5 networks are described in section 2.2.1.2 and s hown in Figures 2-5 and 2-6, respectively. It 11 is important to note that there ar e few sites in these recent datase ts with colocated monitors for 12
the different size fractions. As described in the IS A, at 18 urban sites (without specification as to 13 proximity to Pb sources) with at least 30 co-located Pb-TSP and Pb-PM 10 samples collected 14 during various time periods (nearly all between 1990 and 2000), approximately 80% of the Pb 15 mass, on average, is captured by the Pb-PM 10 measurements (ISA, sections 3.5.3.1 and 3.8.6). 16 The data distributions in Figures 2-11 through 2-13 indicate reduced variability in concentration 17 for non-source-oriented sites and for part iculate Pb of smaller size fractions. 18January 2013 Draft – Do Not Quote or Cite2-291Figure 2-11.Distribution of maximum 3-month meanconcentrations of Pb-TSP, Pb-PM10and Pb-PM2.5at different site types,22009-2011.3 Concentration (μg/m 3 )0.00.10.20.30.40.50.60.70.80.91.01.11.2All Pb-TSPsites(n=215)Pb-TSPsourceorientedsites(n=112)Pb-TSPnot sourceoriented sites(n=91)Pb-TSPprevioussourceoriented sites(n=12)Pb-PM10urbansites(n=35)Pb-PM2.5urbanCSN sites(n=198)Pb-PM2.5non-urbanIMPROVEsites(n=106)January 2013 Draft – Do Not Quote or Cite2-301Figure 2-12.Distribution of annual mean concentrations of Pb-TSP, Pb-PM10and Pb-PM2.5at different site types, 2009-2011.20.00.10.20.30.40.50.60.7

Concentration (μg/m 3 )All Pb-TSPsites(n=215)Pb-TSPsourceorientedsites(n=112)Pb-TSPnot sourceoriented sites(n=91)Pb-TSPprevioussourceoriented sites(n=12)Pb-PM10urbansites(n=35)Pb-PM2.5urbanCSN sites(n=198)Pb-PM2.5non-urbanIMPROVEsites(n=106)January 2013 Draft – Do Not Quote or Cite2-311Figure 2-13.Distribution of maximum monthly meanconcentrations of Pb-TSP, Pb-PM10and Pb-PM2.5at different site types,22009-2011.30.00.10.20.30.40.50.60.70.80.91.01.11.21.31.41.51.61.71.8All Pb-TSPsites(n=215)Pb-TSPsourceorientedsites(n=112)Pb-TSPnot sourceoriented sites(n=91)Pb-TSPprevioussourceoriented sites(n=12)Pb-PM10urbansites(n=35)Pb-PM2.5urbanCSN sites(n=198)Pb-PM2.5non-urbanIMPROVEsites(n=106)

Concentration (μg/m 3 )January 2013 Draft – Do Not Quote or Cite 2-32 2.3 AMBIENT AIR LEAD IN OTHER MEDIA 1 Lead emitted into the ambient air, depending on its chemical and physical characteristics, 2 deposits out of air onto surfaces in the environmen t. The environmental fate of atmospherically 3 emitted Pb once deposited, is influenced by the t ype of surface onto which the particles deposit 4 and by the type and activity level of transport fo rces in that location. Deposited Pb can be 5 incorporated into soil matrices in terrestrial ecosystems or transported (by direct deposition or 6 stormwater runoff) to water bodies and into a quatic sediments, which may serve as aquatic 7 ecosystem sinks. Particles deposited onto impe rvious surfaces, such as roadway or urban 8 surfaces, are more available for human contac t while they remain on such surfaces. For 9 example, they may be available for adherence onto skin or they may be resuspended into the air 10 and inhaled. Precipitation and ot her natural, as well as human-i nfluenced, proce sses contribute 11 to the fate of such particles and their potential transport to areas or environments of lesser or 12 greater likelihood for human contact, e.g., transport with surface runoff into nearby water bodies 13 or tracking into nearby h ouses (ISA, section 3.3). 14
Lead from current and histori cal air emissions sources, in addition to a range of nonair 15 sources (e.g., land disposal of wastes as well as surface runoff and releas es to surface waters), 16 contribute to Pb in outdoor dust, soil and aquatic systems. Because of its persistence, Pb from all 17
of these sources can contribute to media concentra tions into the future. The pattern of resulting 18 Pb concentrations changes over time in respons e to changes in new Pb contributions to the 19 systems (e.g., in types and rates of addition), as well as environmental processes (chemical, 20 biological and physical) particular to each type of media and ecosystem. Accordingly, media 21 and ecosystems differ with regard to Pb concentr ations and changes in th ose concentrations in 22 response to airborne Pb. These di fferences relate to ecosystem pro cesses as well as Pb source or 23 emissions characteristics and proximity. 24 The initial section below (s ection 2.3.1) summarizes sali ent information regarding 25 atmospheric deposition and how it is monitored. Subsequent sections describe the current 26 information related to the pres ence of ambient air Pb in nonair media and what it indicates 27 regarding impacts of current patterns of Pb in and being emitted to ambient air, including 28 relationships to impacts in the past and to ot her Pb sources. Section 2.3.2 focuses on terrestrial 29 media, while section 2.3.3 discusses aquatic media. 30

2.3.1 Atmospheric Deposition 31 Deposition is the pathway by which Pb partic les are removed from the atmosphere and 32
transferred to other environmental media. Ther e are several approaches by which atmospheric 33 deposition, or the transfer of Pb from the atmos phere to soil or water bodies, can be assessed. 34
These include measurements of Pb in rainfall (wet deposition) and on collection surfaces during 35January 2013 Draft – Do Not Quote or Cite 2-33 dry periods (dry deposition); dry deposition is also estimated from measurements of airborne Pb 1 particles coupled with estimates of deposition ve locity (see 2006 CD, Sec tion 2.3.2). Less direct 2 approaches include monitoring changes in Pb co ncentration in various biological or physical 3 media such as lichen or mosses, snowpack, soil and aquatic sediments (ISA, sections 3.6.2, 3.6.4 4 and 3.6.6). Approaches for the latter three media may involve repeated measurements of surface 5 samples over time or core samples coupled with isotope dating. To gain information on 6 atmospheric deposition, unaffected by contributions from direct nonair environmental releases, 7 such studies are generally conducted in somewhat remote areas. As there are currently no 8 nationwide Pb atmospheric deposition monitori ng programs, the discussion of atmospheric 9 deposition in this and subsequent sections is drawn from this range of approaches (2006 CD, 10 sections 2.3, 8.2.2 and AX7.1.2.3; ISA, sections 3.3.1.2 and 3.6 ). Geographic differences in 11 deposition generally relate to differences in the amount and size distribution of airborne Pb 12 particles in that location, as well as meteorology a nd other site-specific factors. For example, the 13 size of particles, as well as solubility in rainwa ter, can also influence wet deposition rates (ISA, 14 section 3.3.1.2; 2006 CD, p. 2-59). Factors that pa rticularly influence dry deposition are the 15 level of atmospheric turbulence, especially in the layer nearest the ground, particle size 16 distributions and density, and the nature of the surface itself, such as smooth or rough (2006 CD, 17 pp. 2-55 to 2-57). 18 Evidence for the temporal pattern of U.S. lead deposition generally indicates a peak 19 during the middle twentieth cen tury (e.g., 1940s through 1970s) followed by substantial declines 20 in the latter part of the cent ury (ISA, section 3.3.1; 2006 CD s ection 2.3.1; Jackson et al., 2004). 21 This pattern reflects the increased use of Pb in th e industrial age (including its use in gasoline in 22 the twentieth century) and declines in response to environmen tal controls on ga soline and metals 23
industries in the latte r part of the twentieth cen tury. Studies continue to document declines in 24 atmospheric deposition since the 1980s in ar eas remote from industrial areas (e.g., Watmough 25 and Dillon, 2007). As would be expected, stationa ry sources of Pb continue to contribute to 26 relatively higher deposition rates in industrial areas as compared to other areas, although rates in 27 those areas appear to have also declined since the 1970s-80s (ISA, section 3.3.1.2; Sabin and 28 Schiff, 2008). 29

2.3.2 Terrestrial Media 30
Lead in the terrestrial media discussed here ma y originate from current or historical air or 31
other sources. Other sources to these media incl ude historical use of indoor and outdoor leaded 32 paint, more prevalent in areas with older bui ldings, and the processi ng of lead-containing 33 materials. Further, the concentr ations of Pb in each media, as well as the relative contributions 34 from various types of sources to those con centrations, vary among media and among locations 35January 2013 Draft – Do Not Quote or Cite 2-34 for any one media. Differences among locations in 0air-related Pb are generally related to the 1 current and historical magnitude of Pb emissions and depositi on at that location, as well as 2 location- and media-specif ic removal factors. 3

2.3.2.1 Indoor Household Dust 4 Household dust arises from particulate matte r generated indoors and outdoors and Pb in 5
household dust can reflect a combination of these sources. Airborne particles can be transported 6 indoors with ambient air, while particles deposited outdoors from am bient air may be carried in 7 on humans and their clothing or other items tran sported indoors. Depending on factors such as 8 the proximity of the residence to current or histor ical metals industries, leaded paint usage, and 9 age of the residence, Pb in indoor residential dust can re flect current or historical atmospheric Pb 10 or nonair-related sources, such as leaded paint. Another indoor source is tobacco smoking (ISA, 11 section 4.1.3.2; Gaitens et al., 2009; 2006 CD, p. 3-15; Mannino et al., 2003) . The age of the 12 residence may be an indicator of the potential for the presence of leaded paint and, in areas of 13 significant levels of airborne Pb in the past, such as near mining or smelting industries, may also 14 indicate the potential for the residual presence of historically emitted Pb (ISA, sections 4.1.1 and 15 4.1.3.2; 2006 CD section 3.2.3). A study of househol ds in the Baltimore metropolitan area (in 16 which there are no areas designated non- attainment for the current Pb NAAQS) 25 indicated 17 indoor air Pb concentrations to be significantly a ssociated with outdoor air Pb concentrations but 18 did not show a statistically signi ficant relationship of outdoor air Pb with indoor dust Pb, perhaps 19 indicating the greater ro le of sources other than current airborne concentrations in those 20 households (ISA, 4.1.3.2; Egeghy et al., 2005). 21 As discussed in chapter 4 below, indoor dust is a major pathway for air-related Pb 22 exposure for pre-school children, larg ely related to prevalent hand-to-m outh behavior at that age. 23

2.3.2.2 Outdoor Dust in Areas of Human Activity 24 Lead in particulate matter occurring on outdoor surfaces (outdoor dust) may reflect 25
current or historical Pb emissions , as well as the historical uses of lead in products on buildings 26 and infrastructure in surrounding area. The concen trations of air-relate d Pb in outdoor dust and 27
the relative contribution of air-r elated Pb to the total Pb conc entrations in outdoor dust varies 28 depending on the location-specific characteristics of air–related (and other) Pb sources. The role 29
of air-related sources in outdoor dust Pb has been documented in areas near industrial sources, 30 such as smelters, where Pb concentrations in outdoor dust have been doc umented to decline in 31 response to reduced emissions. For example, out door dust Pb concentrations in a long-time 32 Canadian smelter town were found to track smelter Pb emissions, as a new smelting technology 33

25 http://www.epa.gov/air/oaqps/greenbk/mnc.htmlJanuary 2013 Draft – Do Not Quote or Cite 2-35 which reduced airborne Pb concentrations by 75% resulted in a 50% re duction in outdoor dust 1 Pb loading rate and concentrations (2006 CD, p. 3-23; Hilts, 2003). 2 Rates of dry deposition of Pb in large metropo litan areas during the past decade are much 3 lower than those reported for the 1970s (ISA, sections 3.3.1 and 3.6.1; Table 2-4, below). For 4 example, dry deposition of Pb into Los A ngeles harbor during 2002-2006 was more than an 5 order of magnitude lower than rates reported for the same location in 1975 (ISA section 3.3.1.2; 6 Sabin and Schiff, 2008; Lim et al., 2006). Across the Los Angeles metropolitan area, average 7 rates generally ranged from 10 to 32 micr ograms per square meter per day (μg/m 2 /day) and down 8 to 0.3 μg/m 2 /day for the non-urban site of Malibu dur ing 2002-2003 (Lim et al., 2006). Rates 9 within this range are reported from studies in Manhattan and a non-industria l area of New Jersey, 10 with a somewhat higher rate reported for a majo r industrial location with in the New York City 11 metropolitan area. Although rates have not been reported recently for smelter locations in the 12 U.S., the outdoor dustfall deposition rate repor ted in a Canadian smelter town after the 13 installation of new technology that reduced averag e airborne Pb-TSP concentrations to a level 14 still at least twice the current U.S. NAAQS (0.3 μg/m 3 from prior av erage of 1.1 μg/m 3 ) was 15 several orders of magnitude hi gher than those reported for New York, Los Angeles and Chicago 16 urban areas (Table 2-4). 17 From the few studies reporting levels of Pb loading or concentration in outdoor dust 18 within the past decade or so, loading to surfaces of pedestrian traffic signals in New York City 19 was on average approximately 15% the loading repor ted on sidewalks in olde r, residential areas 20 of downtown Baltimore (e.g., approximately 250 ug/ft 2 as compared to 1500 ug/ft 2 ), an order of 21 magnitude or more below that reported in the lo ng-time Canadian smelter town (Caravanos et al., 22 2006b; Farfel et al 2005; Hilts, 2003). 23January 2013 Draft – Do Not Quote or Cite 2-3 6 Table 2-3. Dry deposition of lead in large metr opolitan areas and in a smelter town. 1

Description Dry Deposition Rate ( μ g Pb/m 2 /day) Study

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

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

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

24 Sabin et al., 2006 Los Angeles, I-405, near Westwood (upwind side), spring 2003 C 7.3 “ Jersey City, NJ, 2001- 2002 50 Yi et al., 2006 New Brunswick, NJ, 2001- 2002 9 “
Manhattan, NYC, 2 nd

story rooftop (unprotected), 2003-2005 22 Caravanos et al., 2006a Chicago, 1993-95 (most recent available) 38-71 Yi et al 2001; Paode et al., 1998
Trail, British Columbia, Canada, historical smelter town, 1999 D

31000 Hilts, 2003

A - 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

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

. D - Average Pb-TSP = 0.3 μ g/m 3 , this reflects new technology (previously 1.1 μ g/m 3 ) for smelter that existed in this town for past 95 years.
2

2.3.2.3 Soil 3 As is the case for Pb in outdoor dust, occu rring in surface soils can be derived from 4
current or historical Pb emissions , as well as leaded paint usage in older residential areas. The 5
relative role of these sources ma y vary with the type of enviro nment and proximity to industry 6 and population centers. 7 In forested areas away from old urban ar eas, the role of leaded gasoline in soil 8 contamination is illustrated by the documented reduc tions in Pb in surface soils subsequent to the 9 leaded gasoline phasout. For example, forest su rface soil (litter) concentrations in a transect 10 from Vermont, through Maine and up to Gaspe in Quebec, which in 1979 exhibited a significant 11 spatial trend, ranging from 200 milligrams pe r kilogram, dry weight (mg/kg dw) at its 12 southernmost point down to 60 mg/kg dw at its no rthernmost and most remote point in Quebec, 13 declined to 32-66 mg/kg dw (with no spatial tre nd) in 1996 (ISA, section 3.6.1; Evans, 2005). In 14
forests from the mid-Atlantic to southern New England, a reduction in litter Pb concentration 15 was observed between 1978 and 2004-05 (ISA, secti on 3.6.1; Johnson and Richter, 2010). In the 16 latter study, the authors observed less change in concentration in the more northern sampling 17 sites, which they attribute to reduced rates of organic matter decomposition in those colder 18 temperature areas. Similarly, an additional New England stu dy by Kaste et al (2006) also 19January 2013 Draft – Do Not Quote or Cite 2-37 documented a pattern in temporal reductions in soil Pb (o-horizon) related to decomposition 1 activity. These recent findings are generally consiste nt with findings reported in the last review 2 which indicated the gradual migration of depos ited Pb into mineral soils (e.g., Miller and 3 Friedland, 1994; Kaste et al., 2003; Wang and Benoit, 1997; Johnson et al., 1995; Zhang, 2003). 4 Few studies have investigated temporal trends of surface soil Pb concentrations in more 5 populated areas in relation to re ductions in usage of leaded gasoline and paint. Current 6 concentrations in areas of past heavy traffic powered by leaded gasoline are generally elevated 7 above areas more distant from these areas (ISA, section 3.6.1). Current roadway-related sources 8 of Pb, while substantially less significant than leaded gasoline, con tinue to provide some 9
contribution to surface dust/soil in these areas (ISA, section 3.2.2.6). Surface soil and dust 10 concentrations are much higher in such areas in large, olde r cities than surrounding suburban 11 areas (ISA, section 3.6.1). In ol der residential areas, the use of leaded ho use paint is another 12 contributor to surface soil concentrations (IS A, sections 3.6.1 and 3.7.7.2; Yesilonis et al., 2008; 13 Brown et al., 2008; Clark et al., 2006). 14 Areas of long-term Pb emissions from point sources appear to be the areas of highest 15 surface soil Pb concentrations (ISA, secti ons 3.6 and 3.6.1). For example, Pb surface soil 16 concentrations within approximate ly 100-250 meters of long-establis hed lead smelters have been 17 five to ten times higher than those at 3-5 km distance (ISA, section 3.6.1; 2006 CD, Table 3-4). 18
Surface soil concentrations near U.S. mines that are no longer active have also been found to be 19 elevated above more distant areas (2006 CD, Ta ble 3-6). Information described in the 2006 CD 20 for areas surrounding smelters after implement ation of pollution cont rols, although showing 21
declines in Pb concentrations in outdoor dustfall, stre et dust and indoor dustfa ll, has not indicated 22
a noticeable decline in soil Pb concentrations (2006 CD, pp. 3-23 to 3-24). The continued Pb 23 emissions in such industrial areas likely influence the dynamics of Pb concentrations in the soil, 24 affecting any response to emissions reductions. Es timates of associated steady-state surface soil 25 Pb concentrations or the expected longer-term tem poral pattern for this situation have not been 26
made. 27 In summary, findings to date indicate th at many of those systems less influenced by 28 current point sources have and may still be resp onding to reduced Pb deposition rates associated 29 with reduced atmospheric emissions of Pb, incl uding those associated wi th the phase-out of 30 leaded gasoline, while potentia l responses of soils near point sources and those involving 31 historically deposited Pb near road ways are less well characterized. 32

2.3.2.4 Biota 33
Measurements of Pb in some biota indicate re ductions in biologically available Pb over 34 the past 30 years in some remote locations. Fo r example, measurements of Pb in lichen from 35January 2013 Draft – Do Not Quote or Cite 2-38 Golden Lake in Mount Ranier National Park (2005) and Emerald Lake basin in Sequoia/Kings 1 Canyon National Parks (2004) indica te significant reduc tions (approximately 3-5-fold) since 2 samples were previously collect ed in those locations in 1984 (ISA, section 3.6.6; Landers et al., 3 2008). Further, Pb in teeth of juvenile and adu lt moose in Isle Royale National Park in northern 4 Michigan have also declined substantia lly (ISA, section 3.6.8; Vucetich et al., 2009). 5
Biota measurements have also documented sources of Pb deposition in mining areas 6 including the transportation of materials along haul roads. Le ad deposition from these mining7
related activities has been documented in remote wilderness areas in Alas ka. For example, Pb 8 concentration in moss in Cape Krusenstern Nation al Monument declines with distance from the 9 road on which product from Red Dog mine 26 in northwest Alaska is transported (ISA, section 10 3.3.1.2; Hasselbach et al., 2005). In summer 2001, the median Pb concentration measured within 11
10 meters of the haul road was more then 20 time s higher than sites at greater distance from the 12 road and nearly three orders of magnitude grea ter than those reported for this moss in other 13
Alaska locations in 1990-1992. Concentrations in moss within 10 meters of the haul road ranged 14 from 271-912 mg/kg dw (Hasselbach et al., 2005). 15

2.3.3 Aquatic Media 16

2.3.3.1 Surface Waters 17 In addition to delivery by atmospheric depositio n, Pb is also carried into surface waters 18 via wastewater effluent from municipalities and industry, stormwater runoff, erosion, and 19 accidental discharges (2006 CD, p. AX7-142; ISA section 3.3.2). As a result of the phasing out 20 of leaded gasoline, reductions in Pb concentrations have been documented in surface waters of 21 the North Atlantic Ocean, as well as the relativ ely less remote areas of the Great Lakes (2006 22 CD, p. 7-23). The availability of studies investigating historical trends in surface waters is 23 limited, in part due to analytical issues that challenged many monitoring programs in the past 24 (2006 CD, AX7.2.2.2). Thus, tempor al trends reported in many aquatic systems are based on 25 sediment analyses (see section 2.3.3.2 below). 26 Most Pb occurring in aquatic systems is associ ated with particles, with the distribution 27 between particle-bound and dissolved form bei ng influenced by water chemistry as well as 28 suspended sediment levels (ISA, 3.3.2; 2006 CD, pp. AX7-117 to AX7-118, Section AX7.2.2). 29
Water columns have been described as “transie nt reservoirs” for pollutants (ISA, section 3.7.2; 30 2006 CD, p. 2-75). Once deposited to sediments, whether Pb is available for resuspension back 31 into the water column with potential transport further down a watershed ve rsus being buried into 32 deeper sediments depends on the aquatic system. In open ocean waters (generally characterized 33

26 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.January 2013 Draft – Do Not Quote or Cite 2-39 by depth and distance from continental sources), re suspension to surface waters is unlikely. In 1 more shallow systems, and additionally those in fluenced by land sources (e.g., stormwater runoff 2 as well as point sources), resusp ension may play a role in wate r column concentrations. For 3 example, studies in San Francisco Bay, the southe rn arm of which has an average depth of 2 m, 4 have indicated that Pb particles may be rem obilized from surface sediments into the water 5 column (2006 CD, AX7-141). 6 The distribution of Pb dissolved in many U. S. surface waters has been reported by the 7 United States Geological Survey (USGS) National Water-Quality Assessment (NAWQA) 8 program. The NAWQA data set encompa sses data, collected from 1991-2003 on Pb 9 concentrations in flowing surface waters for more than 50 river basins and aquifers throughout 10 the country (2006 CD, Section AX7.2.2.3). Thes e data indicate a mean dissolved Pb 11
concentration in U.S. surface waters of 0.66 μ g/L (range 0.04 to 30 μ g/L) in waters affected by a 12
combined contribution of natura l and anthropogenic sources, as compared to a mean of 0.52 13

μ g/L (range 0.04 to 8.4 μ g/L) for waters in “forest”, “ra ngeland”, and “reference” sites (2006 14 CD, Section AX7.2.2.3). The highest surface water Pb concentrations were observed in sites 15 impacted by land uses such as mining (2006 CD, p. AX7-131). The role of surface runoff in 16 delivering contamination to waters near meta ls industries presents a challenge to the 17 disentangling of atmospheric deposition contributi ons from those associated with surface runoff. 18

2.3.3.2 Sediments 19 Many studies have investigated temporal tre nds in sediment Pb concentrations, using 20
sediment cores or surface sediment Pb concentr ation, with declines documented in many systems 21 and usually attributed to the phasing out of leaded gasoline (I SA, section 3.6.2; 2006 CD, section 22 AX7.2.2). Several studies documenting the increa sed Pb deposition of the industrial age, 23 including specifically leaded gasoline usage, and the subsequent declines associated with leaded 24 gasoline phase-out were reporte d in the 2006 CD. They include investigations involving 25 sediment cores from the Okefenokee Swamp in Ge orgia as well as from 35 reservoirs and lakes 26 in urban and reference locations (ISA, secti on 3.6.2; 2006 CD, p. AX7-141). In the latter, the 27
median reduction in Pb mass accumulation rate in the cores, adjusted for background 28 concentrations, was 246%, with the largest decreases in lakes locat ed in dense urban watersheds 29 (ISA, section 3.6.2; 2006 CD, p. AX7-141; Mahler et al, 2006). A third study of sediment cores 30
in 12 lakes in the Great Lakes area also documente d a peak in Pb concentrations consistent with 31 peak use of leaded gasoline in the U.S. in th e mid 1970’s and declining co ncentrations in most 32 lake sediments through the mid 1990’s (2006 CD, p. 2-55; Yohn et al., 2004). Sediment surveys 33 by the USGS NAWQA have reported the highest Pb concentrations in Idaho, Utah, and 34January 2013 Draft – Do Not Quote or Cite 2-40 Colorado, with seven of the highest concentratio ns at sites classified as mining land use (2006 1 CD, p. AX7-133). 2 Among the more recent investigation of temporal trends in aquatic sediments described in 3
the ISA is that associated with the Western Ai rborne Contaminants Assessment Project which 4
documented Pb in sediment cores from 14 lakes in eight U.S. national parks in western states, 5 including three in Alaska (ISA, section 3.6.2; Lande rs et al., 2010). Among the Alaska cores, in 6 which concentrations were ge nerally on the order of 20 μ g/kg, dw, there was little variation in Pb 7 concentration, flux or enrichment factor. The ot her park cores, with few exceptions, generally 8
exhibited an increase in concentration comme ncing in the mid-nineteenth century, which 9 transitioned to declining trends in the past few decades, with lower concentrations in more 10 recent, surface material. The highest concentra tion was recorded at core depth corresponding to 11 the mid-1970s, in one of the Sequoia/Kings Canyon lake cores (Figure 2-16; ISA, section 3.6.2; 12 Landers et al., 2010 27 ). 13
14

27 Figure created from database for Landers et al (1980); http://www.nature.nps.gov/air/St udies/air_toxics/wacap.cfm.January 2013 Draft – Do Not Quote or Cite 2-41 1
Figure 2-14. Temporal trend in sediment concentrat ion from core samples in 12 lakes at 2 eight National Parks or Preserves. 3

Analyses of cores taken in several lake s and reservoirs along the Apalachicola, 4 Chattahoochee, and Flint River Basin from north of the Atlanta, GA metropolitan area to the 5 Gulf of Mexico indicate changes in sediment c oncentration both with time and in relation to 6 influence of the large metropol itan area of Atlanta (ISA, s ection 3.6.2; Callender and Rice, 7 2000). Highest concentrations were documented ju st downstream from Atlanta at the core depth 8 corresponding to the 1975-1980 tim e period; the corresponding concentration for the most 9 recent time period (1990-1995) at that location was approximately 50% lower (ISA, section 10 3.6.2; Callender and Rice, 2000). These data may re flect changes in surface water discharges of 11 Pb in the Atlanta area, during this time period, as well as changes in air deposition. The smaller 12 reduction (on the order of 20%) observed across the 20 year time period at the upstream site is 13 likely more generally reflective of changes in air deposition. 14 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 Ranie r -Golden (mid Washington) Mt Ranier-LP19 (mid Washington)

Glacie r -Snyder (Montana)

Glacie r -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)January 2013 Draft – Do Not Quote or Cite 2-42 2.4 REFERENCES 1

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Callender, E; Rice, KC. (2000). The urban environmental gradient: Anthropogenic influences on the spatial and 5 temporal distributions of lead and zinc in sediments. Environ Sci Technol 34: 232-238. 6 http://dx.doi.org/10.1021/es990380s. 7

Caravanos, J.; Weiss, A.L.; Jaeger, R.J. (2006a) An exterior and interior leaded dust deposition survey in New York 8 City: results of a 2-year study. Environ. Res. 100: 159-164. 9

Caravanos, J; Weiss, AL; Blaise, MJ; Jaeger, RJ. (2006b). A survey of spatially distributed exterior dust lead 10 loadings in New York City. Environ Res 100: 165-172. http://dx.doi.org/10.1016/j.envres.2005.05.001

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Clark, HF; Brabander, DJ; Erdil, RM. (2006). Sources, sinks, and exposure pathways of lead in urban garden soil. J 15 Environ Qual 35: 2066-2074. http://dx.doi.org/10.2134/jeq2005.0464

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Farfel, MR; Orlova, AO; Lees, PSJ; Rohde, C; Ashley, PJ; Chisolm, JJ, Jr. (2005). A study of urban housing 24 demolition as a source of lead in ambient dust on side walks, streets, and alleys. Environ Res 99: 204-213. 25 http://dx.doi.org/10.1016/j.envres.2004.10.005. 26

Gaitens, JM; Dixon, SL; Jacobs, DE; Nagaraja, J; Strauss, W; Wilson, JW; Ashley, PJ. (2009). Exposure of US 27 children to residential dust lead, 1999-2004: I. Housing and demographic factors. Environ Health Perspect 28 117: 461-467. http://dx.doi.org/10.1289/ehp.11917

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Hasselbach, L; Ver Hoef, JM; Ford, J; Neitlich, P; Crecelius, E; Berryman, S; Wolk, B; Bohle, T. (2005). Spatial 32 patterns of cadmium and lead deposition on and adjacent to National Park Service lands in the vicinity of 33 Red Dog Mine, Alaska. Sci Total Environ 348: 211-230. http://dx.doi.org/10.1016/j.scitotenv.2004.12.084. 34

Hilts, S. R. (2003) Effect of smelter emission reductions on children's blood lead levels. Sci. Total Environ. 303: 51- 35 58. 36

Jackson, B.P., P.V. Winger, P.J. Lasi er (2004) Atmospheric lead deposition to Okefenokee Swamp, Georgia, USA. 37 Environ Poll. 130: 445-451. 38January 2013 Draft – Do Not Quote or Cite 2-43 Johnson, C. E.; Siccama, T. G.; Dris coll, C. T.; Likens, G. E.; Moeller, R. E. (1995) Changes in lead 1 biogeochemistry in response to decreasing atmospheric inputs. Ecol. Appl. 5: 813-822. 2

Johnson, AH; Richter, SL. (2010). Organic-horizon lead, copper, and zinc contents of Mid-Atlantic forest soils, 3 1978-2004. Soil Sci Soc Am J 74: 1001-1009. http://dx.doi.org/10.2136/sssaj2008.0337. 4

Kaste, JM; Bostick, BC; Friedland, AJ; Schroth, AW; Si ccama, TG. (2006). Fate and speciation of gasoline-derived 5 lead in organic horizons of the northeastern USA. Soil Sci Soc Am J 70: 1688-1698. 6 http://dx.doi.org/10.2 136/sssaj2005.0321. 7

Kaste, J.; Friedland, A.; Stürup, S. (2003) Using stable and ra dioactive isotopes to trace atmospherically deposited 8 Pb in montane forest soils. Environ. Sci. Technol. 37: 3560-3567. 9

Kenny L; Beaumont G, Gudmundsson A, Thorpe A, Koch W. (2005) Aspiration and sampling efficiencies of the 10 TSP and louvered particulate matter inlets. J Environ Monit. May 2005. 7 481-487. 11

Landers, DH; Simonich, SL; Jaffe, DA; Geiser, LH; Campbe ll, DH; Schwindt, AR; Schrec k, CB; Kent, ML; Hafner, 12 WD; Taylor, HE; Hageman, KJ; Usenko, S; Ackerman, LK; Schrlau, JE; Rose, NL ; Blett, TF; Erway, MM. 13 (2008). The fate, transport, and ecological impacts of airborne contaminants in western national parks 14 (USA). (EPA/600/R-07/138). Corv allis, Oregon: U.S. Environmen tal Protection Agency, NHEERL, 15 Western Ecology Division. http://www.nature.nps.gov/air/studies/air_toxics/WACAPreport.cfm. 16

Landers, DH; Simonich, SM; Jaffe, D; Geiser, L; Campbell, DH; Schwindt, A; Schreck, C; Kent, M; Hafner, W; 17 Taylor, HE; Hageman, K; Usenko, S; Ackerman, L; Schr lau, J; Rose, N; Blett, T; Erway, MM. (2010). The 18 Western Airborne Contaminant Assessment Project (W ACAP): An interdisciplinary evaluation of the 19 impacts of airborne contaminants in western U.S. National Parks. Environ Sci Technol 44: 855-859. 20 http://dx.doi.org/10.1021/es901866e. 21

Lim, JH; Sabin, LD; Schiff, KC; Stolzenbach, KD. (2006). Concentration, size distribution, and dry deposition rate 22 of particle-associated metals in the Los Angeles region. Atmos Environ 40: 7810-7823. 23 http://dx.doi.org/10.1016/j.atmosenv.2006.07.025. 24

Mahler, B. J.; Van Metre, P. C.; Callender, E. (2006) Trends in metals in urban and reference lake sediments across 25 the United States, 1970 to 2001. Environ. Toxicol. Chem. 25: 1698-1709. 26

Mannino, D.M.; Albalak, R.; Grosse, S.; Repace, J. (2003) Second-hand smoke exposure and blood lead levels in 27 U.S. children. Epidemiology 14(6): 719-727. 28

Miller, E. K.; Friedland, A. J. (199 4) Lead migration in forest soils: response to changing atmospheric inputs. 29 Environ. Sci. Technol. 28: 662-669. 30

Osterberg, E; Mayewski, P; Kreutz, K; Fisher, D; Handle y, M; Sneed, S; Zdanowicz, C; Zheng, J; Demuth, M; 31 Waskiewicz, M; Bourgeois, J. (2008). Ice core record of rising lead pollution in the North Pacific 32 atmosphere. Geophys Res Lett 35: L05810. http://dx.doi.org/10.1029/2007gl032680 33

Paode, RD; Sofuoglu, SC; Sivadechathep, J; Noll, KE; Holsen, TM; Keeler, GJ. (1998). Dry deposition fluxes and 34 mass size distributions of Pb, Cu, and Zn measured in southern Lake Michigan during AEOLOS. Environ 35 Sci Technol 32: 16291635. http://dx.doi.org/10.1021/es970892b

. 36

Russell A. and Samet, J.M. (2010) Letter from Dr. A. Ru ssell, Chair, Clean Air Scientific Advisory Committee, 37 Ambient Air Monitoring Methods Subcommittee and J.M. Samet, Chair, Clean Air Scientific Advisory 38 Committee, to Administrator Lisa P. Jackson. Re: CASAC Review of EPA’s White Paper Approach for 39 the Development of a new Federal Reference Method (FROM) for Lead in Total Suspended Particulates 40 (Pb-TSP). November 30, 2010. 41January 2013 Draft – Do Not Quote or Cite 2-44 Sabin, LD; Schiff, KC. (2008). Dry atmo spheric deposition rates of metals along a coastal transect in southern 1 California. Atmos Environ 42: 6606-6613. http://dx.doi.org/10.1016/j.atmosenv.2008.04.042 2

U.S. Environmental Protection Agency. (1996-2011) . AP-42, Compilation of Air Pollutant Emission Factors, 5th 3 Edition. Volume 1: Stationary Point and Area Sources, Chapter 13: Miscellaneous Sources. Available at: 4 http://www.epa.gov/ttn/chief/ap42/ch13/index.html 5

U.S. Environmental Protection Agency. (2012) National Emissions Inventory for 2008, version 3. Office of Air 6 Quality Planning and Standards, Resear ch Triangle Park, NC. November 2012. 7 http://www.epa.gov/ttn/chief/net/2008inventory.html 8

Vucetich, JA; Outridge, PM; Peterson, RO; Eide, R; Isrenn, R. (2009). Mercury, lead and lead isotope ratios in the 9 teeth of moose (Alces alces) from Isle Royale, U.S. Upper Midwest, from 1952 to 2002. J Environ Monit. 10

Wang, E. X.; Benoit, G. (1997) Fate and transport of contaminant lead in spodosols: a simple box model analysis. 11 Water Air Soil Pollut. 95: 381-397. 12

Watmough, SA; Dillon, PJ. (2007). Lead biogeochemistry in a central Ontario forested watershed. Biogeochemistry 13 84: 143-159. http://dx.doi.org/10.1007/s10533-007-9110-6 14

Yesilonis, ID; Pouyat, RV; Neerchal, NK . (2008). Spatial distribution of metals in soils in Baltimore, Maryland: 15 Role of native parent material, proximity to major roads, housing age and screening guidelines. Environ 16 Pollut 156: 723-731. http://dx.doi.org/10.1016/j.envpol.2008.06.010. 17

Yi, SM; Totten, LA; Thota, S; Yan, S; Offenberg, JH; Eisenreich, SJ; Graney , J; Holsen, TM. (2006). Atmospheric 18 dry deposition of trace elements measured around the urban and industrially impacted NY-NJ harbor. 19 Atmos Environ 40: 6626-6637. http://dx.do i.org/10.1016/j.atmosenv.2006.05.062. 20

Yohn, S., Long, D., Fett, J., Patino, L. (2004) Regional versus local influences on lead and cadmium loading to the 21 Great Lakes region. Appl. Geochem. 19: 1157-1175. 22

Zhang, Y.-H. (2003) 100 years of Pb deposition and transpor t in soils in Champaign, Illinois, U.S.A. Water Air Soil 23 Pollut. 146: 197-210. 24January 2013 3-1 Draft - Do Not Quote or Cite 

### 3 HEALTH EFFECTS AND EXPO SURE/RISK INFORMATION 1

This chapter presents key aspects of the curr ent evidence of lead-rel ated health effects 2 and presents exposure/risk information from th e quantitative assessment performed in the last 3 review in the context of the currently available evidence. Staff has drawn from EPA’s synthesis 4 of the scientific evidence presented in the draft Integrated Science Assessment for Lead (USEPA, 5 2012; henceforth referred to as the ISA) and 2006 Air Quality Criteria Document for Lead 6 (USEPA, 2006; henceforth referred to as th e 2006 CD), and from the documentation of the 2007 7 human exposure and health risk assessment (doc umented in USEPA, 2007a; henceforth referred 8 to as the 2007 REA). The chapter is organize d into sections considering the information on 9 blood Pb as a biomarker (section 3.1), the nature of Pb effects on health (section 3.2), public 10 health implications and at-risk populations (s ection 3.3), and exposure and risk information 11 (section 3.4). Presentation within these sections is organized to address key policy-relevant 12 questions for this review concerning the evid ence and exposure/risk information, building upon 13 the questions included in th e IRP (IRP, section 3.1). 14

3.1 INTERNAL DISPOSITION AND BIOMARK ERS OF EXPOSURE AND DOSE 15 The health effects of Pb, di scussed in detail in the IS A and summarized in Section 3.2 16 below, are remote from the portals of entr y to the body (i.e., the respiratory system and 17 gastrointestinal tract). Consequent ly, the internal disposition and di stribution of Pb is an integral 18 aspect of the relationship between exposure and e ffect. Inhaled lead-bear ing particles, depending 19 on size and solubility, may be absorbed into th e systemic circulation or transported to the 20 gastrointestinal tract (ISA, section 4.2.1.1). The absorption efficiency of Pb from the 21 gastrointestinal (GI) trac t varies with characteristics asso ciated with the ingested Pb (e.g., 22 particle size and chemical form or matrix), as well as with an individual’s physiology (e.g., 23 maturity of the GI tract), nut ritional status (e.g., iron, calcium, and zinc deficiencies increase 24 absorption), and the presence of food in the GI tract (ISA, section 4.2.1.2). Once in the blood 25 stream, where approximately 99% of the Pb is associated with red blood cells (mostly bound to 26 aminolevulinic acid dehydratase, the predomin ant ligand), Pb is quick ly distributed throughout 27 the body (e.g., within days) and is available for exchange with the soft and skeletal tissues, 28 conceptually viewed as the fast and slow tu rnover pools, respectively (ISA, section 4.2.2). 29 Skeletal tissue serves as the largest storage compar tment, with much less Pb stored in soft tissues 30 (e.g., kidney, liver, brain, etc) (ISA, section 4.2.2.2). 31 The role of the bone as the main storage comp artment is related to the ability of Pb to 32 form stable complexes with phosphate and repl ace calcium in the salt comprising the primary 33 crystalline matrix of bone (ISA, section 4.2.2.2). In infants le ss than a year old, the bone is 34January 2013 3-2 Draft - Do Not Quote or Cite estimated to contain approximately 60% of th e total body burden of Pb (ISA, section 4.2.2.2; 1 Barry, 1975). Circulating Pb is taken up into the bone regions of active calcification. 2 Accordingly, during early childhood there is rapi d uptake of Pb into mineralizing bone, with 3 somewhat more than 70% of total body burden Pb estimated to reside in bone of children aged 2 4 to 16, increasing up to more than 90% by adul thood (ISA, section 4.2.2.2; Barry, 1975). The net 5 accumulation of Pb in bone over a person’s lifetime results in bone lead concentrations generally 6 increasing with age (ISA, section 4.2.2.2). 7
The distribution of Pb in the body is dynamic. Throughout life, Pb in the body is 8 exchanged between blood and bone, and between blood and soft tissues (ISA, sections 4.3.5 and 9 4.2.2; 2006 CD, section 4.3.2). The rates of thes e exchanges vary with age, exposure and 10 various physiological variables. For example, resorption of bone, which results in the 11
mobilization of Pb from bone in to the blood, is a gradual proce ss in later adulthood. Resorption 12 rate is appreciably increased in pregnant or nursing women, and in association with osteoporosis 13 in postmenopausal women or, to a lesser magn itude, in older men (IS A, sections 4.3.5.2). 14 Changes in Pb exposure circumstances can also influence these exchanges, e.g., substantial 15 reductions in exposure levels cont ribute to increased release of Pb from the bone into the blood 16 (ISA, section 4.3.5). The studies that address th e relative contributions of bone Pb and current 17 Pb exposure to blood Pb are limited to a few human studies during the 1980s and early 1990s, 18 when leaded gasoline usage wa s common, and a primate study. These studies indicate an 19 appreciable contribution from bone Pb stores to Pb in blood, on the order of 40-70% of blood Pb 20 contributed from bone, under circumstances with higher concurrent exposure than exposures 21 common today (ISA, section 4.3.5; Smith et al ., 1996; Gulson et al., 1995; Manton, 1985; 22 Franklin et al., 1997). 23 During bone resorption that occu rs in pregnancy, Pb is released from bone, increasing the 24 bone contribution to maternal blood Pb levels, an d maternal Pb circulates across the placenta, 25 posing risk to the developing fetus and provi ding the fetal body burden (ISA, sections 4.2.2.4, 26 4.3.5, 4.7.2 and 4.7.3; 2006 CD, 6.6.2; Chuang et al., 2001). The relative size of contributions of 27 maternal bone Pb and current maternal exposur e to maternal blood Pb and fetal body burden, are 28 influenced by the relative magnitude of curre nt and historical expos ures. In various study 29 populations with mean maternal blood Pb levels ranging from 1.7 to 8.6 μg/dL, average blood Pb 30
concentration in the umbilical co rd (as representative of newbor n blood) has been reported to 31 range from 70% to 100% of av erage maternal blood Pb (ISA, section 4.2.2.4); the range is 32 similar for four study populations with mean maternal blood Pb level below 4 μg/dL (Amaral et 33 al., 2010; Patel and Prabhu, 2009; Lagerkvist et al., 1996; Jedrychowski et al., 2011). The 34 relationship for individual mothe r-child pairs is more variable. In a low income population with 35 mean maternal blood Pb of 1.9 μg/dL, factors as sociated with occurrences of relatively higher 36January 2013 3-3 Draft - Do Not Quote or Cite cord blood Pb level to maternal blood Pb leve l pairs included maternal blood pressure and 1 alcohol consumption, while factors associated with relatively lowe r ratios of cord blood Pb to 2 maternal blood Pb included maternal hemoglobin a nd sickle cell trait (Harv ille et al., 2005). As 3
a result of the contributions of maternal bone Pb to matern al blood Pb during pregnancy, the 4 contribution to fetal body burden from maternal bone Pb relative to maternal concurrent 5 exposure is appreciable. This maternal bone Pb contribution to feta l body burden is likely to 6 vary, however, in response to differences betwee n maternal historical ex posures and those during 7 pregnancy, among other factors (2006 CD, sec tions 4.3.1.5 and 4.3.2.5; ISA, section 6.1; Chuang 8 et al., 2001; Gulson et al., 1999; Gulson et al., 2003; Gulson et al., 2004a ; Rothenberg et al., 9 2000). 10
Limited data indicate that blood Pb levels in some newborns may decline during the 11 period extending through the first few months of life; the extent to which this may occur may be 12 influenced by the magnitude of blood Pb level at birth and of subseque nt exposure during early 13 infancy (ISA, section 4.2.2.1; Carbone et al ., 1998; Simon et al., 2007; Gulson et al., 1999, 14 2001). As infants become more mobile and engage in hand-to-mouth behavior, blood Pb levels 15 then commonly increase to a peak around two years of age (ISA, sections 4.4.1 and 6.2.1.1). 16

 Does the current evidence continue to support blood Pb level as a useful indicator 17 of Pb exposure and dose for purposes of characterizing Pb health effects, with 18 well recognized strengths and limitations? To what extent does the evidence 19 suggest alternatives? 20 As discussed in past CDs and in the ISA, blood Pb is the most commonly used indicator 21 of human Pb exposure. For exam ple, given the association with exposure and the relative ease of 22 collection, blood Pb levels are exte nsively used as an index or biomarker of exposure by national 23 and international health agencies, as well as in epidemiological and toxicological studies of Pb 24 health effects and dose-response relati onships (ISA, sections 4.3.2, 4.4.1, 5.3, 5.4, 5.5, 5.6, 5.7, 25 and 5.8). Since 1976, the U.S. Centers for Dis ease Control and Preven tion (CDC) has been 26 monitoring blood Pb levels nationally through th e National Health and Nutrition Examination 27 Survey (NHANES). This survey has documented the dramatic decline in mean blood Pb levels 28 in all ages of the U.S. population that has occu rred since the 1970s, as shown in Figure 3-1, and 29
that coincides with actions on l eaded fuels, leaded paint, l ead in food packaging, and lead30 containing plumbing materials that have reduced Pb exposure in the U.S. (ISA, section 4.4.1; 31 Pirkle et al., 1994; Schwemberger et al., 2005). This decline ha s continued over the more recent 32 past. For example, the 2009-2010 geometric mean blood Pb level in U.S. children aged 1-5 33 years is 1.17 μg/dL, as compared to 1.51 μg /dL in 2007-2008 (ISA, section 4.4.1) and 1.8 μg/dL 34 in 2003-2004, the most recent data available at the time of the last review (73 FR 67002); 35January 2013 3-4 Draft - Do Not Quote or Cite somewhat less dramatic declines have also been reported in the upper tails of the distribution and 1 in different groups with higher levels than the general child population (ISA, Figure 4-19). 2

3
Source: Adapted from data fr om the NHANES (NCHS, 2010) 4 Note: The means of logged blood Pb were weighted to represent national averages. Data were from the publically NHANES II, NHANE S III for 5 1988 1991 and 1992 1994, and the continuous NHANES in 1999 2000, 2003 2004, 2005 2006, 2007 2008. Continuous NHANES data from 6 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 7 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 8 the continuous NHANES. 9 Figure 3-1. Temporal trend in mean blood Pb levels for NHANES cohorts. 10

The CDC, and its predecessor agencies, have for many years used blood Pb level as a 11 metric for identifying highly exposed children at risk of adverse health effects for whom 12 recommendations might be made for their protection (e.g., CDC, 1991; CDC, 2005). In 1978, 13 when the current Pb NAAQS was established, the CDC recognized a blood Pb level of 30 μ g/dL 14 as a level warranting individua l intervention (CDC, 1991). In 1985, the CDC recognized a level 15
of 25 μ g/dL for individual child intervention, and in 1991, they recognized a level of 15 μ g/dL at 16
which individual intervention actions were recommended, and a level of 10 μ g/dL at which more 17 general community-wide preven tion activities were to be implemented (CDC, 1991; CDC, 18 2005). In 2005, with consideration of a review of the evidence by their advisory committee, 19January 2013 3-5 Draft - Do Not Quote or Cite CDC revised their statement on Preventing Lead Poisoning in Young Children , specifically 1 recognizing the evidence of adve rse health effects in children with blood Pb levels below 10 2

μ g/dL and emphasizing the importance of preventive measures (CDC, 2005). 1 Consistent with 3 this statement, the CDC revised their appr oach in 2012 to one that relies on the 97.5 th percentile 4 of blood Pb concentrations in U.S. children (currently 5 μg/dL) 2 as a reference level for 5 identifying children for whom they recomme nd particular follow-up actions (CDC, 2012). 6 Multiple studies of the relationship between Pb exposure and blood Pb in children (e.g., 7 Lanphear and Roghmann 1997; Lanphear et al., 1998) , have shown blood Pb levels to reflect Pb 8 exposures, including exposures to Pb in surface dus t. These and studies of child populations 9
near active sources of air emi ssions (e.g., metal smelters), further demonstrate the effect of 10
airborne Pb on interior dust and on blood Pb (ISA, sections 4.4.1, 4.5.1 and 4.5.3; Hilts, 2003; 11 Gulson et al., 2004b). Accordingly, blood Pb leve l was the index of expos ure in the assessment 12 of young children’s risk performe d in the last Pb NAAQS revi ew (described in section 3.4 13 below). 14 A well recognized strength of using childre n’s blood Pb to investigate relationships 15 between Pb exposure and health effects is the relatively lesser uncertainty in the causality 16 aspects of such relationships than might be associated with such relationships based, for 17 example, on media concentration. Blood Pb is an integrated marker of aggregate exposure 18 across all pathways. For example, the bl ood Pb-response relationships described in 19 epidemiological studies of l ead-exposed populations do not dis tinguish among different sources 20 of Pb or pathways of Pb exposure (e.g., inhala tion, ingestion of indoor dust, ingestion of dust 21 containing leaded paint). Given our focus on ambient air contributi ons to Pb exposures, 22 discussion in response to the question below c onsiders the available information regarding 23 relationships between Pb in ambient air and the associated Pb in blood. Additionally, the 24 exposure assessment performed for the last review of the Pb NAAQS (and described in section 25 3.4 below), employed biokinetic modeling to estimate blood Pb levels associated with aggregate 26 Pb exposure to inform our estimates of contributi ons to blood Pb arising from ambient air related 27
Pb. 28 The response of adult blood Pb levels to a ppreciable changes in exposure circumstances 29 is generally slower than that of blood Pb levels in young child ren. For example, simulations 30 using biokinetic models indicate that blood Pb levels in adults achieve a new quasi-steady state 31

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).January 2013 3-6 Draft - Do Not Quote or Cite within 75-100 days (approximately 3-4 times th e blood elimination half- life) subsequent to 1 abrupt increases in Pb intake (ISA, section 4.3.5.2); similar models indicate a much quicker 2 response of blood Pb levels in child ren both with regard to abrupt increases and reductions in Pb 3 exposure (ISA, section 4.3.5.1). The response in young children may reflect their much more 4 labile bone pool associated with the rapid turnover of bone mine ral in response to their rapid 5 growth rates (ISA, section 4.3.5). As a result of these physiological pr ocesses in young children, 6 their blood Pb levels tend to more quickly refl ect changes in their tota l body burden (associated 7 with their shorter exposure hist ory), and can also reflect chan ges in recent exposures (ISA, 8 section 4.3.5). 9
The extent to which blood Pb measurements represent current e xposure circumstances 10 may be uncertain, particularly where histories include exposures largel y different from those 11 occurring more recently (ISA, s ection 4.3.2). This uncertainty may be greater for blood Pb 12
measurements taken in older children 3 and adults that those for young children as a re sult of their 13 longer exposure histories. For example, the bone of adults has accumulated decades of Pb 14 exposures (with past exposures of ten greater than current ones fo r current U.S. populations) such 15 that the bone may be a significant source of Pb in blood in later ye ars, after exposure has ended. 16 Thus, in populations with past exposures that we re appreciably elevated in comparison to more 17 recent exposures, current blood Pb levels may pred ominantly reflect their exposure history rather 18 than current exposures (ISA, sections 4.3.5.2 a nd 4.4.1). Accordingly, the extent to which 19 studies using cross-sectional blood Pb measurem ents as the exposure biomarker inform our 20 understanding of relationships between recent Pb exposures and various hea lth effects, can differ 21 across age groups, and is greatest for very young children, as discussed in section 3.3 below. 22 Alternative biomarkers of Pb exposure incl ude bone Pb, teeth Pb, and hair Pb (ISA, 23 section 4.3.1, 4.3.3 and 4.3.4). Given the role of bone as the repository of more than 90% of an 24 adult body’s Pb burden, bone Pb levels are re cognized as indicators of body burden and 25 cumulative exposure history (ISA, sections 4.2.2 .2 and 4.3). The currently available evidence 26 does not, however, indicate these or any other alternatives to be superior to blood Pb in young 27 children or as commonly used for the purposes of tracking recent Pb expos ures and for assessing 28 potential health risk for this age group (ISA, section 4.7.3). In summary, the current evidence 29 continues to support our conclusions from the last review regardi ng the use of blood Pb levels as 30 an internal biomarker of Pb exposure and dose info rmative to characterizing Pb health effects in 31 young children. 32

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 4.3).January 2013 3-7 Draft - Do Not Quote or Cite  To what extent has new information alt ered scientific conclusions regarding the 1 relationships between Pb in ambient air and Pb in children’s blood? 2 As described above, blood Pb is an integrat ed marker of aggregate exposure across all 3 pathways and a reflection of exposure history. Thus, our interpretation of the health effects 4 evidence for purposes of this review necessitates characterization of the relationships between Pb 5 from those sources and pathways of interest in this review (i.e., those related to Pb emitted into 6 the air) and blood Pb. The evidence in this re gard derives from analyses of datasets for 7 populations residing in areas w ith differing air Pb concentrations, including datasets for 8
circumstances in which blood Pb levels have ch anged in response to changes in air Pb. The 9
control for variables other than air Pb that can affect blood Pb varies across these analyses. 10
Lead in ambient air contributes to Pb in blood by multiple exposure pathways by both 11 inhalation and ingestion exposure routes (ISA, section 4.1.1). The qua ntitative relationship 12 between ambient air Pb and blood Pb, which is often termed a slope or ratio, describes the 13 increase in blood Pb (in μg/dL) estimated to be a ssociated with each unit increase of air Pb (in 14 μg/m 3 ). Ratios are presented in the form of 1:x, with the 1 representing air Pb (in μg/m3) and x 15 representing blood Pb (in μg/dL). Description of rati os as higher or lower re fers to the values for 16 x (i.e., the change in blood Pb pe r unit of air Pb). Slopes are pres ented as simply the value of x. 17
At the conclusion of the last review in 2008, the EPA interpreted the evidence as 18 providing support for use (in informing the Admini strator’s decision on st andard level) of a 19 range “inclusive at upper end of estimates on the or der of 1:10 and at the lower end on the order 20 of 1:5” (73 FR 67002). This conclusion reflec ted consideration of the air-to-blood ratios 21 presented in the 1986 CD 4 and associated observations regardin g factors contribu ting to variation 22 in such ratios, ratios reported subsequently and ratios estimate d based on modeling performed in 23 the REA, as well as advice from CASA C (73 FR 66973-66975, 67001-67002). The information 24 available in this review, which is assessed in the ISA and is largely, although not completely, 25 comprised of studies that were av ailable in the last review, does not alter the primary scientific 26
conclusions drawn in the last re view regarding the relationships between Pb in ambient air and 27
Pb in children’s blood. The ratios summarized in the ISA in this review span a range generally 28 consistent with the range concl uded in 2008 (ISA, section 4.5.1). 29 The air-to-blood ratios for children, or for popul ations inclusive of children, discussed in 30 the ISA for this review are summarized in Table 3-1. The evidence pertaining to this 31 quantitative relationship between air Pb and children’s blood Pb is now, as in the past, limited by 32
the circumstances in which the data are collected. These estimates are generally developed from 33 studies of populations in a va riety of Pb exposure circumstances. Accordingly, there is 34

4 The 2006 CD did not include an assessment of then-current evidence on air-to-blood ratios.January 2013 3-8 Draft - Do Not Quote or Cite significant variability in air-to-blood ratios among the differe nt study populations exposed to Pb 1 through different air-related exposur e pathways and at different expos ure levels. This variability 2
in air-to-blood estimates can relate to the representation of air-related pathways and study 3 populations, including, for example, relatively na rrow age ranges for the population, to reduce 4 age-related variability in blood Pb or includi ng populations with narro wly specified dietary 5 sources. It can also relate to the precisi on of air and blood measurements and of the study 6 circumstances, such as with regard to spatial an d temporal aspects. Additionally, in situations 7 where exposure to nonair sources covaries with air-related exposures that are not accounted for 8 in deriving ratio estimates, uncertainties may relate to the potential for confounding by nonair 9 exposure covariance (ISA, section 4.5). 10 As was noted in the last review, populat ion age is an important influence on the 11 magnitude of air-to-blood ratio estimates derived. Ratios for children ar e generally higher than 12 those for adults, and higher for young children than older children, perhaps due to behavioral 13 differences between the age groups, as well as th e more rapid response of children’s blood Pb to 14 exposure and body burden changes (as discussed above ) and shorter exposure history. Similarly, 15 given the common pattern of higher blood Pb levels in pre-school aged children than during the 16 rest of childhood, related to behaviors that in crease environmental exposures, ratios would be 17 expected to be highest in earlier childhood. A dditionally, estimates of air-to-blood ratios that 18 include air-related ingestion pa thways in addition to the inhalation pathway are “necessarily 19 higher”, in terms of blood Pb response, than those estimates based on inhalation alone (USEPA 20 1986, p. 11-106). Thus, the extent to which studi es account for the full set of air-related 21 inhalation and ingestion exposure pathways affect s the magnitude of the resultant air-to-blood 22 estimates, such that including fewer pathways as “air-related” yields lowe r ratios. Estimates of 23 air-to-blood ratios can also be influenced by population characteristics th at may influence blood 24 Pb; accordingly, some analyses include adjustments. 25 Given the recognition of young children as a ke y at-risk population in section 3.3 below, 26 as well as the influence of age on blood Pb levels , the studies presented in Table 3-1 are grouped 27 with regard to the extent of their inclusion of young children (e.g., children barely school age). 28 Among the first group of studies, focused exclus ively on young children, is the only study that 29 dates from the end of or after the phase-out of leaded gasoline usage (Hilts, 2003). This study 30 reports changes in children’s blood Pb levels associated with reduced Pb emissions and 31
associated air concentrations near a Pb smelter in Canada (for children through age five). Given 32 the timing of this study, after the leaded gasoline phase-out, and its setting near a smelter, the 33 ambient air Pb in this study may be somewhat more comparable to that near sources in the U.S. 34January 2013 3-9 Draft - Do Not Quote or Cite today than other studies discusse d here. The study authors repor t an air-to-blood ratio of 1:6. 5 1 An EPA analysis of the air and blood data re ported for 1996, 1999 and 2001 results in a ratio of 2 1:6.5, and the analysis focused only on th e 1996 and 1999 data (pre- and post- the new 3 technology) yields a ratio of 1:7 (ISA, section 4.5.1; Hilts, 2003). 6 The two other studies that 4 focused on children of age 5 or younger analyze varia tions in air Pb as a re sult of variations in 5 leaded gasoline usage in Chicago, Illinois. Th e study by Hayes et al. (1994) compared patterns 6
of ambient air Pb reductions and blood Pb re ductions for large numbers of children, aged 6 7 months - 5 years, in Chicago between 1974 a nd 1988, a period when significant reductions 8 occurred in both measures. The study reports a better fit for the log-log model which describes a 9 pattern of higher ratios with lower ambient air Pb and blood Pb levels (Hayes et al., 1994). 10 Based on the log-log model, the ratio derived for the relationship of quarterly mean air 11
concentration with blood Pb duri ng the period is 1:8 (Table 3-1). Another analysis for a Chicago 12 dataset, performed by Schwartz and Pitcher (198 9) focused on the association of blood Pb in 13 black children (aged < 5 years) with the use of leaded gasoline from 1978 through 1980. Given 14 that leaded gasoline exposure o ccurs by air-related pa thways, additional analyses have related 15 the leaded gasoline usage for this period to air co ncentrations. Using the resulting relationship of 16 blood Pb with air Pb (adjusted for age and a numbe r of other covariates) yields a ratio of 1:8.6 17 (ISA, table 4-12, section 4.5.2). The blood Pb concen trations in the two l eaded gasoline studies 18 are appreciably higher (a factor of two or more) than those in the study near the smelter (Hilts, 19 2003). 20 The second group of studies in Table 3-1 (com prised of studies including but not limited 21 to children less than or equal to five years of age) includes a complex statistical analysis and 22
associated dataset for a cohort of children born in Mexico City from 1987 through 1992 (Schnaas 23 et al., 2004). This study, which was not assessed in the last review, en compasses the period of 24

5 Sources of uncertainty include the role of factors other than ambient air Pb reduction in influencing decreases in blood Pb (ISA, section 4.5.1). 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 he notes that these prog rams were in place in 1992, s uggesting 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 previous years (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 4.5.1).January 2013 3-10 Draft - Do Not Quote or Cite leaded gasoline usage and further informs our understanding of f actors influencing the 1 quantitative relationship between air Pb and children’s blood P b. Air-to-blood ratios developed 2 from this study are influenced by a number of f actors and appear to range from roughly 2 to 6, in 3 addition to an estimate of 9 (ISA, section 4.5.1), a lthough this is derived fro m data set restricted 4 to the latter years of the study wh en little change in air Pb con centration occurred, such that the 5 role of air Pb may be more unc ertain. Estimates associated w ith the developmental period of 6 highest exposure – e.g., age 2 y ears - range up to approximately 6, illustrating the influence of 7 age on the ratio (ISA, section 4.5.1 ). Also in the Table 3-1 second group are two much older 8 studies of populations compri sing age ranges extending well beyond 6 years. The first is the 9 review and meta-analysis by Brunekreef (1984) usi ng datasets available at the time for variously 10 aged children as old as 18 years with identifi ed air monitoring methods and reliable blood Pb 11 data for 18 locations in the U.S. and internationally. 7 The author discusse s potential confounders 12 of the relationship between air Pb and blood Pb, recognizing the desira bility of taking them into 13 account when deriving an air-to-blood relations hip from a community study, but noting that was 14 not feasible in such an analysis. Two models we re produced, one based on the full pooled dataset 15
and a second limited to blood Pb-air Pb data pairs with blood Pb levels below 20 μg/dL (r 2 16 values were 0.692 and 0.331, respecti vely). From these two log n -log n models, air-to-blood ratio 17
estimates were derived for air concentrations corresponding to the geometric means of the two 18 sets of data pairs. At thos e concentrations (1.5 and 0.54 μg/m 3 , respectively), the resultant ratios 19 both round to 5. The study by Schwartz and Pitc her (1989) described above also analyzed the 20 relationship between U.S. NHANES II blood Pb levels for white subjects, aged < 74 years, and 21 national usage of leaded gasoline. A separate, less specifically desc ribed, air Pb dataset was used 22 to convert the relationship of blood Pb with gas Pb to one for blood Pb with air Pb, with a 23 resultant ratio on the order of 9, adjusted for age and other covariates (Henderson, 2007, pp. D-2 24 to D-3; ISA, Table 4-12). 25
The last two studies included in Table 3-1 ar e focused on older children (ages 6-11). The 26
methods for characterization of air Pb concentr ations (and soil Pb for latter study) also differ 27
from other studies in Table 3-1. The first st udy regressed average blood Pb concentrations for 28 multiple locations around Mumbai, India on averag e air Pb concentrations at those locations 29 (Tripathi et al., 2001). The valu es in the linear regression we re 13 pairs of location-specific 30 geometric means of all the da ta collected over the 13-year period from 1984 to 1996; the 31 reported slope was 3.6 (Tripathi et al., 2001). The location-spec ific geometric mean blood Pb 32

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 et al. (1984) used multiple regression to control for several confounders (73 FR 66974).January 2013 3-11 Draft - Do Not Quote or Cite levels in this study (8.6-14.4 μg /dL) indicate blood Pb distribu tions in this age group much 1 higher than those pertinent to similarly aged children in the U.S. today. The second study 2 analyzed air, soil and children’s blood Pb concentrations in Duisburg, Germany during the 3 leaded gasoline phase-out (Ranft et al., 2008). Av erage blood Pb levels declined over the nearly 4 20-year study period from 9 μg/dL in 1983 (345 child ren average age of 9 years) to 3 μg/dL in 5 2000 (162 children average of 6 years). 8 Average air Pb concentr ation declined from 0.45 μg/m 3 6 to 0.06 μg/m 3 over the same period, with the largest re duction occurring between the first study 7 year (derived from tw o monitoring sites for full study area ) and the second study year, 1991, for 8
which air concentrations were derived from a combination of dispersion modeling and the two 9 monitoring sites. 9 For a mean air Pb concentration of 0.1 μg/m 3 , the study’s multivariate log10 linear regression model predicted air to blood ratios of 3.2 and 6.4 for “background” blood Pb 11 concentrations of 1.5 and 3 μg/dL, respectively. In this study, background referred to Pb in 12 blood from other sources; the bl ood Pb distribution over the study pe riod, including levels when 13 air Pb concentrations are lowest, indicates 3 μg /dL may be the better es timate of background for 14 this study population. Inclusion of soil Pb as a variable in the model may have contributed to an 15
underestimation of the these blood Pb-air Pb ratios for this study because some of the Pb in soil 16 likely originated in air and the blood Pb-air Pb slope does not in clude the portion of the soil/dust 17 Pb ingestion pathway that derive s from air Pb. The ISA also pr esents somewhat higher air-to18 blood ratio estimates derived using univariate linear, log-log and log-linear models on the 19 median air and blood Pb concentrations reported fo r the five years include d in this study (ISA, 20 section 4.5.1; Ranft et al., 2008, Table 2). Uncertain ties related to this study’s estimates include 21
those related to the bulk of air concentrati on reduction occurring between the first two time 22 points (1983 and 1991) and the difference among the year’s air datasets (e .g., two data sources 23 [air monitors] in 1983 and multiple geographical poi nts from a combination of the monitors and 24 modeling in subsequent years). 25

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).January 2013 3-12 Draft - Do Not Quote or Cite Table 3-1. Empirically derived air-to-b lood ratios for populations inclusive of children. 1

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 mean PbB and PbA [unadjusted] PbB: 10-28 μg/dL (quarterly mean) 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 et al. (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 Ave 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); ave~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, Table4-12; Hayes et al., 1994) C - See discussion in text and ISA, section 4.5.1. D - Based on data for U.S. (1986 Pb CD). See I SA, section 4.5.1. 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 4.5.1). GM, geometric mean; AM, arithmetic mean; GSD, geometric standard dev iation; PbB, blood Pb concentration, μg/dL; PbA, air Pb con centration, μg/m 3 2January 2013 3-13 Draft - Do Not Quote or Cite In the 2008 review, in addition to considering the evidence presented in the published 1
literature and that reviewed in the 1986 CD, we also considered air-to-blood ratios derived from 2 the exposure assessment (73 FR 66974; 2007 REA, section 5.2.5.2). In the exposure assessment 3 (summarized in section 3.4 below), current mode ling tools and informati on on children’s activity 4 patterns, behavior and physiology were used to estimate blood Pb leve ls associated with 5 multimedia and multipathway Pb exposure. The results from the various case studies assessed, 6 with consideration of the context in which they were derived (e.g., the extent to which the range 7 of air-related pathways were si mulated, and limitations associated with those simulations), and 8 the multiple sources of uncertainty (see secti on 3.4.7 below) are also informative to our 9 understanding of air-to-blood ratio s. Estimates of air-to-blood ratios for the two REA case 10 studies that represent localized population expo sures exhibited an increasing trend across air 11 quality scenarios representing decr easing air concentrations. For example, across the alternative 12 standard levels assessed, which ranged from a calendar quarter average of 1.5 μg/m 3 down to a 13 monthly average of 0.02 μg/m 3 , the ratios ranged from 1:2 to 1:9 for the general urban case 14 study, with a similar trend although of generally higher ratio for the primary smelter case study 15 subarea. This pattern of model- derived ratios is generally cons istent with the range of ratios 16
obtained from the literature. We continue to recognize a numbe r of sources of uncertainty 17
associated with these model-derived ratios which may contribute to high or low biases. 10 18 The evidence on the quantitativ e relationship between air Pb and air-related Pb in blood 19 is now, as in the past, limited by the circumstan ces (such as those related to Pb exposure) in 20
which the data were collected. Previous reviews have recognized the significant variability in 21
air-to-blood ratios for different populations exposed to Pb thr ough different air-related exposure 22 pathways and at different air and blood levels, with the 1986 CD noting that ratios derived from 23 studies involving the higher blood and air Pb levels pertaining to workers in lead-related 24 occupations are generally smaller than ratios from studies involving lower blood and air Pb 25 levels (ISA, p. 4-129; 1986 CD, p. 11–99). Consiste nt with this observation, slopes in the range 26 of 3 to 5 were estimated for child population datasets assessed in the 1986 CD (ISA, p. 4-129; 27

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 Risk Assessment Report, 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 ra tios 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.January 2013 3-14 Draft - Do Not Quote or Cite 1986 CD p. 11–100; Brunekreef, 1984; Tr ipathi et al., 2004). Additi onal studies considered in 1 the last review and those assessed in the ISA pr ovide evidence of ratios above this older range 2 (ISA, p. 4-130). For example a ratio of 6.5-7 is indicated by the study by Hilts (2003), one of the 3
few studies that evaluate the air Pb-blood Pb re lationship in conditions that are closer to the 4 current state in the U.S. ( ISA, p. 4-130). We add itionally note the variety of factors identified in 5 the ISA that may potentially affect estimates of various ratios (including potentially coincident 6 reductions in nonair Pb sources during the course of the studies), and for which a lack of 7 complete information may preclude any adjustment of estimates to account for their role (ISA, 8 section 4.5). 9 In summary, as at the time of the last review of the NAAQS for Pb, the currently 10
available evidence includes estimates of air-to-bl ood ratios, both empirically- and model-derived, 11
with associated limitations and related uncertain ties. These limitations and uncertainties, which 12 are summarized here and also noted in the ISA, usually include uncertainty associated with 13 reductions in other Pb sources during study pe riod. The limited amount of new information 14
available in this review has not appreciably altered the scientific conclusions reached in the last 15 review regarding relationships between Pb in ambient air and Pb in children’s blood or with 16 regard to the range of ratios. The currently available evidence conti nues to indicate ratios 17 relevant to the population of young children in th e U.S. today, reflecti ng multiple air-related 18 pathways in addition to inhalation, to be generall y consistent with the approximate range of 1:5 19 to 1:10 given particular atten tion in the 2008 NAAQS decision, incl uding the “generally central 20 estimate” of 1:7 (73 FR 67002, 67004; ISA, pp. 4-129 to 4-130). 21

3.2 NATURE OF EFFECTS 22 Lead has been demonstrated to exert a broad array of deleterious effects on multiple 23 organ systems as described in the assessment of the evidence available in this review and 24 consistent with conclusions of past CDs (ISA, section 2.6; 2006 CD, section 8.4.1). A sizeable 25
number of studies on Pb health effects are newly available in th is review and are critically 26 assessed in the ISA as part of the full body of evidence. The ne wly available evidence reaffirms 27 conclusions on the broad array of effects recognized for Pb in the last review (see ISA, section 28 2.10). Consistent with those conclusions, th e ISA determines that causal relationships 11 exist for 29

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).January 2013 3-15 Draft - Do Not Quote or Cite Pb 12 with effects on the nervous system (cognitiv e function decrements and attention-related 1 behavioral problems in children), hematological system (altered heme synthesis and decreased 2 red blood cell survival and function), and cardi ovascular system (hypertension and coronary 3 heart disease), and on reproduction and develo pment (postnatal development and male 4 reproductive function) (ISA, table 2-2). Additio nally, the ISA describes relationships between 5 Pb and effects on kidney and immune system function, and with cancer 13 as likely causal 14 (ISA, 6 table 2-2, sections 2.6.3, 2.6.4 and 2.6.7). 7 In some categories of health effects, ther e is newly available evidence regarding some 8 aspects of the effects described in the last review or that stre ngthens our conclusions regarding 9 aspects of Pb toxicity on a pa rticular physiological system. Am ong the nervous system effects of 10 Pb, the newly available evidence is consistent wi th conclusions in the previous review which 11 recognized that “[t]he neurotoxi c effects of Pb exposure are am ong those most studied and most 12 extensively documented among human population groups” (2006 CD, p. 8-25). Nervous system 13 effects that receive prominence in the current review, as in previous reviews, include those 14 affecting cognitive function and behavior in childre n (ISA, section 5.3), with conclusions that are 15 consistent with findings of the last review. 16 Across the broad array of Pb effects for sy stems and processes other than the nervous 17 system, the evidence base has been augmented with additional epidemiological investigations in 18 a number of areas, including developmental outcome s, such as puberty onset, and adult outcomes 19 related to cardiovascular function, for which se veral large cohorts have been analyzed (ISA, 20 Table 2-8 and sections 5.4 and 5.8). Conclusi ons on these other systems and processes are 21
consistent with conclusions reached in the last review, while also extending our conclusions on 22 some aspects of these effects. For example, evidence in this review for the cardiovascular 23 system includes information on the role of inte ractions of cumulative Pb exposure with other 24
factors such as stress in cont ributing to hypertension, and on a role for Pb in contributing to 25 coronary heart disease (ISA, section 5.4 and Table 2-8). 26

12 In determining that a causal relationship exists fo r 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. lxiv)
13 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 5.10). In this assessment, EPA concludes that there is a likely causal relationship between Pb exposure and cancer, based primarily on animal studies, with limited human evidence of suggestive associations (ISA, section 5.10.6).
14 In determining a likely causal relationship exists fo r Pb with specific health effects, EPA has concluded that “[e]vidence is sufficient to conclude that a causal relationship is likely to exist with relevant pollutant exposures, but important uncertainties remain” (ISA, p. lxiv).January 2013 3-16 Draft - Do Not Quote or Cite Based on the extensive assessmen t of the full body of evidence available in this review, 1 the major conclusions drawn by the ISA regarding health effects of Pb in children include the 2 following (ISA, section 1.3.1). 3 Multiple epidemiologic studies conducted in diverse populations of children 4 consistently demonstrate the harmful e ffects of Pb exposure on IQ, academic 5 performance, learning and memory. Epidem iologic studies also demonstrate the 6 effect of Pb exposure on i nattention, impulsivity, and hy peractivity in children. 7 The evidence in children is supported by findings in animal studies demonstrating 8 analogous effects and biological plausibility at relevant exposure levels. Evidence 9 suggests that some Pb-related cognitive effects may not be reversible and that 10 neurodevelopmental effects of Pb may persist into adulthood (section 2.9.4). 11 Lead exposure also causes hematologic ef fects (such as effects on blood cells or 12 blood producing organs) in children and is a ssociated with an increased risk of 13 internalizing behaviors (e.g., withdrawn behavior and depressive symptoms), 14 sensory and motor function decrements, atopic and inflammatory conditions (e.g., 15 asthma and allergy) in children, as we ll as misconduct in older children and 16 young adults. Uncertainties arising from the lack of information about the specific 17 Pb-exposure histories which contribute to observed blood Pb l evels are greater in 18 adults and older children than in young children (section 2.9.5). 19 20
Based on the extensive assessmen t of the full body of evidence available in this review, 21 the major conclusions drawn by the ISA regarding health effects of Pb in adults include the 22 following (ISA, section 1.3.1). 23 A large body of evidence from both epidemiologic studies of adults and 24 experimental studies in anim als demonstrates the effect of long-term Pb exposure 25 on increased blood pressure (BP) and hype rtension (Section 2.6.2). In addition to 26 its effect on BP, Pb expos ure leads to coronary hear t disease and death from 27 cardiovascular causes and is likely to cause cognitive function decrements, 28 symptoms of depression and anxiety, redu ced kidney function, and immune effects 29 in adults. The extent to which the effects of Pb on the cardiova scular system are 30 reversible is not well characterized. It is also important to note that the 31 frequency, timing, level and dur ation of Pb exposure causing the effects observed 32 in adults has not been pinpointed, an d higher past exposures may well have 33 contributed to the development of hea lth effects measured later in life. 34 35 As in prior reviews of the Pb NAAQS, this review is focused on those effects most 36 pertinent to ambient air Pb exposures. Given th e reductions in ambient air Pb levels over the 37 past decades, these effects are ge nerally those associated with th e lowest levels of Pb exposure 38 that have been evaluated. Additionally, we recognize the limitations on our ability to draw 39 conclusions regarding the exposure conditions cont ributing to the findings from epidemiological 40 analyses of blood Pb levels in populations of olde r children and adults, particularly in light of 41 their history of higher Pb exposures. In the la st review, while recognizi ng the range of health 42January 2013 3-17 Draft - Do Not Quote or Cite effects in variously aged populati ons related to Pb exposure, we focused on the health effects for 1 which the evidence was strongest with regard to relationships with the lowest exposure levels, 2 neurocognitive effects in young childre n. The policy-relevant questions on health effects for this 3 review (identified in the IRP) were framed in r ecognition of the conclusions of the last review. 4
Our consideration of the health effects evidence in this review is framed by policy-relevant 5 questions building on those identified in the IRP. 6

 To what extent is there new scientif ic evidence available to improve our 7 understanding of the health effects associ ated with various time periods of Pb 8 exposures at various stages of life? 9 As in the last review, we base our current und erstanding of health effects associated with 10 different Pb exposure circumstances at various stages of life on the full body of available 11 evidence which includes epidemiological studies of health effects associated with population Pb 12 biomarker levels as well as laboratory animal st udies in which the effects of different exposures 13 on different lifestages are assessed under controlled conditions. Th e epidemiological evidence is 14 overwhelmingly comprised of studies that rely on blood Pb for the exposure metric, with the 15 remainder largely including a focus on bone Pb. Because these metrics reflect Pb in the body 16 (e.g., as compared to Pb exposure concentratio ns) and, in the case of blood Pb, reflect Pb 17 available for distribution to targ et sites, they strengthen th e evidence base for purposes of 18 drawing causal conclusions with regard to Pb generally. The complexity of Pb exposure 19 pathways and internal dosimetry tends to limit the extent to which these types of studies inform 20 our more specific understanding of the Pb exposure circumstances (e.g., timing, duration, 21 frequency and magnitude) elici ting the various effects. 22 The specific exposure circumstances, including timing during the lifetime, that contribute 23 to the blood Pb (or bone Pb) measurements with which associations have been analyzed in 24 epidemiological studies are unknown. This is particularly the case with regard to the 25 contributing role of recent exposures for which uncer tainty is greater in a dults and older children 26 than in younger children (ISA, s ection 1.4). For example, a crit ical aspect of much of the 27 epidemiological evidence, particularly that focu sed on older adults in the U.S. today, is the 28 backdrop of generally declini ng environmental Pb exposure th at is common across many study 29 populations. An additional complication pertaining to older children and younger adults is the 30 common behaviors of younger children (e.g., hand to mouth contact) which generally contribute 31 to relatively greater environmental exposures earlier in life (ISA, sections 4.1.1, 6.2.1). Such 32 exposure histories complicate our ability to draw conclusions regarding critical time periods and 33January 2013 3-18 Draft - Do Not Quote or Cite lifestages for Pb exposures eliciting the effects w ith which associations with Pb biomarkers have 1 been observed in populations of adults a nd older children (e.g., ISA, section 2.9.5). 15 2 As at the time of the last review, assessm ent of the full evidence base, including evidence 3 newly available in this review, demonstrates that Pb exposure prenatally and also in early 4 childhood can contribute to neurocognitive impact s in childhood, with evidence also indicating 5 the potential for effects pers isting into adulthood (ISA, s ections 2.9.5, 2.9.6, and 2.10). In 6
addition to the observed associatio ns of prenatal and childhood bl ood Pb with effects at various 7 ages in childhood, there is also evidence of lead-related cogni tive function effects in non8 occupationally exposed adults (ISA, section 5.3.12) . This includes eviden ce of associations of 9
such effects in adulthood with childhood blood Pb levels and, in other cohorts, with concurrent 10 (adult) blood Pb levels (ISA, sections 5.3.2.1, 5.3.2.7 and 5.3.12). As the studies finding 11
associations of adult effects with childhood blood Pb levels did not examine adult blood Pb 12 levels, the relative influence of adult Pb exposure cannot be ascertained, and a corresponding 13 lack of early life exposure or biomarker measurem ents for the latter studies limit our ability to 14 draw conclusions regarding spec ific Pb exposure circumstances eliciting the observed effects 15 (5.3.12). Findings of stronger associations fo r adult neurocognitive effects with bone Pb, 16 however, indicate the role of historical or cumulative exposu res for those effects (ISA, section 17 5.3). 18 Given the relatively short exposure hist ories of young children, th ere is relatively 19 reduced uncertainty regarding th e lifestages in which exposures contribute to effects for 20 associations of early childhood effects with ear ly childhood blood Pb levels (ISA, sections 2.9.5 21 and 5.3.12). In considering our understanding of the relative impact on neurocognitive function 22 of additional Pb exposure of children by school ag e or later we recognize increasing uncertainty 23 associated with limitations of the currently avai lable evidence, including epidemiological cohorts 24 with generally similar temporal patterns of e xposure. We take note, additionally, of evidence 25 from experimental animal studies and a small body of epidemiologic studies that indicates that 26 Pb exposures during different lifestages can induce cognitiv e impairments. The limited 27 epidemiological evidence is of populations with blood Pb levels that are not strongly correlated 28 over time and that can, accordingl y, address the issue of the role of exposure subsequent to the 29

15 The evidence from experimental animal studies can be informative with regard to key aspects of exposure circumstances in eliciting specific effects. Accord ingly, for health effects wh ere the animal evidence base is extensive with regard to investigation of different patterns of exposure, it informs our interpretation of the epidemiological evidence. For example, the animal evidence base is particul arly extensive with regard to Pb effects on blood pressure, demonstrating the etiologically-relevant role of long-term exposure (ISA, section 5.4.1). This finding then informs consideration of epidemiological stud ies of adult populations for whom historical exposures were likely more substantial than concurrent ones to sugg est that the observed effects may be related to the past exposure (ISA, section 5.4.1). For other health effects, the anim al evidence base may be less extensive with regard to the role of specific exposure circumstances and thus less informative with regard to key exposure aspects.January 2013 3-19 Draft - Do Not Quote or Cite earliest lifestages (ISA, sect ion 5.3.12; Hornung et al., 2009). Some animal evidence 1 demonstrates impaired learning with infancy only, from infancy into adulthood, and postinfancy 2 only Pb exposure (Rice, 1990; Rice and Gilbert 1 990; Rice, 1992). Further, evidence that Pb 3 exposure presents a risk during different lifestages is also consistent with our broader 4 understanding that nervous system developm ent continues throughout childhood. The limited 5 analyses of this issue that are newly availabl e in this review do not appreciably change our 6 understanding or conclusions on th is from those of the prior review (ISA, section 5.3.12). 7 As in the last review, there is also substant ial evidence of other neurobehavioral effects in 8 children, such as attention-related behavioral problems, conduct problems or internalizing 9 behaviors. The evidence for many of these endpoints, as with neurocognitive effects, also 10
includes associations of effects at various ages in childhood and, for some effects, into 11 adulthood, with blood Pb levels reflective of se veral different lifesta ges (e.g., prenatal and 12 several different ages in chil dhood) (ISA, sections 5.3.3 and 5.3.4). There is similar or relatively 13
less extensive evidence to inform our understanding of such effect s associated with specific time 14 periods of exposure at specific lifestages than is the case for effects on cognitive function. 15 Across the range of Pb effects on physiologi cal systems and processes other than the 16 nervous system, the full body of evidence on etiologi cally relevant circumst ances of Pb exposure 17 eliciting increases in blood pre ssure and hypertension is somewhat more informative than is the 18 case with regard to many other effects. In the case of lead-induced in creases in blood pressure, 19
the evidence indicates an im portance of long-term exposure (ISA, sections 2.6.2 and 5.4.7.1). 20 In summary, as in the last review, we con tinue to recognize a numb er of uncertainties 21 regarding the circumstances of Pb exposure, in cluding timing or lifestage s, eliciting specific 22
health effects. Consideration of the evidence newly available in this review has not appreciably 23 changed our understanding on this to pic. Across the full evidence base, the effects for which our 24 understanding of relevant exposure circumstance s is greatest are neurocognitive effects in 25 children, and to a lesser degree, hypertension and increased bl ood pressure. Thus, we continue 26 to recognize and give particular attention to the role of Pb expos ures relatively early in childhood 27 in contributing to neurocognitive effect s which may persist into adulthood. 28

 At what levels of Pb exposure do health effects of concern occur? 29

 Is there evidence of effects at exposure leve ls lower than previously observed and 30 what are important uncertai nties in that evidence? 31 In considering the question posed here, we r ecognize, as discussed in section 3.1 above, 32 that the epidemiological evidence base for our co nsideration in this review, as in the past, 33
includes substantial focus on intern al biomarkers of exposure, such as blood Pb, with relatively 34 less information specific to exposure levels, includ ing those derived from air-related pathways. 35January 2013 3-20 Draft - Do Not Quote or Cite Given that blood and bone Pb are integrated ma rkers of aggregate expo sure across all sources 1 and exposure pathways, our interpretation of stud ies relying on them is informed by what is 2 known regarding the historical context and expos ure circumstances of the study populations. For 3 example, a critical aspect of much of the epidemiological evid ence is the backdrop of generally 4 declining Pb exposure over the past severa l decades. Thus as a generality, recent 5 epidemiological studies of populatio ns with similar characteristics as those studied in the past 6 tend to involve lower overall Pb exposures and accordingly lower blood Pb levels (e.g., ISA, 7 sections 3.5 and 4.4.1; 2006 CD, section 3.4). This ha s been of particular not e in the evidence of 8 blood Pb associations with nervous system effect s, particularly impacts on cognitive function in 9 children, for which we have seen associations with progressively lower childhood blood Pb 10 levels across past reviews (ISA, sec tion 5.3.13; 1986 CD; USEPA, 1990; 2006 CD; 73 FR 11 66976). 12 The evidence currently available with rega rd to the magnitude of blood Pb levels 13 associated with neurocognitive effects in children is generally consistent with that available in 14 the review completed in 2008. Nervous system effects in children, sp ecifically effects on 15 cognitive function, continue to be the effects that are best substantiated as occurring at the lowest 16 blood Pb concentrations (ISA, sect 1.5). Asso ciations of blood Pb with effects on cognitive 17 function measures in children have been repo rted in many studies across a range of childhood 18 blood Pb levels, including study group (mean/media n) levels ranging down to 2 μg/dL (e.g., ISA, 19 sections 1.5 and 5.3.2). 16 Studies in which such findi ngs were reported for childhood study 20 group blood Pb levels below 5 μg/d L are summarized in Table 3-2. 17 In recognition of the 21 influence of age on blood Pb levels, the analyses in Table 3-2 are listed in order of age at which 22 the blood Pb measurements were taken. Findings fo r studies newly availabl e in this review are 23
indicated in bold text. 24

16 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).
17 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 5.3.2.1 and 5.3.3.5; 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).January 20133-21Draft - Do Not Quote or CiteTable 3-2.Associations with neurocognitive functionmeasures in analyses with child study group blood lead levels <5 μg/dL.1MeasureAStudy Group Dataset DescriptionBlood Pb LevelsAdditional Information on AnalysesAgeMeanB(μg/dL)RangeB(μg/dL)NCStudies discussed in ISA (section 5.3.2) with findings ofeffects onneurocognitivemeasuresreported forchildhood 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 200324mo3.81 -9.348Regression, PbB as continuous variable; statistically significant negativeassociationBSID/MDI Mexico 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 mo4.81-1657,678Linear 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 mo4.2221% <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])FSIQ Rochester, prospective cohort, age 5 yrSubgroup with peak PbB <10 μg/dLCanfield et al., 20035 yr3.320.5–8.4(LOD=1)71Regression, PbB as continuous variable; statistically significant negativeassociationFSIQ Pooled International, age 6-10 yrSubgroup with peak PbB <7.5 μg/dLLanphear et al 2005E5-7yr3.240.9–7.4103Regression, PbB as continuous variable; statistically significant negativeassociationFSIQLM, EFAcadPerfNew England, 2 areas, age 6-10, ,Full dataset,Surkan et al., 20076-10 yr2.31–10389Regression, 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 yr1.730.4–4.9261Regression, 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 yr1.94,853Continuous (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 yr1.95766-80Regression 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).C - Bolded measures and studies are newly available in this review.D - In practice, 337-425 cases were included in analysis (Chandramouli et al., 2009).E - Blood Pb measurements of subgroup with peak PbB <7.5μg/dL comprised of 13.6% age 5 (Boston, Cleveland), 67.0% age 6 (Rochester), 19.4% 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.January 2013 3-22 Draft - Do Not Quote or Cite Among the analyses of lowest study group blood Pb levels at the youngest ages in Table 1 3-2 are analyses available in the last review of Pb associations with neurocognitive decrement in 2 study groups with mean levels on the order of 3- 4 μg/dL in children aged 24 months, or ranging 3 from 5 to 7 years (73 FR 66978-66969; ISA, section 5.3.2.2; Bellinger and Needlemann, 2003; 4 Canfield et al., 2003; Lanphear et al., 2005; Tellez-Rojo et al., 2006; Bellinger, 2008; Canfield, 5 2008; Hornung, 2008; Tellez-Rojo, 2008). 18 Newly available in this review are two studies 6 reporting association of blood Pb levels prior to three years of age with academic performance 7 on standardized tests in primary school; mean bl ood Pb levels in these studies were 4.2 and 4.8 8 μg/dL (ISA, section 5.3.2.5; Chandramouli et al., 2009; Miranda et al., 2009). One of these two 9 studies, which represented integer blood Pb levels as categorical variab les, indicated a small 10 effect on end-of-grade reading score of blood Pb le vels as low as 2 μg/dL, after adjustment for 11 age of measurement, race, sex, enrolled in fr ee or reduced lunch program, parental education, 12 and school type (Miran da et al., 2009). 13 In a newly available study of blood Pb leve ls at primary school age, a significant 14 association of blood Pb in children aged 8-11 years and concurrently measured full scale IQ 15 (FSIQ) was reported for a cross- sectional cohort in Korea with a mean blood Pb level of 1.7 16 μg/dL and range of 0.43-4.91 μg/dL (Kim et al., 2009). 19 In considering the blood Pb levels in 17 this study, we note that blood Pb le vels in children aged 8-11 are generally lower than those in 18 pre-school children, for reasons related to beha vioral and other factors (ISA, sections 4.3.5, 4.4.1 19 and 6.2.1.1). 20 It is likely that the blood Pb levels of this study group at earlier ages, e.g., prior to 20 school entry, were higher and the available inform ation does not provide a basis to judge whether 21 the blood Pb levels in this study represent lowe r exposure levels than those experienced by the 22 younger study groups. In still older children, a la rge cross-sectional investigation of blood Pb 23
association with effects on memo ry and learning, that was available in the last review was 24 focused on children aged 6-16 years, born during 1972-1988, with a mean blood Pb of 1.9 25 μg/dL. A study newly available in this review, focused on a subset of the earlier study cohort 26 (ages 12-16, born during 1975-1982), also reports a si gnificant negative association of blood Pb 27

18 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, however, these tests 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.
19 Limitations of this study included a lack of consid eration of potential confounding by parental caregiving quality or IQ (ISA, Table 5-3).
20 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 5.3.2). Separate analysis of the full study group found a significant negative association of IQ with blood Mn (Kim et al., 2009).January 2013 3-23 Draft - Do Not Quote or Cite with learning and memory test results with mean blood Pb levels of approximately 2 μg/dL (ISA, 1 section 5.3.2.3; Lanphear et al., 2000; Krieg et al., 2010). In considering these study findings 2 with regard to the question of exposure levels eliciting effects, we recognize, however, that blood 3 Pb levels are, in general, lower among teenagers than young children and also that, for these 4 subjects specifically, the ma gnitude of blood Pb levels dur ing the earlier childhood (e.g., pre5 school ages) was much higher. For example, the mean blood Pb levels for the 1-5 year old age 6 group in the NHANES 1976-80 sample was 15 μg/dL, declining to 3.6 μg/dL in the NHANES 7 1988-1991 sample (Pirkle et al., 1994; ISA, section 4.4.1). 8 With regard to other nervous system effects in children, the evidence base at lower blood 9
Pb levels is somewhat extended since the last review with re gard to the evidence on Pb and 10 attention-related behavioral problems, such as inattention, impulsi vity, hyperactivity and 11 attention deficit hyperactivity disorder (ISA, section 5.3.3 and table 5-17). Several newly 12 available studies investigating th e role of blood Pb levels in ol der children (primary school age 13 and older) have reported signi ficant associations of attenti on-related behavior or conduct 14 problem measures with concurrent blood Pb levels, with mean levels generally on the order of 5 15 μg/dL or higher (ISA, section 5.3.3). One excep tion is the newly available cross-sectional, 16 categorical analysis of the NHANES 2001-2004 sample of children aged 8-15 years, which 17 found higher prevalence of conduct disorder in th e subgroup with concurrent blood Pb levels of 18 0.8-1.0 μg/dL as compared to the <0.8 μg/dL group (ISA, section 5.3.4 and Table 5-12). As 19 noted above, we recognize that many of thes e children, born between 1986 and 1996, are likely 20 to have had much higher Pb exposures (and associat ed blood Pb levels) in their earlier years than 21 those commonly experienced by young children toda y, thus precluding a conclusion regarding 22 evidence of effects associated with lower exposur e levels than provided by evidence previously 23
available. 24 As summarized earlier in this section, blood Pb has been associated with a range of health 25 effects on multiple organ systems or processes. As is the case for studies of nervous system 26 effects in children, newly available studies of ot her effects in child and adult cohorts include 27
cohorts with similar or somewhat lower mean blood levels than in previous ly available studies. 28 Categories of effects for which a causal relati onship has been concluded in the ISA and for 29 which there are a few newly available epidemiol ogical studies indicating blood Pb associations 30 with effects in study groups with somewhat lower blood Pb levels than previously available for 31 these effects include effects on development (delayed puberty onset) and reproduction (male 32 reproductive function) and on the cardiovascular system (hypertension) (ISA, sections 5.4 and 33 5.8; 2006 CD, sections 6.5 and 6.6). With regard to the former category, study groups in the 34 newly available studies include groups comprised of older child ren ranging up to age 18 years, 35 for which there is increased uncertainty regardin g historical exposures and their role in the 36January 2013 3-24 Draft - Do Not Quote or Cite observed effects. 21 An additional factor that handicaps our consideration of exposure levels 1 associated with these findings is the appreciabl e uncertainty associated with our understanding of 2 Pb biokinetics during this lifestage (ISA, secti ons 4.3, 5.8.6). The evidence newly available for 3 Pb relationships with cardiovascular effects in a dults include some studies with somewhat lower 4
blood Pb levels than in the last review. The l ong exposure histories of these cohorts, as well as 5 the generally higher Pb exposures of the past co mplicate conclusions regarding exposure levels 6 that may be eliciting observed e ffects (ISA, sections 5.4.2.4 and 5.4.7). 22 7 In summary, our conclusions regarding exposure levels at which Pb health effects occur, 8 and particularly with regard to such levels that might be common in the U.S. today, are 9 complicated now, as in the last review, by several factors. These factors include the scarcity of 10 information in epidemiological studies on cohort exposure histories, as well as by the backdrop 11 of higher past exposure levels which frame the hi story of some study cohorts. Recognizing the 12 complexity, as well as the potenti al role of higher exposure levels in the past, we continue to 13 focus our consideration of this question on th e evidence of effects in young children for which 14 our understanding of exposure hi story is less uncertain. 23 Within this evidence base, we 15 recognize the lowest study group blood Pb levels to be associated with effects on cognitive 16 function measures, indicating that to be the most sensitive en dpoint. As described above, and 17 summarized in Table 3-2, the evidence available in this review is generally consistent with that 18 available in the last review with regard to blood Pb levels at which such effects had been 19 reported (ISA, section 5.3.2; 2006 CD, section 8.4.2.1; 73 FR 66976-66979). As blood Pb levels 20 are a reflection of exposure hi story, particularly in early childhood (ISA, section 4.3.2), we 21 conclude, by extension, that the currently available evidence does not indicate Pb effects at 22 exposure levels appreciably lower than recognized in the last review. 23 We additionally note that, as in the last re view, a threshold blood Pb level with which 24 nervous system effects, and specifically neur odevelopmental effects, occur in young children 25 cannot be discerned from the currently ava ilable studies (ISA, s ections 2.9.4 and 5.3.13). 26 Epidemiological analyses have reported blood Pb associations with neurocognitive effects (FSIQ 27
or BSID MDI 24 ) in young child population subgroups, wh ich included individual blood Pb 28

21 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 5.8.6).
22 Studies from the late 1960s and 1970s suggest that adult blood Pb levels during that period ranged from roughly 10 to 30 μ g/m3 (ISA, section 5.4.1).
23 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 5.3, 5.4, 5.5, 5.6, 5.7, 5.8).
24 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 5.3.16.1).January 2013 3-25 Draft - Do Not Quote or Cite measurements as low as approximately 1 μg/dL and mean concentrations as low as 2.9 to 3.8 1 μg/dL (ISA, section 5.3.13; Bellinger and Need leman, 2003; Bellinger, 2008; Canfield el al., 2 2003; Canfield, 2008; Tellez-Rojo et al., 2006; Telle z-Rojo et al., 2008). As concluded in the 3 ISA, however, “the current evidence does not preclude the possibility of a threshold for 4 neurodevelopmental effects in ch ildren existing with lower blood levels than those currently 5 examined” (ISA, section 5.3.13). 6 Important uncertainties associated with the ev idence of effects at low exposure levels are 7 similar to those recognized in the last review, incl uding the shape of the concentration-response 8 relationship for effects on neurocognitive function at low blood Pb levels in today’s young 9 children. Also of note is our interpretation of a ssociations between blood Pb levels and effects in 10 epidemiological studies, with wh ich we recognize uncertainty w ith regard to the specific 11 exposure circumstances (timing, duration, magnitude and frequency) that have elicited the 12 observed effects, as well as uncertainties in re lating ambient air concentrations (and associated 13 air-related exposures) to blood Pb levels in early childhood, as discussed in section 3.1 above. 14 We additionally recognize uncertainties associated with conclusions drawn with regard to the 15 nature of the epidemiological associations w ith blood Pb (e.g., ISA, s ection 5.3.14), but note that 16
based on consideration of the full body of evidence for neurocognitive effects, the EPA has 17 determined a causal relationship to exist between relevant blood Pb levels and neurocognitive 18 impacts in children (ISA, section 5.3.16.1). 19

 To what extent does the newly available evidence alter our understanding of the 20 concentration-response relationship for neur ocognitive effects (IQ) with blood Pb 21 levels in young children? 22 Based primarily on studies of FSIQ, the assessm ent of the currently available studies, as 23 was the case in the last review, continues to recognize a nonlinear rela tionship between blood Pb 24 and effects on cognitive function, with a greater incremental effect (greater slope) at lower 25 relative to higher blood Pb levels within the range thus far stud ied, extending from well above 10 26 μg/dL to below 5 μg/dL (ISA, section 5.3.13). Th is was supported by the evidence available in 27 the last review, including the an alysis of the large pooled inte rnational dataset comprised of 28 blood Pb measurements concurrent with the IQ te sts that ranged from 2.5 μg/dL to 33.2 μg/dL 29 (Lanphear et al., 2005; Rothenberg and Rothe nberg, 2005; ISA, section 5.3.13). The study by 30 Lanphear et al (2005) additionally presented anal yses that stratified the dataset based on peak 31 blood Pb levels (e.g., with cutpoints of 7.5 μg/d L and 10 μg/dL peak blood Pb) and found that 32
the coefficients from linear models of the asso ciation for IQ with concurrent blood Pb were 33 higher in the lower peak blood Pb level subset s than the higher groups (ISA, section 5.3.13; 34 Lanphear et al., 2005). Stratified analyses of se veral individual cohorts also observed higher 35 coefficients for blood Pb relationships with m easures of neurocognitive function in lower as 36January 2013 3-26 Draft - Do Not Quote or Cite compared to higher blood Pb subgroups (ISA, se ction 5.3.13; Canfield et al., 2003; Bellinger and 1 Needleman, 2003; Kordas et al., 2006; Tellez-Rojo et al., 2006). Of these subgroup analyses, 2 those involving the lowest mean blood Pb levels and closest to the cu rrent mean for U.S. 3 preschool children are listed in Table 3-3 below (drawn from Table 3 of the 2008 final 4 rulemaking notice [73 FR 67003]). These analys es were important inputs for the evidence5 based, air-related IQ loss framework which informed decisions on a revised standard in the last 6 review (73 FR 67005), discussed in section 4.1.1 below. 7

Table 3-3. Summary of quantitative relationships of IQ and blood Pb for analyses with 8 blood Pb levels closest to those of young children in the U.S. today. 9

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 3.24 0.9 – 7.4 Lanphear et al (2005) C , subgroup with peak blood Pb <7.5 μ g/dL -2.94 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 to7 years.
10 Several studies newly available in the current review have, in all but one instance, also 11 found a nonlinear blood Pb-cognitive function relati onship in nonparametric regression analyses 12 of the cohort blood Pb levels analyzed (ISA, section 5.3.13). These studies, however, used 13 statistical approaches that did not produce qua ntitative results for each blood Pb group (ISA, 14 section 5.3.13). Thus, newly available studies ha ve not extended the range of observation for 15 quantitative estimates of this relationship to lo wer blood Pb levels than those of the previous 16 review. The ISA further notes that the potential for nonlinearity has not been examined in detail 17 within a lower more narrow range of blood Pb le vels than those of th e full cohorts thus far 18 studied in the currently availabl e evidence base (ISA, section 5.3.13) . Such an observation in the 19 last review supported the consider ation of linear slopes with regard to blood Pb levels at and 20 below those represented in Table 3-3. In summary, the newly available evidence does not 21 substantively alter our unders tanding of the concentration -response relationship (including 22 quantitative aspects) for neurocognitive impact , such as IQ with blood Pb in young children. 23January 2013 3-27 Draft - Do Not Quote or Cite 3.3 PUBLIC HEALTH IMPLICATIONS AND AT-RISK POPULATIONS 1 There are several potential publ ic health impacts associated with Pb exposure. In 2 recognition of effects causally related to blood Pb levels somewhat near those most recently 3 reported for today’s population and for which the wei ght of the evidence is greatest, the potential 4 public health impacts most prominently rec ognized in the ISA are population IQ impacts 5 associated with childhood Pb exposure and preval ence of cardiovascular e ffects in adults (ISA, 6 section 2.9.1). With regard to the latter category, as discussed above, the full body of evidence 7 indicates a role of long-term cumulative exposur e, with uncertainty re garding the specific 8 exposure circumstances contributing to the effect s in the epidemiological studies which focused 9 largely on adult populations for whom historical Pb exposures were likely much higher than 10 exposures that commonly occur today (ISA, secti on 5.4). There is less un certainty regarding the 11 exposure patterns contributing to the blood Pb levels reported in studies of younger populations 12 (ISA, section 2.10). Accordingly, we focus the disc ussion of public health implications relevant 13 to this review predominantly on nervous system effects, including IQ de crements, in children. 14 We focus this discussion on IQ in recogniti on of IQ being a well established, widely 15 recognized and rigorously standardized measure of neurocognitive function, as well as a global 16 measure reflecting the integrati on of numerous processes (ISA, section 5.3.2; 2006 CD, sections 17 6.2.2 and 8.4.2). We recognize, however, that IQ is one of several measures of cognitive 18 function negatively associated with Pb exposur e. Other examples include other tests of 19 intelligence and cognitive development, and tests of other cognitive abilities, such as learning, 20 memory, and executive functions, as well as academic performance and achievement (ISA, 21 section 5.3.2). In consid ering the public health significance of neurocognitive effects of Pb in 22 children, we recognize that, althoug h some may be transient, so me effects may persist into 23 adulthood (ISA, section 2.9.5). 25 We also note that deficits in neurodevelopment early in life 24 may have lifetime consequences as “[n]eurodeve lopmental deficits meas ured in childhood may 25 set affected children on trajectories more pr one toward lower educational attainment and 26 financial well-being” (ISA, section 5. 3.15). Thus, population groups for which 27 neurodevelopment is affected by Pb exposure in early childhood are at risk of related impacts on 28
their success later in life. 29 There are important distinctions between popul ation and individual risk such that “small 30 shifts in population means are of ten significant from a public hea lth perspective” (ISA, p. 2-63). 31 For example, if lead-related decrements are mani fested uniformly across the range of IQ scores 32

25 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, section 2.9.5; Bellinger et al., 1990).January 2013 3-28 Draft - Do Not Quote or Cite in a population, “a small shift in th e population mean IQ may result in a substantial increase in 1 the number of individuals functioning in the low ra nge of the IQ distributi on, which is associated 2 with increased risk of educational, vocational, an d social failure” as well as a decrease in the size 3 of the subgroup achieving very high scores (ISA, section 2.9.1). 4 In the discussion below, we use the term at -risk populations to r ecognize populations that 5 have a greater likelihood of experiencing lead -related health effects, i.e., groups with 6
characteristics that contribute to an increased risk of Pb-related h ealth effects. These populations 7 are also sometimes referred to as sensitive groups, as in section 1.2.1 above. This increased 8
likelihood of lead-related effects can result from many factors, incl uding lifestage or age, gender, 9 race or ethnicity, diet, pre-existing disease stat e, or increased exposure (ISA, chapter 6). 10 Accordingly, in identifying factors that increase risk of lead-related health effects, there has been 11 consideration of evidence rega rding factors contributing to in creased susceptibility (i.e., 12 physiological or intrinsic factor s contributing to a greater resp onse for the same exposure), and 13 those contributing to increased exposure (inclu ding that resulting from behavior leading to 14 increased contact with contaminated media). As noted in the ISA, “definitions of susceptibility 15 and vulnerability vary across studies, but in most instances ‘susceptibility’ refers to biological or 16 intrinsic factors (e.g., age, sex) while ‘vulnerabi lity’ refers to nonbiologica l or extrinsic factors 17 (e.g., socioeconomic status [SES])” and the terms “at-risk” and “sensitive” populations have in 18 various instances been used to encompass these concepts more generally (ISA, p. 6-1). Although 19 we emphasize the term “at-risk”, we rely on the othe r terms in particular instances below; in so 20 doing, our usage is consistent with these definitions. 21
Factors that increase risk of lead-related effects include , among others, behavioral 22 physiological factors. A behavior al factor of great impact on Pb exposure is the incidence of 23 hand-to-mouth activity that is prevalent in very young children and by which they transfer Pb in 24 settled particles to their mouths (ISA, secti ons 4.7.1 and 6.2.1.1). Physiol ogical factors include 25 both conditions contributing to a gr oup’s increased risk of effects at a given blood Pb level, and 26
those that contribute to blood Pb levels higher than those otherw ise associated with a given Pb 27 exposure (ISA, sections 6.3 and 6.1, respectively). We also considered evidence encompassing 28 situations of elevated exposure, such as residi ng in old housing with Pb-containing paint or near 29 sources of ambient Pb, as well as socioeconomic f actors, such as reduced access to health care or 30 low socioeconomic status (SES) that can contribute to increased risk of adverse health effects 31 from Pb (ISA, sections 2.9.7, 6.2, and 6.4). 32
33January 2013 3-29 Draft - Do Not Quote or Cite  Has new information altered our understanding of human populations that are 1 particularly at risk of health effects from Pb exposures? 2 The information newly available in this review has not substa ntially altered our 3 understanding of at-risk populations . As in the last review, the factor most prominently 4 recognized to contribute to increas ed risk of Pb effects is age (ISA, section 2.9.7). As noted in 5 section 3.2 above, although the specific ages or life stages of greatest susceptibility have not been 6 established (e.g., ISA, section 5.3.12), the susceptibility of young children to the 7 neurodevelopmental effects of Pb is we ll recognized (e.g., ISA, sections 2.9.7, 5.3, 6.2.1, 6.3.1, 8 and 6.4). The evidence indicates that prenatal blood Pb levels are causally associated with 9 nervous system effects, including mental deve lopment in very young children and can also be 10 associated with cognitive decrements in older children (ISA, section 5.3). The coincidence 11 during early childhood of behavior s that increase exposure, such as hand-to-mouth contact, and 12 the development of the nervous system contributes increased risk during this time (ISA, sections 13 5.3.2.6, 6.2.1.1, and 6.3.1.1). The evidence also indicates a causal relationship of postnatal blood 14 Pb levels (through early childhood to school age) with cognitive function decrement in older 15 children and adolescence (ISA, section 5.3). In ep idemiological studies, associations have been 16 observed of neurocognitive, and some other nervous system effects, at various ages from early 17 childhood to school age with prenatal, early-ch ildhood, lifetime average, and concurrent blood 18
Pb levels as well as with childhood tooth Pb levels (ISA, section 5.3). Consideration of 19 epidemiological study results for different lifestages of exposure, particularly later in childhood, 20 is complicated by the fact that blood Pb leve ls in children, although highly affected by recent 21 exposure, are also influenced by their history of Pb exposure due to rapid growth-related bone 22 turnover in children (ISA, section 4.3.5). Thus, bl ood Pb level in children also may reflect past 23 Pb exposures and, to some extent, maternal Pb, w ith relative contributions varying with child and 24 maternal exposure history (ISA, sect ion 4.2.2.4, 4.4.1 and 5.3.16; 2006 CD, section 6.6.2). 25 Collectively, however, the evidence indicates both the susceptibility of the developing fetus and 26 early postnatal years, as well as the potentia l for continued susceptib ility through childhood as 27 the human central nervous system continues to ma ture and be vulnerable to neurotoxicants (ISA, 28 sections 2.9.5 and 5.3.16; 2006 CD, section 6.2.12). 29 In the collective body of eviden ce of nervous system effects in children, it is difficult to 30 distinguish exposure in later lifes tages (e.g., school age), and its as sociated risk, from prenatal 31 and early childhood (ISA, section 5.3.12). While early childhood is reco gnized as a time of 32 increased susceptibility, a difficu lty in identifying a discrete period of susceptibility from 33 epidemiological studies has been that the period of peak exposur e, reflected in peak blood Pb 34 levels, is around 18-27 months when hand-to-mout h activity is at its maximum (ISA, section 35 4.4.1 and 6.2.1.1; 2006 CD, p. 6-60). The task is additionally complicated by the role of 36January 2013 3-30 Draft - Do Not Quote or Cite maternal exposure history in contributing Pb to the developing fetus (ISA, section 4.2.2.4.). 1 Epidemiological analyses evaluating risk of ne urocognitive impacts (e.g., reduced IQ) associated 2
with different blood Pb metrics in cohorts with differing exposure patterns (including those for 3
which blood Pb levels at differe nt ages were not highly correlate d) indicate associations with 4 blood Pb measurements concurrent with FSIQ tests at ages of approximate ly 6-7 years, although 5 the analyses did not conclusive ly demonstrate stronger findings for early (e.g., age 2 years) or 6 concurrent blood Pb (ISA, section 5.3.12). The experimental animal evidence additionally 7 indicates early life susceptibility (ISA, section 5. 3.16). Thus, the full evid ence base continues to 8 indicate prenatal and early chil dhood lifestages as periods of in creased lead-related risk. In 9 summary, while uncertainties remain with regard to the role of Pb exposures during a particular 10 age of life in eliciti ng nervous system effects, such as cognitive function decrements, the 11
evidence continues to in dicate the at-risk status of pre- and postnatal childhood lifestages (ISA, 12 sections 5.3.12 and 5.3.16). 13 Several physiological factors incr ease risk of lead-related hea lth effects by contributing to 14
increased blood Pb levels over those otherwise associated with a given Pb exposure (ISA, 15 sections 4.2, 4.3 and 6.1). These include nutritiona l status, which plays a role in Pb absorption 16 from the GI tract (ISA, section 4.2.1.2). For exampl e, diets deficient in ir on, calcium or zinc can 17 contribute to increased Pb absorption and asso ciated higher blood Pb levels (ISA, sections 18 4.2.1.2, and 6.1). Evidence is suggestive of some gene tic characteristics as potential risk factors, 19 such as presence of the δ -aminolevulinic acid dehydratase-2 (ALAD-2) allele which has been 20
indicated to increase blood Pb levels and or lead-related risk (ISA, sections 4.3.2 and 6.1). 21 Risk factors based on increased exposure in clude spending time in proximity to sources 22
of Pb to ambient air or other environmenta l media (e.g., large active metals industries or 23 locations of historical Pb contamination) (ISA, section 2.9.7, 6.2.5). Residential factors 24 associated with other sources of Pb exposure (e .g., leaded paint or plumbing with Pb pipes or 25 solder) are another exposure-r elated risk factor (ISA, s ection 2.9.7, 6.2.6). The role of 26 socioeconomic status (SES) with regard to lead-r elated risk is somewhat complicated. SES often 27
serves as a marker term for one or a combin ation of unspecified or unknown environmental or 28
behavioral variables. Lower SES has been asso ciated with higher Pb exposure and higher blood 29 Pb concentration (ISA, sections 5.3.16, 6.2.4 and 6.4) . Further, it is independently associated 30 with an adverse impact on neurocognitive development and a few studies have examined SES as 31 a potential modifier of the a ssociation of childhood Pb exposure with cognitive function with 32 inconsistent findings regarding lo w SES as a potential risk factor. Although the differences in 33 blood Pb levels among children of lower as compar ed to higher income levels have lessened, 34 blood Pb levels continue to be higher among lo wer income children indicating higher exposure 35January 2013 3-31 Draft - Do Not Quote or Cite and/or greater influence of fact ors independent of exposure, su ch as nutritional factors (ISA, 1 sections 2.9.7, 6.2.1.1 and 6.4). 2 In considering risk factors associated with increased Pb exposure or increased blood Pb 3 levels, we note that the currently available ev idence continues to support a nonlinear relationship 4 between neurocognitive effects and blood Pb that indicates incrementally greater impacts at 5 lower as compared to higher blood Pb levels (IS A, section 5.3.13), as described in section 3.2 6 above. An important implication of this findi ng is that while children with higher blood Pb 7 levels are at greater risk of lead-related effects than children with lower blood Pb levels, on an 8 incremental basis (e.g., per μg/dL), the risk is greater for children at lower blood Pb levels. This 9 was given particular attention in the last review of the Pb NAAQS, in which the standard was 10
revised with consideration of the incremental impact of air-related Pb on young children in the 11 U.S and the recognition of greater impact for those children with lower absolute blood Pb levels 12 (73 FR 67002). Such consideration included a fo cus on those C-R studies involving the lowest 13 blood Pb levels, as described in section 4.1.1 below. 14 Some racial or ethnic backgr ounds have been identified as fa ctors that may increase risk 15 of lead-related health effects (ISA, secti ons 2.9.7, 6.2.3 and 6.3.7). For example, although blood 16 Pb levels in the U.S. general population (e.g., geom etric mean level in children aged 1-5) have 17 declined, mean levels reported in recent NHANE S samples continue to differ among children of 18 different ethnic backgrounds, w ith higher levels in non-white pe rsons as compared to whites 19 (ISA, sections 4.4.1, 6.2.1.1 and 6.2.3). Additionally, a study of lead-related risk of hypertension 20 among adults reported greater risk associated with blood Pb levels above 1 μg/dL among 21 Mexican Americans and non-Hispanic blacks th an among non-Hispanic whites (ISA, section 22 6.3.7; Muntner et al., 2005). The ev idence available in the current review, consis tent with that in 23 the last, also suggests that health status or pre-existing disease is potentially a phys iological risk 24
factor for lead-related effects (ISA, section 2.9.7). Populations with pre-existing health 25 conditions, such as hypertension, may be more susceptible (as compared to the general 26 population) for particular Pb-associ ated effects (ISA, section 6.3.4). For example, increased risk 27
of lead-related renal effects and heart rate va riability have been reported among hypertensive 28 individuals compared to those that are normote nsive (ISA, section 2.9.7). Additionally, African 29 Americans, as a group, have a higher frequency of hypertension than the general population or 30 other ethnic groups (NCHS, 2011), and as a result may face a greater risk of adverse health 31 impact from Pb-associated cardiovascular effects. 32
Older adulthood has been identified as a life stage of potentially gr eater risk of lead33 related health effects based primarily on the eviden ce of increases in blood Pb levels during this 34 lifestage, and of potential for effects, su ch as (ISA, sections 6.2.1.2, 6.3.1.2, and 6.4). 35 Contributing to blood Pb levels in the studied populations of older adults are likely to be their 36January 2013 3-32 Draft - Do Not Quote or Cite exposure histories, which included younger years during the time of leaded gasoline usage and 1 other sources of Pb exposures which were more prevalent in the past than today (e.g., ISA, 2 Figure 3-1 and section 3.4.3.2). Exposure history has a contributing role to blood Pb levels 3 throughout life, and the increased rate of bone remodeling during late r adulthood increases 4
contributions of Pb from bone stores into the systemic circulation during that lifestage (ISA, 5 sections 4.3.5 and 6.2.1.2). Additionally, limited an imal evidence has indicated specific brain 6 pathology in older animals that had substantial Pb exposures ear lier in life (ISA, sections 7 5.3.10.1 and 6.3.1). Further, the full body of eviden ce includes observed associations of various 8 health effects, such cardiovascular and neurol ogical effects with bone and blood Pb in older 9 populations, with biological plausibility for th e role of Pb provided by experimental animal 10 studies (ISA, sections 5.3.6, 5.3.8, 5.3.10 and 5.4). 11 In summary, the information newly available in this review has not appreciably altered 12 our understanding of human populations that are part icularly sensitive to Pb exposures. In the 13 current review, as at the time of the last re view of the Pb NAAQS, we recognize young children 14 as an important at-risk populat ion, with sensitivity extending to prenatal exposures and into 15 childhood development. Additional risk factors in clude deficiencies in dietary minerals (iron, 16 calcium and zinc), some racial or ethnic b ackgrounds, and spending ti me in proximity to 17 environmental sources of Pb or residing in ol der houses. The evidence for SES continues to 18
indicate increased blood Pb levels in lower income children, although its role with regard to an 19
increased risk for same blood Pb level is unclear . Additionally, the curren tly available evidence 20 continues to indicate a potential for increased risk associated with several other factors, including 21 older adulthood, pre-existing di sease (e.g., hypertension), varian ts for certain genes and 22
increased stress. 23

 Is there new evidence on health effect s beyond neurocognitive endpoints in 24 children that suggest additional at-ris k populations should be given increased 25 focus in this review? 26 The evidence newly available in this revi ew supports or strengthens our previous 27 conclusions regarding the broad array of health effects of Pb (see ISA, section 2.10 which 28 compares key conclusions drawn in the last re view with conclusions drawn in the current 29 assessment). Additionally, in some categories of health effects, the newly available studies 30 extend the evidence for some aspects of the health effects described in the last review. For 31 example, among the nervous system effects, th e newly available eviden ce continues to support 32 the conclusions from the last review regard ing Pb and neurocognitive and neurobehavioral 33 effects (ISA, section 5.3). Across the array of neurocognitive and beha vioral effects, we 34 recognize the sensitivity of the prenatal period and se veral lifestages of childhood, and 35January 2013 3-33 Draft - Do Not Quote or Cite particularly recognize young child ren as an important at-risk population in light of current 1 environmental exposure levels. 2 As discussed in section 3.2 above, the blood Pb levels of populations studied in newly 3 available epidemiological studies that report associations of bl ood Pb with effects for systems 4 and processes other than the nervous syst em (e.g., cardiovascular, developmental and 5 reproductive) are similar, or in a few cases, so mewhat lower than those assessed in the last 6 review (ISA, sections 5.4, 5.6, 5.7, and 5.8). Th e greater uncertainties regarding the time, 7 duration and magnitude of expos ure contributing to these obser ved health effects complicate 8 identification of sensitive lifestages and associat ed exposure patterns that might be compared 9 with our understanding of the sensitivity of young children to neurocognitive impacts of Pb. 10 Thus, while augmenting the evidence base on th ese additional endpoints, the newly available 11 evidence does not lead us to identify a health en dpoint expected to be more sensitive to Pb 12 exposure than neurocognitive endpoints in children, l eading us to continue to conclude that the 13 appropriate primary focus for our review is on neurocognitive e ndpoints in children. 14 In summary, there are a vari ety of ways in which lead-exposed populations might be 15
characterized and stratified for cons ideration of public health impact s. Age or lifestage was used 16 to distinguish potential groups on which to focus in the last review in re cognition of its role in 17 exposure and susceptibility, and young children were selected as the priority population for the 18 risk assessment (see section 3.4 below) in consider ation of the health eff ects evidence regarding 19 endpoints of greatest public hea lth concern and in recognition of effects on the developing 20 nervous system as a sentinel endpoint for public health impacts of P b. This identification 21 continues to be supported by the eviden ce available in th e current review. 22

 What does the information about air Pb concentrations available in this review 23 indicate with regard to the size of a t-risk populations and their distribution 24 across the U.S.? 25 The magnitude of a public health impact is dependent upon the size of populations 26 affected, as well as type or se verity of the effect. As summarized above, the population group 27 that may be most at risk of health effects asso ciated with exposure to Pb is young children. The 28 2010 census indicates nearly 310 million people residing in the U.S., 74 million of which 29 approximately are children under the age of 18, with some 20 million under the age of five years. 30 Children at greatest risk from air-related Pb are cons idered to be those children living in areas of 31 higher air Pb exposures. Accordingly, the discus sion below considers the information available 32 to inform our understanding of areas of childre n potentially at risk from air-related Pb. 33 In considering the extent of this at-risk populat ion, we turn first to consideration of those 34
areas in the U.S. with air Pb concentrations above the current sta ndard (e.g., section 2.2.2.2 35 above). Using the available monitoring data a nd U.S. census information, Table 3-4 summarizes 36January 2013 3-34 Draft - Do Not Quote or Cite the size of populations within 0.5 km of monitors in our current Pb NAAQS surveillance 1 network at which Pb concentrations were highe r than the current standard during the recent 2 period from 2009-2011. The distance to which co ncentrations exceeding the standard might 3 extend will vary with the magnitude of the Pb concentrations and particle size, among other 4 factors; a half kilometer distance was selected for purposes of illustration here. This analysis 5 indicates approximately 2,400 childre n aged 5 or under to reside within 0.5 km of monitors 6 exceeding the current standard. To also account for the population in areas with air 7 concentrations just at (or very near) the curren t standard, we have also identified an additional 8 nine Pb-TSP monitors with 3-month average concen trations within 10% of the current standard 9 (Appendix 2D). Based on the 2010 U.S. census, 265 children aged 5 or under reside within 0.5 10
km of these additional sites. 11

Table 3-4. Number of children aged 5 and under in areas of elevated ambient Pb 12 concentrations relative to the NAAQS. 13

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; recent Pb-TSP dataset presented in Figure 2-10 above (dataset criteria and summaries included Appendices 2C and 2D, respectively). 14 As the current air quality da ta set (analyzed in section 2.2.2 above) may not be inclusive 15 of all of the newly sited monito rs, as discussed in section 2.2.1 above, we recognize there may be 16 other areas of the country where concentrations are above or just meet the current standard but 17 for which such data are not yet available. To co nsider the potential for ther e to be additional, not 18 yet identified, areas with elevated Pb concentra tions, we have separately quantified the size of 19 young child populations residing in ar eas near large Pb sources in Table 3-5. In so doing, we 20 recognize uncertainties and potenti al limitations associated with these emissions estimates for 21 these purposes, uncertainties both with regard to the accuracy of such estimates and also with 22 regard to the role of specific source charac teristics and meteorology, not explicitly considered 23 here, in influencing ambient air Pb concentrations and contributing to substantial variation in air 24 Pb concentrations at source locations (e.g., Figur e 2-11 above). Accordi ngly, while the summary 25 in Table 3-5 is informative to considering the pot ential prevalence of airb orne Pb emissions and 26 potential exposure of human populations, it is lim ited with regard to its ability to identify 27January 2013 3-35 Draft - Do Not Quote or Cite populations living in areas of elevat ed ambient air Pb concentrations . We interpret this analysis 1 to indicate that fewer than about 7,800 young child ren (aged 5 or younger) live in areas with air 2
Pb concentrations near or above the current standard, with the current mon itoring data indicating 3 the size of this population to be approximately 2,700. 4

Table 3-5. Population size near larger sources of lead emissions. 5

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/n et/2008neiv2/2 008_neiv2_ts d_draft.pdf. 6
7January 2013 3-36 Draft - Do Not Quote or Cite 3.4 EXPOSURE AND RISK 1
This risk information available for this revi ew and described here is based primarily on 2 the exposure and risk assessment developed in th e last review of the Pb NAAQS (henceforth 3 referred to as the 2007 REA [USEPA, 2007a]), in the context of the evidence newly available in 4 this review, as presented in the ISA. As de scribed in the REA Planning Document, careful 5
consideration of the information newly available in this review , with regard to designing and 6 implementing a full REA for this review, led us to conclude that performance of a new REA for 7
the review was not warranted. We did not find the information newl y available in this review to 8 provide the means by which to develop an upda ted or enhanced risk model that would 9 substantially improve the utility of risk estimat es in informing the current Pb NAAQS review 10 (REA Planning Document, section 2.3). Based on their consideration of the REA Planning 11 Document analysis, the CASAC Pb Review Panel generally concur red with the conclusion that a 12
new REA was not warranted in this review (Frey, 2011). 26 Accordingly, the information 13 described here is drawn primarily from the 2007 REA, augmented by a limited new case study14 specific analysis focused on risk associated with the current standard, as described in section 15
3.4.3.3 below. 16 The focus for the risk assessment and associated estimates presented here is on Pb 17 derived from sources emitting Pb to ambient air. As discussed in section 1.3 above (and 18 conceptually illustrated in Figure 1-1), the multimedia and persistent nature of Pb, the role of 19 multiple exposure pathways, and the contributions of nonair sources of Pb to human exposure 20 media all present challenges and co ntribute significant additional complexity to the health risk 21 assessment that goes far beyond the situation for similar assessments typically performed for 22 other NAAQS pollutants (e.g., that focus only on th e inhalation pathway). Limitations in the 23
available data and models affected our character ization of the various complexities associated 24 with exposure to ambient air Pb. As a result , the assessment includes a number of simplifying 25 assumptions in a number of areas and, as descri bed in section 3.4.4 below, our estimates of air26 related Pb risk are approximate and ar e characterized by upper and lower bounds. 27 The conceptual model developed to in form planning for the 2007 REA, including 28 identification of key exposure media, target population, health endpoint and risk metric is 29
described in section 3.4.1. The 2007 REA relied on a case study approach to provide estimates 30 that inform our understanding of air-related exposure and risk in different types of air Pb 31 exposure situations; the case stud ies included are described in s ection 3.4.2. In section 3.4.3, the 32

26 In our evaluation presented in the REA Planning Document and consultation with CASAC, we indicated our conclusion that the information newly available in this review did not provide the means by which to develop an updated or enhanced risk model that would substantially improve the utility of risk estimates in informing the current Pb NAAQS review.January 2013 3-37 Draft - Do Not Quote or Cite analysis approach and general aspects of expos ure and risk assessment methods are summarized, 1 and the air quality scenarios simulated are desc ribed. In section 3.4.3, we also summarize the 2 2007 REA risk model and the interpolation approach used in the limited new analyses performed 3 for purposes of this review. Section 3.4.4 identifi es key aspects in exposure assessment and risk 4 estimates are presented in section 3.4.5. Treatment of key sources of vari ability in exposure and 5
risk estimates is described in section 3.4.6 and the characterizati on of uncertainty is summarized 6 in 3.4.7. An updated interpretation of the risk estimates for our purposes in this Pb NAAQS 7 review section is presented in section 3.4.8. 8

3.4.1 Conceptual Model for Air-Rela ted Lead Exposure and Risk 9 The focus in consideration of public health ri sks associated with Pb from ambient air is 10 on Pb derived from those sources emitting Pb to ambient air. The multimedia and persistent 11 nature of Pb, illustrated in Figure 1-1 above, as well as the existence of many nonair sources of 12 Pb to the environment, contribute multiple comple xities to the consideration of exposure and risk 13 for ambient air-related Pb. The conceptual model that informed planning for the 2007 REA 14 identified sources, pathways, routes, exposed populations, and health endpoints, focusing on 15 those aspects of Pb exposure most relevant to th e review, while also recognizing the role of Pb 16 exposure pathways unrelated to Pb in ambient air (2007 REA, section 2.1). 17 As recognized in section 1.3 above, sources of human Pb exposure include current and 18 historical air emissions sources, as well as mis cellaneous nonair sources, wh ich can contribute to 19 multiple exposure media and associated pathways (e.g., inhalation of ambi ent air, ingestion of 20 indoor dust, outdoor soil/dust and diet or drinking water). 27 Figure 3-2 illust rates these human 21 exposure pathways from an analytical perspec tive, drawing on the conceptual model for the 22 assessment (2007 REA, Figure 2-1). As shown in Figure 3-2, in addition to airborne emissions 23 (recent or those in the past), so urces of Pb to these pathways also include old leaded paint, 24 including Pb mobilized indoors dur ing renovation/repair activities, and contaminated soils. Lead 25 in diet and drinking water may have air pathway related contributions as well as contributions 26 from nonair sources (e.g., Pb solder on water dist ribution pipes and Pb in materials used in food 27 processing). Limitations in our data and modeling tools handicappe d our ability to separate the 28 nonair contributions to Pb exposure from estim ates of air-related Pb exposure and risk. 28 29
30

27 We did not explicitly consider Pb exposure related to consumer products (e.g., toys, cosmetics, dishes) in the 2007 REA.
28 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.January 2013 3-38 Draft - Do Not Quote or Cite 1

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

Identification of exposure populations, exposur e/dose metric, health effects endpoint and 3
risk metric to be included in the 2007 REA we re based on consideration of the then-currently 4
available evidence as assessed in detail in th e 2006 CD. As discussed in the REA Planning 5 Document (USEPA, 2011), these selections continue to be supported by the evidence now 6
available in this review as described in the ISA. 7 In the REA, we focused on IQ loss in childre n exposed up to age 7 years. This focus 8 reflected the evidence for young children with re gard to air-related exposure pathways and 9 susceptibility to Pb health impacts (e .g., ISA, sections 4.1.1, 5.3, 6.2.1, 6.3.1, and 6.4). For 10 example, the hand-to-mouth activity of young child ren contributes to their Pb exposure (i.e., 11
incidental soil and indoor dust ingestion) and ambient air-related Pb has been shown to 12
contribute to Pb in outdoor so il and indoor house dust. Accord ingly, the Agency maintains a 13 biokinetic blood Pb model for estimating blood Pb levels in young children (through age 7), 14
which was used in this risk assessment. 29 In addition, our focus on young children reflects the 15 evidence that the developing nervous system in children is among, if not, the most sensitive of 16 the endpoints associated with Pb expos ure (ISA, sections 2.6 and 2.10). 17 In terms of internal disposition and the biom etrics used to assess Pb exposure, blood Pb 18 (PbB) levels continue to be ex tensively used as an index or biomarker of exposure by national 19

29 The pathways represented in this modeling includei ng childhood inhalation and ingestion pathways, as well as maternal contributions to newborn body burden (2007 REA, Appendix H, Exhibit H-6). 

### Pb in ambient air

Indoor air

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

Paint Pb Historic Pb Deposition outdoors 

## (p )

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 

### *January 2013 3-39 Draft - Do Not Quote or Cite and international health agencies. This reflects the association of PbB with exposure, particularly 1 recent exposure in young children, and the relative ease of collecting PbB measurement. 2 Although bone Pb measurements have become easie r to collect and conseq uently, their use has 3 been more widespread, epidemiological and toxico logical studies of Pb health effects and dose4 response relationships (particula rly for neurodevelopmental effects in children) tend to be 5 dominated by PbB as the exposure metric. Th erefore, we focused on modeling PbB in young 6 children, developing estimates for two PbB metrics: “concurrent” and “lifetime average”. For 7 the former we estimated PbB at age 7 years, wh ile lifetime average was estimated as the average 8
of PbB levels across the 7 year period. 9 At the time of the last review, we noted th at limitations precluded prediction of changes 10 in adult PbB levels (or bone Pb levels) given cha nges in ambient Pb levels. This reflects the fact 11 that the presence of substantial hi storic Pb stores in most adults introduces uncertainty into the 12 prediction of changes in blood or bone Pb in th ese adult populations resu lting from changes in 13 ambient air Pb exposure. Additionally, in cons idering concentration-response relationships for 14 adult PbB and adult health outcomes, we recognized the uncertainty with regard to the role of 15 historic compared to recent exposures in eliciting the observed outcomes. 16 Based on conclusions regarding the scientific evidence available in the last review 17 (presented in the 2006 CD), the assessment focuse d on risk to the central nervous system in 18
childhood as the most sensitive effect that could be quantitatively assessed, with decrement in IQ 19
used as the risk metric. 20

3.4.2 Case Studies 21 Lead exposure and associated risk was estimat ed for multiple case studies that generally 22 represent two types of re sidential population exposures to ai r-related Pb (see Table 3-6): (1) 23 location-specific urban populati ons of children with a broad ra nge of air-related exposures, 24 reflecting existence of urban con centration gradients; and, (2) child ren residing in localized areas 25 with air-related exposures representing air con centrations specif ically reflecting the standard 26 level being evaluated. Thus, the two types of case studies differed with regard to the extent to 27 which they represented population variability in air-related Pb e xposure (as discussed further in 28 section 3.4.7 below). Three location-specific ur ban case studies focused on residential areas 29 within Cleveland, Chicago, and Los Angeles, pr oviding representations of urban populations 30 with a broad range of air-related exposures due to spatial gradient s in both ambient air Pb levels 31 and population density. For example, the highest ai r concentrations in these case studies (i.e., 32
those closest to the standard be ing assessed) were found in very small parts of the study areas, 33 while a large majority of the case study populati ons resided in areas with much lower air 34 concentrations. The case studies representing th e children most highly exposed via air-related 35January 2013 3-40 Draft - Do Not Quote or Cite pathways were the generalized (local ) urban case study (also referred to as general urban case 1 study ) and the primary Pb smelter case study subarea. The generalized (loc al) urban case study 2 was not based on a specific geographic location an d reflected several simplifying assumptions in 3 representing exposure incl uding uniform ambient air Pb levels associated with the standard of 4 interest across the hypot hetical study area and a uniform st udy population. The primary Pb 5 smelter case study provides risk estimates for children living in a specific area that, at the time of 6 the 2007 REA, was not meeting the then current NAAQS. In addition to characterizing risks 7
within a 10 km radius area surr ounding the smelter (fu ll area), we focused particularly on a 8
subarea within 1.5 km of the faci lity, where airborne Pb concen trations were closest to the 9
current standard and where child ren’s air-related exposures ar e most impacted by emissions 10
associated with the Pb smelter from which air Pb concentrations were estimated. Based on the 11 nature of the population exposures represen ted by the two categor ies of case study, the 12 generalized (local) urban and primary Pb smelte r case study subarea includ e populations that are 13 relatively more highly exposed by way of air pathwa ys to air Pb concentrations near the standard 14 level evaluated, compared with th e populations in the th ree cities or the fu ll area of the primary 15 smelter case study. 30,31 16

Table 3-6. Types of population exposures assessed. 17

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)

30 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).
31 In addition to the case studies included in the Risk Assessment Report, the pilot phase of the 2007 REA also included a near-roadway case study, focused on subset of urban population exposed immediately near roadways (ICF International, 2006). Based on the pilot results and advice from CASAC, however, this case study was not carried into the full-scale analysis. As an alternative, we developed the generalized (local) urban case study to represent urban residents in a localized area exposed to air-r elated Pb associated with the standard being assessed.January 2013 3-41 Draft - Do Not Quote or Cite 3.4.3 Analysis Approach 1 The approach to assessing exposure and risk for the two categories of case studies was 2 comprised of four main analytic al steps: (a) estimation of ambi ent air Pb concentrations, (b) 3 estimation of Pb concentrations in other key ex posure media, including outdoor soil and indoor 4 dust, (c) use of exposure media Pb concentrations, with other pathway Pb intake rates (e.g., diet), 5 to estimate PbB levels in children using biokinetic modeling, and (d) use of concentration6 response functions derived from epidemiology studi es to estimate IQ loss associated with the 7 PbB levels. In implementing these steps for the primary smelter case study, air concentrations 8 were estimated using dispersion modeling; indoo r dust concentrations were estimated for the 9 case study subarea using a site-spe cific regression model. The approach for the generalized 10 (local) urban case study and loca tion-specific urban case studies is somewhat simpler, since it 11 does not involve fate and transport modeling for air concentration estimates and, instead, uses 12
ambient monitor levels to charac terize the gradient in air Pb le vels across the study area. All 13 steps are somewhat simpler in the generalized (local) urban case study which includes a single 14 exposure zone. Figure 3-3 identifies the key inpu t data sets, modeling steps and intermediate 15 model output in each of the four analytical steps. The first three steps were employed in the 16 exposure assessment (discussed in section 3.4.3.1), wh ile the fourth is the risk assessment step 17 (discussed in section 3.4.3.3). 18January 2013 3-42 Draft - Do Not Quote or Cite 1 Drawn from 2007 REA, Figure 3-3 (USEPA, 2007). 2

Figure 3-3. Overview of analysis approach. 3 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 CHARACTERIZATIONJanuary 2013 3-43 Draft - Do Not Quote or Cite 3.4.3.1 Estimating Exposure 1
Concentrations of Pb were estimated in ambient media and indoor dust using a 2 combination of empirical data and modeling projectio ns. The use of empirica l data brings with it 3 uncertainty related to the potential inclusion of nonair source si gnals in these measurements (e.g., 4 house paint contributions to indoor dust and outdoor soil Pb). Conversely, the use of modeling 5
tools introduces other uncerta inties (e.g., model and parameter uncertainties). The 6 characterization of uncertainty a ssociated with the risk assessment is discussed in section 3.4.7. 7 Table 3-7 summarizes the exposur e modeling approaches and data used to characterize Pb 8 concentrations or input associated with each exposure pathway for each of the case studies. 9
Characterization of Pb in ambient air relied on (a) dispersion modeling of facility-related 10 (including fugitive) Pb emissions for the primar y Pb smelter case study, (b) the use of ambient 11 monitor data for the location-sp ecific urban case studies, and (c) an assumption of uniform 12 ambient air Pb levels (matching the standard le vel being considered) for the generalized (local) 13 urban case study. The use of dispersion modeling for the primary Pb smelter case study allowed 14 us to capture more spatially re fined patterns of ambient air Pb over residential areas in the 15 vicinity of the facility, where am bient Pb levels were dominated by Pb released from the facility. 16 For the location-specific urban case studies, we used Pb monito rs within each of the urban study 17 areas to characterize spatial grad ients. By contrast, the genera lized (local) urban case study is 18 designed to assess exposure a nd risk for a smaller group of residents (e.g., neighborhood) 19 exposed at the level of the standa rd and therefore, did not rely on monitor data in characterizing 20 levels, since ambient air Pb was fixed at the standard being assessed. While ambient air Pb 21 concentrations in the primary Pb smelter case st udy reflected only contributions from direct and 22 fugitive emissions associated with the facility, co ncentrations in the location-specific urban study 23 areas, which relied on empirical (monitor-based) da ta to define ambient air Pb concentrations, 24
reflected contributions from a ll contributing sources, be they currently active stationary or 25 mobile sources, resuspension of previously de posited Pb or other. Additional detail on 26 estimation of ambient (outdoor) and indoor air con centrations is presented in section 5.2.2 and 27 Appendices A through D of the 2007 REA. 28
Characterization of Pb concentrations in outdoor surface soil/dust, resulting from 29 deposition of airborne Pb was based on the us e of (a) existing site-specific measurements 30 (primary Pb smelter case study), and (b) nationall y representative resident ial soil measurements 31 obtained from the literature (general and location-sp ecific urban case studies). In the case of the 32 primary Pb smelter case study, soil Pb concentrati on data were available for a zone close to the 33 facility and statistical extrapolat ion from these data was used to predict soil levels for portions of 34 the study area beyond this zone. Additional detail on estimation of Pb concentrations in outdoor 35 surface soil or dust is presented in sec tions 3.1.3 and 5.2.2.2 and Appendix F of 2007 REA. 36January 2013 3-44 Draft - Do Not Quote or Cite To predict concentrations of ambient Pb in indoor dust, we relied on a combination of (a) 1 regression-based models that rela te indoor dust to outdoor air Pb and/or outdoor soil Pb and (b) 2 mechanistic models that predic t indoor dust Pb based on key mechanisms (e.g., infiltration of 3 outdoor air indoors, deposition rates of Pb from indoor air to indoor surfaces, house cleaning 4 rates). For the point source case study, a combin ation of regression-base d models obtained from 5 the literature and developed ba sed on site-specific data were used, and a customized hybrid 6 empirical-mechanistic model was developed for the general and location-specific urban case 7
studies. This reflected the fact that availabl e regression-based models had been developed 8 largely based on residential e xposures near large point sour ces and were not considered 9 representative of more genera l urban exposures. Consequently, a mechanistic model, augmented 10 with empirical data, was developed for the ge neralized (local) urban case study. Additional 11
detail on estimation of Pb concentrations in indoor dust is presente d in sections 3.1.4 and 5.2.2.2 12 and Appendix G of 2007 REA. 13

Table 3-7. Summary of approaches used to estima te case study media concentrations. 14

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

15 Blood Pb levels were predicted from estimat es of Pb contained in various media (e.g., 16 ambient air, diet, water, indoor dust), and estimates of Pb intake from dietary and drinking water 17 pathways, using the Integrated Exposure and Uptake Biokinetic (IEUBK) model (2007 REA, 18January 2013 3-45 Draft - Do Not Quote or Cite sections 3.2.1.1 and 5.2.4). 32 Diet and drinking water intake an d concentrations, as well as other 1 model inputs, were based on the most current information (2007 REA, Appendix H). Detail on 2
methods used to characterize media Pb concentr ations and all IEUBK inputs for each case study 3 are in the 2007 REA, sections 3.1, 3.2, 5.2.3 and 5.2.4 and Appendices C through H. As the 4 shortest temporal scale accepted for inputs to the IEUBK is a y ear, all model inputs, developed 5 for each exposure zone in each case study, were a nnual average values. For media concentration 6 inputs, the same values were used for each ye ar of the seven-year simulation. Other model 7 inputs varied as appropriate with the age of the simulated child (2007 REA, Appendix H). 8 To simulate population variability in Pb inta ke and uptake, we used the IEUBK model to 9 first generate a central-tendency estimate of the PbB levels for the group of children within a 10 given exposure zone of a study area. 33 Outside the IEUBK model, we then combined this central11 tendency estimate with a geometric standard devi ation (GSD) reflecting vari ability in PbB levels 12 for groups of children to generate a distribution of PbB levels for a study area. The procedure 13 for combining the IEUBK-based central tendency blood Pb estimate with a GSD to generate a 14 population distribution of PbB leve ls differs somewhat for the ca tegories of case studies. The 15 approach for the general urban case study is fairly simple in that we have a single IEUBK-based 16 estimate of PbB levels and this is in turn, combin ed with the GSD selected for this study area to 17 produce a population-distribution of PbB levels . For both the primary Pb smelter and the 18 location-specific urban study areas, multiple po lygons within the larger study area (e.g., US 19 Census blocks for the location specific urban st udy areas) are used as the basis for generating 20 distributions of PbB levels for the child populatio n in each study area. These distributions are 21 generated using a MonteCarlo-b ased population-weighted sampli ng method with U.S. Census 22 child counts for each polygon and an adjustment factor distribution based on the chosen GSD 23 (see 2007 REA, sections 3.2.2 and 5.2.2.3). 24 The GSD reflects a number of factors which ope rate together to pr oduce interindividual 25 variability in blood Pb levels, including: (a) bi okinetic variability (differences in the uptake, 26 distribution or clearance of Pb), (b) differences in behavior rela ted to Pb exposure (e.g., varying 27 hand-to-mouth activity, tap water ingestion rate s, and time spent playing indoors) and (c) 28

32 In predicting PbB levels, we assumed that Pb con centrations in exposure media remained constant throughout the 7 year simulation period.
33 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.January 2013 3-46 Draft - Do Not Quote or Cite differences in environmental Pb exposure concen trations (e.g., spatial gr adients in ambient Pb 1 levels of a resolution beyond that simula ted in each case study, differences in 2 cleaning/vacuuming rates a nd air exchanges rates). 34 Note, that for all of the study areas, we 3 assumed that pathway apportionment of PbB le vels based on the modeling of the central4 tendency PbB level (using IEUBK) holds for all percentiles of PbB leve ls derived by combining 5 that central-tendency with the GSD. Blood Pb modeling completed for all case studies included 6
estimates of both concurrent and lifetime-avera ge PbB metrics, although ultimately, we focused 7 on the concurrent PbB metric in estimating risk. 35 8

3.4.3.2 Air Quality Scenarios Included in 2007 Assessment 9 The air quality scenarios assessed in the 2007 REA for the case st udies identified in 10 Table 3-6 above included conditions just meetin g the NAAQS that was current at the time of the 11 last review (1.5 μ g/m 3 , maximum calendar quarter average) and conditions meeting several 12 alternative, lower standards. Additionally, fo r the three location-specific urban case studies, 13
scenarios were included for then-current conditions (2003-2005) in each location. 36 These air 14 quality scenarios are characterized by quarterlyor monthly averaging times and a not-to-be15 exceeded form. Once the air quality dataset re presenting each scenario was developed, the 16 associated annual average concentrations for each exposure zone were derived for input to the 17 IEUBK model, which does not accep t air quality inputs of a tempor al scale shorter than a year 18 (2007 REA, Appendix H). 37 19 As a result of the differing then-current condi tions of the location-sp ecific case studies, 20 the specific alternative standard s assessed for each differed (see Table 3-8). To simulate the 21

34 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).
35 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-associated intellectual deficits than was the maximal measured (peak) or early childhood blood lead concentrations” with the concurrent PbB level exhibiting the strongest relationship (2006 CD, p. 6-29).
36 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).
37 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.January 2013 3-47 Draft - Do Not Quote or Cite previous NAAQS scenario at the primary Pb sme lter location, at which then-current monitoring 1 data indicated exceedance of that standard, a proportional roll-down was performed across the 2 area to achieve conditions that just met that st andard. Additionally, although it was considered 3 an extremely unlikely scenario th at air concentrations in urban areas across the U.S. that were 4 well below the previous NAAQS would increase to just meet that standard (e.g., by way of 5 expansion of existing sources or congregation of multiple sources in adjacent locations), we 6
simulated this scenario in all case studies. In so doing, the air Pb concentrations were rolled up 7 proportionally across the location- specific urban study areas to conditions just meeting the 8
standard. No other scenario simulati ons involved rolling concentrations up . For the primary Pb 9 smelter case study, air Pb concentrations were proportionally rolled down to conditions just 10 meeting each of the potential altern ative standards assessed. In the three location-specific urban 11 case studies, the temporally and spatially varying concentrations were rolled down to conditions 12 just meeting each of the potential alternative standards that they exceeded (2007 REA, section 13 5.2.2.1). 38 14 For the generalized (local) urban case study, wh ich has a single expos ure zone in which 15 air Pb concentrations do not vary spatially, we derived a single air Pb concentration estimate to 16 meet the standard assessed (e.g., specified maximu m monthly or quarterly average). To reflect 17 the variability in air Pb concentrations that occur over time scales less than a year as a result of 18 temporal changes in meteorology and source and em ission characteristics, the annual average air 19 concentration (input for IEUBK and dust model) was derived for the maximum monthly and 20 quarterly average metrics assessed using relati onships based on the ava ilable Pb-TSP monitoring 21 data for large U.S. urban ar eas (2007 REA, Appendix A). 22
23

38 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”.January 2013 3-48 Draft - Do Not Quote or Cite Table 3-8. Air quality scenarios assessed. 1

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. 2 The approaches for estimating Pb concentratio ns in other media varied depending on the 3 type of case study (see section 3.4.3.1 above). Li mitations in the available data and modeling 4 tools precluded simulation of linkages between some media and air Pb, such that the full impact 5 of changes in air Pb conditions associated with attainment of lower stan dards was not simulated. 6 For example, dietary and drinking water Pb con centrations, as well as soil Pb concentrations, 7 were not varied across the air quality scenarios in any case study (see Tabl e 3-7). For all case 8 studies, however, indoor dust Pb concentrations were simulated to change with the different air 9 quality scenarios that also provided differing ambient air Pb concentrations (outdoors and 10 indoors). 11

3.4.3.3 Methods for Deriving Risk Estimates 12 In this section, we first summarize the fu ll risk model employed in the 2007 REA for 13 estimating risk for a broad range of air qual ity scenarios (section 3.4.3.3.1). Then, in section 14 3.4.3.3.2, we summarize approaches by which we have identified risk estima tes pertaining to the 15 current standard, the second of which involves an analysis newly completed in this review in 16 which risk estimates are interpolated for th e current standard based on the 2007 REA risk 17
estimates. 18
19January 2013 3-49 Draft - Do Not Quote or Cite 3.4.3.3.1 Full Risk Model in 2007 REA 1 The risk characterization step employed in the 2007 REA involved generating a 2 distribution of IQ loss estimates for the set of children simulated in the exposure assessment. 3 Specifically, estimated PbB levels (for the concurrent PbB metric) 39 were combined with four 4 PbB concentration-response (C-R) functions for IQ loss based on the analysis by Lanphear et al 5 (2005) of a pooled international dataset of blood Pb and IQ (see 2007 REA, section 5.3.1.1). 6 Four different C-R functions were selected to pr ovide different characteri zations of behavior at 7 low exposures. The decision to use four different functions is in recognition of uncertainty 8 related to modeling this endpoint, particularly at lower PbB leve ls for which there is limited 9 representation in the Lanphear et al (2005) pooled dataset; the 5t h percentile for the concurrent 10 PbB measurements in that dataset is 2.5 μg/dL, and the mean is 9.7 μg/dL (73 FR 66978). The 11
four different functions are eith er based directly on the lognorm al model described in Lanphear 12 et al (2005), or they are derive d from data presented in that study. The four functions are 13 presented in Figure 3-4 and compared in Table 3- 9 with regard to total IQ loss and incremental 14 IQ loss (IQ loss per μg/dL blood Pb) across a ra nge of concurrent PbB levels. A brief 15 description of each of the functions is also here: 16

 Log-linear with cutpoint: log-linear functi on derived from the pooled analysis applied 17 down to 1 μg/dL (concurrent PbB metric) with no IQ loss projected below that 18 exposure level. 19

 Log-linear with low-exposure linearizatio n: log-linear function applied down to 1 20 μg/dL (concurrent PbB metric) with linearizati on of the slope at that point which is 21 used to project IQ loss down to the origin. 22

 Dual linear – stratified at 10 μg/dL: func tion developed by fitti ng a two-piece linear 23 function stratified at 10 μg/d L (peak PbB metric) to the log-linear function developed 24 from the pooled analysis. 25

 Dual linear-stratified at 7.5 μg/dL: as a bove, but based on stratification of the two26 piece function at 7.5 μg/dL (peak PbB metric). 27

39 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 due to the slightly more significant association found for concurrent PbB with IQ by Lanphear et al (2005) in addition to advice from CASAC.January 2013 3-50 Draft - Do Not Quote or Cite 1

Figure 3-4. Comparison of four concentration-respons e functions used in risk assessment. 2

3

Table 3-9. Comparison of total and incremental IQ loss estimates for blood Pb below 10 4 μg/dL based on the four concentration-response functions. 5

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 6 Of the four C-R functions provided above, we have the greatest overall confidence in risk 7 estimates generated using the lo g-linear with low-exposure linear ization (LLL) function because 8 this function is (a) nonlinear, describing greater response pe r unit blood Pb at lower blood Pb 9 levels consistent with multiple studies, (b) is based on fitting a function to the entire pooled 10 dataset (and hence uses all of th e data in describing response ac ross the range of exposures), (c) 11 is supported by sensitivity analyses showing the model coefficients to be robust (Lanphear et al., 12 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 linearizationJanuary 2013 3-51 Draft - Do Not Quote or Cite 2005), and (d) provides an approach for predicting IQ loss at the lowest exposures simulated in 1 the assessment (which for some simulated children yield blood Pb levels below those studied). 2 Risk estimates generated using the other three C-R functions are also presented to provide 3 perspective on the impact of uncertainty in this key modeling step. For additional detail on the 4 rationale for placing greater emphasis on the LLL function, see section 4.2.1 of the 2007 Pb Staff 5 Paper (USEPA, 2007b). 6 Two categories of risk metrics were genera ted for each of the location-specific case 7 studies: 8

 Population risk percentiles: The IQ loss associated with policy-relevant exposure 9 pathways for specific percentiles of the child population (e.g., the 50 th , 90 th and 95 th 10 percentile modeled child ). This category of metric provides perspective on the 11 distribution of IQ loss resulting from po licy-relevant exposure pathways, ranging 12 from the typical or average child (50 th percentile, mean) to children experiencing 13 higher exposures (90 th , 95 th percentiles). Greater empha sis has been placed on the 14 median IQ loss estimates due to increased confidence in these estimates relative to the 15 higher percentile estimates, as noted in section 3.4.7. 16

 Child frequency counts associated with specific ri sk percentiles : Number of children 17 associated with each of the population pe rcentiles (e.g., the nu mber of children 18 predicted to have risk le vels at or above the 95 th percentile). This risk metric provides 19 a perspective on the number of children associ ated with various leve ls of IQ loss for a 20 particular case study. 21 For the generalized (local) urban case study, onl y the first type of risk metric, population 22 risk percentiles, was developed because a specif ic location with associated demographic data 23 was not modeled. In summarizing risk estimates from the 2007 REA in this document, we have 24 focused on the first category of risk metric, a nd specifically, on the median IQ loss estimates. 25

3.4.3.3.2 Air Quality Scenarios Reflecting the Current Standard 26 As the 2007 REA did not include an air quality scenario simulated to just meet the 27 standard selected by the 2008 decision, 40 we have considered two appr oaches for identifying risk 28 estimates pertaining to conditions just meeting the now-current Pb standard for our purposes in 29
this review. We first reviewed all the scen arios analyzed in the 2007 REA and recognize the 30 similarity to the current standa rd of the then-current conditions scenario for the Chicago case 31 study. Accordingly, we consider th e risk estimates for that scenario for our purposes in this 32 review of considering risk associated with the current standard (s ee section 3.4.5 below). 33 Additionally, in recogni tion of the variation among specifi c locations and urban areas with 34

40 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).January 2013 3-52 Draft - Do Not Quote or Cite regard to air quality patterns and exposed populat ion, we have also newly developed estimates 1 for an air quality scenario just meeting the curr ent Pb NAAQS in the cont ext of the generalized 2 (local) urban case study to augment the risk info rmation available in this current review. The 3 newly developed estimates were derived based on interpolation from the risk estimates available 4 for scenarios previously assessed for the generalized (local) urba n case study. Such interpolated 5 estimates were only developed for the generali zed urban case study due to its use of a single 6 exposure zone which greatly simplified the met hod employed, thus contribu ting relatively lesser 7 uncertainty from the interpolation step. 41 8 In newly developing estimates for the current standard in the gene ralized (local) urban 9 case study, the general approach we followed wa s to identify the two alternative standard 10 scenarios simulated in the 2007 REA which repres ented air quality conditions bracketing those 11 for the current standard and then linearly interpol ate an estimate of risk for the current standard 12 based on the slope created from the two bracketing estimates. In representing air quality 13 conditions for these purposes, we focused on the annual average air Pb concentration estimates 14 used as IEUBK model inputs for the various air quality scenarios. An annual average 15 concentration estimate to represent the current standard was identified in a manner consistent 16 with that employed in the 2007 REA for this cas e study (see section 3.4.3.2 above) with the use 17 of currently available monitoring data for relationships between air quality metrics for 18 representation of the current sta ndard. By this method, the air qua lity scenario for the current 19 standard (0.15 μg/m 3 , as a not-to-be-exceeded 3-month average) was found to be bracketed by 20
the scenarios for alternat ive standards of 0.20 μg/m 3 (maximum calendar quarter average) and 21 0.20 μg/m 3 (maximum monthly average). A risk estim ate for the current standard was then 22 derived using the slope relating general ur ban case study IQ loss to annual average Pb 23 concentration used for those two air quality scenar ios. We used this interpolation approach to 24 develop median risk estimates for the current sta ndard based on each of the four C-R functions. 25 Details on the method for the interpolation approach are provided in Appendix 3A. The 26 interpolated median estimates of risk for the cu rrent standard for the ge neralized (local) urban 27 case study are provided be low in Table 3-9. 28

41 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.January 2013 3-53 Draft - Do Not Quote or Cite 3.4.4 Challenges in Characterizing Air-related Exposure and Risk 1 In estimating the portion of total (all-pathway) PbB and IQ loss attributable to air-related 2 pathways, we faced a variety of challenges. A lthough we parsed total estimates into those for 3 diet/drinking water and tw o air-related categories, referred to as “recent air” and “past air”, 4 significant limitations in our modeling tools and data resulted in an inability to parse specific risk 5 estimates into specific pathways. Although Pb in diet and drinking water sources may include 6 Pb derived from Pb in the ambient air (as well as Pb from nonair sources ), limitations precluded 7 explicit modeling of the contribution from air pa thways to these exposure pathways, such that 8 the air-related component of th ese exposures was not estimated. 42 As a result we utilized the 9 estimates from recent and past air categories to create bounds within which we consider air10 related risk to fall, as illustrated in Figure 3-5 and described further below. 11

12

Figure 3-5. Parsing of air-related risk estimates. 13

Those Pb exposure pathways tied most directly to ambient air, which consequently have 14 the potential to respond relatively more quickly to changes in air Pb (i.e., inhalation and 15 ingestion of indoor dust Pb derived from the inf iltration of ambient air Pb indoors), were placed 16 into the "recent air" category. The other air-related Pb exposure pathways, all of which are 17 associated with atmospheric deposition, were pla ced into the “past air” category. These include 18

42 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. 

### “Recent air”

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

• Risk assessment simulated just meeting alternative NAAQS by changing recent air exposures. • Although unquantified, alternative NAAQS expected to also influence, to some extent, past air exposures and diet.

 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 contributionsJanuary 2013 3-54 Draft - Do Not Quote or Cite ingestion of Pb in outdoor dust/so il and ingestion of the portion of Pb in indoor dust that after 1 deposition from ambient air outdoors is carried indoors with humans. Additionally, while we 2 recognized the potential for these other air-rela ted exposures to be affected (over some time 3 frame) by an adjustment to the Pb NAAQS, lim itations in our date a nd tools precluded our 4 simulation of that relationship with air Pb levels. 5 Among the limitations affecting our estimates for the air-relate d categories is the 6 apportionment of nonair pathways. For exampl e, while conceptually indoor Pb paint 7
contributions to indoor dust Pb would be cons idered background and included in a “background” 8 category for this assessment, due to technical li mitations related to i ndoor dust Pb modeling, dust 9 from Pb paint was included as part of "other" ind oor dust Pb (i.e., as part of past air exposure). 10 The inclusion of indoor paint Pb as a component of "other" indoor dust Pb (and consequently as 11 a component of the “past air” category) represents a source of potential high bias in our 12 prediction of exposure and risk as sociated with the “past air” category because, indoor paint Pb 13 is a nonair Pb source. At the same time, Pb in ambient air does contribu te to the drinking water 14 and diet exposure pathways, and is likely a s ubstantial contribution to diet. We could not 15 separate the air contribution from the nonair contributions in the dr inking water and diet 16 pathways. As a result, our ri sk estimate for the drinking wate r/diet category of pathways 17 includes some air-related risk representing a source of potential low bias in our predictions of 18
air-related risk. 19 Further, we note that in simulating reductio ns in exposure associated with reducing 20 ambient air Pb levels through alternative NAAQS (and increases in exposure if the current 21 NAAQS was reached in certain ca se studies) only the exposure path ways categorized as “recent 22 air” (inhalation and ingestion of that portion of indoor dust asso ciated with outdoor ambient air) 23 were varied with changes in ai r concentration. The assessment fr om the previous review did not 24 simulate decreases in “past air” exposure path ways (e.g., reductions in outdoor soil Pb levels 25 following reduction in ambient air Pb levels and a subsequent decr ease in exposure through 26 incidental soil ingestion and th e contribution of outdoor soil to indoor dust). These exposures 27
were held constant across all air quality scenarios. This mo deling/data limitation, accordingly, 28 precluded estimates for this category from reflect ing any impact of altern ative standard levels 29
simulated. 30 In summary, because of limitations in th e assessment design, data and modeling tools, 31 our risk estimates for the “past air” category in th e last review include both risks that are truly 32 air-related and potentially, some nonair risk. Because we could not sharply separate Pb linked to 33
ambient air from Pb from othe r (nonair) sources, some of the three categories of risk are 34
underestimated and others overestimated. On balan ce, we believe this lim itation leads to a slight 35
overestimate of the risks in the “past air” category. At the same time, as discussed above, the 36January 2013 3-55 Draft - Do Not Quote or Cite "recent air" category does not fully represent the ri sk associated with all air-related pathways. 1 Thus, we considered the risk at tributable to air-related exposure pathways to be bounded on the 2 low end by the risk estimated for the “recent ai r” category and on the upper end by the risk 3 estimated for the “recent air” plus “past air” ca tegories. With regard to the latter, we are 4 additionally cognizant of the mode ling and data limitations which reduce the extent to which the 5 upper end of these bounds reflects impacts of alternative air quality conditions simulated. 6

3.4.5 Risk Estimates 7
This section summarizes air-related risk estim ates generated for the previous review and 8 also risk estimates that have been newly derived in this review by interpolation from the previous 9 review estimates for the current standard (see section 3.4.3.3.2 above). Included in this summary 10 is consideration of the following question: 11

 What is the nature and magnitude of air-related risks remaining upon just 12 meeting the current Pb standard? 13 The air-related risk quantifie d in the 2007 REA is for IQ loss associated with Pb 14 exposure. As discussed in section 3.2 above, the evidence in the last review, as well as in the 15 current review, supports identification of neurocognitive effects in young children as a 16 particularly sensitive endpoint fo r the exposure circumstances releva nt to this review and which 17 addresses the important at-risk population, young children. With this support in the evidence for 18 quantification, the risk assessment quantified decr ements in IQ, an established indicator of 19 neurocognitive function. With rega rd to the nature of the risks, in addition to recognizing the 20 role of IQ as an indicator of an array of ne urocognitive function impacts, we additionally take 21 note of the evidence regarding implications of neurocognitive impacts in young children with 22 regard to potential future impacts as the ch ildren age, as recognized in section 3.2 above. 23 In presenting risk estimates here, we focus on the median estimates of air-related IQ loss 24 for each case study. Estimates of air-related risk ar e substantially more uncertain for extremes of 25 the risk distribution, such as the 95 th percentile. Those estimates and estimates for other risk 26 metrics, including population incidence for IQ loss at those case studies with population 27 enumeration, are available elsewhere (2007 REA, s ections 4.2 and 5.3.2). In this section, Table 28 3-10 presents air-related IQ lo ss estimates derived in the 2007 REA for the full set of case 29 studies. Table 3-11 provides a subset of these risk estimates for the generalized (local) urban case 30 study in addition to estimates for air quality cond itions just meeting the current standard, derived 31 by interpolation. A number of details, listed he re, should be kept in mind when reviewing the 32 estimates presented in Tables 3-9 and 3-10. 33

 The risk estimates represent IQ loss associated with air-r elated lead exposure for the 34 median child (exposure is modeled through age seven years). 35January 2013 3-56 Draft - Do Not Quote or Cite  Our estimation of risk attributable to air- related exposure pathways is approximate, as 1 described in sections 3.4.4 and 3.4.7. We cons ider the air-related risk to fall within 2 the ranges presented, bounded on the lo w end by estimates for the pathways 3 categorized as “recent air” and on the uppe r end by the sum of the estimates for both 4 the “recent” and “past air” pathways. 43 5

 The bolded range of risk estimates are derive d using the C-R function in which we 6 have the highest overall confidence (the lo g-linear with low-expos ure linearization – 7 see section 3.4.3.3.1). The wider range of risk estimates presented within the 8 parentheses in both tables reflects the application of all four C-R functions (see 9 section 3.4.3.3.1) to exposure estimates for the recent and recent plus past air 10 categories. Consequently, this range of risk estimates reflects both uncertainty in 11 estimation of air-related exposures as well as uncertainty in th e C-R function for IQ 12 loss in children. 13

14

43 The third category of pathways for which risk was es timated in the 2007 REA was comprised of 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.January 2013 3-57 Draft - Do Not Quote or Cite Table 3-10. Estimates of air-related risk from 2007 risk assessment. 1

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 log-linear wi th low-exposure linearization function. Values in parentheses reflect the range of estimate s associated with all four concentration-response functions. 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. 2
3 4 5January 2013 3-58 Draft - Do Not Quote or Cite Table 3-11. Estimates of air-related risk for the generalized (local) urban case study, 1 including interpolated estimates for current standard. 2

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 values are estimates generated using the log-linear with low-exposure linearization function. Values in parentheses reflect the range of estimates associated with all four concentration-response functions. B – Risk estimates interpolated - see text. 3 Key observations regarding thes e air-related risk estimates across the array of air quality 4
scenarios: 5

All Case Studies 6

 Relative to the previous Pb NAAQS, substant ial reduction in estimates of air- related 7 risk is demonstrated across the full set of potential alternative standards simulated 8 (Table 3-10). This is particular ly the case for the lower bound (the recent air 9 estimates) which reflects only the pathways simulated to respond to changes in air 10 concentrations associated with different air quality scenarios. 11 Generalized (local) Urban Case Study 12

 As described above, the general urban case st udy provides risk estimates for a single 13 group of children residing in a single area where air concentrations throughout area 14 are near the level of the standard being simulated. In this case study, air-related 15 median IQ loss, based on the higher conf idence C-R function (bold), ranged from 16 roughly 2 to 4 IQ points for the 0.5 μg/m 3 , maximum monthly average scenario, to <1 17 to roughly 3 IQ points for the 0.02 μg/m 3 , maximum monthly average scenario. 18 These ranges are expanded somewhat with consideration of the full range of C-R 19 functions considered in the analysis. . 20January 2013 3-59 Draft - Do Not Quote or Cite Location-specific Case Studies 1

 Compared to the other case studies, the air-related risk estimates for the location2 specific urban case studies are lower because of the broader range of air-related 3 exposures and the distribution of the populat ion within the study areas. For example, 4 the majority of the populations in each of the lo cation-specific case st udies reside in 5

area s with ambient air Pb levels wel l below each standard assessed, particularly for 6 standard levels above 0.05 μg/m 3 , as a maximum monthly average. Consequently, 7 risk estimates for these case studies indic at e little response to alternative standard 8 levels above 0.05μg/m 3 maximum monthly average (as shown in Table 3-10). 9

 For the primary Pb smelter subarea, only an upper bound on risk attributable to air10 related exposures is provided due to uncerta inties associated with dust Pb model used 11 for this case study. 44 For all air quality scenarios, the population median recent plus 12 past air risk estimate is generally similar to or slightly higher than those for the 13 general urban case study, likely due to differe nces in the indoor dust models used for 14 the two case studies (discussed in Risk Assessment Report, sections 3.1.4). 15

16 Key observations regarding air- related risk estimates for the current standard : 17

 The median air-related IQ loss estimate fo r then current conditions in Chicago study 18 area, which just met a level of 0.14 μg/m3 as a maximum calendar quarter average, 19 falls somewhere within the lower and upper bounds of 0.6 and 2.9 points IQ loss, 20 respectively (Table 3-10). 21

 The median air-related IQ loss estimate fo r the current standard in the Generalized 22 (local) Urban Case Study, newly derived by interpolation from 2007 REA results, 23 falls somewhere within the lower and upper bounds of 1.5 and 3.4 points IQ loss, 24 respectively (Table 3-11). This estimate is derived by inter polation between the 25 estimates for the 0.2 μg/m 3 maximum quarterly and 0.2 μg/m 3 maximum monthly 26 average scenarios that were derived in 2007 REA. The newly interpolated estimate is 27 essentially the same as the estimate for 0.2 μg/m 3 maximum quarterly average 28 scenario for this case study. 29

 Based on results from the last review fo r a location-specific urban study area and on 30 those newly derived in this review ba sed on interpolation from 2007 REA results, 31 median air-related IQ loss for the curren t standard is estimated, with rounding, to 32 generally fall above a rough lower bound of 1 point IQ loss and below a rough upper 33 bound of 3 points IQ loss. 34

35

36

44 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).January 2013 3-60 Draft - Do Not Quote or Cite 3.4.6 Treatment of Variability 1
This section discusses the de gree to which the design of th e previous risk assessment 2 reflected consideration for key sources of variab ility associated with the scenarios evaluated 3 (e.g., IQ loss in children associated with ambient Pb in various residential settings). In so doing, 4 the following question is address. 5

 How are key sources of variability treated in the assessment? 6

7 Key sources of variability associated with the risk assessment include: 8

 Variation in ambient air Pb level s among U.S. urban residential areas: The location9 specific urban study areas were chosen to provide coverage for diverse residential 10 populations in U.S. urban areas with relativ ely elevated ambient air Pb levels (as 11 characterized using monitoring). We believe that the three cities included in those 12 case studies capture the variability in spatial patterns of ambient air Pb concentrations 13 within and across such areas reasonably we ll. In addition, the generalized (local) 14 urban case study provides coverage for a resi dential population exposed in a localized 15 area with air concentrations somewhat ne ar the standard bein g evaluated, providing 16 coverage for a higher-end population risk sc enario where a subset of urban children 17 are exposed without any spatial gradie nt in ambient air Pb levels. 18

 Variation in the spatial dist ribution of children within an urban area and assignment 19 of ambient air Pb exposure: Exposure of populations within the three location20 specific urban study areas was characterized to the US Census block group-level 21 characterization. Each block group was asso ciated ambient air Pb exposure based on 22 proximity to monitor nearest to bloc k group centroid (Risk Assessment Report, 23 section 5.2.2). While ther e is uncertainty associat ed with these exposures 24 (population-weighted through use of census block groups) - for example, we did not 25 consider time spent by children away from their residential block group - we believe 26 that this approach provides reasonable cove rage for the potential pattern of interaction 27 between resident children located in these urban study areas and th e associated spatial 28 gradients of ambient air Pb levels. 29

 Variation among children in factors other t han media concentrations that influence 30 PbB levels: The inputs to the blood Pb model we re central tendency estimates for 31 each exposure zone within each study area (pathway-specific estimates for central32 tendency child). The IEUBK model then generated PbB levels for that central33 tendency child within each exposure zone. These central-tendency PbB levels were 34 then combined with a GSD reflecting va riability in PbB levels for young children 35 (at/near age 7 years) to ge nerate a distribution of total PbB for a group of children 36 within each exposure zone in a given case study under the specific air quality 37 scenario. We have reasonable confiden ce that this modeling approach captures 38 variability in total Pb ex posure (and consequently total PbB levels) for children 39 modeled for a given study area. As noted in section 3.4.7 below, however, there is 40 uncertainty associated with parsing indi vidual pathway contribu tions to total PbB 41January 2013 3-61 Draft - Do Not Quote or Cite levels (and consequently to total Pb-attributab le risk). This is particularly true for 1 high-end population percentile estimates of IQ loss. 2

 Inter-individual variability in IQ loss related to Pb exposure: The use of C-R 3 functions based on a pooled analysis (La nphear et al., 2005) which combined study 4 populations from a number of different epidemiological stud ies of IQ loss in children 5 likely provides reasonable coverage for va riation across children regarding IQ loss 6 attributable to Pb exposure. Furthermore, our estimation of risk based on several C-R 7 functions provides further coverage for that variability, as well as also addressing 8 uncertainty in the specification of that C- R functional form (see section 3.4.7 below). 9

3.4.7 Characterizing Uncertainty 10 Although the risk assessment utilized a numbe r of innovative modeling elements in order 11 to generate representative estima tes of risk for the various stu dy area populations, like all risk 12 models there was uncertainty associated with the model a nd its output. 13

 What are the important uncertainties associated with any risk/exposure 14 estimates? 15 One overarching area of uncertainty concer ns the precision of our estimation of the 16 neurocognitive risk (as represented by IQ loss) associated with ambient air Pb. For example, 17 because of the evidence for a nonlinear response of PbB to Pb exposure and also for nonlinearity 18 in the C–R relationship for Pb-associated IQ loss, the assessment first estimated PbB levels and 19 associated risk for total Pb exposure (i.e., in cluding Pb from air-re lated and nonair exposure 20 pathways), and then separated out estimates fo r pathways of interest. We separated out the 21 estimates of total (all-pathway) PbB and IQ lo ss into three categories that included two air22 related categories (“past” and “recent”), in ad dition to a third categor y for diet and drinking 23 water. However, significant limitations in our modeling tools affected our ability to develop 24 precise estimates for air-related exposure path ways. As recognized in section 3.4.4 above, we 25 believe these limitations led to a slight overestimation of the risks for the past air category and to 26 an under representation of ai r-related pathways for the recent air category. Thus, we 27
characterized the risk attri butable to air-related exposur e pathways to be bounded by the 28 estimates developed for the past air category and the sum of estimates for the recent air and past 29
air categories. For air quality scenarios other than those for the previous NAAQS, this upper 30 bound is recognized as having a potential upward bi as with regard to its reflection of the 31 simulated air quality conditions because modeli ng and data limitations precluded simulation of 32
the influence of lower air Pb concentrations on the outdoor dust and soil exposure pathways, as 33
noted in section 3.4.4 above. 34 Additional limitations, assumptions and uncertain ties, recognized in various ways in the 35 assessment and presentation of re sults, along with a concise char acterization of their expected 36 impact on results, are listed below. The list be gins with factors rela ted to design of the 37January 2013 3-62 Draft - Do Not Quote or Cite assessment or of the case studies, followed by those related to estimation of Pb concentrations in 1 ambient air, indoor dust, outdoor soil/dust, a nd blood, and estimation of Pb-related IQ loss. 2

 Temporal Aspects: During the 7-year exposure period, media concentrations remain 3 fixed and the simulated child resides at the same residence (although exposure 4 factors, including behavioral and physiologi cal parameters, are adjusted to match the 5 aging of the child). While these aspects of simulation introduce uncertainty into the 6 risk estimates, it is not clear if there is a directional bias. For example, failure to 7 consider population mobility during the simulation period could bias the overall 8 distribution upwards unless ch ildren move to, or from a residential location with 9 higher Pb exposure, in which case this would not be the case. 10

 Generalized (local) Urban Case Study: The design for this case study employs 11 assumptions regarding uniformity that are reasonable in the c ontext of a general 12 description of a small neighborhood populat ion, but would contribute significant 13 uncertainty to extrapolation of these estimates to a specific urban location, 14 particularly a relatively large one. Thus, th e risk estimates for this case study, while 15 generally representative of an urban resi dential population expos ed to the specified 16 ambient air Pb levels, cannot be readily related to a sp ecific large urban population. 17 As long as these important caveats are cons idered in interpreti ng the risk estimates 18 (i.e., these risk estimates are likely repres ent a relatively small portion of the resident 19 child population in any given city just m eeting specific air quality conditions) then 20 the potential error of extrapol ating these results to a la rger child population can be 21 avoided. An additional area of uncertainty is with regard to the representation of 22 variability in air quality. Given the relati vely greater variability common in areas of 23 high Pb concentrations, the approach used to reflect variability may bias the estimates 24 high, although there is uncertainty with re gard to the representativeness of the 25 monitoring dataset used to characterize this. 26

 Location-specific Urban Case Studies: Limitations in the sp atial density of ambient 27 air monitors in the three metropolitan areas simulated limit our characterization of 28 spatial gradients of ambient air Pb levels in these case studies. While this factor 29 introduces uncertainty into the risk estimates for this category of case study, it is not 30 clear if there is a directional bias. 31

 Air Quality Simulation: The proportional roll-up and ro ll-down procedures used in 32 some case studies to simulate air quality conditions just meeting the previous 33 NAAQS and alternative NAAQS, respectivel y, assume proportional changes in air 34 concentrations across those case study areas to create those air quality scenarios. The 35 EPA recognizes the uncertainty with our simulation of hi gher air Pb concentrations 36 that would just meet the previous NAAQS in the urban location-specific case studies, 37 as well as the uncertainty in simulati on of conditions associated with the 38 implementation of emissions reduction actions to meet a lower standard. There is the 39 potential that the use of the proportional approach for adjusting monitor values 40 introduced a degree of high-bias into estimates of risk reduction. This could result if 41 we find that urban areas can target specific Pb sources impacting individual monitors, 42 thereby avoiding the need for more genera lized reduction strategies resulting in a 43 uniform pattern of reduction across all monitors in an urban area. It is important to 44January 2013 3-63 Draft - Do Not Quote or Cite point out however, that the generalized ur ban case study is not effected by this 1 potential bias, since, given the single exposure zone involve d, the single ambient air 2 Pb level is fixed to reflect meeting the standard being considered (i.e., no spatial 3 gradient is simulated in the small, localized residential area being modeled). 4

 Outdoor Soil/Dust Pb Concentrations: Limitations in datasets on Pb levels in surface 5 soil/dust Pb in urban areas and in our ability to simulate the impact of reduced air Pb 6 levels related to lowering the NAAQS cont ributes uncertainty to air-related risk 7 estimates. In this case, it is likely that we have low-biased our estimates of risk 8 reduction associated with alternative (low er) Pb NAAQS levels, since we have not 9 simulated potential changes in soil Pb related to changes in ambient air Pb. 10

 Indoor Dust Pb Concentrations: Limitations and uncertain ty in modeling of indoor 11 dust Pb levels, including the impact of reduc tions in ambient air Pb levels, contributes 12 uncertainty to air-related risk estimat es. Although our modeling of indoor dust does 13 link changes in ambient air Pb to changes in indoor dust Pb (via air exchanges and 14 indoor deposition onto surfaces), the modeling does not include a link between 15 ambient air Pb, outdoor soil Pb and subsequent changes in the leve l of Pb carried (or 16 “tracked”) into the house. This could intr oduce low-bias into our total estimates of 17 air-related Pb exposure and risk. 18

 Interindividual Variability in PbB Levels: Uncertainty related to population 19 variability in PbB levels (i.e., interindivi dual variability in fact ors other than media 20 concentration that influence PbB) and lim itations in modeling of this introduces 21 significant uncertainty into PbB and IQ loss estimates for the 95th percentile of the 22 population. We are not aware of any systematic bias introduced into the analysis from 23 this source of uncertainty. 24

 Pathway Apportionment for Higher Percentile PbB and risks: Limitations, primarily 25 in data, prevented us from characterizi ng the degree of correlation among high-end 26 Pb exposures for the various pathways (e.g., the degree to which an individual 27 experiencing high drinking water Pb exposur e would also experience high Pb paint 28 exposure and high ambient air- related Pb exposure). Our inability to characterize 29 potential correlations between exposure pathways (particularly at the higher 30 percentile exposure levels) limited our abi lity to (a) effectively model high-end Pb 31 risk and (b) apportion that risk betwee n different exposure pathways, including 32 ambient air-related pathways. 33

 IQ Loss Concentration-response Functions: Specification of the quantitative 34 relationship between PbB level and IQ loss is subject to greater uncertainty at lower 35 PbB levels (e.g., particularly below 2.5 μg/d L concurrent PbB). However, we believe 36 that by considering four different models (which each treat the response at low PbB 37 levels in a different manner), we have comp leted a reasonable characterization of this 38 source of uncertainty and its impact on ri sk estimates. Given comparison of risk 39 estimates generated using the four models , it would appear that this source of 40 uncertainty has a potentially significant impact on risk. 41January 2013 3-64 Draft - Do Not Quote or Cite 3.4.8 Updated Interpretation of Risk Estimates 1 As summarized in prior sections, a range of information gaps and areas of uncertainty 2
were associated with the information availabl e in the last review. In the REA Planning 3 document, staff considered the degree to which information newly available since the last Pb 4 NAAQS review, as summarized in the draft ISA, might address specific uncertainties associated 5 with the 2007 REA, such that an updated risk model might be developed with the potential to 6 provide new exposure and risk estimates substantially different 45 from estimates generated in 7 2007 (USEPA, 2011). Staff concluded that the newl y available information did not provide the 8 means by which to develop an updated or enhanced risk model that would substantially improve 9 the utility of risk estimates in informing th e Pb NAAQS review. Speci fically it was concluded 10 that none of the primary sources of uncertainty in dentified to have the greatest impact on risk 11 estimates would be substantially reduced thr ough the use of newly available information 12 (USEPA, 2011). 13 Our ongoing review of the newly av ailable information leads us to conclude at this time, 14 that the key observations regarding air-related Pb risk modeled for the set of standard levels 15 covered in the 2007 REA, as well as the risk esti mates interpolated for th e current standard (as 16 discussed in Section 3.4.5) are not significantly affected by the new information. Our overall 17 characterization of uncertainty and variability associated with those estimates (as described 18 above in sections 3.4.6 and 3.4.7) is not appreciabl y affected by new information. As recognized 19 at the time of the last review, exposure and ri sk modeling conducted for this analysis was 20 complex and subject to significant uncertainties due to limitations, data, and models, among 21 other aspects. Further, limitations in the assessment design, data and modeling tools 22 handicapped us from sharply separating Pb linked to ambient air from Pb that is not air-related. 23 In summary, the estimates of risk attributab le to air-related exposures, with which we 24 recognize a variety of sources of uncertainty, are considered to be approximate, falling within 25 upper and lower bounds which over- and underestimat e, respectively. In scenarios for more 26 restrictive air quality conditions th an those associated with the pr evious Pb standard, substantial 27
reductions in air-related risk were demonstrate d. Focusing on the resu lts for the generalized 28 (local) urban case study, the interpolated estimat es for the scenario representing the current 29 standard are very similar to estimates for the two 0.2 μg/m 3 scenarios (maximum monthly and 30 quarterly averages) simulated in the 2007 REA, 46 and are appreciably lower than those 31

45 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.
46 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.January 2013 3-65 Draft - Do Not Quote or Cite associated with the previous st andard. In characterizing the magnitude of air-related risk 1 associated with the current standard, we fo cusing on median estimates, for which we have 2 appreciably greater confidence than estimates fo r outer ends of risk distribution (see section 3 3.4.7) and on risks derived using the C-R function in which we ha ve greatest confidence (see 4 sections 3.4.3.3.1 and 3.4.7). The risk results for th e current standard from the last review for 5 one of the location-specific urba n study area populations and those newly derived in this review 6 based on interpolation from 2007 RE A results for the generalized (local) urban case study, which 7 is recognized to reflect a generalized high end of air-related exposure fo r localized populations, 8
indicate air-related risk for the current standard of a magnitude generally within the bounds of 9 roughly 1 and 3 points IQ loss. 10January 2013 3-66 Draft - Do Not Quote or Cite 3.5 REFERENCES 1

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Patel, AB; Prabhu, AS. (2009). Determinants of lead le vel in umbilical cord blood. Indian Pediatr 46: 791- 37 793.Pirkle, JL; Brody, DJ; Gunter, EW; Kramer, RA ; Paschal, DC; Flegal, KM; Matte, TD. (1994). The 38 decline in blood lead levels in the United States: The National Health and Nutrition Examination Surveys 39 (NHANES). JAMA 272: 284-291. http://dx.doi.org/10.1001/jama.1994.03520040046039 40January 2013 3-69 Draft - Do Not Quote or Cite Ranft, U; Delschen, T; Machtolf, M; Sugiri, D; Wilhelm, M. (2008). Lead concentration in the blood of children and 1 its association with lead in soil and ambient air: Trends between 1983 and 2000 in Duisburg. J Toxicol 2 Environ Health A 71: 710-715. http://dx.doi.org/10.1080/15287390801985117 3

Rice, DC. (1990). Lead-induced behavioral impairment on a spatial discrimination reversal task in monkeys exposed 4 during different periods of development. Toxicol Appl Pharmacol 106: 327-333. 5 http://dx.doi.org/10.1016/0041-008X(90)90251-O 6

Rice, DC. (1992). Lead exposure during different developmental periods produces different effects on FI 7 performance in monkeys tested as juveniles and adults. Neurotoxicology 13: 757-770. 8

Rice, DC; Gilbert, SG. (1990). Sensitive periods for lead-i nduced behavioral impairment (nonspatial discrimination 9 reversal) in monkeys. Toxicol Appl Pharma col 102: 101-109 . http://dx.doi.org/10.1016/0041- 10 008X(90)90087-BRothenberg, S. J.; Khan, F.; Manalo, M.; Jian, J.; Cuellar, R.; Reyes, S.; Acosta, S.; 11 Jauregui, M.; Diaz, M.; Sanchez, M.; Todd, A. C.; Johnson, C. (2000) Maternal bone lead contribution to 12 blood lead during and after pregnancy. Environ. Res. 82: 81-90. 13

Schnaas, L; Rothenberg, SJ; Fl ores, MF; Martinez, S; Hernandez, C; Osorio, E; Perroni, E. (2004). Blood lead 14 secular trend in a cohort of children in Mexico City (1987-2002). Environ Health Perspect 112: 1110-1115. 15 http://dx.doi.org/10.1289/ehp.6636 16

Schwartz, J., and Pitcher, H. (1989) The relationship betw een gasoline lead and blood lead in the United States. J 17 Official Statistics 5(4):421-431. 18

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Simon, DL; Maynard, EJ; Thomas, KD. (2007). Living in a sea of lead changes in blood- and hand-lead of infants 21 living near a smelter. J Expo Sci Environ Epidemiol 17: 248-259. http://dx.doi.org/10.1038/sj.jes.7500512 22

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### 4 REVIEW OF THE PRIMAR Y STANDARD FOR LEAD 1

This chapter presents preliminary staff conc lusions regarding the primary Pb standard. 2 These preliminary staff conclusions are guided by consideration of key policy-relevant questions 3 and based on the assessment and integrative synt hesis of information presented in the ISA and by 4 staff analyses and evaluations presented in chapte rs 2 and 3 herein. Final evaluations and staff 5 conclusions, to be developed taking into c onsideration CASAC advice and public comment on 6 this draft document, will be presented in the final PA. The final evaluations and staff 7
conclusions will inform the Administrator’s decisi ons on whether to retain or revise the existing 8 primary standard for Pb. 9 Following an introductory section on the ge neral approach for reviewing the primary 10 standard (section 4.1), including a summary of considerations in th e last review, the discussion in 11 this chapter focuses on the central issue of whet her the information available in this review 12 supports or calls into question the adequacy of the current primary standard. Building on the 13 responses to specific policy-rel evant questions on th e scientific evidence and exposure-risk 14 information in chapter 3 above, presentation in sec tion 4.2 is also organized into consideration of 15 key policy-relevant questions framing evidence-b ased and exposure/risk-based considerations. 16 The policy-relevant questions in this document are based on t hose included in the IRP (IRP, 17 section 3.1). In section 4.3, preliminary staff conc lusions are developed. Section 4.4 presents a 18 brief overview of key uncertainties and areas for future research. 19

4.1 APPROACH 20 Staff’s approach in this revi ew of the current primary sta ndard takes into consideration 21 the approaches used in the pr evious Pb NAAQS review. The past and current approaches 22 described below are both based, most fundamenta lly, on using EPA’s assessment of the current 23
scientific evidence and a ssociated quantitative analyses to inform the Administrator’s judgment 24 regarding a primary standard for Pb that protects public health with an adequate margin of safety. 25 We note that the final decision on the adequacy of the current standard is largely a public health 26 policy judgment to be made by the Administrator. The Administrator’s final decision must draw 27 upon scientific information and analyses about he alth effects, population exposure and risks, as 28 well as judgments about how to consider the ra nge and magnitude of uncertainties that are 29 inherent in the scientific evidence and analyses . Our approach to informing these judgments, 30 discussed more fully below, is based on the recogn ition that the available health effects evidence 31 generally reflects a continuum, consisting of ambi ent levels at which scientists generally agree 32 that health effects are likely to occur, through lower levels at which the likelihood and magnitude 33 of the response become increasingly uncertai n. This approach is consistent with the 34January 2013 4-2 Draft - Do Not Quote or Cite requirements of the NAAQS provisions of the Ac t and with how the EPA and the courts have 1 historically interpreted the Act. These provisions require the Ad ministrator to establish primary 2 standards that, in the Administrator’s judgment, ar e requisite to protect pu blic health with an 3 adequate margin of safety. In so doing, the Admi nistrator seeks to establ ish standards that are 4 neither more nor less stringent than necessary fo r this purpose. The Act does not require that 5 primary standards be set at a zero-risk level, but rather at a level that a voids unacceptable risks to 6 public health. The four basic elements of the NAAQS (indicator, averaging time, level, and 7 form) are considered collectively in evaluating the health protection afforded by the current 8
standard. 9 The following subsections include background in formation on the approach used in the 10 previous review of the standard (section 4.1.1) and a discussion of the approach for the current 11 review (section 4.1.2). 12

4.1.1 Approach Used in the Last Review 13 The last review of the NAAQS for Pb was completed in 2008 (73 FR 66964). In 14 consideration of the much-expanded health effect s evidence on neurocognitive effects of Pb in 15 children available at that time, the EPA substa ntially revised the prim ary standard from 1.5 16 μg/m 3 , as a not-to-be exceeded average concentra tion over a calendar quart er, to a level of 0.15 17 μg/m 3 , as a not-to-be-exceeded rolling 3-month average concentration. The 2008 decision to 18 revise the primary standard was based on the extensive body of scientif ic evidence published 19 over almost three decades, from the time the standard was originally set in 1978 through 2005- 20 2006. The 2008 decision considered the body of evidence as assessed in the 2006 CD (USEPA, 21 2006) as well as the 2007 Staff Paper assessment of the policy-relevant information contained in 22 the CD and the quantitative risk/exposure assessment (USEPA, 2007a, 2007b), the advice and 23 recommendations of CASAC (Henderson 2007a , 2007b, 2008a, 2008b), and public comment. 24 While recognizing that Pb has been demonstr ated to exert “a broad array of deleterious 25 effects on multiple organ systems”, the review fo cused on the effects most pertinent to ambient 26 air exposures, which given ambient air Pb reducti ons over the past 30 years are those associated 27 with relatively lower exposures and associated blood Pb levels (73 FR 66975). In so doing, the 28 EPA recognized the general consensus that the developing nervous system in children is among, 29
if not the most sensitive health endpoint associated with Pb e xposures. Thus, primary attention 30 was given to consideration of nervous syst em effects, including neurocognitive and 31 neurobehavioral effects, in chil dren (73 FR 66976). The body of ev idence included associations 32 of such effects in study populati ons of variously-aged children w ith mean blood Pb levels below 33 10 μg/dL, extending from 8 down to 2 μg/dL (73 FR 66976). The public health implications of 34January 2013 4-3 Draft - Do Not Quote or Cite effects of air-related Pb on cognitive function (e.g., IQ) in young children were given particular 1
focus in the review. 2

4.1.1.1 Conclusion Regarding the Need for Revision 3 The conclusions reached by the Administrator in the last review were based primarily on 4 the scientific evidence, with the risk- and exposure-based in formation providing support for 5 various aspects of the decision. In reaching his conclusion on the adequacy of the prior standard, 6 the Administrator placed primary consideration on the large body of scientific evidence available 7 in the review including significan t new evidence concerning effect s at blood Pb concentrations 8 substantially below those identified when th e NAAQS for Pb was initially set in 1978 (73 FR 9 66987; 43 FR 46246). Given particular attention was the robust evidence of neurotoxic effects 10 of Pb exposure in children, rec ognizing: (1) that while blood Pb levels in U.S. children had 11 decreased notably since the late 1970s, newer epidemiologic studies had investigated and 12 reported associations of effects on the neurode velopment of children with those more recent 13 lower blood Pb levels and (2) th at the toxicological evidence included exte nsive experimental 14 laboratory animal evidence substantiating well th e plausibility of the epidemiologic findings 15 observed in human children and expanding our un derstanding of likely mechanisms underlying 16 the neurotoxic effects (73 FR 66987). Additi onally, within the range of blood Pb levels 17 investigated in the available evidence base, a threshold level for neurocognitive effects was not 18 identified (73 FR 66984; 2006 CD, p. 8-67). Fu rther, the evidence in dicated a steeper dose19 response relationship for effects on cognitive functi on at those lower blood Pb levels than at 20 higher blood Pb levels that were more common in the past, “indicating the potential for greater 21 incremental impact associated with exposure at these lower levels” (73 FR 66987). As at the 22 time when the standard was set, the health effects evidence and exposure/risk assessment 23 supported the conclusion that air -related Pb exposure pathways c ontribute to blood Pb levels in 24 young children by inhalation and in gestion (73 FR 66987). The av ailable information also 25 suggested that the air-to-blood ra tio was likely larger, when all in halation and ingestion pathways 26 for air-related Pb are considered, than the ai r-to-blood ratio (of 2 μg/dL blood Pb to 1 μg/m 3 air 27 Pb) estimated when the standard was initially set in 1978 (73 FR 66987). 28 In the Administrator’s decision on the adequ acy of the 1978 standar d, the Administrator 29 considered the evidence using a very specifically defined framework, referred to as an air-related 30 IQ loss evidence-based framework. This framew ork integrates evidence for the relationship 31 between Pb in air and Pb in young children’s bl ood with evidence for the relationship between 32 Pb in young children’s blood and IQ loss (73 FR 77987) , as described in more detail in section 33 4.1.1.2 below. This evidence-based approach co nsiders air-related effects on neurocognitive 34 function (using the quantitative metric of IQ loss) associated with exposure in those areas with 35January 2013 4-4 Draft - Do Not Quote or Cite elevated air concentrations equal to potential al ternative levels for the Pb standard. Thus, the 1 conceptual context for the framework is that it provides estimates of ai r-related IQ loss for a 2 subset of the population of U.S. children (i.e., th e subset living in close proximity to air Pb 3
sources that contribute to elevat ed air Pb concentrations that equal the current level of the 4 standard). This is the subset expected to expe rience air-related Pb exposures at the high end of 5
the national distribution of such exposures, not at the average. This is the case since when a 6 standard of a particular level is just met at a monitor sited to record the highest source-oriented 7 concentration in an area, the la rge majority of children in th e larger surrounding area would 8 likely experience exposures to concen trations well below that level. 9 The two primary inputs to the evidence-base d air-related IQ loss fr amework are air-to10
blood ratios and C-R functions for the relations hip between blood Pb and IQ response in young 11 children. Additionally taken into consideration in applying and drawing conclusions from the 12
framework were the uncertainties inherent in these inputs. App lication of the framework also 13 entailed consideration of an appropriate level of protection from air-related IQ loss to be used in 14 conjunction with the framework. In simplest te rms, the framework provides for estimation of a 15 mean air-related IQ decrement for young children in the high end of the national distribution of 16 air-related exposures by focusing on children exposed to air-rela ted Pb in those areas with 17
elevated air Pb concentrations equal to specific potential standard levels. The framework 18 estimates of mean air-related IQ loss are derive d through multiplication of the following factors: 19 standard level (μg/m 3 ), air-to-blood ratio in term s of μg/dL blood Pb per μg/m 3 air concentration 20 and slope for the C-R function in terms of points IQ decrement per μg/dL blood Pb. 21 Based on the application of the air-related IQ loss framework to the evidence, the 22 Administrator concluded that, for exposures projected for air Pb concentrati ons at the level of the 23 1978 standard, the quantitative estimates of IQ loss associated with air-related Pb indicated risk 24 of a magnitude that in his judgment was significant from a public health pe rspective, and that the 25 evidence-based framework supported a conclusion that the 1978 standard did not protect public 26 health with an adequate margin of safety ( 73 FR 77987). The Administ rator further concluded 27
that the evidence indicated the n eed for a substantially lower standard level to provide increased 28 public health protection, especially for at-risk gr oups (most notably children ), against an array of 29 effects, most importantly including effects on th e developing nervous syst em (73 FR 77987). In 30 addition to giving primary consideration to the much expanded evidence base since the standard 31 was set, the Administrator also took into consideration the expos ure/risk assessments. In so 32 doing, he observed that, while ta king into consideration thei r inherent uncertainties and 33 limitations, the quantitative estimates of IQ loss a ssociated with air-related Pb in air quality 34 scenarios just meeting the then-current standard also indicated risk of a magnitude that in his 35 judgment was significant from a public health pers pective. Thus, the Administrator concluded 36January 2013 4-5 Draft - Do Not Quote or Cite the exposure/risk estimates provi ded additional support to the evid ence-based conclusion that the 1 standard needed revision (73 FR 66987). 2

4.1.1.2 Conclusions on Elements of Revised Standard 3 In considering appropriate revisions to the prior standard in the review completed in 4 2008, each of the four basic elements of the NAAQS (indicator, averaging time, level, and form) 5
were evaluated. The rationale for decisions on those elements is summarized below. 6 With regard to indicator, consideration was given to replacing Pb-TSP with Pb-PM 10
. 7 The EPA recognized, however, that Pb in all pa rticle sizes co ntributes to Pb in blood and 8 associated health effects, addi tionally noting that the difference in particulate Pb captured by 9
TSP and PM 10 monitors may be on the order of a factor of two in some areas (73 FR 66991). 10 Further, the Administrator recognized uncer tainty with regard to whether a Pb-PM 10 -based 11
standard would also effec tively control ultra-coarse 1 Pb particles, which may have a greater 12 presence in areas near sources where Pb c oncentrations are highest (73 FR 66991). The 13
Administrator decided to retain Pb-TSP as the indicator to provide sufficient public health 14 protection from the range of partic le sizes of ambient air Pb, incl uding ultra-coarse particles (73 15 FR 66991). Additionally, a role was provided for Pb-PM 10 in the monitoring required for a Pb16 TSP standard (73 FR 66991) based on the conclusion that use of Pb-PM 10 measurements at sites 17 not influenced by sources of ultr a-coarse Pb, and where Pb concentrations are well below the 18 standard, would take advantage of the increased precision of these measurements and decreased 19 spatial variation of Pb-PM 10 concentrations, without raising the same con cerns over a lack of 20 protection against health risks from all partic ulate Pb emitted to the ambient air that support 21 retention of Pb-TSP as the indicator ( versus revision to Pb-PM 10 ) (73 FR 66991). Accordingly, 22
allowance was made for the use of Pb-PM 10 monitoring for Pb NAAQS attainment purposes in 23 certain limited circumstances, at non-source-oriented sites, where the Pb concentrations are 24 expected to be substantially belo w the standard and ultra-coarse pa rticles are not expected to be 25 present (73 FR 66991). 26 With regard to averaging time and form, consideraton was given to monthly and 3-month 27 averaging times. The Administrator recognized th e complexity related to the multimedia nature 28 of Pb and its multiple pathways of human exposure, in addition to uncertainty remaining over the 29 period of time needed for air Pb co ncentrations to lead to the health effects most at issue in this 30 review (73 FR 77995). Relevant factors pertai ning to the human physiological response to 31 changes in Pb exposures and those pertaining to the response of air-related Pb exposure 32

1 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.January 2013 4-6 Draft - Do Not Quote or Cite pathways to changes in airborne Pb were considered in an integrated manner (73 FR 77996). 1 Key considerations included the limited eviden ce indicating more numer ous factors influencing 2 ingestion (versus inhalation) pathways, which we re considered likely to lessen the impact of 3
month-to-month variations in airborne Pb concentr ations on levels of air -related Pb in children’s 4 blood. Such factors were considered likely to le ad to response times (e.g., for the response of 5 blood to air Pb via these pathways) extending longer than a month (73 FR 66996). The EPA 6 additionally considered the control that a ro lling 3-month averaging time can provide (e.g., 7 compared to a block calendar quarter) on month-to-month variability in air Pb concentrations 8 and in associated exposures (73 FR 66996). Based on this integrat ed consideration of the range 9 of relevant factors, the averaging time was revised to a rolling three-month period with a 10 maximum (not-to-be-exceeded) form, evaluated over a three-year period. As compared to the 11 previous averaging time and form of calendar qua rter (not-to-be exceeded), this revision was 12 considered to be more scientifically appropria te and more health prot ective (73 FR 77996). The 13 rolling average gives equal wei ght to all three-month periods , and the new calculation method 14 gives equal weight to each month within each three-month period (73 FR 77996). Further, the 15 rolling average yields 12 three-month averages ea ch year to be compared to the NAAQS versus 16 four averages in each year for the block calendar quarters pertaining to the previous standard (73 17 FR 77996). 18 Lastly, based on the body of scientific eviden ce and information available, as well as 19 CASAC recommendations and public comment, the Administrator decided on a standard level 20 that, in combination with the specified choice of indicator, averaging time, and form, he judged 21 requisite to protect public health, including the health of sensitive groups, with an adequate 22 margin of safety (73 FR 67006). In reaching th e decision on level for the revised standard, the 23 Administrator considered as a useful guide th e evidence-based framework developed in that 24
review. As described in s ection 4.1.1.1 above, that framework integrates evidence for the 25 relationship between Pb in air and Pb in chil dren’s blood and the rela tionship between Pb in 26 children’s blood and IQ loss. Application of th e air-related IQ loss evidence-based framework 27 was recognized, however, to provide “no evidence- or risk-based bright line that indicates a 28 single appropriate level” for the standard (73 FR 67006). Rather, the framework was seen as a 29 useful guide for consideration of h ealth risks from exposure to ambien t levels of Pb in the air, in 30 the context of a specified averaging time and form , with regard to the Administrator’s decision 31 on a level for a revised NAAQS that provides public health protection that is sufficient but not 32 more than necessary unde r the Act (73 FR 67004). 33 As noted above, use of the evidence-based air-related IQ loss framework to inform 34
selection of a standard level i nvolved consideration of the evid ence with regard to two input 35 parameters. The two input parameters are an air-to-blood ratio and a C-R function for population 36January 2013 4-7 Draft - Do Not Quote or Cite IQ response associated with blood Pb level (73 FR 67004). The evidence at the time of the last 1 review indicated a broad range of air-to-bl ood ratio estimates, each with limitations and 2
associated uncertainties. Based on the then-availa ble evidence, the Administrator concluded that 3 1:5 to 1:10 represented a reasonabl e range to consider and identif ied 1:7 as a generally central 4 value on which to focus (73 FR 67004). With regard to C-R functions, in li ght of the evidence of 5 nonlinearity and of steeper slope s at lower blood Pb levels, the Administrator concluded it was 6 appropriate to focus on C-R analys es based on blood Pb levels th at most closely reflected the 7 then-current population of children in the U.S., 2 recognizing EPA’s identi fication of four such 8 analyses and giving weight to the central estimate or median of the resultant C-R functions (73 9 FR 67003, Table 3; 73 FR 67004). The four study groups from which C-R functions were drawn 10 in 2008, and the associated C-R slopes, are summarized in Table 3-3 above. 3 The median 11 estimate of -1.75 IQ points decrement per μg/dL wa s selected for use with the framework. With 12 the framework, as summarized in section 4.1.1.1 a bove, potential alternativ e standard levels 13 (μg/m 3 ) are multiplied by estimates of air-t o-blood ratio (μg/dL blood Pb per μg/m 3 air Pb) and 14 the median slope for the C-R function (points IQ decrement per μg/dL blood Pb), yielding 15
estimates of a mean air-related IQ decrement for a specific su bset of young children (i.e., those 16 children exposed to air-related Pb in areas with el evated air Pb concentrations equal to specified 17 alternative levels). As such, the application ofthe framework yields estimates for the mean air18 related IQ decrements of the s ubset of children expected to e xperience air-related Pb exposures 19 at the high end of the distribution of such exposures. The associated mean IQ loss estimate is the 20 average for this highly exposed subset and is not the average air-related IQ loss projected for the 21 entire U.S. population of children. Uncertainties and limitations were r ecognized in the use of 22
the framework and in the resu ltant estimates (73 FR 67000). 23 In considering the use of the evidence-based air-related IQ loss framework to inform his 24 judgment as to the appropriate degree of public h ealth protection that should be afforded by the 25 NAAQS to provide requisite protection against risk of neurocognitive effects in sensitive 26 populations, such as IQ loss in children, the Ad ministrator recognized in the 2008 review that 27 there were no commonly accepted guidelines or crit eria within the public health community that 28 would provide a clear basis for such a judgm ent. During the 2008 review, CASAC commented 29

2 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).
3 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.January 2013 4-8 Draft - Do Not Quote or Cite regarding the significance from a public health pe rspective of a 1-2 point IQ loss in the entire 1 population of children and, along with some co mmenters, emphasized that the NAAQS should 2 prevent air-related IQ loss of a significant magnitude , such as on the order of 1-2 IQ points, in all 3 but a small percentile of the population. Similarl y, the Administrator stated that “ideally air4 related (as well as other) exposures to environmental Pb would be reduced to the point that no IQ 5 impact in children would occur” (73 FR 66998). The Administrator further recognized that, in 6 the case of setting a NAAQS, he was required to make a judgment as to what degree of 7 protection is requisite to protec t public health with an adequate margin of safety (73 FR66998). 8 The NAAQS must be sufficient but not more stringe nt than necessary to achieve that result, and 9 does not require a zero-risk standard (73 FR 66998). The Administrator additionally recognized 10
that the evidence-based air-relate d IQ loss framework did not provi de estimates pertaining to the 11 U.S. population of children as a whole. Ra ther, the framework provides estimates (with 12
associated uncertainties and limitati ons) for the mean of a subset of that population, the subset of 13 children assumed to be exposed to the level of th e standard. As describe d in the final decision 14 “[t]he framework in effect focuses on the se nsitive subpopulation that is the group of children 15 living near sources and more likely to be exposed at the level of the standard” (73 FR 67000). 16
As further noted in the final decision (73 FR 67000): 17 EPA is unable to quantify the pe rcentile of the U.S. popula tion of children that 18 corresponds to the mean of this sensi tive subpopulation. Nor is EPA confident in 19 its ability to develop quantified estimates of air-related IQ loss for higher 20 percentiles than the mean of this sub population. EPA expects that the mean of 21 this subpopulation represents a high, but not quantifiable, perc entile of the U.S. 22 population of children. As a result, EPA expects that a standard based on 23 consideration of this framework would provide the same or greater protection 24 from estimated air-related IQ loss for a high, albeit unquantifiable, percentage of 25 the entire population of U.S. children. 26 27 In reaching a judgment as to the appropria te degree of protection, the Administrator 28
considered advice and recommendations from CA SAC and public comments and recognized the 29
uncertainties in the health effects evidence and re lated information as well as the role of, and 30 context for, a selected air-related IQ loss in the application of the framework. In so doing, the 31 Administrator identified an air-related IQ loss of 2 points to be used in conjunction with the 32 evidence-based framework in considering an ap propriate level for the standard (73 FR 67005). 4 33
Given the various uncertainties associated with the framework and the scientific evidence base, 34
and the focus of the framewor k on the sensitive s ubpopulation of more hi ghly exposed children, 35

4 Also noted that “in determining what level of estimated IQ loss should be used for evaluating the results obtained from this specific evidence-based framework, the Administrator is not determining that such an IQ loss is appropriate for use in other contexts”. (73 FR 67005)January 2013 4-9 Draft - Do Not Quote or Cite a standard level selected using this air-relate d IQ loss, in combination with the selected 1 averaging time and form, was exp ected to significantly reduce a nd limit for a high percentage of 2 U.S. children the risk of experiencing an air-re lated IQ loss of that magnitude (73 FR 67005). At 3 the standard level of 0.15 μg/m 3 , with the combination of the gene rally central estimate of air-to4
blood ratio of 1:7 and the median of the four C-R functions (-1.75 IQ point decrement per μg/dL 5 blood Pb), the framework estimates of air-relat ed IQ loss were below 2 IQ points (73 FR 67005, 6 Table 4). 7 In reaching the decision in 2008 on level for th e revised standard, th e Administrator also 8 considered the results of the qua ntitative risk assessment to provide a useful perspective on risk 9 from air-related Pb. In light of important uncer tainties and limitations for purposes of evaluating 10 potential standard levels, however, the Administ rator placed less weight on the risk estimates 11
than on the evidence-based assessment. Ne vertheless, in recognition of the general 12 comparability of quantitative risk estimates for th e case studies considered most conceptually 13 similar to the scenario represented by the evid ence-based framework, he judged the quantitative 14 risk estimates to be “roughly consistent with and generally supportive” of the evidence-based 15 framework estimates (73 FR 67006). 16
Based on consideration of the entire body of evidence and in formation available in the 17 review, as well as the recommendations of CASAC and public comments, the Administrator 18 decided that a level for the pr imary Pb standard of 0.15 μg/m 3 , in combination with the specified 19 choice of indicator, averaging time and form was requisite to protect pub lic health, including the 20 health of sensitive groups, with an adequate margin of safety (73 FR 67006). In reaching 21
decisions on level as well as the other elements of the revise d standard, the Ad ministrator took 22 note of the complexity associated with consid eration of health effects caused by different 23
ambient air concentrations of Pb and with uncertainties with rega rd to the relationships between 24 air concentrations, exposures, and health effects For example, selection of a maximum, not to 25 be exceeded, form in conjunction with a rolling 3-month averaging time over a three year span 26 was expected to have the effect that the at -risk subpopulation of children would be exposed 27 below the standard most of the time (73 FR 67005). The Administrator additionally noted his 28 consideration of the provision of an adequate margin of safety in making decisions on each of the 29 elements of the standard, including, for exampl e “selection of TSP as the indicator and the 30 rejection of the use of PM 10 scaling factors; selection of a maxi mum, not to be exceeded form, in 31 conjunction with a 3-month averaging time that em ploys a rolling average, with the requirement 32 that each month in the 3-month period be we ighted equally (rather than being averaged by 33 individual data) and that a 3-year span be used for comparison to the standard; and, the use of a 34 range of inputs for the evidence-based framew ork, that includes a focus on higher air-to-blood 35
ratios than the lowest ratio considered to be s upportable, and steeper ra ther than shallower C-R 36January 2013 4-10 Draft - Do Not Quote or Cite functions, and the consideration of these inputs in selection of 0.15 μ g/m 3 as the level of the 1 standard” (73 FR 67007). 2 He additionally noted that a standard with this level would reduce the risk of a variety of 3 health effects associated with exposure to Pb, including effects indicated in the epidemiological 4 studies at lower blood Pb levels, particularly including neurological effects in children, and the 5 potential for cardiovascular a nd renal effects in adults ( 73 FR 67006). The Administrator 6 additionally considered higher a nd lower levels for the standar d, concluding that a level of 0.15 7 μg/m 3 provides for a standard that is neither more or less stringent than necessary for this 8 purpose, recognizing that the Clea n Air Act does not require that primary standards be set at a 9 zero-risk level, but rather at a level that reduces risk sufficientl y so as to protect public health 10 with an adequate margin of safety (73 FR 67007). For example, the Administrator additionally 11 considered potential public health protecti on provided by standard levels above 0.15 μg/m 3

, 12 which he concluded were insufficient to protect pub lic health with an adequa te margin of safety. 13
The Administrator also noted that in light of all of the evidence, including the evidence-based 14 framework, that the degree of public health prot ection likely afforded by standard levels below 15 0.15 μg/m 3 would be greater than what is necessary to protect public safety with an adequate 16 margin of safety. 17 The Administrator concluded, based on review of all of the evid ence (including the 18 evidence- based framework), that when taken as a whole the selected standard, including the 19 indicator, averaging time, form, and level, would be “sufficient but not more than necessary to 20 protect public health, including the health of sensitive subpopulations, with an adequate margin 21 of safety” (73 FR 67007). 22

4.1.2 Approach for the Current Review 23
To evaluate whether it is appropriate to consider reta ining the current primary Pb 24 standard, or whether considerati on of revision is appropriate, we have adopted an approach in 25 this review that builds upon the general approach used in the last review and reflects the broader 26 body of evidence and information now available. As summarized above, the Administrator’s 27 decisions in the prior review were based on an integration of information on health effects 28 associated with exposure to Pb, relationships between ambient air Pb and blood Pb; expert 29 judgments on the adversity and public health si gnificance of key health effects; and policy 30 judgments as to when the standard is requisite to protect public h ealth with an adequate margin 31 of safety. These considerations were informed by air quality and relate d analyses, quantitative 32 exposure and risk assessments, and qualitative assessment of impacts that could not be 33 quantified. 34January 2013 4-11 Draft - Do Not Quote or Cite In conducting this assessment, we draw on the current evid ence and quantitative 1 assessments of exposure pertaining to the public health risk of Pb in ambient air. In considering 2 the scientific and technical information, we consider both the information available at the time of 3 the last review and information newly available since the last review, including the current ISA 4 (USEPA, 2012), as well as the quantitative exposure/ risk assessments from the last review that 5 estimated Pb-related IQ decrements associated w ith different air quality conditions in simulated 6 at-risk populations in multiple case studies (U SEPA, 2007a). Figure 4-1 illustrates the basic 7 construct of our two part appro ach in developing conclusions re garding options appropriate for 8
the Administrator to consider in this review with regard to the adequacy of the current standard 9 and, as appropriate, potential alte rnate standards. In the boxe s of Figure 4-1, the range of 10 questions considered in chapter 3 above and se ction 4.2 below are represented by a summary of 11 policy-relevant questions that frame our c onsideration of the scientific evidence and 12 exposure/risk information. 13January 2013 4-12 Draft - Do Not Quote or Cite 1

Figure 4-1. Overview of approach for review of current primary standard. 2 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 ConsiderationJanuary 2013 4-13 Draft - Do Not Quote or Cite 4.2 ADEQUACY OF THE CURRENT STANDARD 1 In considering the adequ acy of the current Pb standa rd, the overarching question we 2
consider is: 3

 Does the currently available scientific evidence- and exposure/risk-based 4 information, as reflected in the ISA a nd REA, support or call into question the 5 adequacy of the protection afforded by the current Pb standard? 6 In considering the scientific and technical information, we gi ve our attention to both the 7
information available at the time of the last revi ew and information newly available since the last 8 review, including most particularly that which has been critically analyzed and characterized in 9 the ISA. In chapter 3 above, at tention was given to addressing specific questions on key aspects 10 of this information. To assist us in interpreti ng the currently available scientific evidence and 11 results of quantitative exposure/ri sk analyses to address the over arching question here, we draw 12 on discussions in chapter 3 above in our cons ideration of broader or more policy related 13 questions, posed within sections 4.2.1 and 4.2.2 below. 14 For the purposes of this draft PA, staff has drawn from EPA’s assessment and integrated 15 synthesis of the scientific evidence presente d in the third draft ISA and on the quantitative 16 exposure and risk information, based on the 2007 REA (USEPA, 2007a), described in section 3.4 17 above. The evidence-based discussions presen ted in this chapter draw upon evidence from 18 epidemiologic studies and experimental animal studies evaluating health effects related to 19 exposures to Pb, as discussed in the ISA. The exposure/risk-bas ed discussions have drawn from 20 the quantitative health risk analyses for Pb perf ormed in the last Pb NAAQS review in light of 21 the currently available evidence (2007 REA, REA Planning Document). Together the evidence22
based and risk-based considerations inform our preliminary conclusions related to the adequacy 23
of the current Pb standard. 24

4.2.1 Evidence-based Considerations 25 In considering the evidence with regard to th e issue of adequacy of the current standard, 26 we address several questions that build on the information summarized in chapter 3 to more 27 broadly address the extent to which the current evidence base supports the adequacy of the 28 public health protection afforded by the current primary standard. The first question addresses 29 our integrated consideration of the health eff ects evidence, in light of aspects described in 30 chapter 3. The second question focuses on our consid eration of associated areas of uncertainty. 31 The third question then integrates our considerat ion of the prior two questions with a focus on 32 the standard, including each of the four elements. 33January 2013 4-14 Draft - Do Not Quote or Cite  To what extent has new information al tered the scientific support for the 1 occurrence of health effects as a result of multimedia exposure associated with 2 levels of Pb occurring in the ambient air? 3
The current evidence continue s to support our conclusions from the previous review 4 regarding key aspects of the health effects evidence for Pb and the health effects of multimedia 5 exposure associated with levels of Pb occurring in ambient air in the U.S. Our conclusions in 6 this regard are based on considerat ion of the assessment of the curr ently available evidence in the 7 ISA, particularly with regard to key aspects summ arized in chapter 3 of this PA, in light of the 8
assessment of the evidence in the last review as described in the 2006 CD and summarized in the 9 notice of final rulemaking (73 FR 66964). Key aspects of these conclusions are summarized 10
below. 11 As at the time of the last review, blood Pb continues to be the predominant biomarker 12 employed to assess exposure and health risk of Pb (ISA, chapters 4 and 5), as discussed in 13 section 3.1 above. This widely accepted role of blood Pb in assessing exposure and risk is 14 illustrated by its established use in programs to prevent both occupational Pb poisoning and 15 childhood Pb poisoning, with the latter program , implemented by the CDC, recently issuing 16 updated guidance on blood Pb measurement interp retation (CDC, 2012). As in the past, the 17
current evidence continues to indicate the clos e linkage of blood Pb levels in young children to 18 their body burden; this linkage is associated with the ongoing bone remodeling during that 19 lifestage (ISA, section 4.3.5). This tight linkage plays a role in the somewhat rapid response of 20 children’s blood Pb to changes in exposure (p articularly to exposure increases), which 21 contributes to its usefulness as an exposur e biomarker (ISA, sections 4.2.2, 4.3.5, and 4.3.5.1). 22 Additionally, the weight of ev idence documenting relationships between children’s blood Pb and 23 health effects, most particularly those on th e nervous and hematological systems (e.g., ISA, 24 sections 5.3 and 5.7) speaks to its usefulness in assessing health risk. 25 As in the last review, the evidence on air-to -blood relationships av ailable today continues 26 to be comprised of studies based on an a rray of circumstances and population groups (of 27 different age ranges), analyzed by a variety of techniques, which together contribute to 28 appreciable variability in the asso ciated quantitative estimates and uncertainty with regard to the 29 relationships existing in the U.S. today. Accordin gly, our interpretation of this evidence base, as 30 discussed in section 3.1 above, al so includes consideration of f actors that may be influencing 31 various study estimates, both with regard to their usefulness for our general purpose of 32 quantitatively characterizing rela tionships between Pb in ambient air and air-related Pb in 33 children’s blood, and with regard to their pe rtinence more specifical ly to conditions and 34 populations in the U.S. today. In so doing, we note that the current evidence, while including 35
two additional studies not available at the time of the last review, is not much changed from that 36January 2013 4-15 Draft - Do Not Quote or Cite available in the last review. The range of estimat es that can be derived from the full dataset is 1 broad and not changed by the inclusion of the newl y available estimates. Further, we recognize 2 significant uncertainties regarding the air Pb to air-related blood Pb relationship for the current 3
conditions where concentrations of Pb in both ambient air and children’s blood are substantially 4 lower than they have been in the past. In cons idering the strengths, lim itations and uncertainties 5 associated with the full dataset, the currently available evidence appears to continue to support a 6 range of estimates for our purposes that is generally consistent with the range given weight in the 7 last review, 1:5 to 1:10 (ISA, section 4.7.4 and Table 4-12; 73 FR 67001-2, 67004). We 8 additionally note that the generally central estimate of 1:7 identified for this range in the last 9
review is consistent with the study involving blood Pb for pre-school children and air Pb 10 conditions near a large source of Pb to ambient air with concentr ations near (and/or previously 11 above) the level of the current Pb st andard (ISA, section 4.5.1; Hilts, 2003). 5 In so noting, we 12 also recognize the general overlap of such circum stances with those repr esented by the evidence13 based, air-related IQ loss framework, 6 for which air-to-blood ratio is a key input. In 14 characterizing the range of air-to- blood ratio estimates, we recognize uncertainty inherent in such 15 estimates as well as the variation in currently available estimates result ing from a variety of 16 factors, including differences in the populations examined, as we ll as in the Pb sources or 17 exposure pathways addressed in thos e study analyses (ISA, section 4.7.4). 18
The scientific evidence conti nues to recognize a broad array of health effects on multiple 19 organ systems or biological pro cesses related to blood Pb, includi ng Pb in blood prenatally (ISA, 20 section 2.6). The currently available evid ence continues to suppor t identification of 21 neurocognitive effects in young child ren as the most sensitive endpoint associated with blood Pb 22 concentrations (ISA, section 2.6.1), which as an integrated index of exposure reflect the 23 aggregate exposure to all sources of Pb through multiple pathways (inhalation and ingestion). 24
Evidence continues to indicate that neuroc ognitive effects in young children may not be 25 reversible and may have effect s that persist into adulthood (I SA, section 2.9.6). Thus, as 26 discussed in section 3.2 above, we continue to consider the eviden ce of Pb effects at the low end 27 of the studied blood Pb levels (closest to those co mmon in the U.S. today) to be strongest and of 28 greatest concern for effects on th e nervous system, most particul arly those on cognitive function 29
in children. 30 As in the last review, evidence on risk fact ors continues to support the identification of 31 young children as an important at-risk population for Pb health effects (ISA, section 6.4). The 32

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.January 2013 4-16 Draft - Do Not Quote or Cite current evidence also continues to indicate important roles as factors that increase risk of lead1
related health effects for: nutri tional factors, such as iron and calcium intake; elevated blood Pb 2 levels; and proximity to sources of Pb exposure, su ch as industrial releases or buildings with old, 3 deteriorating, leaded paint. Further, some races or ethnic groups continue to demonstrate 4
increased blood Pb levels relative to others, which may be related to these and other factors (ISA, 5 sections 6.1, 6.2 and 6.4). 6 With regard to our understanding of the rela tionship between exposur e or blood Pb levels 7 in young children and neurocognitive effects, the evid ence in this review, as in the last, does not 8
establish threshold blood Pb le vel for neurocognitive effects in young children (ISA, sections 9 2.9.4 and 5.3.13). The lowest blood Pb levels at which associations with neurocognitive impacts 10 have been observed in pre-school and school age children continue to range down below 5 11 μg/dL, with lowest group levels that have been associated with such effects ranging down to 2 12 μg/dL (ISA, sections 2.6.1.1 and 5.3.16.1). Additionally, as in the last review, there is evidence 13 that the relationship of young child ren’s blood Pb with neurocognitiv e impacts, such as IQ, is 14 nonlinear across a wide range of blood Pb, with gr eater incremental impacts at lower vs. higher 15 blood Pb levels (ISA, sections 2.9.4 and 5.3.13). Accord ingly, as in the last review, we continue 16 to focus our interest on C-R relationships from study groups with blood Pb levels closest to those 17 in children in the U.S. today, which are genera lly lower than epidemiological study groups. The 18 currently available evidence does not identify additional C-R slopes for study groups of young 19 children (e.g., < 7 years) with mean blood Pb levels belo w that of groups iden tified in the last 20 review, 2.9 – 3.8 μg/dL, as discussed in secti on 3.2 above (ISA, section 5.3.13). Thus, the blood 21 Pb concentration - IQ response f unctions or slopes identified in this review for epidemiological 22 study groups of young children with mean blood Pb leve ls closest to that of children in the U.S. 23 today include the same set recogni zed at the time of the last revi ew (see Table 3-3 above), the 24 median of which is 1.75 points decrement per μg/dL blood Pb (73 FR, 67003). 25

 To what extent have important uncertaint ies identified in the last review been 26 reduced and/or have new uncertainties emerged? 27 In our consideration of the evidence, as su mmarized in discussing the previous question 28 and in chapter 3 above, we have not identified any new uncertain ties as emerging since the last 29 review. However, we continue to recognize import ant uncertainties identifi ed in the last review 30 that remain today. Importantly, given our focus in this review , as in the last review, on 31 neurocognitive impacts associated with Pb e xposure in early childhood, we recognize remaining 32 uncertainties in our understanding of the C-R rela tionship of neurocognitive impacts, such as IQ 33 decrements, with blood Pb level in young children, particularly across the range of blood Pb 34 levels common in the U.S. today. With rega rd to C-R relationships for IQ, the evidence 35
available in this review does not include studies that appreciab ly extend the range of blood Pb 36January 2013 4-17 Draft - Do Not Quote or Cite levels studied beyond those availa ble in the last review. As in the last review, the early 1 childhood (e.g., 2 to 6 or 7 years of age) blood Pb levels for which associations with IQ response 2 have been reported continue to extend at the low end of the range to study group mean blood Pb 3 levels of 2.9 to 3.8 μg/dL (e.g., 73 FR 67003, Table 3) . The studies at th ese blood Pb levels do 4 not provide evidence of a thresh old level and, as summarized in section 3.2 above, continue to 5 indicate higher C-R slopes in these groups with lower blood Pb levels than in study groups with 6 higher blood Pb levels (ISA, section 5.3.13). 7 Further, we recognize important uncertainti es in our understanding of the relationship 8
between ambient air Pb concentrations and air- related Pb in children’s blood. The evidence 9 newly available in this review ha s not reduced such key uncertainties. As in the last review, air10
to-blood ratios based on the available evidence con tinue to vary, with our conclusions based on 11 the current evidence generally consistent with the range of 1:5 to 1:10 given emphasis in the last 12 review (73 FR 67002; ISA, section 4.7.4). There c ontinues to be uncertainty regarding the extent 13 to which this range represents the relationship between ambient air Pb and Pb in children’s blood 14 (derived from the full set of air-related exposure pathways), and with regard to its reflection of 15 exposures associated with ambient air Pb levels common in the U.S. today and to circumstances 16 reflecting just meeting the current Pb standard (ISA, section 4.7.4). We note additionally the 17 significant uncertainty remaining with regard to th e temporal relationships of ambient Pb levels 18 and associated exposure with occurrence of a health effect (73 FR 67005). 19

 To what extent does newly available info rmation support or call into question any 20 of the basic elements of the current Pb standard? 21 We address this question for each of the elemen ts of the standard in light of the health 22
effects evidence and other relevant information ava ilable in this review. As an initial matter, 23 however, we recognize the weight of the scientif ic evidence available in this review that 24 continues to support our focus on effects on the nervous system of young children, and 25 specifically neurocognitive decrements, as the most sensitive endpoint. Consistent with the 26 evidence available in the last review, the currently available evidence continues to indicate that a 27 standard that provides requisite public health protection against the occurrence of such effects in 28 at-risk populations would also prov ide the requisite public health protection agains t the full array 29 of health effects of Pb. Accordingly, the disc ussion of the elements below is framed by that 30 background. 31
Indicator 32
The indicator for the current Pb standard is Pb-TSP. Exposure to Pb in all sizes of 33 particles passing through ambient air can contribute to Pb in bl ood and associated health effects 34 by a wide array of exposure pathways (ISA, sec tion 4.1). These pathways include the ingestion 35 route, as well as inhalation (ISA, section 4.1), and a wide array of particle sizes play a role in 36January 2013 4-18 Draft - Do Not Quote or Cite these pathways (ISA, section 4.1.1.1). As at the time of the last re view, we continue to recognize 1 the variability of the Pb-TSP FRM in its capt ure of airborne Pb pa rticles (see section 2.2.1.3.1 2 above). As in the last review, we also note th at an alternative appro ach for collection of a 3 conceptually comparable range of particle sizes, including ultra- coarse particles, is not yet 4 available, although we take note of activities under way to remedy that situation in the future, as 5
referenced in section 2.2.1.3.1 above. Additionall y, the limited available information regarding 6 relationships between Pb-TSP and Pb in other size fractions indicates appreciable variation in 7 this relationship, particularly n ear sources of Pb emissions wher e concentrations, and potential 8 exposures, are greatest. Thus, the informati on available in this review does not address 9 previously identified limitations and uncertaintie s for the current indicat or. Nor does the newly 10 available information identify additional limitations or uncertainties. The evidence available in 11
this review continues to indicate th e role of a range of air Pb part icle sizes in contributing to Pb 12 exposure (e.g., ISA, section 4.1.1.1), th at contributes to Pb in blood a nd associated health effects, 13 reinforcing the appropriateness of an indicator for the Pb standard that reflects a wide range of 14 airborne Pb particles. 15 Averaging time and form 16 The averaging time and form of the current standard is a not-to-be-exceeded rolling 17 three-month average (CFR 50.16), derived from thr ee monthly averages calculated in accordance 18 with the current data handling pro cedures (CFR, Appendix R to Part 50). As at the time of the 19 last review, evidence continues to support the importanc e of periods on the order of 3 months 20 and the prominent role of deposition-related exposur e pathways, with uncertainty associated with 21 characterization of precise time periods associating am bient air Pb with air-related health effects. 22 Relevant factors continue to be those pertaini ng to the human physiological response to changes 23 in Pb exposures and those pertaining to the re sponse of air-related Pb exposure pathways to 24 changes in airborne Pb. The newly available evidence in this review does not appreciably 25 improve our understanding of the period of time in which air Pb concentrations would lead to the 26
health effects most at issue in th is review. Thus, there continue to be limitations in the evidence 27
to inform our consideration of these elements of the standard and a ssociated uncertainty. 28 However, there is no newly available information that calls into question this element of the 29
current Pb standard. 30
Level 31 The level of the current standard is 0.15 μg/m 3 (CFR 50.16). As described in section 32 4.1.1 above, this level was selected in 2008 with consideration of, among other factors, an 33 evidence-based air-related IQ loss framework, fo r which there are two primary inputs: air-to34 blood ratios and C-R functions for blood Pb – IQ response in young children. Additionally taken 35
into consideration were the uncer tainties inherent in these inputs. Application of the framework 36January 2013 4-19 Draft - Do Not Quote or Cite also entailed consideration of a magnitude of air-related IQ loss, which as further described in 1 section 4.1.1.2 above, is used in conjunction with this specific framework in light of the 2 framework context, limitations and uncertainties . Additionally, selecti on of a level for the 3 standard in 2008 was made in conj unction with decisions on indica tor, averaging time and form. 4 As an initial matter, we consider the extent to which the evidence-based, air-related IQ 5
loss framework which informed the Administrator’s decision in the last review is supported by 6 the currently available evidence and information. In so doing, we recognize the support provided 7 by the currently available evidence for the key conc lusions drawn in the last review with regard 8 to health effects of greatest c oncern, at-risk populations, the influe nce of Pb in ambient air on Pb 9
in children’s blood and the association betw een children’s blood Pb and decrements in 10 neurocognitive function (e.g., IQ). We additi onally note the complexity associated with 11 interpreting the scientific evidence with regard to specific levels of Pb in ambient air, given the 12 focus of the evidence on blood Pb as the key biom arker of children’s aggregate exposure. The 13 need to make such interpretations in the face of the associated complex ity supported use of the 14
evidence-based framework in the last review. In considering the currently available evidence for 15 the same purposes in this review, we conclude that the evidence-based framework continues to 16 provide a useful tool for consider ation of the evidence w ith regard to the level of the standard. 17 We next turn to consideration of the primary inputs to the framework: air-to-blood ratios 18 and C-R functions for blood Pb – IQ response in young children. With regard to the former, the 19 limited newly available information assessed in th e ISA, and discussed in section 3.1 above, is 20 generally consistent with the information in this area that was available at the time of the last 21 review. We additionally recogni ze the variability and uncertainty associated with quantitative 22
air-to-blood ratios based on this in formation, as also existed in the last review. As in the last 23 review, we recognize that factor s contributing to the variabil ity and uncertainty of these 24 estimates are varied, and incl ude aspects of the study populati ons (e.g., age and Pb exposure 25 pathways) and the study circumstances (e.g., length of study period and vari ations in sources of 26 Pb exposure during the study period). We note that the full range of estimates associated with 27 the available evidence is wide, and consider it appropriate to give emphasis to estimates 28 pertaining to circumstances closest to those in the U.S. today with regard to ambient air Pb and 29
children’s blood Pb concentrati ons, while recognizing the limita tions associated with the 30 available information with regard to this emphasis. With that in mind, we consider the currently 31 available evidence to continue to support the rang e of estimates concluded in the last review to 32 be most appropriate for the current population of young children in the U.S., in light of the 33 multiple air-related exposure pathways by which children are exposed, in addition to inhalation 34 of ambient air, and of the levels of air and bl ood Pb common today. Identification of this range 35
also included consideration of the limitations associated with the available information and 36January 2013 4-20 Draft - Do Not Quote or Cite inherent uncertainties. This range of air-to-blood ratios included 1:10 at th e upper end and 1:5 at 1 the lower end. We further recogni ze that the limited evidence fo r air Pb and children’s blood Pb 2
concentrations closest to those in U.S. today continues to prov ide support for the Administrator’s 3 emphasis in the 2008 decision on the rela tively central estimate of 1:7. 4 With regard to the second input to the ev idence-based framework, C-R functions for the 5 relationship of young children’s bloo d Pb with neurocognitive impacts (e.g., IQ decrements), we 6 consider several aspects of the evidence. First, as discussed in section 3.2 above, the currently 7 available information continues to provide evidence that this C-R relationship is nonlinear across 8 the range of blood Pb levels from the higher concen trations more prevalent in the past to lower 9 concentrations more common today. Thus, we conti nue to consider it partic ularly appropriate to 10
focus on the evidence from studies with blood Pb le vels closest to those of today’s population, 11
which in the last review included studies with study group mean blood Pb levels ranging roughly 12 from 3 to 4 μg/dL in children aged 24 months to 7 years (Table 3-3 above). As discussed in 13 sections 3.2 above, this is also consistent with the evidence currently avai lable for this age group 14 of young children, and the currently available evidence does not include additional C-R slopes 15 for incremental neurocognitive decrement with blood Pb levels at or below this range. In 16 considering whether this set of functions continues to be well supported by the evidence, as 17 assessed in the ISA (ISA, section 5.3.2), we note the somewhat wide range in slopes 18 encompassed by these study groups, while also noting the stability of the median. For example, 19 omission of any of the four slope s considered in the last review does not appreciably change the 20 median (e.g., the median would change from - 1.75 IQ points per μg/dL blood Pb to -1.71 or - 21 1.79). Thus, we conclude that wh ile differing judgments might be ma de with regard to inclusion 22 of each of the four study groups, these estimates ar e generally supported by the current review of 23
the evidence in the ISA. Furthe r, the stability of the median to modifications to this limited 24
dataset lead us to conclude that the currently availabl e evidence continues to support 25 consideration of -1.75 IQ points per μg/dL blood Pb as a well founded and stable estimate for 26 purposes of describing the neurocognitive impact quantitatively on this age group of U.S. 27
children. 28 In summary, in considering the evidence a nd information available in this review 29 pertaining to the level of the current Pb standar d, we note that the evidence available in this 30 review, as summarized in the ISA, continues to support the air-related IQ loss evidence-based 31 framework, with the inputs that were used in the last review. These include estimates of air-to32 blood ratios ranging from 1:5 to 1:10, with a gene rally central estimate of 1:7. Additionally, the 33
C-R functions most relevant to blood Pb levels in U.S. children today continue to be provided by 34 the set of four analyses consider ed in the last review for whic h the median estimate is -1.75 IQ 35 points per μg/dL Pb in young children’s blood. Thus , we observe that the evidence available in 36January 2013 4-21 Draft - Do Not Quote or Cite this review has changed little if at all with regard to the aspect s given weight in the conclusion on 1
level for the new standard in the last review and would not appear to call into question any of the 2 basic elements of the standard. In so doing, we additionally recognize that the overall decision 3 on adequacy of the current standard is a public health policy judgment by the Administrator; we 4
discuss considerations that inform su ch judgments in section 4.3 below. 5

4.2.2 Exposure/Risk-based Considerations 6 Our consideration of the issue of adequacy of public health protection provided by the 7 current standard is also informed by the quantita tive exposure/risk asse ssment completed in the 8 last review, augmented as described in section 3.4 above. We have organized the discussion that 9 follows around two questions to assist us in in terpreting the results of the assessment of case 10 studies simulated to meet several different air qu ality conditions, including those just meeting the 11
current standard. 12

 What is the level of confidence associat ed with estimates of air-related risk 13 generated for simulations just meeting the current Pb standard? 14 As an initial matter, we recognize the signifi cant limitations and complexity associated 15 with the risk/exposure assessmen t for Pb that are far beyond those associated with similar 16 assessments typically performed for other criteria pollutants. In completing the assessment we 17 were constrained by significant limitations with rega rd to data and tools particular to the problem 18 at hand. Further, the multimedia and persistent nature of Pb and the role of multiple exposure 19 pathways contribute significant additional complexity to the assessment as compared to other 20 assessments that focus only on the inhalation path way. As a result, our estimates of air-related 21 exposure and risk are approximate, presente d as upper and lower bounds within which we 22 consider air-related risk likely to fall. We ba se our description of overall confidence in this 23
characterization of air-related ri sk on our consideration of the ove rall design of the analysis (as 24 described in section 3.4 above), the degree to which key sources of variability are reflected in the 25 design of the analysis, and our characteri zation of key sources of uncertainty. 26 In considering the degree to which key sources of variability (discussed in section 3.4.6 27 above) are reflected in the design of the analys is, we note the following aspects addressed by the 28
risk assessment. 29

 Variation in distributions of potential urban residential exposure and risk across U.S. 30 urban residential areas. This is addressed by the inclus ion of three different (location31 specific) urban study areas that reflect a di verse set of urban areas in the U.S. 32

 Representation of a more highly-exposed subset of urban residents potentially exposed at 33 the level of the standard. This is addressed by the incl usion of the generalized (local) 34 urban study area. 35January 2013 4-22 Draft - Do Not Quote or Cite  Variation in residential exposure to ambient air Pb within an urban area. This is 1 addressed through the partitio ning of the location-specific study areas into exposure 2 zones to provide some representation of sp atial gradients in ambient air Pb and their 3 interaction with population dist ribution and demographics. This was done in a somewhat 4 more precise manner in the primary Pb smelter case study, which relied on dispersion 5 modeling to describe gradient s, as compared with the ma nual assignment of gradients 6 related to air concentration differe nces among monitors in an area. 7

 Inter-individual variability in blood Pb levels. This is addressed though the use of 8 empirically-derived GSDs to develop blood Pb distribution for the child population in 9 each exposure zone, with GSDs selected pa rticular to each case study populations. 10

 Inter-individual variability in IQ response to blood Pb. This is addressed through the use 11 of C-R functions for IQ loss based on a pool ed analysis reflecti ng studies of diverse 12 populations. 13 We also considered key sources of uncerta inty (discussed in section 3.4.7 above), in 14 particular the overarching area co ncerning the precision of the ai r-related risk estimates, as 15 mentioned above. Associated sources of uncertainty include our inab ility to simulate changes in 16 air-related Pb as a function of changes in ambien t air Pb in exposure pathways other than those 17 involving inhalation of ambient air and ingestion of indoor dust. Th is contributes to the positive 18 bias of the upper bound for the air-related risk estimates. We a dditionally recognize the 19 significant uncertainty associated with estima ting upper percentiles of the distribution of air20
related blood Pb concentration estimates (and associat ed IQ loss estimates) due to limitations in 21 available information. Lastly, we recognize the un certainty associated with application of the C22
R function at the lower blood Pb levels in th e distribution; this relates to the limited 23 representation of blood Pb levels of this magnitude in the dataset from which the C-R function is 24
derived. 25 In the quantitative risk information available in this review, we ha ve air-related risk 26 estimates for simulations just meeting the current standard from one of the location-specific 27 urban case studies (Chicago) and fr om the generalized (local) urba n case study. With regard to 28 the latter, we note its simplified design that does not include multiple exposure zones, thus 29 reducing the dimensions simulated. We have a r easonable degree of confidence in aspects of the 30 generalized (local) urban case study for the specific situation we consider it to represent (i.e., a 31 temporal pattern of air Pb concentrations that ju st meets the level of the standard), and when the 32
associated estimates are characterized as approximate, within upper and lower bounds (as 33 described in section 3.4.4 above), while also reco gnizing considerable asso ciated uncertainty. 34January 2013 4-23 Draft - Do Not Quote or Cite  To what extent are the air-related risk s remaining upon just meeting the current 1 Pb standard important from a public health perspective? 2 In considering public health importance of estim ated air-related risks, we consider here 3 the nature and magnitude of such estimated risk s (and attendant uncertain ties), including such 4 impacts on the affected population, and we addi tionally consider the size of the affected 5 population. Based on the evidence available in the la st review and consistent with that available 6 today, the quantitative risk estimates developed in the 2007 REA and augmented slightly in this 7 review are for decrements in IQ, an estab lished indicator of neur ocognitive function. In 8 considering these estimates, we recognize that although some neurocognitive effects may be 9 transient, some effects may persist into adult hood, affecting success later in life (ISA, sections 10 2.9.5 and 5.3.15). We additionally recognize the poten tial population impacts of small changes 11 in population mean values of metrics such as IQ, presumi ng a uniform manifestation of lead12 related decrement across the range of population IQ (ISA, section 2.9.1), as noted in section 3.3 13
above. 14 Exposures and risks associated with air-re lated Pb under several different air quality 15
conditions were estimated in the 2007 REA. As summarized in section 3.4 above, limitations in 16 our modeling tools and data affected our ability to develop precise estimates for air-related 17 exposure pathways and contributed uncertainties. The results are approximate estimates which 18 we describe through the use of rough upper a nd lower bounds within which we estimate air19 related risk to fall. We have recognized a number of uncertainties in the underlying risk 20 estimates from the 2007 REA and in the interpolation approach employed in the new analyses 21 for this review. We have characterized the magn itude of air-related risk associated with the 22
current standard with a focus on median estim ates, for which we have appreciably greater 23
confidence than estimates for outer ends of ri sk distribution (see section 3.4.7) and on risks 24 derived using the C-R function in which we ha ve greatest confidence (s ee sections 3.4.3.3.1 and 25 3.4.7). These risk estimates include estimates fr om the last review for one of the location26 specific urban study area populations as well as estimates newly de rived in this review based on 27 interpolation from 2007 REA results for the ge neralized (local) urban case study, which is 28 recognized to reflect a generalized high end of air-related exposure for localized populations. 29 Taken together, these estimates indicate air-related risk associated with just meeting the current 30 standard of a magnitude generally within th e bounds of roughly 1 and 3 points IQ loss. 31 In considering the importance of such risk from a public health perspective, we also 32 consider the size of at-risk populations represen ted by the REA case studies. As discussed in 33 section 3.4 above, the generalized (l ocal) urban case study is consid ered to represent a localized 34 urban population exposed near th e level of the standard, such as a very small, compact 35 neighborhood near a source contributing to air Pb c oncentrations just meeting the standard. This 36January 2013 4-24 Draft - Do Not Quote or Cite case study provides representation in the risk assessment for such small populations at the upper 1 end of the gradient in ambient ai r concentrations expected to o ccur near sources; thus estimates 2 for this case study reflect exposures nearest the standard being evaluated. While we do not have 3 precise estimates of the number of young children living in such area s of the U.S. today, we have 4 information that informs our understanding of thei r magnitude. For example, as discussed in 5 section 3.3 above (Table 3-3), we estimate th ere to be approximately 2,400 children, aged 5 6 years and younger, residing within 0.5 km of a monitor with ai r Pb concentrations above the 7
current standard. We further observe several additional monitors with maximum 3-month Pb 8
concentrations that fall below but within 10% of the current standard level (as noted in section 9 3.3 above); an estimated 265 young children reside near these monitors. Thus, together we 10 estimate some 2700 children, aged 5 years and younge r, living in localized areas with elevated 11
air Pb concentrations that ar e above or near the current st andard. Based on the 2010 census 12 estimates of approximately 24.3 million children in the U.S. aged five years or younger, this 13 represents approximately one hundredth of one percent of this age group in the U.S. 7 This 14 indicates the size of the popul ation of young children of this age living in areas in close 15 proximity to areas where air Pb concentrations ma y be above or near the current standard to be 16 approximately 2700, which is approximately a hundred th of one percent of the full population of 17 correspondingly aged children. 8 18 In summary, we recognize substantial uncerta inty inherent in the REA estimates of air19 related risk associated with conditions just meeting the current standard, which we characterize 20 as approximate and falling somewhat above the rough lower bound of 1 and below the rough 21 upper bound of 3 IQ points. 9 This approximate estimate of risk for children living in such areas 22 is generally overlapping with and co nsistent with the evidence-based air-related IQ loss estimates 23 summarized in section 4.2.1 above. With regard to the the importance of the estimated risks 24 from a public health perspective, we note, based on the currently available monitoring and 25 census data, the estimated size of the aff ected population to be approximately 2700 young 26 children, representing slightly more than one one hundredth of a percent of the full population of 27

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 gr oup that the subset represents.
8 This estimate includes children in areas where r ecent information indicates the standard is exceeded because areas not in atttainment 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 ai r Pb concentrations near the current standaard.
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).January 2013 4-25 Draft - Do Not Quote or Cite similarly aged children. In cons idering the exposure/risk estima tes during the last review, the 1 Administrator took note of the important uncerta inties and limitations associated with these 2 assessments and, while placing less weight on th e assessment estimates, he recognized the 3 quantitative risk estimates to be “roughly cons istent with and genera lly supportive” of those 4 estimated by the evidence-based framework. In our consideration of the risk estimates 5 considered in the last review, as well as the es timates for the current standard that have been 6 newly developed in this review for the gene ralized (local) urban case study (see section 7 3.4.3.3.2), we agree with the previous characteriza tion. As would be expected by the use of 8 interpolation, the newly derived es timates are consistent with the estimates for similar air quality 9
scenarios that were available in the last review. 10

4.3 PRELIMINARY STAFF CONCLUSIONS ON THE PRIMARY STANDARD 11 This section describes preliminary staff conc lusions regarding ade quacy of the current 12 primary Pb standard. These conclusions are base d on considerations described above and in the 13 discussion below regarding the currently available scientific evidence summarized in the third 14 draft ISA and prior CDs and the risk and expos ure information drawn from the 2007 REA. The 15 final PA will draw upon the final ISA, devel oped after CASAC review and public comment on 16 the third draft ISA. Further, staff conclusions presented in the final PA will take into account 17 advice from CASAC and public comment on the draft PA and the preliminary conclusions. 18 Taking into consideration the discussions res ponding to specific ques tions above in this 19 and the prior chapter, this section addre sses the following overar ching policy question. 20

 Does the currently available scientific evidence- and exposure/risk-based 21 information, as reflected in the ISA a nd REA, support or call into question the 22 adequacy of the protection afforded by the current Pb standard? 23 Our response to this question takes into c onsideration the discussions responding to the 24 specific policy-relevant questions in prior sections of this document (see sections 3.1-3.4, 4.2.1, 25 and 4.2.2). In so doing, we focus first on consid eration of the evidence, including that newly 26 available in this review, and th e extent to which it alters ke y conclusions suppor ting the current 27
standard. We then turn to consideration of th e quantitative risk estimates drawn from the 2007 28 REA, and associated limitations and uncertainties . We additionally cons ider the public health 29 policy judgments and judgments about the uncertain ties inherent in the scientific evidence and 30 quantitative analyses that are i nherent in decisions on the adequacy of the current primary Pb 31
standard. 32 We first recognize the complexity involved in considering the adequ acy of protection in 33 the case of the primary Pb standard, which di ffers substantially from that involved in 34 consideration of the NAAQS for ot her pollutants. Unlike the case for Pb, the other pollutants for 35January 2013 4-26 Draft - Do Not Quote or Cite which NAAQS are set involve only inhalation e xposure pathways, a relatively simpler context. 10 1 In addition, generally an important component of the scientific evidence base considered in 2 reviewing the adequacy of NAAQS for other pollutants is the availability of studies that have 3 investigated associations betw een current concentrations of the pollutant in ambient air 4 (including in circumstances where the current st andard is met) and th e occurrence of health 5 effects judged plausibly relate d to ambient air exposure to th e NAAQS pollutant. While such 6 studies, targeting locations near air Pb sources such as smelters, were available at the time the Pb 7 NAAQS was initially set in 1978, and to a much more limited degree at the time of the last 8 review, such studies of health effects under air quality conditi ons near those reflecting the 9
current standard are not available in this review . Rather, the evidence ba se that supports our 10
conclusions in this review includes most prominently epid emiological studies reporting 11 associations of blood Pb levels in U.S. populatio ns, including the partic ularly at-risk population 12 of young children with health eff ects judged plausibly related to Pb exposures. Support for our 13 conclusions regarding the plausibili ty for ambient air Pb to play a role in such findings derives, 14 in part, from studies linking Pb in ambient air w ith the occurrence of health effects. However, 15 such studies (dating from the past or from other countries) involv e ambient air Pb concentrations 16 many times greater than those that would meet th e current standard. T hus, in considering the 17 adequacy of the current Pb standard, rather th an considering studies th at have investigated 18 current concentrations of Pb in ambient air (inc luding in locations where the current standard is 19 met) and the occurrence of health effects, we primarily consider the evidence for, and risk 20 estimated from, models based upon key relationships, such as those between ambient air Pb, Pb 21 exposure, blood Pb and health effects. This evidence, with its asso ciated limitations and 22 uncertainties, contributes to our conclusions re garding a relationship between ambient air Pb 23
conditions under the current st andard and health effects. 24 In considering the currently available eviden ce, staff gives great weight to the long25 standing body of evidence on the hea lth effects of Pb, augmented in some aspects since the last 26 review, which continues to support identificatio n of neurocognitive effects in young children as 27 the most sensitive endpoint associated with Pb exposure, as discussed in sections 3.2 and 3.3 28
above. The evidence continues to indicate that a standard that provides protection from 29 neurocognitive effects in young child ren additionally provides protec tion for other health effects 30 of Pb, such as cardiovascular eff ects later in life. Application of the evidence-ba sed, air-related 31 IQ loss framework, developed in the last review, continues to provide a useful approach for 32

10 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).January 2013 4-27 Draft - Do Not Quote or Cite considering and integrating the evidence on relati onships between Pb in ambient air and Pb in 1 children’s blood and risks of neurocognitive effects (IQ loss). The currently available evidence 2 base, while somewhat expanded since the last re view, is not appreciabl y expanded or supportive 3 of appreciably different conclusions with regard to air-to-blood ratios (section 3.1 above) or C-R 4 functions for neurocognitive decrements (section 3.2 above) in young children. 5 As in the last review, uncertainties remain in our understanding of important aspects of 6 ambient air Pb exposure and associated health e ffects. For example, important uncertainties 7 remain, both with regard to air-to-blood ratios that refl ect the relationship between 8
concentrations of Pb in ambient air and air-related Pb in children’s blood, and to estimates of the 9 slope of the C-R function for neurocognitive impact s (IQ loss) at lower blood Pb levels. With 10 regard to the former, we note par ticularly the limitations associated with the available studies and 11 gaps in the evidence base with regard to studi es that have investig ated such quantitative 12 relationships under conditions pertai ning to the current standard (e .g., in localized areas near air 13
Pb sources where the standard is met in the U.S. today). Further, in considering our reliance on 14 the evidence in performing quantitative modeli ng of exposure and risk we additionally note 15 important uncertainties associated with rela tionships between ambient air Pb and outdoor 16 soil/dust Pb and indoor dust Pb that particularly affect our quantitative estimates of air-related 17
risk under conditions of lower am bient air Pb levels and lower blood Pb levels (73 FR 66981). 18 These critical exposure pathways are also inherent in the evid ence-based air-related IQ loss 19 framework, encompassed within the estimates of air-to-blood ratios . Thus, we recognize 20 uncertainties related to our understanding of th ese and other processes that also contribute 21 uncertainty to our application of the evidence-based framework. We consider this uncertainty to 22 be increased with application of the framework for levels below the current standard given the 23 weaker linkage with existing evidence, as noted below. 24 We additionally take note of the role of public health policy judgments in the 25 Administrator’s setting of the current standard in 2008, as summa rized in section 4.1.1.2 above. 26 Such judgments are inherent in setting the standard, a nd particularly in us ing the evidence-based 27
framework to inform the decision on level for the standard, and in consid ering the exposure/risk 28 information. We recognize that publ ic health policy judgments always play an important role in 29 each NAAQS review for each pollutant. One type of public health policy judgments focuses on 30 how to consider the nature and magnitude of the array of uncertainties that are inherent in the 31 scientific evidence and analyses. These judgments are traditionally made with a recognition that 32 our understanding of the relationshi ps between the presence of a pollutant in ambient air and 33
associated health effects is based on a broad body of information encompassing not only more 34 established aspects of the evidence but also aspects in which there may be substantial 35 uncertainty. In the case of the Pb NAAQS review, we recognize incr eased uncertainty in 36January 2013 4-28 Draft - Do Not Quote or Cite characterizing the IQ response to blood Pb levels below those represente d in the evidence base. 1 We also recognize increased uncertainty in pr ojecting the magnitude of blood Pb response to 2
ambient air Pb concentrations at and below the le vel of the current standard. We recognize this 3 increased uncertainty particularly in light of the multiple factors that play a role in such a 4 projection (e.g., meteorology, atmospheric disp ersion and deposition, human physiology and 5 behavior), for each of which we recognize attendan t uncertainties. Collectively, these aspects of 6
the evidence and associated uncer tainties contribute to a recogn ition that for Pb, as for other 7 pollutants, the available health effects evidence generally reflects a continuum, consisting of 8
ambient levels at which scientists generally agree that health eff ects are likely to occur, through 9 lower levels at which the likelihood and magn itude of the response become increasingly 10
uncertain. 11 Reviews may also require judgments as to the point at which health effects become 12 important from a public health perspective. In th e case of Pb, such a judgment is explicitly made 13 in considering the public health significance of one to two points IQ loss in at-risk populations, 14 such as young children. This type of judgment also includes consider ation of the IQ loss 15 estimates yielded by the air-rela ted IQ loss evidence-based framework for specific combinations 16 of standard level, air-to-blood ratio and C-R func tion. With regard to public health significance 17 of one to two points IQ loss in young children, st aff gives weight to th e comments of CASAC 18 and some public commenters in the last review which recognized such a magnitude of IQ loss to 19 be of public health significance and recommended that a very high percen tage of the population 20 be protected from such a magnitude of IQ loss (73 FR 67000). 11 With this objective in mind, we 21
consider the extent to which the air-relate d IQ loss evidence-based framework informs 22 consideration of standards that might be conclude d to provide such a leve l of protection. In so 23 doing, we first recognize that the IQ loss estimat es produced with the evidence-based framework 24 do not correspond to a specific quantitative public h ealth policy goal for air-related IQ loss that 25 would be acceptable or unacceptable for the entire population of children in the U.S. Rather, the 26 conceptual context for the evidence-based framew ork is that it provides estimates for the mean 27 air-related IQ loss of a subset of the population of U.S. children (i.e., the subset living in close 28 proximity to air Pb sources that contributed to elevated air Pb concentrations that equal the 29 current level of the standard). This is the subs et expected to experience air-related Pb exposures 30 at the high end of the national distribution of such exposures. The associated mean IQ loss 31 estimate is the average for this highly exposed s ubset and is not the aver age air-related IQ loss 32

11 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 5.3.2; 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.January 2013 4-29 Draft - Do Not Quote or Cite projected for the entire U.S. population of children. Further, we recognize uncertainties 1 associated with those estimates, which increase with estimates associated with successively 2
lower standard levels. 3 For the current standard level of 0.15 μg/m 3 , an air-to-blood ratio estimate of 7 μg/dL per 4 μg/m 3 (which we note as reasonably representative of the range supported by the evidence) and a 5 C-R slope of -1.75 IQ points per μg/dL, the IQ loss estimate using the evidence-based 6 framework is 1.8 points. 12 As noted above, this value is c onsidered to be an estimate, with 7 attendant uncertainties, of mean ai r-related IQ loss of a subset of the population of U.S. children 8 in the high end of the exposure distribution for air-related Pb. 13 As noted in section 4.2.2 above, 9 our current information on numbers of young childre n living near monitors above or within 10% 10
of the current Pb standard indicates the size of this population subset to be on the order of 2700 11 children aged 5 years or younger, which would correspond to approximately one hundredth of 12 one percent of the U.S. population of this age children (estimated at approximately 24 million in 13 2010 census). A primary objective of the monitoring network for Pb is to identify and monitor 14
sites of maximum concentration in areas antic ipated to be at risk of exceeding the NAAQS. 15 While we acknowledge the possibility that the monitoring data thus far available may not 16 identify every occurrence of elevated Pb concen trations, the size of such a population subset can 17
still be concluded to fall well below one tenth of one percent of the full population of children 18 aged 5 years or younger in the U.S. today. Thus , we conclude that the current evidence, as 19 considered within the conceptual and quantitative context of the evidence-based framework, and 20 current air monitoring information indicates that the current standard would be expected to 21 achieve the public health policy goal recommen ded by CASAC in the last Pb NAAQS review 22 that IQ loss on the order of one to two IQ points be “prevented in all but a small percentile of the 23 population” (73 FR 67000). 24 In drawing conclusions from application of the evidence based framew ork with regard to 25 adequacy of the current standard, we further recognize the degree to which IQ loss estimates 26
drawn from the air-rela ted IQ loss evidence-based framework reflect mean blood Pb levels 27 below those represented in the currently available evidence for young children. For example, in 28 the case of the current standard level of 0.15 μg/m 3 , multiplication by the air-to-blood ratio of 7 29

12 Using an air-to-blood ratio estimate of 8 μg/dL per μg/m 3 also yields an IQ loss estimate of approximately 2 IQ points.
13 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.January 2013 4-30 Draft - Do Not Quote or Cite yields a mean air-related blood Pb level of 1.05 μg/d L, which is half the le vel of the lowest blood 1 Pb subgroup of pre-school children in which ne urocognitive effects have been observed (Table 2 3-2 above; Miranda et al., 2009) and well below the means of subgroups for which continuous C3 R functions have been estimated (Table 3-3 above). 14 Such an extension below the lowest 4 studied levels may be viewed as appropriate give n the lack of identified blood Pb level threshold 5 in the current evidence base for neurocognitive effects and the need for the NAAQS to provide a 6 margin of safety. 15 We note, however, that the framew ork IQ loss estimates for still lower 7 potential standard levels represen t still greater extrapolations from the current evidence base with 8 corresponding increased uncertainty. 9 In recognition of the role of public health policy judgments in drawing conclusions as to 10 adequacy of the Pb NAAQS, we consider the av ailability of new information or new commonly 11 accepted guidelines or criteria with in the public health community with regard to the public 12 health significance of specific IQ decrements in exposed, at-risk populations that might inform 13 public health policy judgments on the appropriate degree of public health protection that should 14 be afforded to protect against risk of su ch neurocognitive effects in at-risk populations, 16 such as 15 children living near air Pb sources. As an init ial matter, we note that no such new information, 16 guidelines or criteria are described in the ISA. In further c onsidering the occurrence of any new 17 actions by public health agencies that might indicate the availability of new information, 18 guidelines or criteria for interp reting public health signi ficance of such effects, we note that the 19
CDC has revised the blood Pb level used to prioritize young children for whom they recommend 20

14 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 risk per increment of blood Pb is greater for children with the lowest blood Pb levels, as noted in section 3.2 above. Thus, 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.
15 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.
16 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.January 2013 4-31 Draft - Do Not Quote or Cite particular follow-up health protective actio ns, as summarized in section 3.1 above. 17 The CDC 1 decision, while emphasizing the critical importa nce of primary prevention of Pb exposure, 2 provides no new guidelines or criter ia with regard to the significance of specific IQ decrements 3 or judgments on appropriate public health protec tion from risk of neurocognitive effects, and 4
their consideration of the evidence base at the time of their decision does not substantively differ 5 from that presented in the current draft ISA (CDC, 2012). Thus, we are aware of no new 6 information or new commonly accepted guidelines or criteria within the public health 7 community for interpreting public health significan ce of neurocognitive eff ects in the context of 8 a decision on adequacy of the current Pb standard. 9 With respect to exposure/risk-based consider ations, we recognize th e complexity of the 10 REA modeling analyses and the associated limitati ons and uncertainties. We additionally note 11 the differences among the case studies included in the REA and the extent to which they inform 12 our understanding of different aspects of the risk associated with ai r-related Pb in the U.S. For 13 example, the location-specific case studies indica te the distribution of population risk in urban 14 areas with differing types of Pb sources and gradie nts in air Pb concentrations as well as in 15 population density, while the generalized urban (l ocal) case study indicates the magnitude of air16 related risk associated with those specific loca lized circumstances where air concentrations just 17 meet the Pb standard (regardless of source type ). We agree with conclusions drawn in the 2008 18 review that the quantitative risk estimates, with a focus on those for the generalized (local) urban 19 case study, are “roughly consistent with and ge nerally supportive” of estimates from the 20 evidence-based air-related IQ loss framework ( 73 FR 67006). We further take note of the 21 increasing uncertainty recognized for air quality scenarios involving air Pb concentrations 22 increasingly below the current c onditions for each case study, recognizing that such uncertainty 23 is due in part to modeling limitations deriving fr om uncertainty regardi ng relationships between 24
ambient air Pb and outdoor soil/dust Pb and i ndoor dust Pb (as noted in section 3.4 above). 25 Based on the above considerations, we reach the preliminary conclusion that the current 26 body of evidence, in combination with the e xposure/risk information, supports a primary 27 standard as protective as the current standar d. Further consideration of the evidence and 28 exposure/risk information available in this revi ew and its attendant uncertainties and limitations, 29
as well as consideration of the availability of other informati on that might also inform public 30 health policy judgments by the Administrator, leads us to reach the additional preliminary 31 conclusion that it is appropriate to consider retaining the current stan dard without revision. 32 These preliminary conclusions are based on cons ideration of the hea lth effects evidence, 33 including consideration of this evidence in the co ntext of the evidence-bas ed, air-related IQ loss 34

17 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).January 2013 4-32 Draft - Do Not Quote or Cite framework, and in combination with the exposure/ risk information (chapt er 3 and sections 4.2.1 1 and 4.2.2 above) and the uncertainties attendant with both, recognizing the complexities and 2 limitations in the evidence base in reaching c onclusions regarding the magnitude of risk 3 associated with the current standard, as well as the increasing uncertainty of risk estimates for 4
lower air Pb levels. Based on these consideratio ns, these preliminary conclusions also recognize 5 what may be considered reasonable judgments on the public health implications of the blood Pb 6
levels and risk estimated for air-related Pb under the current standard, incl uding the public health 7 significance of the Pb effects bei ng considered, as well as aspect s of the use of the evidence8 based framework that may be considered to contribute to the margin of safety. 9 In reaching these preliminary conclusions, we additionally note that different public 10 health policy judgments could lead to different conclusions regarding the extent to which the 11 current standard provides protecti on of public health with an ade quate margin of safety. Such 12 public health policy judgments include those rela ted to the appropriate degree of public health 13 protection that should be afforded to protect against risk of neurocognitive effects in at-risk 14 populations, such as IQ loss in young children, as we ll as with regard to the appropriate weight 15 to be given to differing aspects of the evid ence and exposure/risk information, and how to 16
consider their associated uncertainties. For ex ample, different judgments might give greater 17 weight to more uncertain aspects of the evidence or reflect a diffe ring view with regard to margin 18 of safety. As noted in section 4.1 above, in es tablishing primary standard s under the Act that, in 19 the Administrator’s judgment, are requisite to protect public health with an adequate margin of 20 safety, the Administrator seeks to establish standard s that are neither more nor less stringent than 21 necessary for this purpose. The Act does not requ ire that primary standards be set at a zero-risk 22 level, but rather at a level that avoids unacceptable risks to public health, ev en if the risk is not 23 precisely identified as to nature or degree. The requirement that primary standards provide an 24 adequate margin of safety was intended to addr ess uncertainties associated with inconclusive 25
scientific and technical informati on available at the time of standard setting. It was also intended 26 to provide a reasonable degree of protection from hazards that research has not yet identified. 27 In this context, we recognize that the uncertainties and limitations associated with the 28 many aspects of the estimated relationships between air Pb concentrations and blood Pb levels 29 and associated health effects are amplified w ith consideration of increasingly lower air 30
concentrations. We believe th e current evidence supports the conclusion that the current 31 standard is requisite to protect publ ic health with an adequate marg in of safety. In staff’s view, 32 based on the current evidence there is apprec iable uncertainty associated with drawing 33 conclusions regarding whether ther e would be reductions in risk to public health from alternative 34 lower levels as compared to the level of the curre nt standard. Thus, we conclude that the basis 35 for any consideration of alternat ive lower standard levels would reflect different public health 36January 2013 4-33 Draft - Do Not Quote or Cite policy judgments as to the appr opriate approach for weighing un certainties in the evidence and 1 for providing requisite protecti on of public health with an ad equate margin of safety. 2 In summary, the newly available health effects evidence, critically assessed in the ISA as 3 part of the full body of evidence, reaffirms conc lusions on the broad arra y of effects recognized 4 for Pb in the last review. Further, staff obser ves the general consistency of the current evidence 5
with the evidence available in th e last review with regard to key aspects on which the current 6 standard is based, including those particular to the evidence-based framework developed in the 7 last review. Staff additionally observes that quantitative risk estimates associated with the 8 current standard, based on the risk assessment perf ormed in the last review, indicate a level of 9 risk generally consistent with conclusions drawn from the evidence using the evidence-based 10 framework. Staff additionally recognizes the lim itations and uncertainties associated with the 11 currently available information. These considera tions provide the basis for the preliminary staff 12 conclusion that consideration should be given to retaining the current stan dard, without revision. 13 Accordingly, and in light of staff preliminary c onclusions that it is appr opriate to consider the 14 current standard to be adequate , we have not identified any pote ntial alternative standards for 15
consideration in this review. 16

4.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND DATA 17 COLLECTION 18 In this section, we highlight key uncertainties associated w ith reviewing a nd establishing 19 NAAQS for Pb. Such key uncertainties and areas for future health-related research, model 20 development, and data gathering are outlined below. In some cases, research in these areas can 21 go beyond aiding standard setting to aiding in the development of more efficient and effective 22 control strategies. We note, however, that a full set of research recommendations to meet 23 standards implementation and strategy developmen t needs is beyond the scope of this discussion. 24 Rather, listed below are key uncertainties and res earch questions and data gaps that have been 25 thus far highlighted in this review of the health-based primary standard. 26

 A critical aspect of our cons ideration of the evidence and th e quantitative risk assessment 27 in this review is our understanding of the C-R relationship between blood Pb levels in 28 young children and neurodevelopmental effects, specifically IQ decrement. Additional 29 epidemiological research involving substant ially-sized populations with mean blood Pb 30 levels closer to those comm on in today’s population of young children, particularly those 31 less affected by higher Pb exposures ear lier in childhood, would help to reduce 32 uncertainty in our estimates of IQ decrement associated with these lower blood Pb levels, 33 and accordingly, in characterizing Pb health effects. 34

35

 There remains uncertainty in the evidence base with regard to the exposure circumstances 36 (timing, duration, magnitude and frequency) elic iting effects in older children and adults. 37January 2013 4-34 Draft - Do Not Quote or Cite Effects of particular focus include eff ects on the nervous system later in life, 1 cardiovascular function, and delayed onset of puberty. 2

 Alzheimer’s-like pathology has been reporte d in aged laboratory animals (non-human 3 primates and rodents) exposed to Pb early in life, however uncertainty remains with 4 regard to relationships of such pat hology with altered f unction/behavior. 5

 Epidemiologic studies indicate detrimental effects of Pb on sperm production and quality, 6 often in occupational cohorts. Uncertainty re mains regarding these effects in otherwise 7 healthy cohorts without occupational Pb exposure or other underlying medical 8 conditions. 9

 Quantitative estimation of blood Pb levels in children and other at-risk subgroups in 10 response to various exposure circumstances , including air-related exposure pathways, 11 would benefit from research in a number of areas including: 12

o Factors affecting relationships between Pb in ambient air and Pb in blood; 13

o Temporal aspects of changes in blood Pb levels associated with changes in 14 ambient air Pb; 15

o Interindividual variability in blood Pb levels and methods for characterizing 16 interindividual variability, including consideration of both empirical and 17 mechanistic methods; 18

o Apportionment of blood Pb levels with re gard to exposure pathway contributions, 19 particular distinctions pertinent to policy-relevant expos ures and background 20 sources; and 21

o Blood Pb model performance evaluati ons, with emphasis on applications 22 pertaining to blood Pb response to ambient air-related pathways and responses to 23 changes in exposures for those pathways. 24

 An important aspect of exposure and risk posed by ambient air Pb is the contribution of 25 ambient air Pb to indoor dust Pb. Research on the relationship betw een Pb in these two 26 media, both generally, as well as in specific en vironments, and also with regard to aspects 27 associated with mechanistic modeling (e.g., ai r exchange rates, home cleaning frequency 28 and efficiency) would reduce uncertainty in m odels and methods applied in consideration 29 of this pathway in future reviews. 30

 An understanding of the spatial gradient of am bient air Pb concentra tions, and associated 31 particle sizes, in urban residen tial areas, as well as near Pb sources, is an important aspect 32 to our implementation of the NAAQS for Pb and a key element in assessing exposure and 33 risk. Additional research in this area is needed. 34

o Current limitations in this area addi tionally contribute uncertainty to 35 characterization of ambient air Pb levels in the risk assessment and associated 36 exposure and risk estimates. Research in the area of characterizing spatial 37 variation in air Pb concentra tions in different environmen ts and related to different 38 air sources would help to reduce this uncer tainty. Of particular interest is the 39 potential for systematic trends in th e relationship between ambient air Pb 40 concentrations and distribution of urban residential populations. Examples of 41January 2013 4-35 Draft - Do Not Quote or Cite locations of interest incl ude neighborhoods downwind of airports with substantial 1 leaded aviation gasoline usage or in the vi cinity of older roads with substantial 2 historical use of leaded ga soline, as well as inner city neighborhoods, both those in 3 which substantial reconstr uction has occurred and mo re static areas. 4

 An important aspect to this review is the relationship betw een ambient air Pb and outdoor 5 dust and surface soil Pb concentrations, including the temporal dynamics of that 6 relationship and variation in that for differe nt environments. Research to improve our 7 understanding of these areas w ould contribute to reducing as sociated uncertainty with 8 regard to characterization of the relationship between air an d soil Pb and the impact of 9 changes in air Pb on outdoor so il Pb levels over time. 10January 2013 4-36 Draft - Do Not Quote or Cite 4.5 REFERENCES 1

Bellinger, D. C. and Needleman, H. L. (2003) Intellectual impairment and blood lead levels [letter]. N. Engl. J. Med. 2 349: 500. 3

Canfield, R. L.; Henderson, C. R., Jr.; Cory-Slechta, D. A.; Cox, C.; Jusko, T. A.; Lanphear, B. P. (2003) 4 Intellectual impairment in children with blood lead concentrations below 10 μ g per deciliter. N. Engl. J. 5 Med. 348: 1517-1526. 6

Centers for Disease Control and Prevention (2012) CDC Response to Advisory Committee on Childhood Lead 7 Poisoning Prevention Recommendations in “Low Le vel Lead Exposure Harms Children: A Renewed Call 8 of Primary Prevention”. Atlanta, GA: U.S. Department of Health and Human Services, Public Health 9 Service. June 7. 10

Henderson, R. (2007a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to 11 Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of 12 the 1st Draft Lead Staff Paper and Draft Lead Exposure and Risk Assessments. March 27, 2007. 13

Henderson, R. (2007b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to 14 Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of 15 the 2nd Draft Lead Human Expo sure and Health Risk Assessments. September 27, 2007. 16

Henderson, R. (2008a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to 17 Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of 18 the Advance Notice of Proposed Rulemaking (ANPR) for the NAAQS for lead. January 22, 2008. 19

Henderson, R. (2008b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to 20 Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of 21 the Notice of Proposed Rulemaking for the NAAQS for lead. July 18, 2008. 22

Hilts, S. R. (2003) Effect of smelter emission reductions on children's blood lead levels. Sci. Total Environ. 303: 51- 23 58. 24

Lanphear, B. P.; Hornung, R.; Khoury, J.; Yolton, K.; Baghurst, P.; Bellinger, D. C.; Canfield, R. L.; Dietrich, K. 25 N.; Bornschein, R.; Greene, T.; Rothenberg, S. J. ; Needleman, H. L.; Schnaas, L.; Wasserman, G.; 26 Graziano, J.; Roberts, R. (2005) Low-level enviro nmental lead exposure and children's intellectual 27 function: an international pooled analysis. Environ. Health Perspect. 113: 894-899. 28

Téllez-Rojo, M. M.; Bellinger, D. C.; Arroyo-Quiroz, C.; Lamadrid-Figuero a, H.; Mercado-García, A.; Schnaas29 Arrieta, L.; Wright, R. O.; Hernández-Avila, M.; Hu, H. (2006) Longitudinal associations between blood 30 lead concentrations < 10 μ g/dL and neurobehavioral development in environmentally-exposed children in 31 Mexico City. Pediatrics 118: e323-e330. 32

U.S. Environmental Protection Agency. (2006) Air Qu ality Criteria for Lead. Washington, DC, EPA/600/R33 5/144aF. Available online at: www.epa.gov/ncea/ 34

U.S. Environmental Protection Agency. (2007a) Lead: Huma n Exposure and Health Risk Assessments for Selected 35 Case Studies, Volume I. Human Exposure and Hea lth Risk Assessments – Full-Scale and Volume II. 36 Appendices. Office of Air Quality Planning and Stan dards, Research Triangle Park, NC. EPA-452/R-07- 37 014a and EPA-452/R-07-014b. 38

U.S. Environmental Protection Agency. (2007b) Review of the National Ambient Air Quality Standards for Lead: 39 Policy Assessment of Scientific and Technical Information, OAQPS Staff Paper. EPA-452/R-07-013. 40 Office of Air Quality Planning and Standards, Research Triangle Park. 41January 2013 4-37 Draft - Do Not Quote or Cite U.S. Environmental Protection Agency. (2012) Integrated Science Assessment for Lead (Third External Review 1 Draft). Washington, DC, EPA/600/R-10/075C. Available online at: 2 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_isa.html 3January 2013 5-1 Draft - Do Not Quote or Cite 

### 5 WELFARE EFFECTS AND EXPOSURE/RISK INFORMATION 1

This chapter presents key aspects of the curr ent evidence of lead-rel ated welfare effects, 2 and presents exposure and risk information from th e last review in the co ntext of the currently 3
available information. Staff has drawn from th e EPA’s synthesis of th e scientific evidence 4 presented in the third draft Integrated Science Assessment for Lead (USEPA, 2012; henceforth 5 referred to as the ISA) and the 2006 Air Quality Criteria Document for Lead (USEPA, 2006; 6 henceforth referred to as the 2006 CD), and from the screening level risk assessment performed 7
in the last review and described in Lead Human Exposure and Health Risk Assessments and 8 Ecological Risk Assessment for Selected Areas. Pilot Phase (documented in ICF, 2006; 9 henceforth referred to as the 2006 REA). This ch apter is organized into two sections regarding 10 the currently available welfare effects eviden ce (section 5.1) and the exposure and risk 11 information (section 5.2) interpreted in light of cu rrently available evidence. Presentation within 12 these sections is organized to address key polic y-relevant questions for this review concerning 13 the evidence and exposure/risk information, building upon the questions included in the IRP 14 (IRP, section 3.2). 15

5.1 WELFARE EFFECTS INFORMATION 16
Lead has been demonstrated to have harm ful effects on reproduction and development, 17 growth, and survival in many species as described in the assessment of the evidence available in 18
this review and consistent with the conclusions drawn in past CDs (ISA, section 2.7; 2006 CD). 19 A number of studies on Pb ecological effects are newly available in this review and are critically 20 assessed in the ISA as part of the full body of evidence. The newly available evidence reaffirms 21 conclusions on the array of effect s recognized for Pb in the last review (ISA, section 2.7). The 22 current ISA, unlike the 2006 CD , makes causal determinations for the effects of Pb on 23 organisms. The ISA determines that causal or likely causal relationships 1 exist in both 24 freshwater and terrestrial ecosystems for Pb 2 with effects on reproduction and development in 25 vertebrates and invertebrates; grow th in plants and invertebrates; and survival in vertebrates and 26 invertebrates (ISA, table 2-3). Based on thes e determinations and a weight of evidence 27 approach, the ISA concludes that higher level community and ecosystem effects in freshwater 28

1 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).
2 In determining that a causal relationship exists for Pb with specific ecological effects, the EPA has concluded that “[e]vidence is sufficient to conclude that there is a cau sal relationship with relevant po llutant exposures (i.e., doses o r exposures generally within one to two orders of magnitude of current levels)” (ISA, p. lxiv)January 2013 5-2 Draft - Do Not Quote or Cite and terrestrial systems are likely to result from the above described popu lation-level endpoints. 1 The ISA also presents evidence for saltwater eco systems but concludes that current evidence is 2 inadequate to make causality determinations for most organisms and communities but finds the 3 evidence to be suggestive linking Pb and eff ects on reproduction and development in marine 4 invertebrates (ISA, section 1.5, Tabl e 2-3, section 7.3.12 and section 7.4.21). 5
Based on the extensive assessmen t of the full body of evidence available in this review, 6 the major conclusions drawn by the ISA regarding ecological effects of Pb include the following 7 (ISA, section 1.5). 8 With regard to the ecological effect s of Pb, uptake of Pb into fauna and 9 subsequent effects on reproduction, growth and survival are established and are 10 further supported by more recent evidence. These may lead to effects at the 11 population, community, and ecosystem level of biological organization. In both 12 terrestrial and aquatic organisms, gradien ts in response are observed with 13 increasing concentration of Pb and some st udies report effects w ithin the range of 14 Pb detected in environmental media. Sp ecifically, observations from controlled 15 studies on reproduction, growth, and surv ival in sensitive freshwater 16 invertebrates are well-characterized at concentrations at or near Pb 17 concentrations occasionally encountered in U.S. surface waters.... However, in 18 natural environments, modifying factors a ffect Pb bioavailabi lity and toxicity and 19 there are considerable uncertainties associ ated with generali zing effects observed 20 in controlled studies to effects at hi gher levels of biological organization. 21 Furthermore, available studies on co mmunity and ecosystem-level effects are 22 usually from contaminated areas where Pb concentrations are much higher than 23 typically encountered in the environment. The contribution of atmospheric Pb to 24 specific sites is not clear and the connec tion between air concentration of Pb and 25 ecosystem exposure continues to be poorly characterized. Furthermore, the level 26 at which Pb elicits a specific effect is difficult to establis h in terrestrial and 27 aquatic systems, due to the influence of other environmental variables (e.g., pH, 28 organic matter) on both Pb bioavailability and toxicity, and also to substantial 29 species differences in Pb sensitivity. 30 31 As in prior reviews of the Pb NAAQS, this review is focused on those effects most 32 pertinent to ambient air Pb exposures. Given th e reductions in ambient air Pb levels over the 33 past decades, these effects are ge nerally those associated with th e lowest levels of Pb exposure 34 that have been evaluated. Additionally, we recognize the limitations on our ability to draw 35 conclusions about environmental exposures from eco logical studies of orga nism-level effects as 36 most studies were conducted in laboratory sett ings which may not accurately represent field 37 conditions or the multiple vari ables that govern exposure. 38
Our consideration of welfare effects eviden ce in this review is framed by key policy39 relevant questions drawn from t hose included in the IRP. In the following sections, we discuss 40 the pathways by which Pb exposure occurs in ecos ystems, the mechanisms that distribute Pb in 41January 2013 5-3 Draft - Do Not Quote or Cite the environment and the bioavailability of Pb in different ecosystems. Understanding the 1 movement of Pb in the environment is importa nt to understanding expos ure and bioavailability 2 and, thus, informs the subsequent discussion of the effects of Pb on terrestrial and aquatic 3 ecosystems. Finally, we discuss the association of ambient air Pb with effects and the important 4 role critical loads play in assessing the overall ability of ecosystems to recover from past Pb 5 exposures and the degree to which newly de posited Pb may affect ecosystem function and 6

recovery. 7

 To what extent has the newly available evidence altered our understanding of the 8 movement and accumulation of air-depo sited Pb through ecosystems over time? 9
There is little new information on fate and tr ansport in ecosystems specifically related to 10 air-derived Pb. Nonetheless, some new studies are available that provide additional information, 11 briefly summarized below, on Pb cycling, flux and retention. This new information does not 12 fundamentally change our understanding from the last review of Pb movement or accumulation 13 through ecosystems over time but rather improves our understanding of some of the underlying 14 processes and mechanisms in so il, water and sediment. The newly available information also 15 adds to the evidence base with regard to th e timing of ecosystem recovery from historic 16 atmospheric deposition of Pb. 17 Overall, recent studies in terrestrial ecosyst ems provide deposition data consistent with 18 deposition fluxes reported in the 2006 CD, and demonstrate consis tently that Pb deposition to 19 soils has decreased since the phase-out of l eaded on-road gasoline (ISA, section 3.3.3.1). 20 Although follow-up studies in severa l locations at high elevation s ites indicate littl e change in 21
soil Pb concentrations since the phase-out of leaded on-road gasoline in surface soils, consistent 22 with the high retention reportedly associated with reduced microbial activity at lower 23 temperatures associated with hi gh elevation sites, amounts of Pb in the surface soils at some 24
lower altitude sites were reduced over the same time period in the same study (ISA, section 25 3.3.3.1). New studies in the ISA also enhance our understanding of Pb se questration in forest 26 soils by providing additional information on the role of leaf litter as a Pb reservoir and the effect 27 of decomposition on Pb dist ribution and sequestration (ISA, section 3.3.3.2). 28 Recent research on Pb transport in aqua tic systems has provided a large body of 29 observations confirming that Pb transport is dom inated by colloids rich in iron and organic 30 material (ISA, section 3.3.2.1). In sediments, rece nt research on Pb flux provides greater detail 31 on resuspension processes than was available in the 2006 CD, including research on resuspended 32 Pb largely associated with organi c material or iron and manganese particles, and research on the 33 important role played by anoxic or depleted oxygen environments in Pb cycling in aquatic 34 systems. This newer research is consistent with prior evidence in indicating that appreciable 35 resuspension and release from sediments largely o ccurs during discrete even ts related to storms. 36January 2013 5-4 Draft - Do Not Quote or Cite It has also confirmed that resuspension is an important process that strongly influences the 1
lifetime of Pb in bodies of wa ter. Finally, there have been advances in understanding and 2 modeling of Pb partitioning between organic material and sediment in complex aquatic 3 environments (ISA, section 3.7.2). 4 In summary, the newly available evidence builds on our understanding of some specific 5 aspects of processes involved in the movement and accumulation of air-deposited Pb through 6 ecosystems over time. This new information, how ever, does not substantially alter our overall 7 understanding of fate and transport of Pb in ecosystems. 8

 Does the newly available evidence furt her inform our understanding of the 9 bioavailability of Pb in different types of ecosystems and organisms? 10 As discussed in the ISA, bioavailability of Pb is an important component of 11 understanding the effects Pb is likely to have on organisms a nd ecosystems (ISA, section 7.3.3). 12
It is the amount of Pb that can interact within the organism that leads to toxici ty and there are 13 many factors which govern this in teraction. Bioavailability is defined in the Framework for 14 Metals Risk Assessment (USEPA, 2007) as “the extent to which bioaccessible metals absorb 15 onto, or into, and across biological membranes of or ganisms, expressed as a fraction of the total 16 amount of metal the organism is proximately e xposed to (at the sorption surface) during a given 17
time and under defined conditions.” The bioavailability of metals varies widely depending on the 18 physical, chemical, and biological conditions un der which an organism is exposed (USEPA, 19 2007). Characteristics of the toxicant itself that aff ect bioavailability are: (1) chemical form or 20 species, (2) particle size, (3) la bility, and (4) source. The bioava ilability of a metal is also 21 dependent upon the fraction of meta l that is bioaccessible. The bi oaccessible fraction of a metal 22 is the portion (fraction or percentage) of environmentally available metal that actually interacts at 23 the organism’s contact surface and is potentially available for absorption or adsorption by the 24 organism (USEPA, 2007; ISA, section 7.3.3). 25 New studies provide additional insight into factors that influence the bioavailability of Pb 26 to specific organisms (ISA, section 7.3.3). In ge neral, this evidence, briefly summarized below, 27 is supportive of previous conclusions and does no t identify significant new variables from those 28 identified previously. Section 7.3.3 of the ISA provi des a detailed discussion of bioavailability in 29 terrestrial systems. With regard to aquatic sy stems, a detailed discussion of bioavailability in 30 freshwater systems is provided in sections 7.4.3 and 7.4.4 of the ISA a nd section 7.4.14 of the 31 ISA discusses bioavailability in saltwater systems. 32 In terrestrial systems, the bioavailability of Pb has a far greater impact on the adverse 33
effects of Pb than does the tota l Pb burden (ISA, section 7.3.11). In such ecosystems, Pb is 34 deposited either directly onto plant surfaces or on to soil where it can bind with organic matter or 35January 2013 5-5 Draft - Do Not Quote or Cite dissolve in pore water. 3 The Pb dissolved in pore water is particularly bioavailable to organisms 1 in the soil and thereby influences the impact of soil Pb on terre strial ecosystems to a much 2 greater extent than the total amount of Pb present (ISA, sect ion 7.3.11). Several soil variables 3
control the amount of Pb that is dissolved in pore water, and the ISA presents new evidence that 4
has advanced scientific understand ing of some of these variable s (ISA, section 7.4.21). Studies 5 have shown that the two most important determinan ts of both Pb solubility and toxicity in soils 6 are pH and cation exchange capacity (ISA, sectio n 2.7.1). Also, evidence newly available in this 7 review has confirmed the important influence of organic matter on Pb sequestration, leading to 8 relatively longer retention in soil s with higher organic matter conten t, with the potential for later 9 release of deposited Pb (ISA, section 2.7.1). In ge neral, soils with higher organic matter content 10 have the capacity for greater retention of Pb in the soil matrix and lesser availability of Pb for 11 release into pore water. Subs equent reduction in soil organi c material, such as through 12 decomposition, can contribute to subsequent increas ed availability. Aging of Pb in soils, both 13
under natural conditions and si mulated through leaching, has al so been shown to reduce 14 bioavailability to plants and soil or ganisms (ISA, sections 7.3.2.3 and 7.3.11). 15 In aquatic systems as in terrestrial systems, the amount of Pb bioavailable to organisms is 16 a better predictor of effect on organisms than the overall amount of Pb in the system. Once 17 atmospherically-derived Pb enters surface water bodi es through deposition or runoff, its fate and 18 bioavailability are influenced by many water qua lity characteristics, such as pH, suspended 19 solids loading and organic content (ISA, section 7.4.2). In sediments, bioavailability of Pb to 20 sediment-dwelling organisms may be influenced by the presence of other metals, sulfides, iron 21 oxides and manganese oxides and also by physical disturbance (ISA, se ction 2.7.2). For many 22 aquatic organisms Pb dissolved in the water colu mn can be the primary exposure route, while for 23 others sediment ingestion is significant (ISA, section 2.7.2). As recognized in the 2006 CD and 24 further supported in the ISA, th ere is a body of evidence showing that uptake and elimination of 25 Pb varies widely between species. 26 Although in freshwater systems the presence of humic acid in dissolved organic material 27 (DOM) is considered to reduce the bioavailable fr action of metals in the water column, there is 28 evidence presented in the ISA that dissolved organic carbon and DOM do not have the same 29
effect on free Pb ion concentration in saltwater systems (ISA, section 7.4.24). Recent studies 30 have broadened previous understandings of the role of DOM in Pb bioavailability and have 31 shown that different components of DOM have different effects on Pb bioavailability in 32 saltwater systems. For example, the ISA discusses two new studies that sugge st that in saltwater 33 aquatic systems, surface water DOM increases (rathe r than decreases) uptake of Pb by fish gill 34

3 The term “pore water” refers to the water occupy ing the spaces among the grains of sediment or soil.January 2013 5-6 Draft - Do Not Quote or Cite structures, potentially through the alteration of membrane permeability. This recent evidence 1 supports the conclusion from the la st review that factor s that modify bioavailability of Pb in 2
saltwater environments are not identical to those in freshwat er systems (ISA, section 7.4.14). 3 There is new evidence about bioavailability in some ecosystems, briefly summarized 4 above, which further informs our understanding of bioavailability of Pb in different ecosystems 5 and organisms, building on our fundamental understa nding in the last review. Bioavailability 6 remains an important considerati on in Pb toxicity and a signifi cant source of uncertainty relating 7
ambient Pb and adverse effects. 8

 Does the current evidence alter our conc lusions from the previous review 9 regarding the ecological effects associated with exposure to Pb? Does the newly 10 available evidence indicate new exposure levels at which ecological systems or 11 receptors are expected to experience effects? 12
There is a substantial amount of new evidence in this review regarding the ecological 13 effects of Pb on specific terrestr ial and aquatic organisms. On th e whole, this evidence supports 14 previous conclusions that Pb has effects on gr owth, reproduction and survival, and that under 15
some conditions these effects can be adverse to organisms and ecosystems. The ISA provides 16 evidence of effects in additional species, and in a few cases, at lower exposures than reported in 17 the previous review, but does not substantially alter the effect s endpoints from the previous 18 review. Looking beyond organism-level evidence, the evidence of adversity in natural systems 19 remains sparse due to the difficulty in determin ing the effects of conf ounding factors such as 20 multiple metals or factors influencing bioavailability in field studies. The following is a brief 21 comparison of the newly available evidence to evidence considered in the 2006 review. 22 Terrestrial Ecosystems 23
The evidence available in the last review indicated a range of biological effects of Pb on 24 terrestrial organisms that varied with type of organism and life st age, duration of exposure, form 25 of Pb, and soil characteristics. New res earch since the 2006 CD has broadened our 26 understanding of the evidence of damage to photos ynthetic ability in plants exposed to Pb, and 27 provided additional evidence of oxidative stress in response to Pb exposure (ISA, section 28 7.3.4.1). Reactive oxygen species have been found to increase in plant tissue grown in Pb29 contaminated soil; with increasing Pb exposure, the plant tissue responded with increased 30 antioxidant activity (ISA, section 7.3.4.1). In ad dition, reduced growth has been observed in 31 some experiments, as well as evidence of genotoxicity, decreased germination, and pollen 32 sterility (ISA, section 7.3.4.1). 33 In terrestrial invertebrates, previous CDs have reported adverse effects of Pb on 34 neurological and reproductive endpoints. R ecently published studies have shown some 35 additional evidence of neurological changes in nematodes at relatively low concentrations of 36January 2013 5-7 Draft - Do Not Quote or Cite soil Pb (2.5 μ M) but given the study design the relevan ce to environmental exposure is unclear 1 (ISA, section 7.3.4.2). Increased mortality was found in recent studies of earthworms at 2
concentrations similar to those in studies review ed previously, but additio nal evidence indicated 3 that effects were strongly dependent on soil characteristic s including pH, cation exchange 4 capacity, and aging (ISA, section 7.3.4.2). There is also newly available evidence for adverse 5 effects in snails and arthropods exposed through soil or diet (ISA, section 7.3.4.2). The effects 6 vary with species and exposur e conditions, and include diminished growth and fecundity, 7 endocrine and reproductive anomalies, and body de formities. Increasing concentration of Pb in 8 the exposure medium generally resulted in increased effects with in each study, but the 9 relationship between concentrati on and effects is highly variable between studies, even when 10 the same medium, e.g. soil, was used. Current evidence suggests that aging and pH are 11 important modifiers of Pb toxicity (ISA, section 7.3.11). 12 In terrestrial vertebrates, some new evidence is available for effects of Pb on amphibians 13 and reptiles as well as birds. Effects reported in reptiles and amphibians include decreased white 14 blood cell counts, decreased testis weight, a nd behavioral anomalies (ISA, section 7.3.4.3). 15 However, depending on various fact ors, studies report large differe nces in effects in different 16 species at the same concentrati on of Pb in soil, and effects we re generally smaller when field17 collected soils were used. In some birds, recen t studies have found maternal elevated blood Pb 18
level to be associated with d ecreased hatching success, smaller cl utch size, high corticosteroid 19 level, and abnormal behavior. Stud ies on some species show little or no effect of elevated blood 20 Pb level. Effects of dietary exposure have b een studied in several mammalian species, with 21 cognitive, endocrine, immunological , and growth effects observed (ISA, section 7.3.11) in some 22
studies. 23 Experimental evidence of organism-level eff ects presented in the ISA demonstrates that 24 increased exposure to Pb is genera lly associated with increases in observed effects in terrestrial 25 ecosystems (ISA, section 7.3.11). It also demonstrat es that many factors, including species and 26 various soil physiochemical properti es, interact strongly with Pb concentration to modify those 27 effects (ISA, section 7.3.11). In terrestrial ec osystems, where soil is generally the main 28 component of the exposure route, Pb aging is a particularly important factor, and one that may 29 be difficult to reproduce experiment ally. Given that in natural settings, thes e modifying factors 30 are highly variable, the ISA notes that “[w] ithout quantitative char acterization of those 31 interactions, characterizations of exposure-r esponse relationships would likely not be 32 transferable outside of experi mental settings” (ISA, section 2.7.1). The results of the few 33 exposure-response studies conducte d since the 2006 CD have been inconsistent (ISA, section 34 2.7.1). 35January 2013 5-8 Draft - Do Not Quote or Cite As reported in both the ISA and the 2006 CD, most direct eviden ce of community- and 1 ecosystem-level effects is from releases by near sources of Pb to the environment, where Pb 2 concentrations are much higher than typically observed environmental co ncentrations and often 3 derive from separate releases to multiple media. Impacts of Pb on terrestrial ecosystems near 4 smelters, mines, and other industrial sources have been studied for several decades (ISA, section 5 7.3.12.7). Emissions of Pb from smelting and other industrial activities are commonly 6 accompanied by other trace metals (e.g., Zn, Cu, Cd) and SO 2 that may cause toxic effects 7 independently or in concert with Pb. Those impa cts have been long shown to include decreases 8 in species diversity and changes in floral a nd faunal community composition. Ecosystem-level 9 field studies are complicated by these confounding exposures and the inherent variability in 10 natural systems (ISA, section 7.3.12.7). 11
New evidence of effects of Pb at the co mmunity and ecosystem scales has been 12 reported. This evidence includes several studies of the ameliorative effect s of mycorrhizal fungi 13 on plant growth with Pb exposure as well as recently published rese arch on soil microbial 14 communities, which have been shown to be impacted by Pb in both composition and activity 15 (ISA, sections 2.7.1 and 7.3.6). Many recent studies have been conducted using mixtures of 16 metals, which have attempted to separate the e ffects of individual metals when possible. In 17 studies that included only Pb, or where effects of Pb could be separated, soil microbial activity 18 was generally diminished, and was shown in some of those cases to r ecover with time (ISA, 19 section 7.3.6). Regardless of the recovery of such microbial communities, species and 20 genotypical composition were consistently altered after Pb exposure, and findings indicate that 21 those alterations were long-lasting or permanent (ISA, section 7.3.11). 22
A recent review has examined differences in species sensitivity, using blood Pb level in 23 birds and mammals as an exposure index rath er than external dose (ISA, section 7.3.9.1; 24 Buekers et al., 2009). In this analysis, varia tion across organisms was reduced with the blood 25 Pb index and variation of Pb absorption from th e diet of the organism largely accounted for the 26 variation seen in the blood Pb. The analysis al so suggests that the asso ciation between blood Pb 27 concentration and toxicity is different betw een birds and mammals (ISA, section 7.3.9.1). 28 Overall, new studies in this review support previous conclusions a bout the effects of Pb 29 on terrestrial ecosystems, namely that increa sing soil Pb concentrations in areas of Pb 30 contamination (e.g. mining sites and industrial s ites) can cause decrea ses in microorganism 31 abundance, diversity, and function. Specifically, shifts in bacteria l species and fungal diversity 32 have been recently observed near long-establish ed sources of Pb contamination (ISA, section 33 7.3.12.7). Most evidence for Pb toxicity to terres trial plants, invertebrates and vertebrates, 34 however, is from single-species assays in laboratory studies wh ich do not capture the 35January 2013 5-9 Draft - Do Not Quote or Cite complexity of bioavailability and other modifier s of effect in natural systems (ISA, section 1 7.3.12.7). 2 Freshwater Ecosystems 3 In fish, while there are species differences in the rate of Pb accu mulation and distribution 4 of Pb within the organism, the g ills and diet are the primary rout es of uptake. Recent studies 5
have identified the anterior in testine as an additional site of uptake of Pb through dietary 6 exposure (ISA, section 7.4.4.3). While there ar e few new studies on Pb uptake through 7 freshwater exposure by amphibians and mammals, there are some new studi es presented in the 8 ISA which seem to provide new information on trophic transfer of Pb (ISA, section 7.4.4.4). 9
Evidence summarized in the 2006 CD indicated that measured concentrations of Pb in the 10 tissues of aquatic organisms were generally hi gher in algae and benthic organisms than in 11 higher trophic-level consumers, indicating that Pb was bioconcentrated but not biomagnified 12 (ISA, section 2.7.2). Some recent studies indicate transfer of Pb in aquatic food webs; recent 13
studies that have traced Pb in freshwater aquatic food webs ha ve found that Pb concentration 14 decreases with increasing tr ophic level (biodilution) (IS A, sections 2.7.2 and 7.4.4.4). 15 Evidence presented in the ISA further suppor ts the findings of past CDs that Pb in 16 freshwater can be highly toxic to aquatic organisms, with toxici ty varying with species and life 17 stage, duration of exposure, form of Pb, a nd water quality charac teristics. The 2006 CD 18 identified evidence of adverse growth effects on several species of fres hwater algae from Pb 19 exposure (2006 CD, Section 7.2.4). The ISA desc ribes several new studies which expand the 20 list of algal species for which these adverse e ffects have been identified (ISA, section 7.4.5.1). 21 For vascular plants, the ISA describes additi onal evidence that oxidative damage, decreased 22 photosynthesis and reduced growth occur with Pb exposure (ISA, section 7.4.5.2). 23 Since the 2006 CD, there is some additional evidence for Pb effects on cellular processes 24 in aquatic invertebrates. Recent studies of repr oductive and developmental effects of Pb provide 25 further support for findings in the 2006 CD and add additional species information on 26 reproductive endpoints for rotifers and freshwater snails as well as multig enerational effects of 27 Pb in mosquito larvae (ISA, section 7.4.5.2). In the 2006 CD, study concentrations cited at 28 which effects were observed in aquatic invert ebrates reflected an e xpansive range from 5 μ g/L 29 (for acute toxicity to Pb nitrate in a test system at a har dness of 18 mg/L calcium carbonate) to 30 greater than 8000 μg/L (for acute toxicity to Pb chloride at a hardne ss of 280-300 mg/L calcium 31 carbonate) (ISA, p.2-38; 2006 CD, Table AX7-2.4.1). Recent studies cited in the ISA provide 32 additional evidence of effects from chronic exposu res. These findings are generally consistent 33 with those of the previous review and reflect the variability of Pb t oxicity under different 34 environmental conditions and in species with varying sensitivity. 35January 2013 5-10 Draft - Do Not Quote or Cite Evidence of effects in aquatic vertebrates pr esented in the ISA reite rates the findings of 1 reproductive, behavioral, and gr owth effects stated in prev ious CDs. Some additional 2 mechanisms of Pb toxicity in the gill and the rena l system of fish have been elucidated since the 3 2006 CD as well as the identification of potentia l new molecular targets for Pb neurotoxicity 4 (ISA, section 2.7.2). Recent studies reported subl ethal effects on tadpole growth, deformity, and 5 swimming ability at concentrations within two orders of magnitude of environmental levels of 6 Pb (ISA, section 7.4.5.3) based on nominal concentrations. 7 As in terrestrial organisms, evidence presen ted in the ISA and prior CDs demonstrates the 8 toxicity of Pb in aquatic ecosystems and the ro le of many factors, incl uding Pb speciation and 9 various water chemistry propert ies in modifying toxicity (IS A, section 2.7.2). Since the 2006 10 CD, additional evidence for community and ecosystem level effects of Pb is available, primarily 11
in microcosm studies or field studies with other metals present (ISA, section 7.4.11). Such 12 evidence described in previous CDs includes al teration of predator-prey dynamics, species 13 richness, species composition, and biodiversity. New studies availa ble in this review provide 14 evidence in additional habitats for these community and ecological-scale eff ects, specifically in 15 aquatic plant communities and sediment-associat ed communities at both acute and chronic 16 exposures involving concentrations similar to previously reported (ISA, section 7.4.4.1). In 17 many cases it is difficult to characterize the na ture and magnitude of effects and to quantify 18 relationships between ambient con centrations of Pb and ecosystem response due to existence of 19 multiple stressors, variability in fi eld conditions, and to differences in Pb bioavailability at that 20 level of organization (ISA, section 2.7.3.7). In these field studies, the degree to which air 21
concentrations contribute to such effects is largely unknown. 22 Saltwater Ecosystems 23 Recently available evidence in the ISA on toxic ity of Pb to marine algae augments the 24 2006 CD findings of variation in sensitivity across marine species. Recent studies on Pb 25 exposure include reports of growth inhibition and oxidative stress in a few additional species of 26 marine algae (ISA, section 7.4.15). 27 Recent literature provides little new ev idence of endpoints or effects in marine 28 invertebrates beyond those reported in the 2006 CD. For example, some recent studies 29 strengthen the evidence of Pb effects on enzymes and antioxidant activity in marine 30
invertebrates and have identified an additional behavioral endpoint (i.e., valve closing speed in 31 juveniles of a marine scallop was affected by 20 -day exposure to 40-400 μg/L Pb nitrate) from 32 those discussed previously (ISA, section 7.4.15.2). Also, as noted in the 2006 CD and supported 33 by new studies reviewed in the ISA, Pb expos ure negatively affects th e growth of marine 34 invertebrates (ISA, section 7.4.15.2). Recent studie s also identify several species exhibiting 35 particularly low sensitivity to hi gh acute exposures (ISA, section 7.4.15.2). 36January 2013 5-11 Draft - Do Not Quote or Cite Little new evidence is available of Pb effects on marine fish and mammals for 1 reproductive, growth and survival endpoints that are particularly relevant to population-level of 2 biological organization and higher (ISA, section 7.4.15). Evidence for effects at higher levels of 3 biological organization in saltwater habitats is primarily supported by observations in a small 4
number of microcosm and field studies where shifts in community structure are the most 5 commonly observed effects of Pb (ISA, section 7. 4.20). These types of studies were presented 6 in the 2006 CD and while there are new studies pr esented in the ISA, they primarily expand the 7 types of communities for which data exist but reach similar conclusions about community 8 structure as the 2006 CD. However, there is no evidence of adverse effects in saltwater 9
environments from current ambient air concen trations and linkages between any level of 10 ambient exposure and effects are unk nown in all but a few organisms. 11 New studies on organism-level effects from Pb in saltwa ter ecosystems provide little 12 evidence to inform our understanding of linkage s between atmospheric concentrations, ambient 13 exposures in saltwater systems and such effects or our conclusions regarding the likelihood of 14
adverse effects under conditions associated w ith the current NAAQS for Pb. Nor does the 15 currently available evidence indicate significantly different exposure levels at which ecological 16 systems or receptors are expected to experience effects. The new evidence, as outlined above, 17 serves to support previous conc lusions regarding effects evidence and provides information on 18 additional species, but does not significantly improve our understanding of ecological effects 19
levels of Pb. 20

 To what extent is there new informat ion that informs our understanding of 21 critical loads of Pb, including criti cal loads in sensitive ecosystems? 22
Critical loads are an es pecially powerful tool that can link Pb input into an ecosystem, 23 including atmospheric deposition, with ecologica l impairment. Critical load calculations are 24 dependent on data relating Pb released into an ecosystem from vari ous sources with an 25 understanding of the level of Pb in an ecosystem th at is likely to result in measurable effects. 26 Importantly, with these data, critical loads can a ccount for heterogeneity in ecosystem sensitivity 27 and exposure which often results in critical lo ad values that vary by ecosystem (e.g., aquatic28 water; aquatic-sediment; terrestrial), and di ffer by endpoint of concern (ISA, section 7.1.3). 29 During the last review, the 2006 CD assessed the available informa tion on critical loads for Pb 30 which was drawn primarily from Europe. Analys es were not available for U.S. locations, and 31 the European critical load values for Pb that had been developed were highly specific to the 32 bedrock geology, soil types, vegetation, and hist orical deposition trends in each European 33 country (2006 CD, p. E-24). As a result, the 2006 CD concluded that “[a]t this time, the methods 34 and models commonly used for the calculation of critical loads have not been validated for Pb” 35 and that “[m]any of the methods neglect the speciation of Pb when estimating critical limits, the 36January 2013 5-12 Draft - Do Not Quote or Cite uptake of Pb into plants, and out flux of Pb in drainage water, limiting the utility of current 1 models” (2006 CD, p. 7-46). Acco rdingly, the quantitative assessment for the last Pb NAAQS 2 review did not involve critical load analyses. 3
There are no critical loads fo r Pb reported in the ISA or 2006 CD for any ecosystems in 4 the U.S.; however, as reported in the 2006 CD and further discussed in section 7.3.7 of the ISA, 5 work has been conducted in terrestrial systems in Europe and aquatic ecosystems in Canada 6 (ISA, section 7.3.7 and section 7.4.8). Given that lo cal conditions (including historic loading, soil 7 transport and transformation processes) are key elemen ts to critical load ca lculation, the utility of 8 critical loads that are develope d from other countries for app lication to U.S. ecosystems is 9 unclear. Given the heterogeneity of ecosyst ems affected by Pb, and the differences in 10 expectations for ecosystem services attached to different land uses, it is expected that there 11 would be a range of critical load values for Pb for soils and freshwaters within the U.S. 12 In the short term, metal emissions generally have greater effects on biota in freshwater 13 systems than in terrestrial systems because metals are more readily immob ilized in soils than in 14 sediment. However, over the longer term, terrestri al systems may be more affected by increasing 15 concentrations, particularly by t hose metals with a long soil residence time, such as Pb (ISA, 16 section 7.4.8). There is no new ev idence regarding critical loads fo r Pb in saltwater ecosystems. 17

 To what extent is there information that improves our understanding of the 18 portion of environmental Pb derived from ambient air and the associated effects 19 on sensitive ecosystems? 20
As stated in the last review , the role of ambient air Pb in contributing to ecosystem Pb 21 has been declining over the past several decades . However, it remains difficult to apportion 22 exposure between air and other sources to better inform our understanding of ecosystem effects 23 that might be associated with air emissions. Co nsiderable uncertainties also remain in drawing 24
conclusions from evidence of effects observed unde r laboratory conditions with regard to effects 25 expected at the ecosystem level in the environmen t. In many cases it is difficult to characterize 26 the nature and magnitude of effects and to quant ify relationships between ambient concentrations 27 of Pb and ecosystem response due to the existenc e of multiple stressors, variability in field 28 conditions, and to differences in Pb bioavailabil ity at that level of or ganization (ISA, section 29 7.5). There is no new evidence th at substantially improves our unde rstanding of the relationship 30 between ambient air Pb and measurable ecological effects. 31
32January 2013 5-13 Draft - Do Not Quote or Cite 5.2 EXPOSURE AND RISK INFORMATION 1
This risk information available for this revi ew and described here is based primarily on 2 the pilot ecological risk assessmen t developed in the last review of the Pb NAAQS (henceforth 3 referred to as the 2006 REA [ICF, 2006]), which is described within the c ontext of the evidence 4 presented in the ISA that is newly available for this review. As described in the IRP, careful 5 consideration of newly available information in th is review led us to conclude that developing a 6
new REA for this review was not warranted. In light of critical limitations and uncertainties that 7 are still unresolved in the current evidence, sta ff concluded that currentl y available information 8 does not provide the basis for developing a new qua ntitative risk and exposure assessment with 9 substantially improved utility for informing the Agency’s consideration of welfare effects and 10 evaluation of the adequacy of th e current secondary standard or alternatives (IRP, section 3.3). 11
Based on their consideration of the IRP, the CASAC Pb Review Panel generally concurred with 12
the conclusion that a new REA was not wa rranted in this review (Frey, 2011). 4 Accordingly, the 13
information described here is drawn primarily from the 2006 REA. 14 The focus for the risk assessment and associated estimates presented here is on Pb 15 derived from sources emitting Pb to ambient air. While there is some new evidence that 16 improves our understanding of some of the envi ronmental variability affecting the disposition 17 and toxicity of Pb in the environment, the information and methods to support a quantitative 18 assessment of the role of atmospheric Pb in th e U.S are limited. Specific constraints include the 19 limited availability of location-specific data describing a range of U.S. ecosystems and their 20 pertinent environmental characteri stics as well as the ability to apportion effects between air and 21 non air sources, and a more complete understanding of bioavailability and its modifiers. These 22 data gaps and areas of uncerta inty in the current evidence re strict our ability to assess 23 quantitatively the relationship between concentrati ons of Pb in ambient air and terrestrial and/or 24 aquatic systems, and their effect on welfare. 25 As discussed in section 1.3 above, the multimedia and persistent nature of Pb, the role of 26 multiple exposure pathways (illustrated in Figur e 1-1 above), and the contributions of nonair 27 sources of Pb to exposure media all present ch allenges and contribute significant additional 28 complexity to the ecological risk assessment that goes far beyond the situation for similar 29 assessments typically performed for other NAAQ S pollutants (e.g., that focus only on a single 30 media pathway or for which air is the only signifi cant source). Limitations in the available data 31
and models affected our characterization of the va rious complexities associated with exposure to 32

4 In our evaluation presented in the REA Planning Document and consultation with CASAC, we indicated our conclusion that the information newly available in this review did not provide the means by which to develop an updated or enhanced risk model that would substantially improve the utility of risk estimates in informing the current Pb NAAQS review.January 2013 5-14 Draft - Do Not Quote or Cite ambient air Pb. As a result, the 2006 assessmen t was conducted as a pilot study with a number 1 of simplifying assumptions with regard to th e representativeness of the case studies for 2 ecological exposures and our ability to isolate case studies where air-derived Pb was the only or 3 most significant source. Therefore, this section presents a brief summary of the screening-level 4 ecological risk assessment conducted in 2006 fo r the Pb NAAQS review completed in 2008 and 5 addresses several questions rela ting to the current evidence a nd understanding that may inform 6
our view of the results of that assessment. Th e discussion here also ta kes into consideration 7
CASAC recommendations in the last review with regard to interp retation of the screening-level 8 assessment (Henderson, 2007a, b), as well as comments received from the CASAC Pb Panel in 9 the current review, as part of the consulta tion on the REA Planning Document (Frey, 2011). 10

5.2.1 Screening Assessment from Last Review 11 The screening-level risk assessment perfor med for the last review was focused on 12 estimating the potential for ecological risks asso ciated with ecosystem exposures to Pb emitted 13 into ambient air (2006 REA, section 7). A natio nal-scale screen was us ed to evaluate surface 14 water and sediment monitoring lo cations across the United States for the potential for ecological 15 impacts that might be associated with atmospheri c deposition of Pb (described in detail in 2006 16 REA, section 7.1.2). In addition to the natio nal-scale screen (2006 REA, section 3.6), the 17 assessment involved a case study approach, with case studies for areas surrounding a primary Pb 18 smelter (2006 REA, section 3.1) and a secondary Pb smelter (2006 REA, section 3.2), as well as 19 a location near a non-urban roadway (2006 REA, s ection 3.4). An additional case study, focused 20 on consideration of gasoline-derived Pb eff ects on an ecologically vulnerable ecosystem 21 (Hubbard Brook Experimental Forest), was iden tified (2006 REA, section 3.5). The Hubbard 22 Brook Experimental Forest (HBEF), in the White Mountain National Forest, near North 23 Woodstock, New Hampshire, was selected as a f ourth case study because of its location and its 24 long record of available data on c oncentration trends of Pb in thr ee media (air or deposition from 25 air), soil, and surface water). While no quantitativ e analyses were performed, summary review of 26
the literature search was incl uded in the assessment report (20 06 REA, Appendix E). For the 27 other three case studies, exposure concentratio ns in soil, surface water, and/or sediment 28
concentrations were estimated from available monitoring data or modeling analysis, and then 29 compared to ecological screening benc hmarks (2006 REA, section 7.1). 30
All three case studies and the national-scale assessment generally cons idered then-current 31
or recent environmental conditions . In all cases but the primary Pb smelter case study, current 32 air quality conditions were below the then-cur rent NAAQS. Air Pb c oncentrations in the 33 primary Pb smelter case study exceeded the then -current NAAQS. A comple te discussion of air 34 quality in each of the case studies can be found in section 4 of the 2006 REA. 35January 2013 5-15 Draft - Do Not Quote or Cite An overview of the approach developed to implement the selected elements of the 1 conceptual model for the ecological risk assessmen t is provided in Figure 5-1. This figure shows 2 the key types of information and models involved in each part of the assessment and how they 3 are related to each other and to the other parts of the analysis. Appendix 5A gives the locations 4 and spatial resolution for each of the case studies and the national scale screen while summarizes 5 the source of the screening values used or each location and media type. As indicated in Figure 6 5-1 and Appendix 5A, the specific approach for e ach case study differed based on the nature of 7 the case study (e.g., type of sour ce, locations of populations) and the site-specific measurements 8
available. 9
10January 2013 5-16 Draft - Do Not Quote or Cite Figure 5-1. Analytical approach for screening-leve l assessment in the last review (2006 1 REA, Exhibit 2-6). 2

3 4
5
6
7January 2013 5-17 Draft - Do Not Quote or Cite To estimate the potential for ecological risk, ecological soil screening values (Eco-SSLs) 1 developed by the EPA’s Superfund program (USEPA, 2003, 2005), the EPA’s recommended 2 ambient water quality criteria (2006 REA, sectio n 7.1) and sediment scre ening values developed 3 by MacDonald and others (2000, 2003) were used, as described in detail in section 7.1.3 of the 4 2006 REA. A hazard quotient (HQ) was calculated for adverse effects on the survival, growth, 5 and reproduction of exposed ecological receptors to determine the potenti al for risk to that 6 receptor. Ecological receptors used in the pilot are discussed in detail in section 7.1 of the 2006 7 REA. The HQ was calculated as the ratio of the media concentration to the ecotoxicity screening 8 value. In each case study, HQ values were calcul ated for each location where either modeled or 9
measured media concentrations were available. Separate soil HQ valu es were calculated for 10 each ecological receptor group for which an ecotoxici ty screening value has been developed (i.e., 11 birds, mammals, soil invertebrates, and plants), as described in detail in section 7.1.2 of the 2006 12 REA. HQ values less than 1.0 were concluded to suggest that Pb concentrations in a specific 13 medium were unlikely to pose significant risks to ecological receptors, while HQ values greater 14 than 1.0 indicated a potentia l for adverse effects. 15

5.2.2 Screening Assessment Results and Interpretation 16 The results for the ecological screening a ssessment for the three case studies and the 17
national-scale screen for surface wa ter and for sediment indicated a potential for adverse effect 18 from ambient Pb to multiple ecological receptor groups in terrestrial and aquatic locations. 19 Below are descriptions of the location-specifi c case studies and the national screening 20 assessment, key findings of the risk assessment fo r each, and an interpretati on of the results with 21 regard to past air conditions as well as the current standard (USEPA, 2007b). 22

 What do the key findings of the 20 06 screening-level a ssessment indicate 23 regarding the likelihood that adverse welf are effects would result from levels of 24 air-related Pb that would meet the current standard? 25 In addressing this question, the findings of the 2006 REA are summarized below. 26
Primary Pb Smelter Case Study 27

 The primary Pb smelter case study location is at one of the largest and longest28 operating primary Pb smelters in the wo rld (since 1892), the only one currently 29 operating in the U. S. (ICF, 2006). 5 30

 Concentrations of total Pb in several of the soil and sedime nt locations within the case 31 study were measured in 2000 and exceeded scre ening values, indica ting a potential for 32 adverse effects to terrestrial a nd sediment dwelling organisms. 33

5 As noted in section 2.1.2 above, this smelter is planning to cease existing smelting operations at this facility by April, 2014.January 2013 5-18 Draft - Do Not Quote or Cite  While the contribution to th ese Pb concentrations from air as compared to nonair 1 sources is not quantified, air emissions from this facility are subs tantial (ICF, 2006). In 2 addition, this facility that has been emitting Pb for many decades, including some 3 seven decades prior to establishment of any Pb NAAQS, such that it is likely air 4 concentrations associated with the facil ity were substantial relative to the 1978 5 NAAQS, which it exceeded at the time of th e last review. Currently, concentrations 6 monitored near this facility exceed the leve l of the current standard. Accordingly, this 7 case study is not informative for consideri ng the likelihood of adve rse welfare effects 8 related to Pb from air sources under air quali ty conditions associated with meeting the 9 current Pb standard. 10 Secondary Pb Smelter Case Study 11

 The secondary Pb smelter location falls w ithin the Alabama Coastal Plain in Pike 12 County, Alabama, in an area of disturbed forest s. The industrial facility in this case 13 study is much younger than the primary Pb sme lter, becoming active less than ten years 14 prior to the establishment of the 1978 Pb standard. 15

 Estimates of total Pb concentration in soils (based on fate and transport modeling using 16 1997-2000 emissions data and data for similar locations measured in a 1995 study) 17 exceeded screening values for plants, birds and mammals, indicating the potential for 18 adverse effects to these groups. 19

 While the contributions from air-related Pb to the total Pb concentrations modeled in 20 soils at this location is uncl ear, the facility co ntinues to emit Pb and the county where 21 this facility is located does not meet the current Pb standard (Appendix 5A). Given the 22 exceedances of the current standard, which lik ely extends back over 4 to 5 decades, this 23 case study also is not informative for cons idering the likelihood of adverse welfare 24 effects related to Pb from air sources unde r air quality conditions associated with 25 meeting the current Pb standard. 26 Near Roadway Non-urban Case Study 27

 This case study comprises two nonurban sites adjacent to established highways for 28 which soil Pb data were available: (1) in Co rpus Christi, Texas (ICF, 2006) and (2) in 29 Atlee, Virginia (ICF, 2006). Measured soil concentration data were used to develop 30 estimates of Pb in soils for each location. 31

 Estimates of total Pb concentrations take n in 1994 and 1998 in soils in this case study 32 exceeded screening values for plants, birds and mammals, indicating the potential for 33 adverse effect to these groups. 34 These case study locations are highly impacted by past deposition of gasoline Pb. It is 35 unknown whether current conditions at these si tes exceed the current Pb standard but 36 given evidence from the past of Pb concentrations near highways that ranged above the 37 previous (1978) Pb standard (1986 CD, s ection 7.2.1), conditions at these locations 38 during the time of leaded gasoline very likely exceeded the current standard. Similarly, 39 those conditions likely resulted in Pb deposition associated with leaded gasoline that 40 exceeds that being deposited unde r current air quality conditi ons that likely meet the 41 current Pb standard. Given this lega cy, consideration of the potential for 42January 2013 5-19 Draft - Do Not Quote or Cite environmental risks from levels of air–rela ted Pb associated with meeting the current 1 Pb standard in these loca tions is highly uncertain. 2 Vulnerable Ecosystem Case Study 3

 This case study was focused on consideration of information available for the Hubbard 4 Brook Experimental Forest (HBEF) in the White Mountain National Forest near North 5 Woodstock, New Hampshire, which incl uded a long record (from 1976 through 2000) 6 of available data on concentra tion trends of Pb in three media (air or deposition from 7 air, soil, and surface water). 8

 While no quantitative analyses were perfor med, summary review of literature search 9 indicated: (1) atmospheric Pb inputs do not directly affect stream Pb levels at HBEF 10 because deposited Pb is almost entirely re tained in the soil profile; (2) soil horizon 11 analysis results showed Pb to have become more concentrated at lower soil depths over 12 time, with the soil serving as a Pb sink, a ppreciably reducing Pb in pore water as it 13 moves through the soil layers to streams (d issolved Pb concentrations were reduced 14 from 5 ppb to about 5 ppt from surface soil to streams). Further, the available studies 15 concluded insignificant contri bution of dissolved Pb from soils to streams (ICF, 2006, 16 Appendix E). It is unlikely that cond itions have changed from the previous 17 conclusions made based on soil data through 2000 and therefore, current ambient air 18 concentrations likely do not directly imp act stream Pb levels under air quality 19 conditions associated with meeting the current standard. 20 National-scale Surface Water and Sediment Screen 21

 The national-scale screen was performed usi ng a national database of surface water and 22 sediment monitoring data (s ee Appendix 5A; ICF, 2006). 23

 The screen identified 15 non-mining sites at which at least one surface water 24 dissolved Pb concentration taken be tween 1994 and 2004 exceeded the chronic 25 screening value, indicating a potential for adverse effect if concentrations were 26 persistent over long time periods. The acute screening value was not exceeded 27 at any of these locations. 28

 Analysis of the sediment concentratio ns for the 15 sites taken from 1991 to 29 2000 analyzed in the surface water scr een identified a subset for which 30 concentrations exceeded the screening va lue, indicating a potential for adverse 31 effects to sediment dwelling organisms. 32

 The extent to which past air emissions of Pb have contributed to surface water or 33 sediment Pb concentrations at the locations identified in the screen is unclear. For 34 some of the surface water loca tions, nonair sources likely contributed significantly to 35 the surface water Pb concentrations. For other locations, a lack of nearby nonair 36 sources indicated a potential role for air so urces to contribute to observed surface water 37 Pb concentrations. Additionally, these concentrations may have been influenced by Pb 38 in resuspended sediments and/or reflect contribution of Pb from erosion of soils with 39 Pb derived from historic as well as current air emissions. 40

41January 2013 5-20 Draft - Do Not Quote or Cite There are multiple sources of uncertainty associated with different aspects of this 1 assessment (discussed in detail in 2006 REA, s ection 7.4). For example, there are significant 2
limitations and uncertainties associated with conc lusions that can be drawn from the primary 3 smelter case study regarding the impact of atmo spheric deposition under conditions associated 4 with meeting the Pb NAAQS (past or present). Additionally, while cas e study locations were 5 chosen with the objective of including locations fo r which recent Pb data were available and for 6 which Pb exposures might be influenced by ai r-related Pb and not be dominated by nonair 7 sources, there is significant un certainty regarding the extent to which nonair sources and 8
conditions associated with histor ic emissions (e.g., prior to establishment of past or present Pb 9 NAAQS) have likely contributed to the Pb exposure estimates in some locations. The screening 10
values available and used in the assessment were also sources of uncertainty with regard to 11 conclusions as to potential for ecological risk as the selected screening values (e.g., ambient 12 water quality criteria, Eco-SSLs, sediment criteria) lacked adjustment for some critical measures 13 of bioavailability. There is also uncertainty regarding the extent to which the screening values 14 could identify potential hazard for some threatened or endangered species or unusually sensitive 15 aquatic ecosystems (ICF 2006). Thus, while the asse ssment results are generally consistent with 16
evidence-based observations of the potential influence of Pb on ecological systems, they are 17 limited with regard to quantitative conclusions and potential hazard or risk associated with the Pb 18 NAAQS, most particularly with rega rd to the current standard. 19

 What are the important uncertainties asso ciated with interpreting the prior 20 assessment in light of newly availa ble evidence in this review? 21 In interpreting the results from the 2006 REA, we consider newly available evidence that 22 may inform our interpretation of risk under the cu rrent standard. Factors necessary to alter our 23 interpretation of risk would include new evidence of harm at lower concentrations of Pb, new 24 linkages that enable us to dr aw more explicit conclusions as to the air contribution of 25 environmental exposures, and/or new methods of interpreting confoundi ng factors that were 26 largely uncontrolled in the pr evious risk assessment. 27 With regard to new evidence of harm at lower concentrations, it is necessary to consider 28 that the evidence of adversity due specifically to Pb in natural systems is limited, in no small part 29 because of the difficulty in determining the e ffects of confounding fact ors such as multiple 30 metals and modifying factors infl uencing bioavailability in field studies. Modeling of Pb related 31 exposure and risk to ecol ogical receptors is subject to a wide array of so urces of both variability 32 and uncertainty. Variability is associated with geographic location, hab itat types, physical and 33
chemical characteristics of soils and water that influence Pb bioavailability, terrestrial and 34 aquatic community composition, Pb uptake rates by i nvertebrates, fish, and plants by species and 35 season. For wildlife, variability also is associated with food ingestion rates by species and 36January 2013 5-21 Draft - Do Not Quote or Cite season, prey selection, and locat ions of home ranges for fo raging relative to the Pb 1 contamination levels (USEPA, 2006b). 2 There are significant difficulties in quantifying the role of air emissions under the current 3 standard, which is significantly lower than the pr evious standard. As recognized in section 1.3.2 4 above, lead deposited before the standard wa s enacted remains in soils and sediments, 5 complicating interpretations regarding the impact of the current standard; historic Pb emitted 6 from leaded gasoline usage continues to move slowly through systems along with more recently 7 deposited Pb and Pb derived from non air sources. The results from the location-specific case 8 studies and the surface and sediment screen performe d in the last review are difficult to interpret 9 in light of the current standard and are not la rgely useful in informing our judgments of the 10 potential for adverse effects at levels of deposition meeting the current standard. Under such 11
constraints it is difficult to a ssess the merit of the risk findi ngs from the previous review. 12January 2013 5-22 Draft - Do Not Quote or Cite 5.3 REFERENCES 1

Buekers, J; Redeker, ES; Smolders, E. (2009). Lead toxicity to wildlife: Derivation of a critical blood 2 concentration for wildlife monitoring based on literature data [Review]. Sci Total Environ 3 407: 3431-3438. http://dx.doi.org/10.1016/j.scitotenv.2009.01.044 4

Frey, C; Samet, JM. (2011). CASAC review of the EPA's integrated science assessment for lead 5 (first external review draft- May 2011). (EPA-CASAC-12-002). Washington, DC: U.S. 6 Environmental Protection Agency, Clean Air Scientific Advisory Committee. 7

Henderson, R. (2007a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory 8 Committee, to Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory 9 Committee’s (CASAC) Review of the 1st Draft Lead Staff Paper and Draft Lead Exposure 10 and Risk Assessments. March 27, 2007. 11

Henderson, R. (2007b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory 12 Committee, to Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory 13 Committee’s (CASAC) Review of the 2nd Draft Lead Human Exposure and Health Risk 14 Assessments. September 27, 2007. 15

ICF International. (2006) Lead Human Exposure and Health Risk Assessments and Ecological Risk 16 Assessment for Selected Areas. Pilot Phase. Draft Technical Report. Prepared for the U.S. 17 EPA's Office of Air Quality Planning and Standards, Research Triangle Park, NC. 18 December. 19

MacDonald, D.D., Ingersoll, C.G., and Berger, T.A. (2000) Development and evaluation of 20 consensus-based sediment quality guidelines for freshwater ecosystems. Archives of 21 Environmental Contamination and Toxicology. 39:20-31. 22 23 MacDonald, D.D., Ingersoll, C.G., Smorong, D.E., Lindskoog, R.A., Sloane, G., and Biernacki, T. 24 (2003) Development and Evaluation of Numerical Sediment Quality Assessment Guidelines 25 for Florida Inland Waters. British Columbia: MacDonald Environmental Sciences, Lt. 26 Columbia, MO: U.S. Geological Survey. Prepared for: Florida Department of Environmental 27 Protection, Tallahassee, FL. January. 28

U.S. Environmental Protection Agency. (2005a) Guidance for Developing Ecological Soil Screening 29 Levels. Washington, DC: Office of Solid Waste and Emergency Response.OSWER Directive 30 9285.7-55. November. 31

U.S. Environmental Protection Agency. (2005b) Ecological Soil Screening Levels forLead, Interim 32 Final. Washington, DC: Office of Solid Waste and Emergency Response. OSWER Directive 33 9285.7-70. Available at http://www.epa.gov/ecotox/ecossl/pdf/eco-ssl_lead.pdf. 34

U.S. Environmental Protection Agency. (2006a) Air Quality Criteria for Lead. Washington, DC, 35 EPA/600/R-5/144aF. Available online at: 36 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr.html 37

U.S. Environmental Protection Agency. (2006b) Analysis Plan for Human Health and Ecological 38January 2013 5-23 Draft - Do Not Quote or Cite Risk Assessment for the Review of the Lead National Ambient Air Quality Standards. 1 Office of Air Quality Planning and Standards, Research Triangle Park, NC. Available at: 2 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_pd.html 3

U.S. Environmental Protection Agency. (2007a). Framework for metals risk assessment [EPA 4 Report]. (EPA 120/R-07/001). Washington, D.C. Available online at: 5 http://www.epa.gov/raf/metalsframework/index.htm 6

U.S. Environmental Protection Agency. (2007b). Review of the National Ambient Air Quality 7 Standards for Lead: Policy Assessment of Scien tific and Technical Information OAQPS Staff 8 Paper. Washington, DC, EPA-452/R-07-013. Available online at: 9 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr.html 10

U.S. Environmental Protection Agency. (2012) Integrated Science Assessment for Lead (Third 11 External Review Draft). Washington, DC, EPA/600/R-10/075C. Available online at: 12 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html 13January 2013 6-1 Draft – Do Not Quote or Cite 

### 6 REVIEW OF THE SECOND ARY STANDARD FOR LEAD 1

This chapter presents preliminary staff conclu sions regarding the secondary Pb standard. 2 These preliminary staff conclusions are guided by consideration of key policy-relevant questions 3 and based on the assessment and integrative synt hesis of information presented in the ISA and by 4 staff analyses and evaluations presented in chapte rs 2 and 5 herein. Final evaluations and staff 5 conclusions, to be developed taking into c onsideration CASAC advice and public comment on 6 this draft document, will be presented in the final PA. The final evaluations and staff 7
conclusions will inform the Administrator’s decisi ons on whether to retain or revise the existing 8 secondary standard for Pb. 9 Following an introductory section on the gene ral approach for reviewing the secondary 10 standard (section 6.1), including a summary of considerations in th e last review, the discussion in 11 this chapter focuses on the central issue of whet her the information available in this review 12 supports or calls into question th e adequacy of the current sec ondary standard. Building on the 13 responses to specific policy-rel evant questions on th e scientific evidence and exposure-risk 14 information in chapter 5 above, presentation in sec tion 6.2 is also organized into consideration of 15 key policy-relevant questions framing evidence-b ased and exposure/risk-based considerations. 16 The policy-relevant questions in this document are based on t hose included in the IRP (IRP, 17 section 3.2). In section 6.3, preliminary staff conc lusions are developed. Section 6.4 presents a 18 brief overview of key uncertainties and areas for future research. 19

6.1 APPROACH 20 Staff’s approach for reviewing the current s econdary standard, which involves translating 21
scientific and technical information into the ba sis for addressing key policy-relevant questions, 22 takes into consideration the appr oaches used in the previous Pb NAAQS review. The past and 23 current approaches described below are al l based most fundamentally on using EPA’s 24
assessment of the current scientific evidence and previous quantitative analyses to inform the 25 Administrator’s judgment with regard to the secondary standard for Pb. 26 Staff final conclusions will be developed for the next version of this document with 27
consideration of CASAC advice and public comment. In drawi ng conclusions regarding the 28 secondary standard for the Administrator’s cons ideration, we note that the final decision on the 29 adequacy of the current secondary Pb standard is largely a public welfar e policy judgment to be 30 made by the Administrator. The Administ rator’s final decision draws upon scientific 31 information and analyses about welfare effects, exposure and risks, as well as judgments about 32 the appropriate response to the ra nge of uncertainties that are inhe rent in the scientific evidence 33 and analyses. This approach is consistent with the requirement s of the NAAQS provisions of the 34January 2013 6-2 Draft – Do Not Quote or Cite Act. Section 109 of the Clean Air Act requires the Administrator to establish a secondary 1 standard that, in the judgment of the Administrator, is “requisite to protect the public welfare 2 from any known or anticipated adverse effects as sociated with the presence of the pollutant in 3 the ambient air”. In so doing, the Administrato r seeks to establish sta ndards that are neither 4 more nor less stringent than necessary for this purpose. 5

6.1.1 Approach Used in the Last Review 6 The current secondary standard for Pb is equa l to the primary standard for human health. 7
As summarized in section 1.2.2 and described in more detail in section 4.1.1, the primary 8 standard was substantially revise d in the last review based on the much-expanded health effects 9 evidence of neurocognitive effects of Pb in children. The level of the revised NAAQS is 0.15 10 μg/m 3 . The averaging time was also revised to a rolling three-month period with a maximum 11 (not-to-be-exceeded) form, evaluated over a three-year period. Compared to the previous 12 averaging time of one calendar qua rter, this revision was considered to be more scientifically 13 appropriate and more protective for human heal th. The indicator of Pb-TSP was retained, 14 reflecting the evidence that Pb particles of all sizes pose health risks (73 FR 67007). 15
The scientific assessment for the last review is described in the 2006 Air Quality Criteria 16 for Lead (AQCD; USEPA, 2006b), multiple drafts of which received review by CASAC and the 17 public. EPA also conducted a pilot ecological risk assessment for the revi ew, after consultation 18 with CASAC and receiving public comment on a dr aft analysis plan (USEPA, 2006c). The pilot 19 ecological risk assessment was released in December 2006 (ICF, 2006) and the policy 20 assessment based on these assessments, air qua lity analyses and key evidence from the AQCD 21 was presented in the Staff Paper (USEPA, 2007b), a draft of which also received CASAC and 22 public review. The final Staff Pa per presented OAQPS staff’s evalua tion of the public health and 23 welfare policy implications of the key studies and scientific information contained in the 2006 24 CD and presented and interpreted results from th e pilot risk/exposure anal yses conducted for this 25
review. Based on this evaluati on, the Staff Paper presented OAQ PS staff recommendations that 26 the Administrator give consideration to subs tantially revising the primary and secondary 27 standards to a range of levels at or below 0.2 μ g/m3. 28 In the previous review, the Administrator considered the evidence-based information 29 presented in the CD and the risk-based info rmation presented in the 2006 REA. It was his 30 conclusion that the available data and evidence, wh ile primarily qualitative, suggested that there 31 was the potential for adverse environmental impa cts under the then-current standard. Given the 32 limited data on Pb effects in ecosystems, it was at the time, as it is now, necessary to look at 33 evidence of Pb effects on organisms and extrapolat e to ecosystem effects. Therefore, taking into 34
account the available evidence and current media concentrations in a wide range of areas, the 35January 2013 6-3 Draft – Do Not Quote or Cite Administrator concluded that th ere was potential for adverse effects occurring under the then1 current standard; however there was insufficient da ta to provide a quantita tive basis for setting a 2 secondary standard different than the primary ( 73 FR 67011). Therefore, ci ting a general lack of 3
data that would indicate the a ppropriate level of Pb in envi ronmental media that may be 4 associated with adverse effects, as well as the comments of the CASAC Pb panel that a 5 significant change to current air concentrations (e.g., via a significant ch ange to the standard) 6 was likely to have significant beneficial eff ects on the magnitude of Pb exposures in the 7 environment, the secondary standard was revise d to be consistent with the revised primary 8 standard (73 FR 67011). 9

6.1.2 Approach for the Current Review 10 In evaluating whether it is appropriate to consider retaining the current secondary Pb 11 standard, or whether considerati on of revision is appropriate, we have adopted an approach in 12 this review that builds on the general approach from the last review and reflects the body of 13
evidence and information now available. As summ arized above, the Administrator’s decisions in 14 the previous review were based on the conclu sion that there was the potential for adverse 15 ecological effects under th e previous standard. In our appr oach here, we intend to focus on 16
consideration of the extent to which a broader body of scientific evidence is now available that 17
would inform decisions on either the potential for adverse effect s to ecosystems under the current 18 standard or the ability to set a more ecologically relevant secondary standard than was feasible in 19 the previous review. In conducti ng this assessment, we draw on the ecological effects evidence 20 presented in detail in the ISA, and aspects summarized above in chapter 5, along with the 21 information associated with the screening-leve l risk assessment also summarized above. Figure 22
6-1 illustrates the basic construc t of our approach in developing conclusions regarding options 23 appropriate for the Administrator to consider in this review with regard to the adequacy of the 24 current secondary NAAQS standard and, as a ppropriate, potential alte rnate standards. 25 In developing preliminary conclusions in th is review, we have taken into account both 26
evidence-based and risk-based considerations fr amed by a series of policy-relevant questions. 27 These questions are outlined in the sections belo w and generally discuss the extent to which we 28
are able to better characterize effects and the likelihood of adve rse effects in the environment 29
under the current standard. Our approach to considering these questions recognizes that the 30 available welfare effects evidence generally refl ects laboratory-based evidence of toxicological 31 effects on specific organisms exposed to concentrati ons of Pb at which scientists generally agree 32 that adverse effects are likely to occur. It is widely recognized, however, that environmental 33 exposures from atmospherically-derived Pb are likely to be lower and/or accompanied by 34January 2013 6-4 Draft – Do Not Quote or Cite significant confounding and modifying factors (e.g., other metals, acidification), which increases 1 our uncertainty about the like lihood and magnitude of organism and ecosystem responses. 2

Figure 6-1. Overview of approach for review of current secondary standard. 3 Evidence-based Considerations

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

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

 Newly identified at-risk ecosystems?

 Changed understanding of lead bioavailability and movement of through ecosystems?

 Effects at lower air-related exposures then previously understood or in conditions that would have likely met current standards? 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 ConsiderationJanuary 2013 6-5 Draft – Do Not Quote or Cite 6.2 ADEQUACY OF THE CURRENT STANDARD 1 In considering the ade quacy of the current Pb standa rd, the overarching question we 2
consider is: 3

 Does the currently available scientific evidence- and exposure/risk-based 4 information, as reflected in the ISA a nd REA, support or call into question the 5 adequacy of the protection afforded by the current Pb standard? 6 To assist us in interpreting the currently av ailable scientific evidence and screening-level 7 risk information to address this question, we have focused on a series of more specific questions, 8 posed within sections 6.2.1 and 6.2.2 below. In so doing, we consider both the information 9
available at the time of the last review and in formation newly available since the last review 10 which has been critically analyzed and characterized in the ISA. 11

6.2.1 Evidence-based Considerations 12 In considering the welfare effects evidence wi th respect to the ade quacy of the current 13 standard, we must consider the array of evidence newly assessed in the ISA and the degree to 14 which the newly available evidence supports previ ous conclusions about the effects of Pb in the 15
environment and the extent to which it reduces areas of uncertainty recognized in decisions on 16 the secondary standard in the la st review. Additionally, as the se condary standard set in 2008 is 17 significantly lower than the prev ious standard, which was the fo cus of evaluation in the last 18 review, we must consider the extent to whic h the current evidence s upports conclusions about 19
the effects of current ambient levels under the current standard and th e extent to which the 20 evidence supports or calls into question the adequacy of prot ection afforded by the current 21
standard. 22

 To what extent does the available informat ion indicate that Pb-related effects are 23 occurring as a result of multimedia pa thways associated with ambient air 24 conditions that would meet the current standard? 25
The current evidence continue s to support our conclusions from the previous review 26 regarding key aspects of the eco logical effects evidence for Pb and the effects of exposure 27 associated with levels of Pb occurring through ec ological media in the U.S. Our conclusions in 28 this regard are based on consider ation of the assessment of the cu rrently available evidence in the 29 ISA, particularly with regard to key aspects summ arized in chapter 5 of this PA, in light of the 30
assessment of the evidence in the last review as described in the 2006 CD and summarized in the 31 notice of final rulemaking (73 FR 67008). Key aspects of these previous conclusions are 32
summarized below. 33

 Deposition of gasoline-derived Pb into fore st soils has produced a legacy of slow 34 moving Pb that remains bound to organic mate rials despite the removal of Pb from 35January 2013 6-6 Draft – Do Not Quote or Cite most fuels and the resulting dramatic re ductions in overall deposition rates (2006 CD, 1 Section AX7.1.4.3). 2

 For areas influenced by point sources of air Pb that meet the standard considered in the 3 previous review, concentrations of Pb in soil may exceed by many orders of magnitude 4 the concentrations which are considered harmful to laboratory organisms (2006 CD, 5 Section 3.2 and AX7.1.2.3). 6

 Some Pb deposited before the previous standard was enacted is still present in soils and 7 sediments; historic Pb from gasoline conti nues to move slowly through systems as does 8 current Pb derived from bot h air and nonair sources. 9

 The evidence of adversity in natural systems is very sparse due in no small part to the 10 difficulty in determining the effects of c onfounding factors such as multiple metals or 11 factors influencing bioavailabi lity in field studies. 12

 Environmental conditions exist in which Pb-associated adverse effects to aquatic 13 organisms and thereby ecosystems may be anticipated given experimental results. 14

 Some areas with long term hist orical deposition of Pb to sediment from a variety of 15 sources as well as areas influenced by poi nt sources have the potential for adverse 16 effects to aquatic communities ( 2006 CD, Sections AX7.2.2.2.2 and AX7.2.4). 17 The range of effects of Pb on terrestrial a nd aquatic organisms based on new information 18
in the current review are summarized in the ISA (ISA, section 2.7 and section 7.3 and 7.4) and 19 largely mirror the conclusions presented above from the previous review. 20 The integrated synthesis contained in the IS A conveys how effects of Pb can vary with 21 species and life stage, duration of exposure, form of Pb, and me dia characteristics such as soil 22 and water chemistry. A wide range of organi sm effects are recognized, including effects on 23 growth, development (particularly of the neur ological system) and reproductive success (ISA, 24 section 7.3 and section 7.4). Lead is recogni zed to distribute from the air into multiple 25 environmental media, as summarized in secti on 1.3 above, contributing to multiple exposure 26 pathways for ecological receptors. As discusse d in section 5.1 above, many factors affect the 27 bioavailability of Pb to receptors in terrestrial and aquatic ecosystems, contributing to differences 28 between laboratory-assessed toxi city and Pb toxicity in th ese ecosystems, challenging our 29 consideration of environmental impacts of Pb emitted to ambient air. 30 In studies in a variety of ecosystems, adverse ecosystem-level effects (including 31 decreases in species diversity, loss of vegeta tion, changes to community composition, decreased 32 growth of vegetation, and increase d number of invasive species) have been demonstrated near 33 smelters, mines and other industries that have released Pb, among other materials (ISA, section 34 7.3.12 and 7.4.12). As noted in section 5.1 above, howev er, our ability to char acterize the role of 35
air emissions of Pb in contributi ng to these effects is complicated because of coincident releases 36 to other media and of other pollutants. Co-rele ased pollutants include a variety of other heavy 37 metals, in addition to sulfur dioxide, which ma y cause toxic effects in themselves and may 38January 2013 6-7 Draft – Do Not Quote or Cite interact with Pb in the environment. There is also some uncertainty as to the extent to which Pb 1 in ambient air is contributing to the exposure. These uncertainties lim it our ability to draw 2 conclusions regarding the extent to which Pb-related effects may be associated with ambient air 3
conditions that would meet the current standard. 4 The role of historically em itted Pb, as discussed in section 1.3.2 above, poses additional 5 complications in addressing this question. The va st majority of Pb in the environment today, 6 particularly in terrestrial ecosystems, was deposited in the past during the use of Pb additives in 7 gasoline (USEPA 2007b, section 6.2.1) although industrial coal use ha s also been documented as 8 a significant source as well (ISA, section 3.2.1). Th is gasoline-derived Pb was emitted in very 9 large quantities (CD, pl AX7-98 and ISA, Figure 3-8) and predominantly in small sized particles 10 which were widely dispersed a nd transported across large dist ances (ISA, section 3.2). As 11 recognized in section 2.3.1 and 2.3.3.2 above, historic al records provided by sediment cores in 12 various environments document the substantially reduced Pb deposition (associated with reduced 13 Pb emissions) in many locations (ISA, section 3. 2.1). As Pb is extremely persistent in the 14 environment, past environmental releases are expected to generally dominate current media 15
concentrations. There is limited evidence to re late specific ecosystem effects with current 16 ambient air concentrations of Pb through deposi tion to terrestrial and aquatic ecosystems and 17 subsequent movement of deposited Pb through the environment (e.g., soil, sediment, water, 18 organisms). The potential for ecosystem effects of Pb from atmospheric sources under conditions 19 meeting the current standard is difficult to asse ss due to limitations on av ailable information not 20 only on bioavailability (as affected by the specific characteristics of the receiving ecosystem), 21 but also information to fully characterize the distribution of Pb from the atmosphere into 22 ecosystems in long-term exposure scenarios. Ther efore, the connection be tween air concentration 23 and ecosystem exposure and associated potential for welfare effects con tinues to be poorly 24 characterized for Pb (ISA, Section 7.5), and is ev en harder to characterize with respect to the 25
current standard than it was in last review with respect to the previous standard. 26

 To what extent have important uncertaint ies identified in the last review been 27 reduced and/or have new uncertainties emerged? 28 With regard to uncertainties in effects associ ated with Pb in the ambient air, the last 29 review illustrated the largest of these uncertainties were the ability to determine the prevalence of 30 effects in the natural environment, the ability to apportion effects between air and nonair sources, 31 and the understanding of the effects in the contex t of the current standard (IRP, section 3.2). 32 While we have some new evidence with regard to bioavailability and its role in determining 33 effects, overall these remain the major sources of uncertainty in evaluating effects and exposure 34 evidence for Pb in ecosystems. 35January 2013 6-8 Draft – Do Not Quote or Cite With regard to the prevalence of effects in the natural environment, it remains difficult to 1
assess the concentration at which Pb elicits a specific effect in terrestrial and aquatic systems, 2
due to the influence of other environmental vari ables on both Pb bioavailabi lity and toxicity, and 3 also due to substantial species di fferences in Pb susceptibility. There is little new information 4 that would facilitate extrapolat ion of evidence on individual speci es, generally from controlled 5 laboratory studies, to conclusions regarding adversity to popula tions or ecosystems within the 6 natural environment. For example, in terrestria l systems, evidence reviewed in the ISA (ISA, 7 Sections 7.2.3 and 7.2.4) demonstrates that exposure to Pb is generally associated with negative 8 effects on growth, reproduction and survival in terrestrial ecosystems. Many factors, including 9 species composition and various soil physiochemi cal properties, intera ct strongly with Pb 10 concentration to modify effects. Also, Pb aging is a particularly important factor in terrestrial 11 systems, where soil is the main route of exposur e, and it is difficult to reproduce experimentally. 12 Without quantitative characteri zation of those interactions, characterizations of exposure13 response relationships would likely not be transferable outside of experimental settings (ISA, 14 Section 2.7.1). 15 As reported in the ISA, th ere continues to be limited evidence linking current ambient 16 air sources of Pb through deposition to envir onmental media (e.g., soil, sediment, water, and 17 biota) and to ecological effects (ISA, section 7.3.1 1). The ability to apportion effects between air 18 deposited Pb and nonair sources is difficult to as sess due to a lack of information not only on the 19 bioavailability of that Pb, which is greatly influenced by the specific characteristics of the 20 receiving ecosystem, but also on Pb distribution in ecosystems in long-term exposure scenarios. 21
Consideration of the environm ental risks associated with the current standard is 22 complicated by the environmental burden associat ed with air Pb concentrations, predominantly 23 in the past, that exceeded the current standa rd (USEPA, 2007b, section 6.4.4.2). For example, a 24 large portion of Pb deposited befo re the standard was enacted is likely still present in soils and 25 sediments and historic Pb from gasoline conti nues to move slowly through systems as does 26
current Pb derived from both air and nonair sources. As a genera l matter, the currently available 27 evidence, as assessed in the ISA, does not significantly reduce any of these areas of uncertainty 28
or inform our consideration of the adequacy of the current standard. 29
30January 2013 6-9 Draft – Do Not Quote or Cite 6.2.2 Exposure/Risk-based Considerations 1

2

 To what extent does risk or exposure information indicate that air-related 3 ecosystem exposures important from a pub lic welfare perspective are likely to 4 occur with air Pb levels that just meet the current standard? 5
The current evidence continues to support our conclusions with regard to interpreting the 6 risk and exposure results from the previous revi ew. Our conclusions in this regard are based on 7
consideration of the scre ening-level ecological risk assessment results from the previous review 8 in light of the currently ava ilable evidence in the ISA and as described in the 2006 REA and 9 summarized in the notice of final rulemaking (73 FR 67009). Key aspects of these results in the 10
context of the current standard are summarized below, drawing from the discussion of the 2006 11 REA results in section 5.2.2 above, which is based on the information in the 2006 REA (ICF, 12 2006). 13 Primary Pb Smelter Case Study 14

 While the contribution to Pb concentrations from air as compared to nonair sources is 15 not quantified, air emissions from this fac ility are substantial (ICF 2006). Currently, 16 the county where this facility is loca ted exceeds the now current Pb NAAQS. 17 Secondary Pb Smelter Case Study 18

 While the contribution from air deposited Pb to the overall Pb concentrations modeled 19 in soils at this location is unclear, the f acility continues to emit Pb and the county 20 where this facility is located exceeds the now current Pb NAAQS (Appendix 5-A). 21 Near Roadway Non-urban Case Study 22

 These case study locations are highly impacted by past deposition of gasoline Pb. It is 23 unknown whether current conditions at these si tes exceed the now current Pb standard 24 but given evidence from the past of Pb con centrations near highways that ranged above 25 the previous (1978) Pb standard (1986 CD, section 7.2.1), conditions at these locations 26 during the time of leaded gasoline very likely exceeded the 1978 standard. 27 Vulnerable Ecosystem Case Study 28

 The previous review concluded that atmospheri c Pb inputs do not dire ctly affect stream 29 Pb levels at Hubbard Brook Experimental Forest because deposited Pb is almost 30 entirely retained in th e soil profile. It is unlikely that conditions have changed from the 31 previous conclusions made based on so il data through 2000 and therefore, current 32 ambient air concentrations likely do not di rectly impact stream Pb levels under air 33 quality conditions associated with meeting the now current standard. 34 National-scale Surface Water and Sediment Screen 35

 The extent to which past air emissions of Pb have contributed to surface water or 36 sediment Pb concentrations at the locations identified in the screen is unclear. For 37 some of the surface water loca tions, nonair sources likely contributed significantly to 38January 2013 6-10 Draft – Do Not Quote or Cite the surface water Pb concentrations. For other locations, a lack of nearby nonair 1 sources indicated a potential role for air so urces to contribute to observed surface water 2 Pb concentrations. Additionally, these concentrations may have been influenced by Pb 3 in resuspended sediments and/or reflect contribution of Pb from erosion of soils with 4 Pb derived from historic as well as current air emissions. 5

6 Although the available risk a nd exposure information continues to be sufficient to 7
conclude that the 1978 standard was not providing adequate pr otection to ecosystems, that 8 information, when considered with regard to air-r elated ecosystem exposures likely to occur with 9 air Pb levels that just meet the now current st andard, does not provide evidence that the current 10 secondary standard is inadequate. 11

6.3 PRELIMINARY STAFF CONCLUSIONS ON THE SECONDARY STANDARD 12 This section describes preliminary staff conc lusions regarding ade quacy of the current 13 secondary Pb standard. These conclusions are based on considerations described above and in 14 the discussion below regarding th e currently available scientific evidence summarized in the 15 third draft ISA and prior CDs and the risk and exposure information drawn from the 2006 REA. 16 The final PA will draw upon the final ISA, deve loped after CASAC review and public comment 17 on the third draft ISA. Staff conclusions presente d in the final PA will take into account advice 18 from CASAC and public comment on this document and these draft conclusions. 19 Taking into consideration the discussions res ponding to specific ques tions above in this 20 and the prior chapter, this section addre sses the following overar ching policy question: 21

 Does the currently available scientific evidence- and exposure/risk-based 22 information, as reflected in the ISA a nd REA, support or call into question the 23 adequacy of the protection afforded by the current secondary Pb standard? 24 With respect to evidence-based considerations, staff gives we ight to the body of evidence 25 on the ecological effects of Pb in the natural e nvironment, expanded in some aspects since the 26 last review, which continues to support identification of ecological effects in organisms relating 27 to growth, reproduction, and survival as the most relevant endpoints associated with Pb 28 exposure. The currently available evidence, wh ile somewhat expanded si nce the last review, 29 does not include evidence of significant effects at lower concentrations or evidence of higher 30 level ecosystem effects beyond t hose reported in the last revi ew. There continues to be 31 significant difficulties in interpreting effects evid ence from laboratory studies to the natural 32 environment and linking those effects to ambient air Pb concentrations. Further, we are aware of 33
no new critical loads information that would in form our interpretation of the public welfare 34 significance of the effects of Pb in various ecosystems. In summary, while new research has 35 added to the understanding of Pb biogeochemistry and expanded the list of organisms for which 36January 2013 6-11 Draft – Do Not Quote or Cite Pb effects have been described, there remains a significant lack of knowledge about the potential 1
for adverse effects from ambient air Pb in the environment and the exposures that occur from 2 such air-derived Pb, particular ly under the current standard. 3 With respect to exposure/risk-based consid erations, we recogni ze the complexity of 4 interpreting the previous risk assessment with respect to ambient air Pb under the current 5
standard and the associated limitations and uncerta inties of such assessments. For example, the 6 location-specific case studies as well as the nati onal screen reflect both current air Pb deposition 7 as well as past air and nonair source contribu tions. We conclude that while the previous 8 assessment is consistent with and generally supp ortive of the evidence-based conclusions about 9
Pb in the environment the limitations of a pportioning Pb between pa st and present air 10
contributions and between air and n onair sources remain significant. 11 In making the decision on revision of the s econdary standard in the last review, the 12 Administrator concurred with the conclusions by CASAC that we lack the relevant data to 13 provide a clear quantitative basi s for setting a secondary Pb NAAQS that differs from the 14 primary in indicator, averaging time, level or fo rm. As a result, the Ad ministrator revised the 15 secondary standard to be identical in all resp ects to the primary standard (73 FR 67012). 16 In now considering the adequacy of the cu rrent standard in this review, we have 17
considered evidence assessed in the ISA and di scussed in sections 5.1, 2.3 and 6.2.1 above, as 18 well as information gained from the 2006 REA discussed in sections 5.2 and 6.2.2 above. As 19
summarized in section 6.2.1 above , the scientific evidence pres ented in detail in the ISA, 20 inclusive of that newly available in this review , is not substantively changed, most particularly 21 with regard to our needs in reviewing the cu rrent standard, from the information that was 22
available in the last review. Further, our updated consideratio n of the screening-level risk 23 information from the 2006 REA, as summarized in section 6.2.2 above, additionally does not 24 provide alternative conclusions with regard to a basis for judging the adequacy of the current 25 standard. Thus, while the current secondary standa rd is not expressed in elements derived from 26 ecological effects evidence, we preliminarily conc lude that the currently available information 27 does not call into question the adequacy of the current standa rd to provide the requisite 28 protection for public welfare. In addition, as in the last review, th ere continues to be insufficient 29 data to provide a quantitative basi s for setting a seconda ry standard different than the primary 30 standard. Accordingly, we reach the preliminary conclusion that it is appropriate to consider 31 retaining the current standard without revision. This pre liminary conclusion is based on 32
consideration of the welfare effects eviden ce in combination with the screening-level 33 exposure/risk information (chapter 5 and s ections 6.2.1 and 6.2.2 above) and staff judgments on 34 the associated public welfare implications. 35January 2013 6-12 Draft – Do Not Quote or Cite 6.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND DATA 1 COLLECTION 2 In this section, we highlight key uncertainties associated with reviewing the secondary 3 NAAQS for Pb. Such key uncertainties and re commendations for ecosystem-related research, 4 model development, and data gath ering are outlined below. In some cases, research in these 5 areas can go beyond aiding standard setting to aiding in the deve lopment of more efficient and 6 effective control strategies. We note, however, that a full set of research recommendations to 7 meet standards implementation and strategy development needs is beyond the scope of this 8 discussion. Rather, listed below are key uncertainties and research questions and data gaps that 9 have been thus far highlighted in this re view of the health-based primary standard. 10

 An important source of uncertainty in characte rizing the effects of air related Pb in the 11 environment is the ability to apportion the sources of Pb to specific ecosystems. 12

 It is difficult to identify the atmospheri c component of Pb deposited in ecosystems 13 from other sources of Pb. Without such in formation, it is not possible to determine 14 the appropriately protective air concentrations of Pb. 15

 Development of critical loads informati on for various ecosystems would allow for a 16 much improved understanding of the si gnificance of air c ontributions to 17 ecosystems. 18

 There is significant uncertain ty regarding the timeframes under which Pb currently in 19 the environment was deposited. 20

 In general, the connection between air c oncentration of Pb and ecosystem exposure 21 continues to be poorly characterized. 22

 There is uncertainty in characterizing the fate and transport of Pb in the 23 environment through air, water, and soil me dia, especially in ecosystems. This 24 limits our ability to account for past Pb exposures in cu rrent media concentrations 25 and to link effects to current air contributions. 26

 Our understanding of the degree of adverse imp act that is occurring in the environment 27 due to Pb is incomplete and leads to uncer tainty in interpreting the significance of 28 effects at specific endpoints. 29

 Critical loads are important to capture the variability of response across ecosystems 30 to determine which ecosystems are most sensitive and additional research is needed 31 to provide inputs for development of critical loads, particularly for a broader range 32 of ecosystem level endpoints. 33

 The available studies on community and eco system-level effects are sparse and 34 usually from contaminated areas where Pb concentrations are much higher than 35 typically encountered in the environment. 36

 The role of modifying factors on Pb toxicity continues to be a source of uncertainty 37 when determining the degree of adverse impact from Pb. 38January 2013 6-13 Draft – Do Not Quote or Cite  Evidence regarding relationships between organism-level effects of Pb (e.g., 1 reproduction, growth, and survival) and e ffects at the population level and higher, 2 is lacking especially in natural systems. 3

 Better indicators of Pb eff ects are needed in estuarine and marine systems to allow 4 us to understand the potential for adverse e ffects from Pb in these environments. 5

6January 2013 6-14 Draft – Do Not Quote or Cite 6.5 REFERENCES 1

Frey, C; Samet, JM. (2011). CASAC review of the EPA's integrated science assessment for lead 2 (first external review draft- May 2011). (EPA-CASAC-12-002). Washington, DC: U.S. 3 Environmental Protection Agency, Clean Air Scientific Advisory Committee. 4

Henderson, R. (2007a) Letter from Dr. Rogene Henderson, Chair, Cl ean Air Scientific Advisory 5 Committee, to Administrator Stephen L. J ohnson. Re: Clean Air Scientific Advisory 6 Committee’s (CASAC) Review of the 1st Dr aft Lead Staff Paper and Draft Lead 7 Exposure and Risk Assessments. March 27, 2007. 8

Henderson, R. (2007b) Letter from Dr. Rogene Hende rson, Chair, Clean Air Scientific Advisory 9 Committee, to Administrator Stephen L. J ohnson. Re: Clean Air Scientific Advisory 10 Committee’s (CASAC) Review of the 2nd Draf t Lead Human Exposure and Health Risk 11 Assessments. September 27, 2007. 12

ICF International. (2006) Lead Human Exposure and Health Risk Assessments and Ecological 13 Risk Assessment for Selected Areas. Pilot Ph ase. Draft Technical Report. Prepared for 14 the U.S. EPA's Office of Air Quality Planni ng and Standards, Research Triangle Park, 15 NC. December. 16

U.S. Environmental Protection Agency. (2006) Air Quality Criteria for Lead. Washington, DC, 17 EPA/600/R-5/144aF. Available online at: 18 http://www.epa.gov/ttn/naaqs/ standards/pb/s_pb_cr.html 19

U.S. Environmental Protection Agency. (2012) In tegrated Science Assessment for Lead (Third 20 External Review Draft). Washington, DC, EPA/600/R-10/075C. Available online at: 21 http://www.epa.gov/ttn/naaqs/ standards/pb/s_pb_index.html 22January 2013 Draft – Do Not Quote or Cite 

### 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-1January 2013 2A-1 Draft - Do Not Quote or Cite 

### APPENDIX 2A 1



### THE 2008 NEI: DATA SOUR CES, LIMITATIONS AND 2 

### CONFIDENCE 3

The process of identifying sour ces that emit Pb into the ai r has been ongoing since before 4 the Clean Air Act of 1970. The comprehensivene ss of emission inventories generally, and the 5 NEI, specifically, depends upon knowledge of sour ce types emit Pb, their locations and their 6 operating characteristics, as well as the reporting of this informa tion to the inventory. As noted 7 above, the NEI relies on information that is av ailable from a variety of sources for this 8 information. There are numerous steps, each with its own uncertainties, associated with the 9 development of this information for use in the em issions inventory. First, the categories emitting 10 Pb must be identified. Second, the sources’ pr ocesses and control devices must be known. 11 Third, the activity throughputs and operating schedules of these s ources must be known. Finally, 12
we must have emission factors to relate em issions to the operati ng throughputs, process 13 conditions and control devices. The proce ss, control device, throughputs and operating 14 schedules are generally available for each sour ce. However, the emission factors represent 15 average emissions for a source type and average emissions may differ significantly from source 16 to source. In some cases, emissions testing pr ovides source-specific information. In others, 17
emissions factors must be estimated from simila r sources or source categories, or from other 18
information. More information on emission factor s and the estimation of emissions is found in 19 the introduction to EPA’s Compilation of Air Pollutant Emissions Factors. 1 20 The Pb emissions information presented in chapter 2 is drawn largely from EPA’s NEI 21
for 2008. The NEI is based on information submitte d from State, Tribal and local air pollution 22 agencies and data obtained during the prepara tion of technical support information for EPA’s 23 hazardous air pollutant regulatory programs. Data in the 2008 NEI for Pb emissions from the 24 use of leaded aviation gasoline were deve loped by EPA using the Federal Aviation 25 Administration’s operations act ivity data, where available. 2 The data were then reviewed by 26 State, Tribal, and local air pollution agencies. W ith some additions, the information presented in 27 this document is primarily based on version 3 of the NEI for 2008, available on the EPA’s 28 CHIEF website at (http://www.ep a.gov/ttn/chief/net/2008inventor y.html). The NEI is limited 29

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.January 2013 2A-2 Draft - Do Not Quote or Cite with regard to Pb emissions estimates for so me sources. For example, we have not yet 1 developed estimates for the NEI of Pb emissions for the miscellaneous categories of on-road 2 emissions (e.g., combustion of fuel with Pb traces, lubricating oil, mechanical wear of vehicle 3 components, etc.) and Pb that may be emitted from wildfires, or for emissions associated with 4 resuspension of Pb residing in roadway dust a nd nearby surface soil in areas not otherwise 5
associated with industrial f acilities (see section 2.1.2). 6
The 2008 NEI underwent extensive external review , including a review of the process for 7 developing the inventory which in cludes extensive quality assurance and quality control steps 8 (QA/QC). We provided feedback reports to point source data providers and we posted several 9 versions of the inventory on our website. We also conducted additional QA targeted at facilities 10 with appreciable Pb emissions in previous year s to ensure that 2008 Pb emissions were reported, 11 and we augmented with TRI where facilities w ith annual emissions greater than 0.5 tpy in 2005 12 were not reported to NEI in 2008 due to Pb emissions reporting thresholds 13 (ftp://ftp.epa.gov/EmisInventor y/20008v2/doc/2008neiv2_issues.xlsx ). Further, there was 14 additional QA/QC conducted for emission inventor y information for facilities that are included 15 in Risk and Technology Re view source categories. 3 As a result we have strong confidence in the 16 quality of the data for these f acilities. In summary, generic limitations to the 2008 NEI include 17 the following. 18

 Consistency: The 2008 NEI for Pb is a com posite of emissions estimates generated by 19 state and local regulatory agencies, in dustry, and EPA. Because the estimates 20 originated from a variety of sources, as well as for differing purposes, they will in turn 21 vary in quality, whether Pb is reported for particular so urce types, method of reporting 22 compound classes, level of deta il, and geographic coverage. 23

 Variability in Quality and Accuracy of Em ission Estimation Methods: The accuracy of 24 emission estimation techniques varies with pol lutants and source categories. In some 25 cases, an estimate may be based on a fe w or only one emission measurement at a 26 similar source. The techniques used and qua lity of the estimates will vary between 27 source categories and between area, major, and mobile source sectors. Generally, the 28 more review and scrutiny given to emissi ons data by states and other agencies, the 29 more certainty and accuracy there is in those estimates. 30

31
32

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 technologies. For more information: http://www.epa.gov/ttn/atw/rrisk/rtrpg.html.January 2013 2B-1 Draft - Do Not Quote or Cite 

### APPENDIX 2B 1

RECENT REGULATORY ACTIONS ON STATIONARY SOURCES OF LEAD 2

The table below identifies recent regulatory actions on stationary sources estimated to 3 result in reductions in lead emissions. 4

Action Source Categories Affected Citation

NESHAP Area Sources: Polyvinyl Chloride and Copolymers Production, Primary Copper Smelting, Secondary Copper Smelting, and Primary Nonferrous Metals (zinc, cadmium, beryllium) 76 FR 22848 (2011)

NESHAP Area Sources: Acrylic and Modacrylic Fibers Production, Carbon Black Production, Chemical Manufacturing: Chromium Compounds, Flexible Polyurethane Foam Production and Fabrication, Lead Acid Battery Manufacturing, Wood Preserving: 72 FR 38864 (7/16/2007)

NESHAP Area Sources: Clay Ceramics Manufacturin g, Glass Manufacturing, and Secondary Nonferrous Metals Processing 72 FR 73179 (12/26/2007) NESHAP Area Sources: Electric Arc Furnace Steelmaking Facilities 72 FR 74088 (12/28/2007) NESHAP Iron and Steel Foundries Area Sources 73 FR 225 (1/2/2008)

NESHAP Area Sources: Acrylic and Modacrylic Fibers Production, Carbon Black Production, Chemical Manufacturing: Chromium Compounds, Flexible Polyurethane Foam Production and Fabrication, Lead Acid Battery Manufacturing, Wood Preserving 73 FR 5923 (3/26/2008)

NESHAP Area Source Standards for Plating and Polishing Operations 73 FR 37728 (7/1/2008) NESHAP Area Source Standards for Nine Metal Fabrication and Finishing Source Categories 73 FR 42978 7/23/2008)

NESHAP Area Source Standar ds for Aluminum, Copper, and Ot her Nonferrous Foundries 74 FR 30366 (6/25/2009) NESHAP, NSPS Portland Cement Manufacturing Industry 75 FR 54970 (9/9/2010) EGES, NSPS Commercial and Industrial Solid Waste Incineration Units 76 FR 15704 (3/21/2011) 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) NESHAP Major Sources: Industrial, Commercial, and Institutional Boilers, and Process Heaters 76 FR 15608 (3/21/2011)
NESHAP Area Sources: Industrial, Commercial, and Institutional Boilers and Process Heaters 76 FR 15554 (3/21/2011) EGES, NSPS Standards of Performance for New Stationary Sources and Emissions Guidelines for Existing Sources: Hospital/Medical/Infectious Waste Incinerators 76 FR 18407 (4/4/2011) NESHAP Ferroalloys Production 76 FR 72508 (11/23/2011) EGES=Emissions Guidelines for Existing Sources NESHAP=National Emission Standards for Hazardous Air Pollutants NSPS= New Source Performance Standards 5January 2013 2C-1 Draft - Do Not Quote or Cite 

### APPENDIX 2C 1



### CRITERIA FOR AIR QUALITY DATA ANALYSIS 2

Criteria for the 2009-2011 data analysis pres ented in Figures 2-10 through 2-13 are as 3 listed below, with abbreviations defined following this list. 4

 Years utilized were 2009-2011. November and December 2008 data were also used for 5 rolling 3-month average analysis. 6

 Data were extracted from EPA’s Air Qualit y System in August and September of 2012. 7

 Data for parameters 12128 (STP) and 14129 (LC) were used for Pb-TSP analysis; data 8 for parameters 84128 (STP) and 88128 (LC) were used for Pb-PM 2.5 analysis; and data 9 for parameters 82128 (STP) and 85128 (LC) were used for Pb-PM 10 analysis. No 10 adjustment was made to the STP or LC data to make them more comparable to each 11 other; based on previous anal ysis, the LC and STP versions of same-site-day samples 12 are extremely similar. Collocated data – for same size cut- were combined to a site 13 basis by using the following hierarchy, evalua ted each site-day: LC parameter data 14 takes precedence over STP parameter data and lower POC numbers take precedence 15 over higher POC numbers. 16

 For maximum rolling 3-month average an alysis, the 2009-2011 databases also 17 encompassed the prior 2 months (i.e., November and December 2008 data): 3 or more 18 observations were needed to make a valid m onthly average (for Pb-TSP, the daily data 19 had to be collected/analyzed via an FRM or FEM); 3 valid consecutive months were 20 required to make a valid rolling 3-month pe riod; 6 valid rolling 3-month periods were 21 required to make a valid year; and 1, 2, or 3 valid years were requi red to make a valid 22 3-month metric. The rolling 3-month aver age metric (by size cut for 2009-2011) was 23 identified as the highest valid 3-month av erage across the valid (1, 2, or 3) years. 24

 For maximum monthly analysis: 3or more obs ervations were needed to make a valid 25 monthly average (for Pb-TSP, the daily data had to be collected/analyzed via an FRM 26 or FEM); 6 valid months were required to make a valid year; and 1, 2, or 3 valid years 27 were required to make a valid monthly metr ic. The maximum monthly metric (by size 28 cut for 2009-2011) was identified as the highest valid monthly average across the valid 29 (1, 2, or 3) years. 30

 For annual average analysis: monthly averages were used to construct annual averages, 31 3 or more observations were required to make a valid month (for Pb-TSP, the daily 32 data had to be collected/analyzed via an FRM or FEM); 6 valid months were required 33 to make a valid year (i.e., annual average) and 1, 2, or 3 valid y ears were required to 34 make a valid annual metric. The annual metric (by size cut for 2009-2011) was 35 identified as the average of the 1, 2, or 3 (2009, 2010, and/or 2011) valid annual means. 36

37January 2013 2C-2 Draft - Do Not Quote or Cite Definitions for Abbreviations 1 FEM – Federal equivalent method 2

FRM – Federal reference method 3

LC – Local conditions 4

POC – Parameter occurrence code 5 STP – Standard temperature and pressure 6Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2009-2011. Appendix 2D - Air Quality Data Analysis Summary

SITE Max 3-month
Mean (ug/m 3 ) A nnual Mean (ug/m 3 ) Max Monthly
Mean (ug/m 3 ) previous

source current

source State County 011090003 1.035 0.564 2.069 0 1 A labama Pike County 040071002 0.267 0.133 0.306 0 1 A rizona Gila County 040078000 0.061 0.033 0.077 0 1 A rizona Gila County 040134018 0.033 0.023 0.042 0 0 A rizona Maricopa County 060250005 0.023 0.016 0.032 0 0 California Imperial County 060371103 0.016 0.011 0.018 0 0 California Los Angeles County 060371302 0.019 0.01 0.026 0 0 California Los Angeles County 060371402 0.044 0.022 0.064 0 0 California Los Angeles County 060371403 0.116 0.061 0.148 0 1 California Los Angeles County 060371404 0.108 0.061 0.14 0 1 California Los Angeles County 060371405 0.667 0.343 0.801 0 1 California Los Angeles County 060371406 0.085 0.049 0.094 0 1 California Los Angeles County 060371602 0.022 0.011 0.04 0 0 California Los Angeles County 060374002 0.01 0.006 0.014 0 0 California Los Angeles County 060374004 0.012 0.007 0.017 0 0 California Los Angeles County 060375005 0.008 0.003 0.01 0 0 California Los Angeles County 060651003 0.011 0.006 0.014 0 0 California Riverside County 060658001 0.011 0.007 0.013 0 0 California Riverside County 060711004 0.011 0.007 0.014 0 0 California San Bernardino County 060719004 0.013 0.008 0.014 0 0 California San Bernardino County 080050007 0.02 0.014 0.028 0 0 Colorado A rapahoe County 080310025 0.01 0.006 0.013 0 0 Colorado Denver County 120570100 0.044 0.026 0.1 0 1 Florida Hillsborough County 120571066 0.979 0.282 1.959 0 1 Florida Hillsborough County 120571073 0.423 0.116 0.977 0 1 Florida Hillsborough County 130150003 0.019 0.014 0.032 0 1 Georgia Bartow County 130890003 0.004 0.003 0.006 0 0 Georgia DeKalb County 132150011 0.071 0.029 0.14 1 1 Georgia Muscogee County 170310001 0.024 0.016 0.028 0 0 Illinois Cook County 170310022 0.051 0.033 0.07 0 0 Illinois Cook County 170310026 0.034 0.023 0.038 0 0 Illinois Cook County 170310052 0.024 0.016 0.032 0 0 Illinois Cook County 170310110 0.294 0.1 0.58 0 1 Illinois Cook County 170310210 0.053 0.037 0.092 0 1 Illinois Cook County 170313103 0.013 0.011 0.016 0 0 Illinois Cook County 170313301 0.027 0.018 0.028 0 0 Illinois Cook County 170314201 0.011 0.01 0.014 0 0 Illinois Cook County 170316003 0.036 0.024 0.04 0 0 Illinois Cook County 171150110 0.199 0.082 0.386 0 1 Illinois Macon County 171170002 0.011 0.01 0.012 0 0 Illinois Macoupin County 171190010 0.416 0.118 0.836 0 1 Illinois Madison County 171193007 0.036 0.018 0.053 0 0 Illinois Madison County 171430037 0.011 0.01 0.013 0 0 Illinois Peoria County 171430110 0.016 0.013 0.024 0 1 Illinois Peoria County 171430210 0.015 0.011 0.026 0 1 Illinois Peoria County
January 2013 2D - 1 Draft - Do Not Quote or CiteTable 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2009-2011. Appendix 2D - Air Quality Data Analysis Summary

SITE Max 3-month
Mean (ug/m 3 ) A nnual Mean (ug/m 3 ) Max Monthly
Mean (ug/m 3 ) previous

source current

source State County 171630010 0.029 0.019 0.038 1 0 Illinois St. Clair County 171950110 0.028 0.02 0.04 0 1 Illinois Whiteside County 172010110 0.063 0.031 0.118 0 1 Illinois Winnebago County 180350008 0.11 0.079 0.141 0 1 Indiana Delaware County 180350009 0.262 0.186 0.427 0 1 Indiana Delaware County 180890023 0.077 0.026 0.087 0 1 Indiana Lake County 180890032 0.06 0.027 0.144 0 1 Indiana Lake County 180890033 0.139 0.054 0.298 0 1 Indiana Lake County 180892008 0.037 0.016 0.049 0 0 Indiana Lake County 180970063 0.079 0.026 0.125 0 1 Indiana Marion County 180970076 0.02 0.01 0.029 0 1 Indiana Marion County 180970078 0.011 0.005 0.013 0 0 Indiana Marion County 181270023 0.022 0.013 0.032 0 1 Indiana Porter County 181630020 0.007 0.004 0.01 0 0 Indiana Vanderburgh County 191550011 0.263 0.122 0.282 0 1 Iowa Pottawattamie County 191630015 0.012 0.01 0.024 0 0 Iowa Scott County 201690004 0.421 0.18 0.488 0 1 Kansas Saline County 210190016 0.004 0.004 0.007 0 1 Kentucky Boyd County 211510003 0.069 0.034 0.121 0 1 Kentucky Madison County 212070001 0.036 0.021 0.076 0 1 Kentucky Russell County 220330014 0.005 0.004 0.007 0 1 Louisiana East Baton Rouge Parish 220950003 0.053 0.037 0.066 0 1 Louisiana St. John the Baptist Parish 250250042 0.01 0.007 0.012 Massachusetts Suffolk County 260670003 0.284 0.126 0.414 0 1 Michigan Ionia County 260810020 0.008 0.005 0.01 0 0 Michigan Kent County 261630001 0.006 0.005 0.007 0 0 Michigan Wayne County 261630033 0.023 0.012 0.034 0 0 Michigan Wayne County 270036020 0.033 0.017 0.054 0 1 Minnesota A noka County 270072303 0.001 0 0.002 0 0 Minnesota Beltrami County 270177416 0 0 0 Minnesota Carlton County 270210001 0.001 0 0.002 0 0 Minnesota Cass County 270370020 0.011 0.005 0.022 0 0 Minnesota Dakota County 270370423 0.002 0.001 0.005 0 0 Minnesota Dakota County 270370442 0.013 0.003 0.007 0 0 Minnesota Dakota County 270370443 0.003 0.002 0.005 0 0 Minnesota Dakota County 270370465 0.259 0.128 0.568 0 1 Minnesota Dakota County 270370470 0.002 0.001 0.004 0 0 Minnesota Dakota County 270530963 0.006 0.003 0.01 0 0 Minnesota Hennepin County 270530966 0.016 0.004 0.044 0 0 Minnesota Hennepin County 270531007 0.004 0.002 0.006 0 0 Minnesota Hennepin County 270532006 0.003 0.001 0.005 0 0 Minnesota Hennepin County 270750005 0 0 0 Minnesota Lake County 271230866 0.016 0.012 0.023 0 0 Minnesota Ramsey County 271230871 0.007 0.002 0.01 0 0 Minnesota Ramsey County 271231003 0.006 0.004 0.008 0 0 Minnesota Ramsey County
January 2013 2D - 2 Draft - Do Not Quote or CiteTable 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2009-2011. Appendix 2D - Air Quality Data Analysis Summary

SITE Max 3-month
Mean (ug/m 3 ) A nnual Mean (ug/m 3 ) Max Monthly
Mean (ug/m 3 ) previous

source current

source State County 271377001 0.003 0.001 0.006 0 0 Minnesota St. Louis County 271377555 0.006 0.002 0.008 0 0 Minnesota St. Louis County 271453053 0.006 0.003 0.01 0 1 Minnesota Stearns County 271630009 0.005 0.003 0.006 0 0 Minnesota Washington County 271630438 0.005 0.002 0.008 0 0 Minnesota Washington County 271630446 0.002 0 0.003 0 0 Minnesota Washington County 290930016 2.07 0.49 1.392 0 1 Missouri Iron County 290930021 1.937 0.622 2.438 0 1 Missouri Iron County 290930027 0.083 0.038 0.121 1 1 Missouri Iron County 290930029 0.115 0.037 0.271 1 1 Missouri Iron County 290930033 0.057 0.027 0.105 0 1 Missouri Iron County 290930034 0.402 0.283 0.509 0 1 Missouri Iron County 290939007 0.581 0.392 0.844 0 1 Missouri Iron County 290939008 0.387 0.256 0.538 0 1 Missouri Iron County 290970005 0.019 0.013 0.024 0 0 Missouri Jasper County 290990004 1.16 0.889 1.576 0 1 Missouri Jefferson County 290990005 0.396 0.231 0.536 0 1 Missouri Jefferson County 290990009 0.067 0.043 0.087 0 1 Missouri Jefferson County 290990011 0.403 0.21 0.509 0 1 Missouri Jefferson County 290990013 0.198 0.116 0.344 0 1 Missouri Jefferson County 290990015 1.079 0.921 1.349 0 1 Missouri Jefferson County 290990020 0.943 0.646 1.28 0 1 Missouri Jefferson County 290990021 0.969 0.585 1.124 0 1 Missouri Jefferson County 290990022 0.63 0.434 0.861 0 1 Missouri Jefferson County 290990023 0.594 0.394 0.724 0 1 Missouri Jefferson County 290990024 0.659 0.374 0.862 0 1 Missouri Jefferson County 290990025 0.085 0.043 0.134 0 1 Missouri Jefferson County 290990026 0.072 0.035 0.114 0 1 Missouri Jefferson County 290999001 1.204 0.824 1.623 0 1 Missouri Jefferson County 290999002 0.431 0.232 0.593 0 1 Missouri Jefferson County 290999003 0.467 0.198 0.605 0 1 Missouri Jefferson County 290999004 0.261 0.119 0.328 0 1 Missouri Jefferson County 290999005 1.432 0.959 2.185 0 1 Missouri Jefferson County 290999006 0.091 0.049 0.131 0 1 Missouri Jefferson County 291790001 0.059 0.033 0.087 0 1 Missouri Reynolds County 291790002 0.068 0.033 0.172 0 1 Missouri Reynolds County 291790003 0.1 0.027 0.268 0 1 Missouri Reynolds County 291790034 0.093 0.068 0.142 0 1 Missouri Reynolds County 291870006 0.132 0.05 0.302 0 0 Missouri St. Francois County 291870007 0.041 0.043 0.364 0 0 Missouri St. Francois County 291892003 0.041 0.007 0.011 0 0 Missouri St. Louis County 310530005 0.072 0.051 0.149 0 1 Nebraska Dodge County 311270002 0.115 0.042 0.206 0 1 Nebraska Nemaha County 360470122 0.019 0.014 0.02 0 0 New York Kings County 360713001 0.101 0.031 0.134 0 1 New York Orange County
January 2013 2D - 3 Draft - Do Not Quote or CiteTable 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2009-2011. Appendix 2D - Air Quality Data Analysis Summary

SITE Max 3-month
Mean (ug/m 3 ) A nnual Mean (ug/m 3 ) Max Monthly
Mean (ug/m 3 ) previous

source current

source State County 360713002 1.027 0.128 2.821 0 1 New York Orange County 360713004 0.012 0.005 0.016 0 1 New York Orange County 390170015 0.009 0.006 0.013 0 0 Ohio Butler County 390290019 0.057 0.022 0.136 0 0 Ohio Columbiana County 390290020 0.025 0.015 0.035 0 0 Ohio Columbiana County 390290022 0.044 0.02 0.065 0 0 Ohio Columbiana County 390350038 0.021 0.013 0.026 0 0 Ohio Cuyahoga County 390350042 0.03 0.014 0.044 0 0 Ohio Cuyahoga County 390350049 0.531 0.165 0.719 0 1 Ohio Cuyahoga County 390350061 0.023 0.015 0.03 1 0 Ohio Cuyahoga County 390350072 0.035 0.014 0.054 0 1 Ohio Cuyahoga County 390490025 0.011 0.008 0.012 0 0 Ohio Franklin County 390510001 0.178 0.073 0.21 0 1 Ohio Fulton County 390910006 0.006 0.004 0.008 1 1 Ohio Logan County 391010003 0.056 0.035 0.097 0 1 Ohio Marion County 391510017 0.023 0.014 0.028 0 1 Ohio Stark County 391550012 0.011 0.007 0.017 0 1 Ohio Trumbull County 391670008 0.007 0.005 0.01 0 0 Ohio Washington County 391670010 0.008 0.005 0.01 0 0 Ohio Washington County 401159006 0.015 0.011 0.022 0 0 Oklahoma Ottawa County 401159007 0.034 0.017 0.056 0 0 Oklahoma Ottawa County 401210416 0.004 0.003 0.006 0 1 Oklahoma Pittsburg County 410711702 0.035 0.018 0.037 0 1 Oregon Yamhill County 420030002 0.016 0.012 0.024 0 0 Pennsylvania A llegheny County 420030008 0.014 0.01 0.02 0 0 Pennsylvania A llegheny County 420030070 0.056 0.022 0.11 0 1 Pennsylvania A llegheny County 420031009 0.138 0.043 0.149 0 1 Pennsylvania A llegheny County 420070006 0.085 0.054 0.198 0 1 Pennsylvania Beaver County 420070007 0.253 0.171 0.393 0 1 Pennsylvania Beaver County 420070505 0.115 0.086 0.17 0 1 Pennsylvania Beaver County 420110005 0.051 0.043 0.07 0 1 Pennsylvania Berks County 420110020 0.196 0.127 0.347 0 1 Pennsylvania Berks County 420110021 0.139 0.049 0.319 0 1 Pennsylvania Berks County 420110022 0.118 0.043 0.261 0 1 Pennsylvania Berks County 420110717 0.116 0.065 0.108 0 1 Pennsylvania Berks County 420111717 0.251 0.133 0.348 0 1 Pennsylvania Berks County 420210808 0.073 0.05 0.128 0 0 Pennsylvania Cambria County 420450002 0.047 0.043 0.048 0 0 Pennsylvania Delaware County 420450004 0.047 0.045 0.048 0 1 Pennsylvania Delaware County 420550002 0.046 0.045 0.047 0 1 Pennsylvania Franklin County 420630005 0.049 0.029 0.058 0 1 Pennsylvania Indiana County 420730011 0.023 0.032 0.046 0 1 Pennsylvania Lawrence County 420790036 0.137 0.095 0.268 0 1 Pennsylvania Luzerne County 421010449 0.03 0.021 0.039 1 0 Pennsylvania Philadelphia County 421011002 0.025 0.022 0.029 0 0 Pennsylvania Philadelphia County
January 2013 2D - 4 Draft - Do Not Quote or CiteTable 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2009-2011. Appendix 2D - Air Quality Data Analysis Summary

SITE Max 3-month
Mean (ug/m 3 ) A nnual Mean (ug/m 3 ) Max Monthly
Mean (ug/m 3 ) previous

source current

source State County 421290007 0.043 0.041 0.043 0 0 Pennsylvania Westmoreland County 421290009 0.046 0.027 0.047 0 1 Pennsylvania Westmoreland County 450190003 0.007 0.005 0.013 0 0 South Carolina Charleston County 450450015 0.006 0.005 0.008 0 0 South Carolina Greenville County 450790007 0.005 0.004 0.007 0 0 South Carolina Richland County 450790019 0.024 0.011 0.061 0 0 South Carolina Richland County 470930023 0.165 0.114 0.208 0 1 Tennessee Knox County 470930027 0.042 0.02 0.078 0 1 Tennessee Knox County 470931017 0.037 0.018 0.063 0 1 Tennessee Knox County 471633001 0.093 0.058 0.115 1 1 Tennessee Sullivan County 471633002 0.06 0.039 0.069 1 1 Tennessee Sullivan County 471633003 0.06 0.041 0.066 1 1 Tennessee Sullivan County 471633004 0.08 0.041 0.124 1 1 Tennessee Sullivan County 471634002 0.038 0.025 0.062 1 1 Tennessee Sullivan County 480610006 0.005 0.004 0.007 0 0 Texas Cameron County 480850003 0.371 0.179 0.625 0 1 Texas Collin County 480850007 0.199 0.105 0.24 0 1 Texas Collin County 480850009 0.774 0.453 1.178 0 1 Texas Collin County 480850029 0.18 0.076 0.335 0 1 Texas Collin County 481410002 0.04 0.023 0.087 0 0 Texas El Paso County 481410033 0.039 0.019 0.057 0 0 Texas El Paso County 481410055 0.014 0.009 0.015 0 0 Texas El Paso County 481410058 0.033 0.017 0.056 0 0 Texas El Paso County 482011034 0.008 0.005 0.009 0 0 Texas Harris County 482570020 0.104 0.06 0.11 0 1 Texas Kaufman County 483750024 0.013 0.005 0.029 0 1 Texas Potter County 484790016 0.026 0.016 0.035 0 0 Texas Webb County 490351001 0.057 0.023 0.086 0 1 Utah Salt Lake County 510090007 0.018 0.004 0.007 0 1 Virginia A mherst County 510270006 0.013 0.01 0.015 0 1 Virginia Buchanan County 510870014 0.004 0.005 0.024 0 0 Virginia Henrico County 517700011 0.109 0.038 0.272 0 1 Virginia Roanoke city 551170008 0.152 0.055 0.225 0 1 Wisconsin Sheboygan County 720130001 0.339 0.188 0.416 0 1 Puerto Rico A recibo Municipio 720210010 0.011 0.005 0.027 0 0 Puerto Rico Bayamón Municipio

January 2013 2D - 5 Draft - Do Not Quote or CiteTable 2D-2. Pb-PM 10 concentrations at urban PM 10 sites, 2009-2011. Appendix 2D - Air Quality Data Analysis Summary

SITE Max 3-month

Mean (ug/m 3 ) Annual Mean (ug/m 3 ) Max Monthly

Mean (ug/m 3 ) State County 040134009 0.005 0.008 A rizona Maricopa County 040139997 0.007 0.004 0.007 A rizona Maricopa County 060371103 0.013 0.006 0.026 California Los Angeles County 060658001 0.013 0.006 0.03 California Riverside County 060850005 0.005 0.002 0.006 California Santa Clara County 080770017 0.004 0.001 0.004 Colorado Mesa County 110010043 0.004 0.003 0.005 District of Columbia District of Columbia 120573002 0.003 0.001 0.003 Florida Hillsborough County 120951004 0.003 0.008 Florida Orange County 121030018 0.003 0.002 0.004 Florida Pinellas County 121030026 0.003 0.002 0.003 Florida Pinellas County 130890002 0.002 0.001 0.003 Georgia DeKalb County 170314201 0.006 0.004 0.01 Illinois Cook County 171639010 0.015 0.031 Illinois St. Clair County 210190002 0.019 0.012 0.028 Kentucky Boyd County 210670014 0.005 0.004 0.009 Kentucky Fayette County 250250042 0.004 0.003 0.004 Massachusetts Suffolk County 261630001 0.006 0.004 0.006 Michigan Wayne County 261630033 0.023 0.011 0.035 Michigan Wayne County 295100085 0.018 0.011 0.026 Missouri St. Louis city 360050080 0.008 0.006 0.012 New York Bronx County 360050110 0.006 0.005 0.008 New York Bronx County 360551007 0.003 0.002 0.004 New York Monroe County 410290133 0.003 0.002 0.005 Oregon Jackson County 410390060 0.003 0.002 0.006 Oregon Lane County 410390062 0.002 0.002 0.003 Oregon Lane County 410510246 0.008 0.004 0.013 Oregon Multnomah County 440070022 0.003 0.003 0.004 Rhode Island Providence County 482011035 0.007 0.005 0.009 Texas Harris County 482011039 0.003 0.002 0.004 Texas Harris County 490110004 0.006 0.003 0.009 Utah Davis County 500070007 0.002 0.001 0.002 Vermont Chittenden County 510870014 0.007 0.003 0.016 Virginia Henrico County 530330080 0.005 0.003 0.006 Washington King County 550790010 0.006 0.01 Wisconsin Milwaukee County

January 2013 2D - 6 Draft - Do not cite or quoteTable 2D-3. Pb-PM 2.5 concentrations at urban CSN PM 2.5 sites, 2009-2011. Appendix 2D - Air Quality Data Analysis Summary

SITE Max 3-month

Mean ( u g /m 3 ) Annual Mean (ug/m 3 ) Max Monthly

Mean ( u g /m 3 ) State County 010730023 0.041 0.017 0.064 A labama Jefferson County 010732003 0.032 0.008 0.078 A labama Jefferson County 010890014 0.003 0.002 0.003 A labama Madison County 011011002 0.007 0.003 0.011 A labama Montgomery County 011130001 0.013 0.004 0.028 A labama Russell County 020900010 0.006 0.003 0.008 A laska Fairbanks North Star Borough 040134009 0.004 0.003 0.005 A rizona Maricopa County 040139997 0.004 0.002 0.004 A rizona Maricopa County 040191028 0.003 0.002 0.003 A rizona Pima County 051190007 0.004 0.002 0.006 A rkansas Pulaski County 060010007 0.005 0.004 0.005 California A lameda County 060010011 0.012 0.005 0.023 California A lameda County 060070002 0.003 0.002 0.003 California Butte County 060190008 0.003 0.002 0.004 California Fresno County 060250005 0.021 0.012 0.029 California Imperial County 060290014 0.003 0.002 0.004 California Kern County 060299001 0.001 0.001 0.001 California Kern County 060371103 0.02 0.005 0.021 California Los Angeles County 060590007 0.042 0.017 0.043 California Orange County 060658001 0.005 0.003 0.006 California Riverside County 060670006 0.004 0.002 0.009 California Sacramento County 060670010 0.003 0.002 0.005 California Sacramento County 060712002 0.037 0.018 0.038 California San Bernardino County 060730003 0.005 0.003 0.006 California San Diego County 060731002 0.004 0.002 0.005 California San Diego County 060850005 0.003 0.002 0.004 California Santa Clara County 060950004 0.007 0.005 0.009 California Solano County 060990005 0.005 0.003 0.009 California Stanislaus County 061072002 0.004 0.002 0.006 California Tulare County 061112002 0.003 0.002 0.003 California Ventura County 080010006 0.003 0.002 0.003 Colorado A dams County 080310025 0.003 0.002 0.005 Colorado Denver County 080770017 0.002 0.002 0.003 Colorado Mesa County 081230008 0.003 0.002 0.003 Colorado Weld County 090090027 0.005 0.003 0.005 Connecticut New Haven County 100010003 0.004 0.002 0.007 Delaware Kent County 100032004 0.004 0.003 0.006 Delaware New Castle County 110010043 0.003 0.002 0.004 District of Columbi a District of Columbia 120111002 0.002 0.002 0.003 Florida Broward County 120573002 0.003 0.002 0.003 Florida Hillsborough County 120730012 0.005 0.003 0.009 Florida Leon County 121030026 0.003 0.002 0.003 Florida Pinellas County 130210007 0.004 0.003 0.007 Georgia Bibb County

January 2013 2D - 7 Draft - Do not cite or quoteTable 2D-3. Pb-PM 2.5 concentrations at urban CSN PM 2.5 sites, 2009-2011. Appendix 2D - Air Quality Data Analysis Summary

SITE Max 3-month

Mean ( u g /m 3 ) Annual Mean (ug/m 3 ) Max Monthly

Mean ( u g /m 3 ) State County 130590001 0.002 0.002 0.003 Georgia Clarke County 130890002 0.003 0.002 0.003 Georgia DeKalb County 131150003 0.006 0.003 0.009 Georgia Floyd County 132150011 0.013 0.005 0.029 Georgia Muscogee County 132450091 0.005 0.003 0.008 Georgia Richmond County 132950002 0.006 0.003 0.009 Georgia Walker County 150030010 0.002 0.002 0.002 Hawaii Honolulu County 150032004 0.008 0.004 0.02 Hawaii Honolulu County 160010010 0.002 0.002 0.003 Idaho A da County 170310057 0.07 0.011 0.199 Illinois Cook County 170310076 0.005 0.003 0.005 Illinois Cook County 170314201 0.004 0.003 0.006 Illinois Cook County 170434002 0.005 0.003 0.008 Illinois DuPage County 171190024 0.02 0.011 0.032 Illinois Madison County 171630900 0.005 0.003 0.006 Illinois St. Clair County 171639010 0.014 0.009 0.019 Illinois St. Clair County 180190006 0.004 0.003 0.005 Indiana Clark County 180390008 0.004 0.003 0.005 Indiana Elkhart County 180890022 0.011 0.006 0.018 Indiana Lake County 180892004 0.022 0.009 0.037 Indiana Lake County 180970078 0.005 0.003 0.007 Indiana Marion County 181630012 0.003 0.002 0.003 Indiana Vanderburgh County 181630021 0.003 0.003 0.004 Indiana Vanderburgh County 191130037 0.003 0.002 0.003 Iowa Linn County 191530030 0.003 0.002 0.005 Iowa Polk County 191630015 0.011 0.006 0.017 Iowa Scott County 201730010 0.004 0.002 0.009 Kansas Sedgwick County 202090021 0.006 0.004 0.01 Kansas Wyandotte County 210190017 0.005 0.003 0.007 Kentucky Boyd County 210670012 0.007 0.003 0.012 Kentucky Fayette County 211110067 0.007 0.004 0.012 Kentucky Jefferson County 211170007 0.006 0.004 0.01 Kentucky Kenton County 220150008 0.006 0.004 0.009 Louisiana Bossier Parish 220330009 0.005 0.003 0.008 Louisiana East Baton Rouge Parish 240053001 0.006 0.003 0.007 Maryland Baltimore County 240330030 0.003 0.002 0.005 Maryland Prince George's County 250130008 0.003 0.002 0.004 Massachusetts Hampden County 250250042 0.003 0.002 0.004 Massachusetts Suffolk County 260810020 0.004 0.003 0.006 Michigan Kent County 261150005 0.005 0.003 0.008 Michigan Monroe County 261470005 0.016 0.004 0.03 Michigan St. Clair County 261630001 0.004 0.003 0.005 Michigan Wayne County 261630015 0.013 0.007 0.027 Michigan Wayne County

January 2013 2D - 8 Draft - Do not cite or quoteTable 2D-3. Pb-PM 2.5 concentrations at urban CSN PM 2.5 sites, 2009-2011. Appendix 2D - Air Quality Data Analysis Summary

SITE Max 3-month

Mean ( u g /m 3 ) Annual Mean (ug/m 3 ) Max Monthly

Mean ( u g /m 3 ) State County 261630033 0.017 0.007 0.029 Michigan Wayne County 270031002 0.009 0.006 0.013 Minnesota A noka County 270530963 0.003 0.002 0.005 Minnesota Hennepin County 271095008 0.004 0.002 0.006 Minnesota Olmsted County 280470008 0.003 0.002 0.003 Mississippi Harrison County 280490019 0.003 0.002 0.004 Mississippi Hinds County 290470005 0.003 0.002 0.003 Missouri Clay County 290990019 0.015 0.005 0.018 Missouri Jefferson County 295100085 0.011 0.006 0.013 Missouri St. Louis city 300630031 0.003 0.002 0.003 Montana Missoula County 310550019 0.004 0.003 0.008 Nebraska Douglas County 320030020 0.002 0.002 0.003 Nevada Clark County 320030540 0.003 0.002 0.004 Nevada Clark County 320310016 0.003 0.002 0.003 Nevada Washoe County 340130003 0.004 0.003 0.006 New Jersey Essex County 340230006 0.003 0.002 0.005 New Jersey Middlesex County 340273001 0.003 0.002 0.003 New Jersey Morris County 340390004 0.004 0.003 0.007 New Jersey Union County 350010023 0.003 0.002 0.005 New Mexico Bernalillo County 360010005 0.005 0.003 0.007 New York A lbany County 360050110 0.004 0.003 0.005 New York Bronx County 360290005 0.011 0.007 0.016 New York Erie County 360551007 0.003 0.002 0.003 New York Monroe County 360610134 0.004 0.003 0.004 New York New York County 360810124 0.005 0.003 0.011 New York Queens County 370210034 0.002 0.002 0.003 North Carolina Buncombe County 370350004 0.003 0.002 0.004 North Carolina Catawba County 370670022 0.006 0.003 0.011 North Carolina Forsyth County 371190041 0.003 0.002 0.003 North Carolina Mecklenburg County 371830014 0.002 0.002 0.003 North Carolina Wake County 380171004 0.003 0.002 0.005 North Dakota Cass County 390171004 0.011 0.006 0.012 Ohio Butler County 390350038 0.009 0.005 0.013 Ohio Cuyahoga County 390350060 0.009 0.006 0.011 Ohio Cuyahoga County 390490081 0.003 0.003 0.005 Ohio Franklin County 390610040 0.01 0.004 0.015 Ohio Hamilton County 390811001 0.009 0.006 0.012 Ohio Jefferson County 390870012 0.007 0.005 0.01 Ohio Lawrence County 390933002 0.01 0.006 0.018 Ohio Lorain County 390950026 0.004 0.003 0.005 Ohio Lucas County 390990014 0.012 0.006 0.018 Ohio Mahoning County 391130032 0.014 0.004 0.034 Ohio Montgomery County 391351001 0.003 0.003 0.004 Ohio Preble County

January 2013 2D - 9 Draft - Do not cite or quoteTable 2D-3. Pb-PM 2.5 concentrations at urban CSN PM 2.5 sites, 2009-2011. Appendix 2D - Air Quality Data Analysis Summary

SITE Max 3-month

Mean ( u g /m 3 ) Annual Mean (ug/m 3 ) Max Monthly

Mean ( u g /m 3 ) State County 391510017 0.013 0.007 0.017 Ohio Stark County 391530023 0.006 0.004 0.01 Ohio Summit County 401091037 0.002 0.002 0.003 Oklahoma Oklahoma County 401431127 0.005 0.003 0.008 Oklahoma Tulsa County 410290133 0.003 0.001 0.002 Oregon Jackson County 410390060 0.003 0.003 0.007 Oregon Lane County 410392013 0.002 0.002 0.004 Oregon Lane County 410510080 0.004 0.003 0.005 Oregon Multnomah County 420030008 0.016 0.009 0.022 Pennsylvania A llegheny County 420030064 0.03 0.017 0.052 Pennsylvania A llegheny County 420110011 0.012 0.006 0.014 Pennsylvania Berks County 420210011 0.01 0.006 0.017 Pennsylvania Cambria County 420270100 0.003 0.002 0.004 Pennsylvania Centre County 420290100 0.004 0.003 0.005 Pennsylvania Chester County 420430401 0.007 0.004 0.011 Pennsylvania Dauphin County 420490003 0.005 0.003 0.007 Pennsylvania Erie County 420692006 0.007 0.003 0.01 Pennsylvania Lackawanna County 420710007 0.005 0.004 0.008 Pennsylvania Lancaster County 420950025 0.008 0.004 0.018 Pennsylvania Northampton County 421010004 0.007 0.003 0.012 Pennsylvania Philadelphia County 421010055 0.003 0.002 0.005 Pennsylvania Philadelphia County 421011002 0.007 0.005 0.009 Pennsylvania Philadelphia County 421255001 0.007 0.004 0.015 Pennsylvania Washington County 421290008 0.004 0.003 0.007 Pennsylvania Westmoreland County 421330008 0.006 0.003 0.01 Pennsylvania York County 440070022 0.004 0.003 0.007 Rhode Island Providence County 440071010 0.003 0.002 0.003 Rhode Island Providence County 450190049 0.003 0.002 0.003 South Carolina Charleston County 450450008 0.003 0.002 0.003 South Carolina Greenville County 450450015 0.006 0.003 0.009 South Carolina Greenville County 450790007 0.003 0.002 0.004 South Carolina Richland County 460990008 0.003 0.002 0.003 South Dakota Minnehaha County 470370023 0.003 0.002 0.004 Tennessee Davidson County 470654002 0.004 0.003 0.006 Tennessee Hamilton County 470931020 0.006 0.003 0.007 Tennessee Knox County 471251009 0.004 0.002 0.005 Tennessee Montgomery County 471570024 0.004 0.002 0.005 Tennessee Shelby County 471570075 0.004 0.003 0.006 Tennessee Shelby County 480612004 0.002 0.002 0.003 Texas Cameron County 481130050 0.005 0.003 0.007 Texas Dallas County 481130069 0.004 0.003 0.008 Texas Dallas County 481390016 0.005 0.003 0.008 Texas Ellis County 481410044 0.006 0.003 0.008 Texas El Paso County

January 2013 2D - 10 Draft - Do not cite or quoteTable 2D-3. Pb-PM 2.5 concentrations at urban CSN PM 2.5 sites, 2009-2011. Appendix 2D - Air Quality Data Analysis Summary

SITE Max 3-month

Mean ( u g /m 3 ) Annual Mean (ug/m 3 ) Max Monthly

Mean ( u g /m 3 ) State County 481410053 0.017 0.007 0.02 Texas El Paso County 482010024 0.006 0.004 0.008 Texas Harris County 482011039 0.002 0.002 0.003 Texas Harris County 482450021 0.003 0.002 0.003 Texas Jefferson County 483030325 0.007 0.003 0.018 Texas Lubbock County 483550034 0.014 0.003 0.036 Texas Nueces County 484530020 0.006 0.002 0.014 Texas Travis County 490110004 0.004 0.003 0.007 Utah Davis County 490353006 0.008 0.003 0.016 Utah Salt Lake County 490494001 0.007 0.003 0.012 Utah Utah County 500070012 0.003 0.002 0.003 Vermont Chittenden County 510870014 0.005 0.002 0.009 Virginia Henrico County 530110013 0.003 0.002 0.004 Washington Clark County 530330057 0.008 0.004 0.013 Washington King County 530330080 0.003 0.003 0.004 Washington King County 530530029 0.005 0.003 0.008 Washington Pierce County 530530031 0.016 0.004 0.033 Washington Pierce County 530611007 0.004 0.003 0.007 Washington Snohomish County 530770009 0.003 0.003 0.004 Washington Yakima County 540390011 0.004 0.002 0.006 West Virginia Kanawha County 540391005 0.005 0.003 0.008 West Virginia Kanawha County 540511002 0.005 0.004 0.006 West Virginia Marshall County 540690010 0.008 0.005 0.01 West Virginia Ohio County 550790026 0.004 0.003 0.006 Wisconsin Milwaukee County 551330027 0.011 0.006 0.013 Wisconsin Waukesha County 560210100 0.002 0.002 0.002 Wyoming Laramie County

January 2013 2D - 11 Draft - Do not cite or quoteTable 2D-4. Pb-PM 2.5 concentrations at non-urban PM 2.5 IMPROVE sites, 2009-2011. Appendix 2D - Air Quality Data Analysis Summary

SITE Max 3-mo Mean (ug/m3) Annual Mean (ug/m3) Max Monthly Mean (ug/m3) State County 020130002 0.002 0.001 0.004 A laska A leutians East Borough 020680003 0.001 0 0.001 A laska Denali Borough 021220009 0.001 0 0.001 A laska Kenai Peninsula Borough 040018001 0.001 0.001 0.001 A rizona A pache County 040038001 0.002 0.001 0.003 A rizona Cochise County 040039000 0.009 0.004 0.012 A rizona Cochise County 040070010 0.004 0.003 0.008 A rizona Gila County 040078100 0.001 0.001 0.002 A rizona Gila County 040170119 0.001 0.001 0.001 A rizona Navajo County 051019000 0.002 0.001 0.002 A rkansas Newton County 051130003 0.001 0.001 0.002 A rkansas Polk County 060150002 0.001 0 0.002 California Del Norte County 060270101 0.001 0.001 0.001 California Inyo County 060430003 0.001 0.001 0.001 California Mariposa County 060519000 0.001 0 0.001 California Mono County 060930005 0.001 0 0.001 California Siskiyou County 061059000 0.001 0 0.001 California Trinity County 080039000 0.001 0 0.001 Colorado A lamosa County 080579000 0.001 0 0.001 Colorado Jackson County 080679000 0.001 0 0.001 Colorado La Plata County 080839000 0.001 0 0.001 Colorado Montezuma County 080979000 0.001 0 0.001 Colorado Pitkin County 081119000 0.001 0 0.001 Colorado San Juan County 090050005 0.002 0.001 0.002 Connecticut Litchfield County 120179000 0.002 0.001 0.002 Florida Citrus County 130499000 0.002 0.001 0.002 Georgia Charlton County 150019002 0.006 0.001 0.01 Hawaii Hawaii County 150099000 0 0 0.001 Hawaii Maui County 160230101 0.001 0 0.001 Idaho Butte County 160370002 0.001 0 0.001 Idaho Custer County 191370002 0.003 0.002 0.003 Iowa Montgomery County 191770006 0.003 0.002 0.005 Iowa Van Buren County 200139000 0.002 0.002 0.003 Kansas Brown County 200170001 0.002 0.001 0.002 Kansas Chase County 201950001 0.001 0.001 0.001 Kansas Trego County 221279000 0.002 0.001 0.002 Louisiana Winn Parish 230031020 0.002 0.001 0.002 Maine A roostook County 230090103 0.002 0.001 0.002 Maine Hancock County 230291004 0.001 0.001 0.002 Maine Washington County 240239000 0.002 0.002 0.002 Maryland Garrett County 250070001 0.001 0.001 0.002 Massachusetts Dukes County 260839000 0.001 0.001 0.002 Michigan Keweenaw County 261539000 0.002 0.001 0.002 Michigan Schoolcraft County

January 2013 2D - 12 Draft - Do not cite or quoteTable 2D-4. Pb-PM 2.5 concentrations at non-urban PM 2.5 IMPROVE sites, 2009-2011. Appendix 2D - Air Quality Data Analysis Summary

SITE Max 3-mo Mean (ug/m3) Annual Mean (ug/m3) Max Monthly Mean (ug/m3) State County 270759000 0.001 0.001 0.002 Minnesota Lake County 271339000 0.002 0.002 0.003 Minnesota Rock County 271699000 0.002 0.002 0.003 Minnesota Winona County 290390001 0.002 0.002 0.002 Missouri Cedar County 292070001 0.003 0.002 0.004 Missouri Stoddard County 292130003 0.002 0.002 0.003 Missouri Taney County 300279000 0.001 0 0.001 Montana Fergus County 300299001 0.001 0 0.001 Montana Flathead County 300479000 0.001 0 0.001 Montana Lake County 300499000 0.001 0 0.001 Montana Lewis and Clark County 300779000 0.001 0 0.001 Montana Powell County 300819000 0.001 0 0.001 Montana Ravalli County 300859000 0.001 0.001 0.001 Montana Roosevelt County 300870762 0.001 0 0.001 Montana Rosebud County 300899000 0.001 0 0.001 Montana Sanders County 300919000 0.001 0.001 0.001 Montana Sheridan County 310699000 0.001 0.001 0.001 Nebraska Garden County 311719000 0.001 0.001 0.001 Nebraska Thomas County 320079000 0.001 0 0.001 Nevada Elko County 320339000 0.001 0 0.001 Nevada White Pine County 330074002 0.001 0.001 0.001 New Hampshire Coos County 350039000 0.001 0.001 0.001 New Mexico Catron County 350059000 0.001 0.001 0.001 New Mexico Chaves County 350279000 0.001 0.001 0.001 New Mexico Lincoln County 350281002 0.001 0 0.001 New Mexico Los Alamos County 350399000 0.001 0 0.001 New Mexico Rio Arriba County 350539000 0.001 0.001 0.001 New Mexico Socorro County 350559000 0.001 0 0.001 New Mexico Taos County 361019000 0.003 0.002 0.006 New York Steuben County 370110002 0.001 0.001 0.002 North Carolina A very County 370959000 0.002 0.001 0.002 North Carolina Hyde County 380070002 0.001 0.001 0.001 North Dakota Billings County 380130004 0.001 0.001 0.001 North Dakota Burke County 391219000 0.005 0.003 0.008 Ohio Noble County 400450890 0.001 0.001 0.001 Oklahoma Ellis County 400719010 0.002 0.001 0.003 Oklahoma Kay County 410330010 0.001 0.001 0.001 Oregon Josephine County 410358001 0.001 0 0.001 Oregon Klamath County 410610010 0.001 0 0.001 Oregon Union County 410630002 0.001 0 0.001 Oregon Wallowa County 420019000 0.003 0.002 0.003 Pennsylvania A dams County 460330132 0.001 0 0.001 South Dakota Custer County 460710001 0.001 0.001 0.001 South Dakota Jackson County

January 2013 2D - 13 Draft - Do not cite or quoteTable 2D-4. Pb-PM 2.5 concentrations at non-urban PM 2.5 IMPROVE sites, 2009-2011. Appendix 2D - Air Quality Data Analysis Summary

SITE Max 3-mo Mean (ug/m3) Annual Mean (ug/m3) Max Monthly Mean (ug/m3) State County 480430101 0.002 0.001 0.002 Texas Brewster County 481099000 0.001 0.001 0.001 Texas Culberson County 490170101 0.001 0 0.001 Utah Garfield County 490379000 0.001 0 0.001 Utah San Juan County 490559000 0.001 0 0.001 Utah Wayne County 500038001 0.001 0.001 0.002 Vermont Bennington County 511139000 0.002 0.001 0.002 Virginia Madison County 511639000 0.004 0.003 0.006 Virginia Rockbridge County 530090020 0.001 0.001 0.002 Washington Clallam County 530370004 0.001 0.001 0.001 Washington Kittitas County 530390010 0.002 0.001 0.002 Washington Klickitat County 530390011 0.001 0.001 0.001 Washington Klickitat County 530410007 0.001 0 0.001 Washington Lewis County 530470012 0.001 0 0.001 Washington Okanogan County 540939000 0.002 0.001 0.002 West Virginia Tucker County 560050123 0.001 0 0.001 Wyoming Campbell County 560199000 0.001 0 0.001 Wyoming Johnson County 560299002 0.001 0 0.001 Wyoming Park County 560359000 0.001 0 0.001 Wyoming Sublette County 560399000 0.001 0 0.001 Wyoming Teton County 780209000 0.001 0.001 0.001

January 2013 2D - 14 Draft - Do not cite or quoteTable 2D-5. Distribution of maximum 3-month means, 2009-2011. Appendix 2D - Air Quality Data Analysis Summary

(units are ug/m3) n min Pct1 Pct5 Pct10 Pct25 mean Pct50 Pct75 Pct90 Pct95 Pct99 max Pb-TSP all 215 0 0.001 0.004 0.006 0.013 0.154 0.04 0.116 0.421 0.943 1.432 2.07 Pb-TSP source 112 0.004 0.004 0.012 0.019 0.05 0.273 0.11 0.355 0.774 1.079 1.937 2.07 Pb-TSP prev source 12 0.006 0.006 0.006 0.023 0.0295 0.057 0.06 0.082 0.093 0.115 0.115 0.115 Pb-TSP not source 91 0 0 0.002 0.003 0.007 0.019 0.012 0.025 0.041 0.047 0.132 0.132 Pb-PM10 urban 31 0.002 0.002 0.002 0.003 0.003 0.007 0.005 0.007 0.013 0.019 0.023 0.023 Pb-PM2.5 urban CSN 198 0.001 0.002 0.002 0.003 0.003 0.007 0.004 0.007 0.013 0.02 0.042 0.07 Pb-PM2.5 non-urban IMPROVE 107 0 0.001 0.001 0.001 0.001 0.002 0.001 0.002 0.002 0.003 0.006 0.009

January 2013 2D - 15 Draft - Do not cite or quoteTable 2D-6. Distribution of annual mean concentrations, 2009-2011. Appendix 2D - Air Quality Data Analysis Summary

(units are ug/m 3 ) n min Pct1 Pct5 Pct10 Pct25 mean Pct50 Pct75 Pct90 Pct95 Pct99 max Pb-TSP all 215 0 0 0.002 0.004 0.008 0.0798 0.022 0.058 0.198 0.434 0.889 0.959 Pb-TSP source 112 0.003 0.003 0.005 0.013 0.027 0.1408 0.053 0.149 0.394 0.622 0.921 0.959 Pb-TSP prev source 12 0.004 0.004 0.004 0.015 0.02 0.0306 0.033 0.04 0.041 0.058 0.058 0.058 Pb-TSP not source 91 0 0 0 0.002 0.004 0.0113 0.008 0.016 0.023 0.041 0.05 0.05 Pb-PM10 urban 35 0.001 0.001 0.001 0.001 0.002 0.0043 0.003 0.005 0.011 0.012 0.015 0.015 Pb-PM2.5 urban CSN 198 0.001 0.001 0.002 0.002 0.002 0.0036 0.003 0.004 0.006 0.009 0.017 0.018 Pb-PM2.5 non-urban IMPROVE 107 0 0 0 0 0 0.0008 0.001 0.001 0.002 0.002 0.003 0.004

January 2013 2D - 16 Draft - Do not cite or quoteTable 2D-7. Distribution of lead concentrations, 2009-2011. Appendix 2D - Air Quality Data Analysis Summary

(units are ug/m 3 ) n min Pct1 Pct5 Pct10 Pct25 mean Pct50 Pct75 Pct90 Pct95 Pct99 max Pb-TSP all 215 0 0.002 0.006 0.008 0.016 0.228 0.056 0.21 0.605 1.178 2.185 2.821 Pb-TSP source 112 0.006 0.007 0.015 0.029 0.0765 0.402 0.16 0.509 1.124 1.623 2.438 2.821 Pb-TSP prev source 12 0.008 0.008 0.008 0.03 0.0385 0.09 0.068 0.1225 0.14 0.271 0.271 0.271 Pb-TSP not source 91 0 0 0.003 0.006 0.01 0.032 0.016 0.035 0.057 0.087 0.364 0.364 Pb-PM10 urban 35 0.002 0.002 0.003 0.003 0.004 0.01 0.007 0.012 0.028 0.031 0.035 0.035 Pb-PM2.5 urban CSN 198 0.001 0.002 0.003 0.003 0.004 0.011 0.007 0.011 0.021 0.033 0.078 0.199 Pb-PM2.5 non-urban IMPROVE 107 0.001 0.001 0.001 0.001 0.001 0.002 0.001 0.002 0.003 0.006 0.01 0.012

January 2013 2D - 17 Draft - Do not cite or quoteTable 2D-8. Pb-TSP metrics (2009-2011). Appendix 2D - Air Quality Data Analysis Summary

Monitoring SITE ID CBSA_gt_1M (2010 Census) (3-yr) - annual

mean (ug/m3) (3-yr) - max 3- month

avg (ug/m3) ratio of 3-yr max 3

- month average to

3-year average annual mean Ratios for CBSA_gt_1M (2010 Census)

011090003 0.564 1.035 1.8351 020200051 021880001 040071002 0.133 0.267 2.0075 040078000 0.033 0.061 1.8485 060250005 0.015 0.023 1.5333 060371103 1 0.011 0.016 1.4545 1.4545 060371302 1 0.01 0.019 1.9000 1.9000 060371402 1 0.022 0.044 2.0000 2.0000 060371403 1 0.061 0.116 1.9016 1.9016 060371404 1 0.061 0.108 1.7705 1.7705 060371405 1 0.343 0.667 1.9446 1.9446 060371406 1 0.049 0.085 1.7347 1.7347 060371602 1 0.011 0.022 2.0000 2.0000 060374002 1 0.006 0.01 1.6667 1.6667 060374004 1 0.007 0.012 1.7143 1.7143 060375005 1 0.003 0.008 2.6667 2.6667 060651003 1 0.006 0.011 1.8333 1.8333 060658001 1 0.007 0.011 1.5714 1.5714 060711004 1 0.007 0.011 1.5714 1.5714 060719004 1 0.008 0.013 1.6250 1.6250 080050007 1 0.014 0.02 1.4286 1.4286 080310025 1 0.006 0.01 1.6667 1.6667 120570100 1 0.026 0.044 1.6923 1.6923 120571066 1 0.282 0.979 3.4716 3.4716 120571073 1 0.116 0.423 3.6466 3.6466 130150003 1 0.014 0.019 1.3571 1.3571 130890003 1 0.003 0.004 1.3333 1.3333 132150010 132150011 0.029 0.071 2.4483 170310001 1 0.016 0.024 1.5000 1.5000 170310022 1 0.033 0.051 1.5455 1.5455 170310026 1 0.023 0.034 1.4783 1.4783 170310052 1 0.016 0.024 1.5000 1.5000 170310110 1 0.1 0.294 2.9400 2.9400 170310210 1 0.037 0.053 1.4324 1.4324 170313103 1 0.011 0.013 1.1818 1.1818 170313301 1 0.018 0.027 1.5000 1.5000 170314201 1 0.01 0.011 1.1000 1.1000 170316003 1 0.024 0.036 1.5000 1.5000 171150110 0.082 0.199 2.4268
January 2013 2D-18 Draft - Do Not Quote or CiteTable 2D-8. Pb-TSP metrics (2009-2011). Appendix 2D - Air Quality Data Analysis Summary

Monitoring SITE ID CBSA_gt_1M (2010 Census) (3-yr) - annual

mean (ug/m3) (3-yr) - max 3- month

avg (ug/m3) ratio of 3-yr max 3

- month average to

3-year average annual mean Ratios for CBSA_gt_1M (2010 Census)

171170002 1 0.01 0.011 1.1000 1.1000 171190010 1 0.118 0.416 3.5254 3.5254 171193007 1 0.018 0.036 2.0000 2.0000 171430037 0.01 0.011 1.1000 171430110 0.013 0.016 1.2308 171430210 0.011 0.015 1.3636 171630010 1 0.019 0.029 1.5263 1.5263 171950110 0.02 0.028 1.4000 172010110 0.031 0.063 2.0323 180350008 0.079 0.11 1.3924 180350009 0.186 0.262 1.4086 180890023 1 0.026 0.077 2.9615 2.9615 180890032 1 0.025 0.06 2.4000 2.4000 180890033 1 0.054 0.139 2.5741 2.5741 180892008 1 0.016 0.037 2.3125 2.3125 180970063 1 0.026 0.079 3.0385 3.0385 180970076 1 0.01 0.02 2.0000 2.0000 180970078 1 0.005 0.011 2.2000 2.2000 181270023 1 0.013 0.022 1.6923 1.6923 181270027 181630006 181630020 0.004 0.007 1.7500 191550011 0.122 0.263 2.1557 191630015 0.01 0.012 1.2000 201690004 0.18 0.421 2.3389 210190016 0.003 0.004 1.3333 211510003 0.034 0.069 2.0294 212070001 0.021 0.036 1.7143 220330014 0.004 0.005 1.2500 220950003 1 0.037 0.053 1.4324 1.4324 250250002 260290011 260670002 260670003 0.126 0.284 2.2540 260810020 0.005 0.008 1.6000 261250013 261570001 261630001 1 0.005 0.006 1.2000 1.2000 261630033 1 0.012 0.023 1.9167 1.9167 270036020 1 0.017 0.033 1.9412 1.9412 270072303 0 0.001 0.0000
January 2013 2D-19 Draft - Do Not Quote or CiteTable 2D-8. Pb-TSP metrics (2009-2011). Appendix 2D - Air Quality Data Analysis Summary

Monitoring SITE ID CBSA_gt_1M (2010 Census) (3-yr) - annual

mean (ug/m3) (3-yr) - max 3- month

avg (ug/m3) ratio of 3-yr max 3

- month average to

3-year average annual mean Ratios for CBSA_gt_1M (2010 Census)

270210001 0 0.001 0.0000 270370020 1 0.005 0.011 2.2000 2.2000 270370423 1 0.001 0.002 2.0000 2.0000 270370442 1 0.003 0.013 4.3333 4.3333 270370443 1 0.002 0.003 1.5000 1.5000 270370465 1 0.128 0.259 2.0234 2.0234 270370470 1 0.001 0.002 2.0000 2.0000 270530963 1 0.003 0.006 2.0000 2.0000 270530966 1 0.004 0.016 4.0000 4.0000 270531007 1 0.002 0.004 2.0000 2.0000 270532006 1 0.001 0.003 3.0000 3.0000 271230866 1 0.012 0.016 1.3333 1.3333 271230871 1 0.002 0.007 3.5000 3.5000 271231003 1 0.004 0.006 1.5000 1.5000 271377001 0.001 0.003 3.0000 271377555 0.002 0.006 3.0000 271453053 0.003 0.006 2.0000 271630009 1 0.003 0.005 1.6667 1.6667 271630438 1 0.002 0.005 2.5000 2.5000 271630446 1 0 0.002 0.0000 0.0000 290930016 0.49 2.07 4.2245 290930021 0.622 1.937 3.1141 290930027 0.038 0.083 2.1842 290930029 0.037 0.115 3.1081 290930032 290930033 0.027 0.057 2.1111 290930034 0.283 0.402 1.4205 290939007 0.392 0.581 1.4821 290939008 0.256 0.387 1.5117 290970005 0.013 0.019 1.4615 290990004 1 0.889 1.16 1.3048 1.3048 290990005 1 0.231 0.396 1.7143 1.7143 290990009 1 0.043 0.067 1.5581 1.5581 290990011 1 0.21 0.403 1.9190 1.9190 290990013 1 0.116 0.198 1.7069 1.7069 290990015 1 0.921 1.079 1.1716 1.1716 290990020 1 0.646 0.943 1.4598 1.4598 290990021 1 0.585 0.969 1.6564 1.6564 290990022 1 0.434 0.63 1.4516 1.4516 290990023 1 0.394 0.594 1.5076 1.5076 290990024 1 0.374 0.659 1.7620 1.7620
January 2013 2D-20 Draft - Do Not Quote or CiteTable 2D-8. Pb-TSP metrics (2009-2011). Appendix 2D - Air Quality Data Analysis Summary

Monitoring SITE ID CBSA_gt_1M (2010 Census) (3-yr) - annual

mean (ug/m3) (3-yr) - max 3- month

avg (ug/m3) ratio of 3-yr max 3

- month average to

3-year average annual mean Ratios for CBSA_gt_1M (2010 Census)

290990025 1 0.043 0.085 1.9767 1.9767 290990026 1 0.035 0.072 2.0571 2.0571 290990027 290999001 1 0.824 1.204 1.4612 1.4612 290999002 1 0.232 0.431 1.8578 1.8578 290999003 1 0.198 0.467 2.3586 2.3586 290999004 1 0.119 0.261 2.1933 2.1933 290999005 1 0.959 1.432 1.4932 1.4932 290999006 1 0.049 0.091 1.8571 1.8571 291790001 0.033 0.059 1.7879 291790002 0.033 0.068 2.0606 291790003 0.027 0.1 3.7037 291790034 0.068 0.093 1.3676 291870006 0.05 0.132 2.6400 291870007 0.027 0.041 1.5185 291892003 1 0.007 0.041 5.8571 5.8571 295100085 310530005 0.051 0.072 1.4118 311270002 0.042 0.115 2.7381 360470122 1 0.014 0.019 1.3571 1.3571 360713001 0.031 0.101 3.2581 360713002 0.128 1.027 8.0234 360713004 0.005 0.012 2.4000 361030024 390170015 1 0.006 0.009 1.5000 1.5000 390290019 0.022 0.057 2.5909 390290020 0.015 0.025 1.6667 390290022 0.02 0.044 2.2000 390350038 1 0.013 0.021 1.6154 1.6154 390350042 1 0.014 0.03 2.1429 2.1429 390350049 1 0.194 0.531 2.7371 2.7371 390350060 390350061 1 0.015 0.023 1.5333 1.5333 390350072 1 0.014 0.035 2.5000 2.5000 390490025 1 0.008 0.011 1.3750 1.3750 390510001 0.073 0.178 2.4384 390910006 0.004 0.006 1.5000 391010003 0.035 0.056 1.6000 391137001 391510017 0.014 0.023 1.6429 391550012 0.007 0.011 1.5714
January 2013 2D-21 Draft - Do Not Quote or CiteTable 2D-8. Pb-TSP metrics (2009-2011). Appendix 2D - Air Quality Data Analysis Summary

Monitoring SITE ID CBSA_gt_1M (2010 Census) (3-yr) - annual

mean (ug/m3) (3-yr) - max 3- month

avg (ug/m3) ratio of 3-yr max 3

- month average to

3-year average annual mean Ratios for CBSA_gt_1M (2010 Census)

391670008 0.005 0.007 1.4000 391670010 0.005 0.008 1.6000 401159006 0.011 0.015 1.3636 401159007 0.017 0.034 2.0000 401210416 0.003 0.004 1.3333 401431127 0.004 0.005 1.2500 410711702 1 0.018 0.035 1.9444 1.9444 420030002 1 0.012 0.016 1.3333 1.3333 420030008 1 0.01 0.014 1.4000 1.4000 420030070 1 0.022 0.056 2.5455 2.5455 420031009 1 0.043 0.138 3.2093 3.2093 420070006 1 0.054 0.085 1.5741 1.5741 420070007 1 0.171 0.253 1.4795 1.4795 420070505 1 0.09 0.115 1.2778 1.2778 420110005 0.043 0.051 1.1860 420110020 0.127 0.196 1.5433 420110021 0.049 0.139 2.8367 420110022 0.043 0.118 2.7442 420110717 0.065 0.116 1.7846 420111717 0.133 0.251 1.8872 420210808 0.05 0.073 1.4600 420450002 1 0.043 0.047 1.0930 1.0930 420450004 1 0.045 0.047 1.0444 1.0444 420550002 0.045 0.046 1.0222 420630005 0.045 0.049 1.0889 420730011 0.019 0.023 1.2105 420790036 0.095 0.137 1.4421 421010449 1 0.021 0.03 1.4286 1.4286 421011002 1 0.022 0.025 1.1364 1.1364 421290007 1 0.041 0.043 1.0488 1.0488 421290009 1 0.027 0.046 1.7037 1.7037 450190003 0.003 0.007 2.3333 450450015 0.003 0.007 2.3333 450790007 0.004 0.005 1.2500 450790019 0.005 0.024 4.8000 470930023 0.114 0.165 1.4474 470930027 0.02 0.042 2.1000 470931017 0.018 0.037 2.0556 471633001 0.058 0.093 1.6034 471633002 0.039 0.06 1.5385 471633003 0.041 0.06 1.4634
January 2013 2D-22 Draft - Do Not Quote or CiteTable 2D-8. Pb-TSP metrics (2009-2011). Appendix 2D - Air Quality Data Analysis Summary

Monitoring SITE ID CBSA_gt_1M (2010 Census) (3-yr) - annual

mean (ug/m3) (3-yr) - max 3- month

avg (ug/m3) ratio of 3-yr max 3

- month average to

3-year average annual mean Ratios for CBSA_gt_1M (2010 Census)

471633004 0.041 0.08 1.9512 471634002 0.025 0.038 1.5200 480610006 0.004 0.005 1.2500 480850003 1 0.179 0.371 2.0726 2.0726 480850007 1 0.105 0.199 1.8952 1.8952 480850009 1 0.453 0.774 1.7086 1.7086 480850029 1 0.076 0.18 2.3684 2.3684 481130069 481410002 0.023 0.04 1.7391 481410033 0.019 0.039 2.0526 481410055 0.009 0.014 1.5556 481410058 0.017 0.033 1.9412 482011034 1 0.005 0.008 1.6000 1.6000 482011039 482570020 1 0.06 0.104 1.7333 1.7333 483750024 0.006 0.013 2.1667 484790016 0.016 0.026 1.6250 490351001 1 0.023 0.057 2.4783 2.4783 510090007 0.004 0.018 4.5000 510270006 0.01 0.013 1.3000 510870014 1 0.004 0.011 2.7500 2.7500 517700011 0.038 0.109 2.8684 530330029 530610013 551170008 0.055 0.152 2.7636 720130001 0.188 0.339 1.8032 720210010 0.005 0.011 2.2000 counts 114 212 212 average ---> 1.9463 1.9203

January 2013 2D-23 Draft - Do Not Quote or CiteJanuary 2013 3A-1 Draft – Do Not Quote or Cite 

### APPENDIX 3A 1



### INTERPOLATED RISK ESTIMA TES FOR THE GENERALIZED 2 

### (LOCAL) URBAN CASE STUDY 3

This Appendix describes the method used to develop risk estimates for conditions just 4 meeting the current standard (0.15 μg/m 3 , as a maximum 3-month average) for the generalized 5 (local) urban case study. These risk estimates were developed by interpolation from the 2007 6 REA results for this case study. The general a pproach was to identif y the two alternative 7
standard scenarios simulated in the 2007 RE A which represented air quality conditions 8 bracketing those for the current st andard and then linearly interpol ate an estimate of risk for the 9 current standard based on the slope created from the two bracketing estimates. In representing 10 air quality conditions for these purposes, we focused on the annua l average air Pb concentration 11
estimates as that is the metric which had been the IEUBK model inputs fo r the various air quality 12 scenarios (IEUBK does not accept air quality inputs of a temporal scale shorter than a year). 1 An 13 annual average concentration estimate to represen t the current standard was identified in a 14 manner consistent with that employed in the 2007 REA for this case study (see section 3.4.3.2 15 above, use of 2003-2005 data) with the use of cu rrently available monitoring data (2009-2011) 16 for relationships between air quality metrics for representation of the current standard. By this 17 method, the air quality scenario fo r the current standard (0.15 μg/m 3 , as a not-to-be-exceeded 3- 18 month average) was found to be bracketed by the scenarios for alternativ e standards of 0.5 and 19 0.20 μg/m 3 (maximum monthly averages). A risk estimate for the current standard was then 20 derived using the slope relating generalized (l ocal) urban case study IQ loss to the annual 21 average Pb concentration used for those two air qu ality scenarios. We us ed this interpolation 22 approach to develop median risk estimates for th e current standard based on each of the four C-R 23
functions. Details on the method for the in terpolation approach are provided below. 24
1. Identify an estimate of annual average air Pb concentration to repr esent each air quality 25 scenario. For the alternative s cenarios, this was done in the 2007 REA using the 2003- 26 2005 Pb-TSP dataset for urban areas of populatio n greater than one million. For analysis 27

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.January 2013 3A-2 Draft – Do Not Quote or Cite of the current standard here, this uses the recent Pb-TSP dataset (2009-2011) for urban 1 areas of population greater than one million. The concentration in terms of the metric 2 being assessed (e.g., maximum 3-month or ca lendar quarter average) was derived per 3 monitoring site, as was the annual average co ncentration and also the ratio of the two 4 (2007 REA, Appendix A; Appendix 2D of this document). From the average of the 5 monitor-specific ratios we derived the annual average estimate. [In the 2007 REA, this 6 was the IEUBK air quality input for each AQ scenario.] With the 2009-2011 data, the 7 average, across monitors in urban areas grea ter than 1 million populat ion, of the ratio of 8 maximum 3-month average to annual average is 1.92 (Appendix 2D in this document). 9

- This ratio was used to derive an an nual average air Pb-TSP concentration 10 estimate to represent the current st andard scenario (annual value = 0.15 μ g/m 3 11 * 1/1.92 = 0.078 μ g/m 3 ). The annual average values for the scenarios 12 included in the 2007 REA and also for the current standard scenario 13 considered in this interpolation are shown in Table 3A-1 below. 14

Table 3A-1. Annual average air Pb-TSP concentratio n estimates for different air quality 15 scenarios. 16

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 2009-2011 air quality dataset. 17 2. Identify the two “bounding” alternative standar d levels that will be used to derive a 18 slope for the risk interpolati on for the current standard level. Based on comparison of 19 the annual ambient air Pb estimates for each of the 2007 REA air qua lity scenarios and 20 for the current standard we determine which scenarios “bound” the current standard (in 21 terms of the annual average ambient Pb estimate). As Table 3A-1 above shows, the 22 bounding scenarios are the scenarios for ju st meeting maximum monthly average 23 concentrations of 0.5 and 0.2 μg/m 3

. 24 25 3. Calculate the slopes of generalized (loc al) urban case study IQ loss per unit annual 26 average Pb estimate for each risk estimate of interest for the two bounding scenarios. 27 This calculation is (IQ Loss Scenario X – IQ Loss Scenario Y )/ (annual average Scenario X – annual 28
average Scenario Y ). The risk estimates for the 4 di fferent C-R functions and two exposure 29 pathway categories of interest ( Recent Air and Recent + Past Air ), with the derived 30 slopes, are in Table 3A-2. 31January 2013 3A-3 Draft – Do Not Quote or Cite Table 3A-2. Risk estimates for bounding air qualit y scenarios and associated slopes. 1

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)

. 2

4. Derive interpolated risk estimates for the current standard scenario. Using the 3 slopes presented in Table 3A-2 and the lower bounding air quality scenario risk 4 estimates, derive corresponding risk estimat es for the current standard scenario: 5 Risk = lower bounding risk + (incre ment annual average Pb * slope) 6
Where: 7

 lower bounding risk = risk for the lower bound air quality scenario (i.e., 8 for 0.2 μg/m 3 maximum monthly average) 9

 increment annual average Pb is the difference between the annual average 10 estimates for the current standa rd and the lower bounding scenario. 11

 slope is the value described in Step 4, which differs across the 8 12 combinations of C-R functions a nd exposure pathway categories. 13 The resulting interpolated risk estim ates are presented in Table 3A-3. 14

Table 3A-3. Interpolated risk estimates for the current NAAQS scenario for the 15 generalized (local) urban case study. 16

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). 17January 2013 5A - 1 Draft - Do Not Quote or Cite APPENDIX 5A 1

ADDITIONAL DETAIL ON 2006 ECOLOGICAL SCREENING 2 ASSESSMENT 3

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, 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 distance 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. 4United StatesEnvironmental ProtectionAgencyOffice of Air Quality Planning and StandardsHealth and Environmental Impacts DivisionResearch Triangle Park, NCPublication No. EPA-452/P-13-001January 2013